esm223_01_bioappend-all

esm223_01_bioappend-all - (EPA-823-R-00-002) Errata 1) page...

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Unformatted text preview: (EPA-823-R-00-002) Errata 1) page 485: Replace paragraph under Human Health Section for Methylmercury with the following: EPA is recommending that the Programs and Regions use 0.1 g/kg/day as an interim RfD for methylmercury until the Agency has had an opportunity to review the work of the National Academy of Science (NAS). NAS is performing an independent assessment of the Agency's reference dose (RfD) for methylmercury (EPA 1999). [U.S. EPA. 1999. Memo: Transmittal of Interim Agency Guidance on the Use of Methylmercury Reference Dose in Making Risk Management Decisions. From: Peter D. Robertson Acting Deputy Administrator, To: Assistant Administrators, General Counsel, Inspector General, Chief Financial Officer, Associate Administrators, Regional Administrators and Staff Office Directors (April 19, 1999)]. 2) pages 7, 23, 35, 45, 61: Add to Human Health: Oral slope factor: 2.0 per mg/kg/d based on environmental mixtures of PCBs in aquatic organisms (EPA 1996) [U.S. EPA. 1996. Cancer Dose-Response Assessment for Application to Environmental Mixtures. EPA/600/P-96/001F. Washington, DC]. 3) The table below provides the latest World Health Organization (WHO ) toxic equivalent factors ( TEFs) for dioxins, furans, and coplanar PCBs. They are more recent than those cited in this document. Congener 2,3,7,8-TCDD 1,2,3,7,8-PeCDD 1,2,3,4,7,8-HxCDD 1,2,3,6,7,8-HxCDD 1,2,3,7,8,9-HxCDD 1,2,3,4,6,7,8,-HpCDD OCDD 2,3,7,8-TCDF 1,2,3,7,8-PeCDF 2,3,4,7,8-PeCDF 1,2,3,4,7,8-HxCDF 1,2,3,6,7,8-HxCDF 1,2,3,7,8,9-HxCDF 2,3,4,6,7,8-HxCDF 1,2,3,4,6,7,8-HpCDF 1,2,3,4,7,8,9-HpCDF OCDF 3,4,4N,5-TCB(81) 3,3N,4,4N-TCB(77) 3,3N,4,4N,5-PeCB(126) 3,3N,4,4N,5,5N-HxCB(169) Toxic Equivalent Factor (TEF) 1 1 0.1 0.1 0.1 0.01 0.0001 0.1 0.05 0.5 0.1 0.1 0.1 0.1 0.01 0.01 0.0001 0.0001 0.0001 0.1 0.01 0.0001 2,3,3N,4,4N-PeCB(105) 0.0005 2,3,4,4N,5-PeCB(114) 0.0001 2,3N,4,4N,5-PeCB(118) 0.0001 2N,3,4,4N,5-PeCB(123) 0.0005 2,3,3N,4,4N,5-HxCB(156) 0.0005 2,3,3N,4,4N,5-HxCB(157) 0.00001 2,3N,4,4N,5,5N-HxCB(167) 0.0001 2,3,3N,4,4N,5,5N-HpCB(189) Van den Berg, et. al. 1998. Toxic Equivalency Factors (TEFs) for PCBs, PCDDs, PCDFs for Humans and Wildlife. Environ. Health Perspect. 106(12):775-792. APPENDIX Chemical-Specific Summary Tables CONTENTS Chemical Page Acenaphthene . . . . . . . . . . . . . . . . . . . . . 1 Aroclor 1016 . . . . . . . . . . . . . . . . . . . . . 7 Aroclor 1242 . . . . . . . . . . . . . . . . . . . . 23 Aroclor 1248 . . . . . . . . . . . . . . . . . . . . 35 Aroclor 1254 . . . . . . . . . . . . . . . . . . . . 45 Aroclor 1260 . . . . . . . . . . . . . . . . . . . . 61 Arsenic . . . . . . . . . . . . . . . . . . . . . . . . . 71 Benzo(a)anthracene . . . . . . . . . . . . . . . 83 Benzo(a)pyrene . . . . . . . . . . . . . . . . . . 89 Benzo(b)fluoranthene . . . . . . . . . . . . . 109 Benzo(g,h,i)perylene . . . . . . . . . . . . . 113 Benzo(k)fluoranthene . . . . . . . . . . . . . 119 Cadmium . . . . . . . . . . . . . . . . . . . . . . 123 Chlordane . . . . . . . . . . . . . . . . . . . . . . 163 Chlorpyrifos . . . . . . . . . . . . . . . . . . . . 179 Chromium (hexavalent) . . . . . . . . . . . 193 Chrysene . . . . . . . . . . . . . . . . . . . . . . . 103 Copper . . . . . . . . . . . . . . . . . . . . . . . . 209 1,2,3,4,6,7,8-HeptaCDD . . . . . . . . . . 231 1,2,3,4,7,8-HexaCDD . . . . . . . . . . . . 241 1,2,3,6,7,8-HexaCDD . . . . . . . . . . . . 249 1,2,3,7,8-PentaCDD . . . . . . . . . . . . . . 259 2,3,7,8-TCDD . . . . . . . . . . . . . . . . . . 269 p,p-DDD . . . . . . . . . . . . . . . . . . . . . . 317 p,p-DDE . . . . . . . . . . . . . . . . . . . . . . 327 p,p-DDT . . . . . . . . . . . . . . . . . . . . . . 351 Diazinon . . . . . . . . . . . . . . . . . . . . . . . 369 Dicofol . . . . . . . . . . . . . . . . . . . . . . . . 377 Dieldrin . . . . . . . . . . . . . . . . . . . . . . . 381 Chemical Page Disulfoton . . . . . . . . . . . . . . . . . . . . . . 399 1,2,3,4,7,8-HexaCDF . . . . . . . . . . . . . 405 1,2,3,7,8-PentaCDF . . . . . . . . . . . . . . 412 2,3,4,7,8-PentaCDF . . . . . . . . . . . . . . 421 2,3,7,8-TCDF . . . . . . . . . . . . . . . . . . . 431 Fluoranthene . . . . . . . . . . . . . . . . . . . . 443 Heptachlor . . . . . . . . . . . . . . . . . . . . . 455 Lead . . . . . . . . . . . . . . . . . . . . . . . . . . 465 Methylmercury . . . . . . . . . . . . . . . . . . 485 Nickel . . . . . . . . . . . . . . . . . . . . . . . . . 525 Oxyfluorfen . . . . . . . . . . . . . . . . . . . . 533 PCB 28 . . . . . . . . . . . . . . . . . . . . . . . . 536 PCB 77 . . . . . . . . . . . . . . . . . . . . . . . . 547 PCB 81 . . . . . . . . . . . . . . . . . . . . . . . . 561 PCB 105 . . . . . . . . . . . . . . . . . . . . . . . 571 PCB 118 . . . . . . . . . . . . . . . . . . . . . . . 585 PCB 126 . . . . . . . . . . . . . . . . . . . . . . . 599 PCB 156 . . . . . . . . . . . . . . . . . . . . . . . 609 PCB 169 . . . . . . . . . . . . . . . . . . . . . . . 621 Pentachlorophenol . . . . . . . . . . . . . . . 631 Phenanthrene . . . . . . . . . . . . . . . . . . . 649 Pyrene . . . . . . . . . . . . . . . . . . . . . . . . . 659 Selenium . . . . . . . . . . . . . . . . . . . . . . . 667 Silver . . . . . . . . . . . . . . . . . . . . . . . . . 685 Tributyltin . . . . . . . . . . . . . . . . . . . . . 693 Terbufos . . . . . . . . . . . . . . . . . . . . . . . 745 Total PCBs . . . . . . . . . . . . . . . . . . . . . 751 Toxaphene . . . . . . . . . . . . . . . . . . . . . 787 Zinc . . . . . . . . . . . . . . . . . . . . . . . . . . 801 BIOACCUMULATION SUMMARY ACENAPHTHENE Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (low molecular weight) Chemical Name (Common Synonyms): ACENAPHTHENE CASRN: 83-32-9 Chemical Characteristics Solubility in Water: Insoluble [1] Log Kow: 3.92 [3] Half-Life: No data [1,2] Log Koc: 3.85 L/kg organic carbon Human Health Oral RfD: 6 x 10-2 mg/kg/day [4] Critical Effect: Hepatotoxicity Oral Slope Factor: No data [4] Carcinogenic Classification: Confidence: Low uncertainty factor = 3000 Wildlife Partitioning Factors: Partitioning factors for acenaphthene in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for acenaphthene in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: The water quality criterion tissue level (WQCTL) for acenaphthene, which is calculated by multiplying the water quality chronic value (710 g/L) by the BCF (389.05), is 276,222 g/kg [5]. Food Chain Multipliers: Food chain multipliers for acenaphthene in aquatic organisms were not found in the literature. Toxicity/Bioaccumulation Assessment Profile Most polynuclear aromatic hydrocarbons (PAHs) occur in sediment as complex mixtures. The toxicities of individual PAHs are additive and increase with increasing Kow, whereas the bioavailabilities of PAHs decrease as a function of their Kows. The 10-day LC50s for Eohaustorius estuarius and Leptocheirus plumulosus in water were 374 g/L and 678 g/L, respectively [6]. Both amphipod species were exposed to acenaphthene-spiked sediments with total organic carbon ranging from 0.82 percent to 4.21 percent. 1 BIOACCUMULATION SUMMARY ACENAPHTHENE The 10-day LC50s ranged from 1,630 to 4,330 g/g for E. estuarius and from 7,730 g/g to >23,500 g/g for L. plumulosus. Bioaccumulation of low-molecular-weight PAHs including acenaphthene from sediments by Rhepoxynius abronius (amphipod) and Armandia brevis (polychaete) was similar; however, a large difference in tissue concentration between these two species was measured for high-molecular-weight PAHs [12]. Meador et al. [12] concluded that the low-molecular-weight PAHs were available to both species from interstitial water, while sediment ingestion was a much more important uptake route for the high-molecular-weight PAHs. The authors also indicated that bioavailability of the high-molecular weight-PAHs to amphipods was significantly reduced due to their partitioning to dissolved organic carbon. 2 Summary of Biological Effects Tissue Concentrations for Acenaphthene Species: Taxa Invertebrates Nereis succinea, Polychaete worm 0.00003 0.001 0.0004 BDL BDL BDL4 BDL BDL 0.025 BDL [7] F Concentration, Units in1: Sediment mol/g Water mol/L Toxicity: Tissue (Sample Type) mol/g Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Corbicula fluminea, Asiatic clam <0.003 <0.003 <0.0005 <0.0007 [8] F Mytilus edulis, Blue mussel -0.35 [9] F Crassostrea virginica, Eastern oyster -0.03 [9] F Macoma balthica, Baltic macoma 0.00003 0.001 0.0004 BDL BDL BDL [7] F Mercenaria mercenaria, Northern quahog -0.44 -0.09 [9] F Mya arenaria, Softshell 3 0.09 [9] F 4 Species: Taxa Decapoda Sediment mol/g 0.034 0.041 0.675 Homarus americanus, American lobster Fishes Fundulus spp., Killifish Poecilia reticulata, Guppy Lepomis sp., Sunfish 0.034 0.041 0.675 Tautogolabrus adspersus, Tautog 1 2 3 4 Summary of Biological Effects Tissue Concentrations for Acenaphthene Concentration, Units in1: Water mol/L Toxicity: Tissue (Sample Type) mol/g Effects 0.001 0.017 0.027 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [10] F -0.89 [9] F -0.33 [9] F 0.14-0.15 0.047 0.027 0.047 0.051 [11] F 0.058 0.038 0.092 [10] F -1.22 [9] F Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. BDL = below detection limit. BIOACCUMULATION SUMMARY ACENAPHTHENE References 1. Merck index, 10th ed., 1983, p. 5. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) 2. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. 3. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. 4. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. 5. Neff, J.M. 1995. Water quality criterion tissue level approach for establishing tissue residue criteria for chemicals. Report to U.S. Environmental Protection Agency. 6. Swartz, R.C. 1991. Acenaphthene and phenanthrene files. Memorandum to David J. Hansen. June 26, 1991. 7. Foster, G.D., and D.A. Wright. 1988. Unsubstituted polynuclear aromatic hydrocarbons in sediments, clams, and clam worms from Chesapeake Bay. Mar. Pollut. Bull. 19:459-465. 8. Harrington, J.M., and D.B. Crane. 1994. Presence of target compounds from creosote impregnated timber in water and tissue of the asiatic clam (Corbicula fluminea) near Ryer Island Ferry, Sacramento River Delta. Report by California Department of Fish and Game Water Pollution Control Laboratory, Rancho Cordova, CA. 9. NOAA. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Technical Memorandum NOS OMA 52. National Oceanic and Atmospheric Administration, Office of Oceanography and Marine Assessment, Rockville, MD. 10. Burkhard, L.P., and B.R. Sheedy. 1995. Evaluation of screening procedures for bioconcentratable organic chemicals in effluents and sediments. Environ. Toxicol. Chem. 14:697-711. 11. Schoor, W.P., D.E. Williams, and N. Takahashi. 1991. The induction of cytochrome P-450-IA1 in juvenile fish by creosote-contaminated sediment. Arch. Environ. Contam. Toxicol. 20:497-504. 5 BIOACCUMULATION SUMMARY ACENAPHTHENE 12. Meador, J.P., E. Casillas, C.A. Sloan, and U. Varanasi. 1995. Comparative bioaccumulation of polycyclic aromatic hydrocarbons from sediments by two infaunal invertebrates. Mar. Ecol. Prog. Ser. 123: 107-124. 6 BIOACCUMULATION SUMMARY AROCLOR 1016 Chemical Category: POLYCHLORINATED BIPHENYLS Chemical Name (Common Synonyms): Aroclor 1016 CASRN: 1336-36-3 Chemical Characteristics Solubility in Water: 225-250 g/L at 25C [1] Log Kow: 5.6 [4] Half-Life: No data [2,3] Log Koc: No data [4] Human Health Oral RfD: 7 x 10-5 mg/kg-day [5] Confidence: Medium [5] Critical Effect: PCBs have been shown to cause reproductive failure, birth defects, lesions, tumors, liver disorders, and death among sensitive species. Their toxicity is further enhanced by their ability to bioaccumulate and to biomagnify within the food chain due to extremely high lipophilicity [2]. Oral Slope Factor: No data [5] Carcinogenic Classification: Unknown [5] Wildlife Partitioning Factors: No partitioning factors for Aroclor 1016 were identified for wildlife. Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and USACE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly waterinsoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. A biomagnification factor of 32 was determined for total PCBs from alewife to herring gull eggs in Lake Ontario [11]. No specific food chain multipliers were identified for Aroclor 1016. Aquatic Organisms Partitioning Factors: No partitioning factors for Aroclor 1016 were identified for aquatic organisms. Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify through the food web. Oliver and Niimi [12], studying accumulation of PCBs in various organisms in the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving 7 BIOACCUMULATION SUMMARY AROCLOR 1016 from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [13] reported that each trophic level contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific food chain multipliers were identified for Aroclor 1016. Toxicity/Bioaccumulation Assessment Profile PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in various processes and products because of the extreme stability of many isomers, particularly those with five or more chlorines [14]. A common use of PCBs was as dielectric fluids in capacitors and transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture. The exception to this code is Aroclor 1016, which contains mono- through hexachlorinated homologs with an average chlorine content of 41 percent [4]. As a result of their stability and their general hydrophobic nature, PCBs released to the environment have dispersed widely throughout the ecosystem [14]. PCBs are among the most stable organic compounds known, and chemical degradation rates in the environment are thought to be slow. As a result of their highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water and at relatively high concentrations in sediment [15]. Individual PCB congeners have different physical and chemical properties based on the degree of chlorination and position of chlorine substitution, although differences with degree of chlorination are more significant [15]. Solubilities and octanol-water partition coefficients for PCB congeners range over several orders of magnitude [16]. Octanol-water partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest for the most chlorinated PCB congeners. Dispersion of PCBs in the aquatic environment is a function of their solubility [15] while PCB mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination [17]. The concentration of PCBs in sediments is a function of the physical characteristics of the sediment, such as grain size [18,19] and total organic carbon content [18,19,20,21]. Fine sediments typically contain higher concentrations of PCBs than coarser sediments because of more surface area [15]. Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [17]. Therefore, it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source [15]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment from reaching the overlying water via diffusion [17]. The persistence of PCBs in the environment is a result of their general resistance to degradation [16]. The rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [22]; other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation to a lesser extent [16]. Photochemical degradation, via reductive dechlorination, is also known to occur in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [21]. Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly 8 BIOACCUMULATION SUMMARY AROCLOR 1016 than higher chlorinated congeners [23]. PCB congeners with no chlorine substituted in the ortho (2 and 2) positions but with four or more chlorine atoms at the meta (3 and 3) and para (4 and 4) positions can assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) [24]. Examples of these more toxic, coplanar congeners are 3,3,4,4-tetrachlorobiphenyl (PCB 77), 3,3,4,4,5-pentachlorobiphenyl (PCB 126), and 3,3,4,45,5hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of mixtures is to use toxic equivalency factors (TEFs) [25]. With this method, relative potencies for individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The following TEFs have been recommended [25,26]: Congener Class 3,3,4,4,5-PentaCB 3,3,4,4,5,5-HexaCB 3,3,4,4-TetraCB Monoortho coplanar PCBs Diortho coplanar PCBs Recommended TEF 0.1 0.05 0.01 0.001 0.00002 Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic organisms have a strong tendency to accumulate PCBs from water and food sources. The log bioconcentration factor for fish is approximately 4.70 [27]. This factor represents the ratio of concentration in tissue to the ambient water concentration. Aquatic organisms living in association with PCB-contaminated sediments generally have tissue concentrations equal to or greater than the concentration of PCB in the sediment [27]. Once taken up by an organism, PCBs partition primarily into lipid compartments [15]. Thus, differences in PCB concentration between species and between different tissues within the same species may reflect differences in lipid content [15]. PCB concentrations in polychaetes and fish have been strongly correlated to their lipid content [28]. Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higherchlorinated congeners [29, 30]. In some species, tissue concentrations of PCBs in females can be reduced during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred PCBs are eliminated from the female during spawning [31,32]. Fish and other aquatic organisms biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners [31]. Consequently, fish and other aquatic organisms may accumulate more of the higher chlorinated PCB congeners than is found in the environment [16]. The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate that PCB toxicity is directly related to the duration of exposure [1]. Toxic responses have been noted to occur at concentrations of 0.03 and 0.014 g/L in marine and freshwater environments, respectively [1]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 g/L [1]. Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [33], although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low 9 BIOACCUMULATION SUMMARY AROCLOR 1016 concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370 g/kg [34]. A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic organisms at low tissue concentrations [16]. Field and Dexter [16] suggest that a number of marine and freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0 mg/kg and as low as 0.1 mg/kg. Spies et al. [35] reported an inverse relationship between PCB concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [36] also reported a significant correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with MFO induction by PCBs at tissue concentrations within the range of environmental exposures [16]. 10 Summary of Biological Effects Tissue Concentrations for Aroclor 1016 Species: Taxa Invertebrates Crassostrea virginica, Oyster 4 mg/kg (whole body)4 32 mg/kg (whole body)4 95 mg/kg (whole body)4 11.2 mg/kg (whole body)4 Growth, ED10 Growth, NA Growth, NA [38] [38] L; reduction in shell growth L; reduction in shell growth L; reduction in shell growth L; delayed molting; less than 50% molted after 96 days starting with T2-stage crabs L; delayed molting; less than 50% molted after 96 days starting with T1-stage crabs L; less than 50% mortality starting with T2-stage crabs Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Limulus polyphemus, Horseshoe Crab Growth, NA [37] 31.9 mg/kg (whole body)4 Growth, NA [37] 11.2 mg/kg (whole body)4 Mortality, NA [37] Fishes Lagodon rhomboides, Pinfish 38 mg/kg (muscle)4 Mortality, ED50 Mortality, ED50 Mortality, ED50 [38] L; 50% mortality 30 mg/kg (muscle)4 72 mg/kg (muscle and skin)4 [38] [38] L; 50% mortality L; 50% mortality 11 12 Summary of Biological Effects Tissue Concentrations for Aroclor 1016 Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 48 mg/kg (muscle and skin)4 205 mg/kg (whole body)4 106 mg/kg (whole body)4 Mortality, ED50 Mortality, ED50 Behavior, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] [38] [38] L; 50% mortality L; 50% mortality L; erratic swimming, stopped feeding, loss of equilibrium L; erratic swimming, stopped feeding, loss of equilibrium L; erratic swimming, stopped feeding, loss of equilibrium L; liver and pancreatic cell alterations L; liver and pancreatic cell alterations L; liver and pancreatic cell alterations L; darkened coloration L; darkened coloration L; darkened coloration 38 mg/kg (muscle)4 Behavior, LOED [38] 72 mg/kg (muscle and skin)4 Behavior, LOED [38] 205 mg/kg (whole body)4 30 mg/kg (muscle)4 Cellular, LOED Cellular, LOED Cellular, LOED Morphology, LOED Morphology, LOED Morphology, LOED [38] [38] 48 mg/kg (muscle and skin)4 106 mg/kg (whole body)4 38 mg/kg (muscle)4 72 mg/kg (muscle and skin)4 [38] [38] [38] [38] Summary of Biological Effects Tissue Concentrations for Aroclor 1016 Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 205 mg/kg (whole body)4 140 mg/kg (muscle)4 Mortality, LOED Mortality, LOED Mortality, LOED Mortality, LOED Mortality, LOED Mortality, LOED Mortality, LOED Mortality, NA Cellular, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] L; statistically significant increase in mortality L; statistically significant increase in mortality L; statistically significant increase in mortality L; statistically significant increase in mortality L; 5% mortality in 96 hours L; statistically significant increase in mortality L; statistically significant increase in mortality L; 18% mortality in 96 hours L; no incidence of pathology (liver and pancreatic alterations) L; no incidence of pathology (liver and pancreatic alterations) [38] 30 mg/kg (muscle)4 [38] 180 mg/kg (muscle and skin)4 48 mg/kg (muscle and skin)4 2.2 mg/kg (whole body)4 620 mg/kg (whole body)4 106 mg/kg (whole body)4 65 mg/kg (whole body)4 [38] [38] [38] [38] [38] [38] 23 mg/kg (muscle)4 Cellular, NOED [38] 13 14 Summary of Biological Effects Tissue Concentrations for Aroclor 1016 Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 49 mg/kg (muscle and skin)4 Cellular, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] L; no incidence of pathology (liver and pancreatic alterations) L; no statistically significant increase in mortality L; no statistically significant increase in mortality L; no statistically significant increase in mortality L; no statistically significant increase in mortality L; no mortality in 96 hours L; no statistically significant increase in mortality L; no statistically significant increase in mortality L; no reduced ability to survive osmotic stress after exposure 111 mg/kg (whole body)4 63 mg/kg (muscle)4 Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Physiological, NOED [38] [38] 23 mg/kg (muscle)4 [38] 76 mg/kg (muscle and skin)4 49 mg/kg (muscle and skin)4 21 mg/kg (whole body)4 170 mg/kg (whole body)4 111 mg/kg (whole body)4 [38] [38] [38] [38] [38] Summary of Biological Effects Tissue Concentrations for Aroclor 1016 Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 23 mg/kg (muscle)4 Physiological, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] L; no reduced ability to survive osmotic stress after exposure L; no reduced ability to survive osmotic stress after exposure L; 33% mortality in 96 hours L; 38% mortality in 96 hours L; 93% mortality in 96 hours L; 8% mortality in 96 hours L; 43% mortality in 96 hours L; uncoordinated swimming, cessation of feeding L; darkened body coloration, body lesions L; lethal to 86% of fry in 28 days L; 88% juvenile mortality in 28 days 49 mg/kg (muscle and skin)4 Physiological, NOED [38] 111 mg/kg (whole body)4 1.1 mg/kg (whole body)4 22 mg/kg (whole body)4 44 mg/kg (whole body)4 3.8 mg/kg (whole body)4 42 mg/kg (whole body)4 1,100 mg/kg (whole body)4 1,100 mg/kg (whole body)4 200 mg/kg (whole body)4 Mortality, LOED Mortality, NA Mortality, NA Mortality, LOED Mortality, NA Behavior, LOED Morphology, LOED Mortality, LOED Mortality, LOED [38] [38] [38] [38] [38] [38] [39] [39] [39] 15 16 Summary of Biological Effects Tissue Concentrations for Aroclor 1016 Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 1,100 mg/kg (whole body)4 Development, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [39] L; no effect on fertilization success, survival of embryos to hatching, and survival of fry two weeks after hatching L; no effect on fertilization success, survival of embryos to hatching, and survival of fry two weeks after hatching L; no effect on fertilization success, survival of embryos to hatching, and survival of fry two weeks after hatching L; no effect on fry mortality in 28 days L; no effect on fry mortality in 28 days L; no effect on fry mortality in 28 days L; no effect on fry mortality in 28 days L; no effect on fry mortality in 28 days 4.2 mg/kg (whole body)4 Development, NOED [39] 17 mg/kg (whole body)4 Development, NOED [39] 66 mg/kg (whole body)4 0.81 mg/kg (whole body)4 4.9 mg/kg (whole body)4 22 mg/kg (whole body)4 38 mg/kg (whole body)4 Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED [39] [39] [39] [39] [39] Summary of Biological Effects Tissue Concentrations for Aroclor 1016 Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 5.9 mg/kg (whole body)4 26 mg/kg (whole body)4 57 mg/kg (whole body)4 2.3 mg/kg (whole body)4 8.9 mg/kg (whole body)4 11 mg/kg (whole body)4 79 mg/kg (whole body)4 230 mg/kg (whole body)4 10 mg/kg (whole body)4 54 mg/kg (whole body)4 220 mg/kg (whole body)4 17 Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [39] [39] [39] L; no effect on fry mortality in 28 days L; no effect on fry mortality in 28 days L; no effect on juvenile mortality in 28 days L; no effect on juvenile mortality in 28 days L; no effect on juvenile mortality in 28 days L; no effect on juvenile mortality in 28 days L; no effect on juvenile mortality in 28 days L; no effect on juvenile mortality in 28 days L; no effect on juvenile mortality in 28 days L; no effect on juvenile mortality in 28 days L; no effect on adult mortality in 28 days [39] [39] [39] [39] [39] [39] [39] [39] 18 Species: Taxa Sediment 1 2 3 4 Summary of Biological Effects Tissue Concentrations for Aroclor 1016 Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.84 mg/kg (whole body)4 1.5 mg/kg (whole body)4 12 mg/kg (whole body)4 46 mg/kg (whole body)4 100 mg/kg (whole body)4 5.4 mg/kg (whole body)4 22 mg/kg (whole body)4 110 mg/kg (whole body)4 Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [39] L; no effect on adult mortality in 28 days L; no effect on adult mortality in 28 days L; no effect on adult mortality in 28 days L; no effect on adult mortality in 28 days L; no effect on adult mortality in 28 days L; no effect on adult mortality in 28 days L; no effect on adult mortality in 28 days [39] [39] [39] [39] [39] [39] [39] Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. BIOACCUMULATION SUMMARY References 1. AROCLOR 1016 USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH. February.) Eisler, R. 1986. Polychlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wild. Serv. Biol. Rep. 85(1.7). MacKay, D., W.Y. Shiu, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons, chlorobenzenes, and PCBs. Lewis Publishers, Boca Raton, FL. Agency for Toxic Substances and Disease Registry. 1993. Toxicological profile for polychlorinated biphenyls. Prepared by Syracuse Research Corporation. Prepared for U.S. Department of Health and Human Services, Public Health Service. April 1993. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Jones, P.D., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. USACE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food chains. Environ. Sci. Technol. 23:699. Hoffman, D.J., C.P. Rice, and T.J. Kubiak. 1996. PCBs and dioxins in birds. In Environmental contaminants in wildlife, ed. W.N. Beyer, G.H. Heinz, and A.W. Redmon-Horwood, pp. 165-207. Lewis Publishers, Boca Raton, FL. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 19 BIOACCUMULATION SUMMARY 12. AROCLOR 1016 Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Rasmussen, J.B., D.J. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J. Fish. Aquat. Sci. 47:2030-2038. Rand, G.M., P.G. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G. M. Rand, pp. 3-67. Taylor and Francis, Washington, DC. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments. In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments. Unpublished document. January 11, 1988. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ. Pollut. 5B:121-132. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ. Sci. Technol. 13:65-71. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop, pp. 273-287. American Society of Testing and Materials, Philadelphia, PA. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls. In PCBs and the environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc., Boca Raton, FL. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL. Bolger, M. 1993. Overview of PCB toxicology. Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93003.U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, 1993, pp. 37-53. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 20 BIOACCUMULATION SUMMARY 24. AROCLOR 1016 Erickson, M.D. 1993. Introduction to PCBs and analytical methods. EPA/823-R-93-003. Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, pp. 3-9. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Critical Reviews in Toxicology 21(1):5188. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group, Inc., Arlington, MA.) Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136. Shaw, G. R., and D. W. Connell. 1982. Factors influencing concentrations of polychlorinated biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution: A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments. Mar. Biol. 91:497-508. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'Itri and M.A. Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL. Mearns, A.J., M. Matta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G. Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric Administration. Seattle, WA. Long, E.R., and L.G. Morgan. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Tech. Memo. NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 21 BIOACCUMULATION SUMMARY 35. AROCLOR 1016 Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success, xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536. Neff, J. M., and C.S. Giam. 1977. Effects of Aroclor 1016 and Halowax 1099 to juvenile horsehoe crabs Limulus polyphemus. Reference Not Available. Hansen, D.J., P.R. Parrish, and J. Forester. 1974. Aroclor 1016: Toxicity to and uptake by estuarine animals. Environ. Res. 7:363-373. Hansen, D.J., S.C. Schimmel, and J. Forester. 1975. Effects of Aroclor 1016 on embryos, fry, juveniles, and adults of sheepshead minnows (Cyprinodon variegatus). Trans. Amer. Fish. Soc. 104:584-588. 36. 37. 38. 39. 22 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED BIPHENYLS Chemical Name (Common Synonyms): Aroclor 1242 AROCLOR 1242 CASRN: 53469-21-9 Chemical Characteristics Solubility in Water: 240 g/L at 25C [1] Log Kow: 5.6 [4] Half-Life: No data [2,3] Log Koc: No data [4] Human Health Oral RfD: No data [5] Confidence: -- Critical Effect: PCBs have been shown to cause reproductive failure, birth defects, lesions, tumors, liver disorders, and death among sensitive species. Their toxicity is further enhanced by their ability to bioaccumulate and to biomagnify within the food chain due to extremely high lipophilicity [2]. Oral Slope Factor: No data [5] Carcinogenic Classification: A2 [5] Wildlife Partitioning Factors: No partitioning factors for Aroclor 1242 were identified for wildlife. Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and USACE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly waterinsoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. A biomagnification factor of 32 was determined for total PCBs from alewife to herring gull eggs in Lake Ontario [11]. No specific food chain multipliers were identified for Aroclor 1242. Aquatic Organisms Partitioning Factors: No partitioning factors for Aroclor 1242 were identified for aquatic organisms. Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify through the food web. Oliver and Niimi [12], studying accumulation of PCBs in various organisms in the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving 23 BIOACCUMULATION SUMMARY AROCLOR 1242 from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [13] reported that each trophic level contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific food chain multipliers were identified for Aroclor 1242. Toxicity/Bioaccumulation Assessment Profile PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in various processes and products because of the extreme stability of many isomers, particularly those with five or more chlorines [14]. A common use of PCBs was as dielectric fluids in capacitors and transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture (e.g., Aroclor 1242 contains biphenyls with approximately 42 percent chlorine). As a result of their stability and their general hydrophobic nature, PCBs released to the environment have dispersed widely throughout the ecosystem [14]. PCBs are among the most stable organic compounds known, and chemical degradation rates in the environment are thought to be slow. As a result of their highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water and at relatively high concentrations in sediment [15]. Individual PCB congeners have different physical and chemical properties based on the degree of chlorination and position of chlorine substitution, although differences with degree of chlorination are more significant [15]. Solubilities and octanol-water partition coefficients for PCB congeners range over several orders of magnitude [16]. Octanol-water partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest for the most chlorinated PCB congeners. Dispersion of PCBs in the aquatic environment is a function of their solubility [15] while PCB mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination [17]. The concentration of PCBs in sediments is a function of the physical characteristics of the sediment, such as grain size [18,19] and total organic carbon content [18,19,20,21]. Fine sediments typically contain higher concentrations of PCBs than coarser sediments because of more surface area [15]. Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [17]. Therefore, it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source [15]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment from reaching the overlying water via diffusion [17]. The persistence of PCBs in the environment is a result of their general resistance to degradation [16]. The rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [22]; other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation to a lesser extent [16]. Photochemical degradation, via reductive dechlorination, is also known to occur in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [21]. Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly than higher chlorinated congeners [23]. PCB congeners with no chlorine substituted in the ortho (2 and 24 BIOACCUMULATION SUMMARY AROCLOR 1242 2) positions but with four or more chlorine atoms at the meta (3 and 3) and para (4 and 4) positions can assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) [24]. Examples of these more toxic, coplanar congeners are 3,3,4,4-tetrachlorobiphenyl (PCB 77), 3,3,4,4,5-pentachlorobiphenyl (PCB 126), and 3,3,4,4,5,5hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of mixtures is to use toxic equivalency factors (TEFs) [25]. With this method, relative potencies for individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The following TEFs have been recommended [25,26]: Congener Class 3,3,4,4,5-PentaCB 3,3,4,4,5,5-HexaCB 3,34,4-TetraCB Monoortho coplanar PCBs Diortho coplanar PCBs Recommended TEF 0.1 0.05 0.01 0.001 0.00002 Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic organisms have a strong tendency to accumulate PCBs from water and food sources. The log bioconcentration factor for fish is approximately 4.70 [27]. This factor represents the ratio of concentration in tissue to the ambient water concentration. Aquatic organisms living in association with PCB-contaminated sediments generally have tissue concentrations equal to or greater than the concentration of PCB in the sediment [27]. Once taken up by an organism, PCBs partition primarily into lipid compartments [15]. Thus, differences in PCB concentration between species and between different tissues within the same species may reflect differences in lipid content [15]. PCB concentrations in polychaetes and fish have been strongly correlated to their lipid content [28]. Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higherchlorinated congeners [29, 30]. In some species, tissue concentrations of PCBs in females can be reduced during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred PCBs are eliminated from the female during spawning [31,32]. Fish and other aquatic organisms biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners [31]. Consequently, fish and other aquatic organisms may accumulate more of the higher chlorinated PCB congeners than is found in the environment [16]. The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate that PCB toxicity is directly related to the duration of exposure [1]. Toxic responses have been noted to occur at concentrations of 0.03 and 0.014 g/L in marine and freshwater environments, respectively [1]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 g/L [1]. Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [33], although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370 g/kg [34]. 25 BIOACCUMULATION SUMMARY AROCLOR 1242 A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic organisms at low tissue concentrations [16]. Field and Dexter [16] suggest that a number of marine and freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0 mg/kg and as low as 0.1 mg/kg. Spies et al. [35] reported an inverse relationship between PCB concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [36] also reported a significant correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with MFO induction by PCBs at tissue concentrations within the range of environmental exposures [16]. 26 Summary of Biological Effects Tissue Concentrations for Aroclor 1242 Species: Taxa Invertebrates Hyalella azteca, Amphipod freshwater 30 mg/kg (whole body)4 Mortality, NOED [38] L; radiolabeled compounds; Exp_conc = 3-100 Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Fishes Oncorhynchus mykiss; Rainbow trout Salmo salar, Atlantic salmon 1.3 mg/kg (whole body)4 Mortality, LOED [39] L; 10% mortality 0.54 mg/kg (eggs)4 Mortality, ED75 [40] L; estimated wet weight; eggs obtained from hatchery stock. 41 g/g lipid L; 40% reduction in mean weight L; 40% reduction in mean weight L; 40% reduction in mean weight L; 40% reduction in mean weight L; increased size of liver Ictalurus punctatus, Channel catfish 3.8 mg/kg (brain)4 14.6 mg/kg (kidney)4 11.9 mg/kg (muscle and skin)4 14.3 mg/kg (whole body)4 3.8 mg/kg (brain)4 Growth, LOED Growth, LOED Growth, LOED Growth, LOED Morphology; LOED [41] [41] [41] [41] [41] 27 28 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Aroclor 1242 Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 14.6 mg/kg (kidney)4 11.9 mg/kg (muscle and skin)4 14.3 mg/kg (whole body)4 1.16 mg/kg (blood)4 Morphology; LOED Morphology; LOED Morphology; LOED Cellular, NOED Cellular, NOED Cellular, NOED Cellular, NOED Cellular, NOED Cellular, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [41] [41] [41] [41] L; increased size of liver L; increased size of liver L; increased size of liver L; no effect on histopathology of liver, brain, kidney L; no effect on histopathology of liver, brain, kidney L; no effect on histopathology of liver, brain, kidney L; no effect on histopathology of liver, brain, kidney L; no effect on histopathology of liver, brain, kidney L; no effect on histopathology of liver, brain, kidney 3.8 mg/kg (brain)4 [41] 14.6 mg/kg (kidney)4 [41] 11.7 mg/kg (kidney)4 [41] 11.9 mg/kg (muscle and skin)4 11.4 mg/kg (muscle and skin)4 [41] [41] Summary of Biological Effects Tissue Concentrations for Aroclor 1242 Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 8.23 mg/kg (ovary)4 Cellular, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [41] L; no effect on histopathology of liver, brain, kidney L; no effect on histopathology of liver, brain, kidney L; no effect on histopathology of liver, brain, kidney L; no effect on histopathology of liver, brain, kidney L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality 5.76 mg/kg (testis)4 Cellular, NOED Cellular, NOED Cellular, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED [41] 14.3 mg/kg (whole body)4 10.9 mg/kg (whole body)4 1.16 mg/kg (blood)4 3.8 mg/kg (brain)4 14.6 mg/kg (kidney)4 11.7 mg/kg (kidney)4 11.9 mg/kg (muscle and skin)4 11.4 mg/kg (muscle and skin)4 29 [41] [41] [41] [41] [41] [41] [41] [41] 30 Species: Taxa Sediment 1 2 3 4 Summary of Biological Effects Tissue Concentrations for Aroclor 1242 Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 8.23 mg/kg (ovary)4 5.76 mg/kg (testis)4 14.3 mg/kg (whole body)4 10.9 mg/kg (whole body)4 Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [41] [41] [41] [41] L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. BIOACCUMULATION SUMMARY AROCLOR 1242 References 1. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.) Eisler, R. 1986. Polychlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.7). MacKay, D., W.Y. Shiu, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons, chlorobenzenes, and PCBs. Lewis Publishers, Boca Raton, FL. Agency for Toxic Substances and Disease Registry. 1993. Toxicological profile for polychlorinated biphenyls. Prepared by Syracuse Research Corporation. Prepared for U.S. Department of Health and Human Services, Public Health Service. April 1993. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Jones, P.D., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. USACE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food chains. Environ. Sci. Technol. 23:699. Hoffman, D.J., C.P. Rice, and T.J. Kubiak. 1996. PCBs and dioxins in birds. In Environmental contaminants in wildlife, ed. W.N. Beyer, G.H. Heinz, and A.W. Redmon-Horwood, pp. 165-207. Lewis Publishers, Boca Raton, FL. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 31 BIOACCUMULATION SUMMARY AROCLOR 1242 12. Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Rasmussen, J.B., D.J. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J. Fish. Aquat. Sci. 47:2030-2038. Rand, G.M., P.G. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G. M. Rand, pp. 3-67. Taylor and Francis, Washington, DC. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments. In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments. Unpublished document. January 11, 1988. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ. Pollut. 5B:121-132. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ. Sci. Technol. 13:65-71. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop, pp. 273-287. American Society of Testing and Materials, Philadelphia, PA. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls. In PCBs and the environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc., Boca Raton, FL. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL. Bolger, M. 1993. Overview of PCB toxicology. Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, 1993, pp. 37-53. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 32 BIOACCUMULATION SUMMARY AROCLOR 1242 24. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, 1993, pp. 3-9. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(1):51-88. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group, Inc., Arlington, MA.) Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136. Shaw, G.R., and D. W. Connell. 1982. Factors influencing concentrations of polychlorinated biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution: A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments. Mar. Biol. 91:497-508. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'Itri and M.A. Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL. Mearns, A.J., M. Matta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G. Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric Administration. Seattle, WA. Long, E.R., and L.G. Morgan. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Tech. Memo. NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success, xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121. 33 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. BIOACCUMULATION SUMMARY AROCLOR 1242 36. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536. Toxscan, Inc. 1990. Technical evaluation of environmental impact potential for proposed ocean disposal of dredged material from Berth 256 Fire Station 111 in Los Angeles Harbor. Toxscan, Inc., Marine Bioassay Laboratories Division, Watsonville, CA. Prepared for the Port of Los Angeles, San Pedro, CA. Borgmann, U., N.P. Norwood, and K.M. Ralph. 1990. Chronic toxicity and bioaccumulation of 2,5,2,5- and 3,4,3,4-tetrachlorobiphenyl and Aroclor 1242 in the amphipod Hyalella azteca. Arch. Environ. Contam. Toxicol., 19:558-564 Hogan, J.W., and J.L. Brauhn. 1975. Abnormal rainbow trout fry from eggs containing high residues of a PCB (Aroclor 1242). Progress. Fish Cult. 37 (4):229-230 Zitko, V., and R.L. Saunders. 1979. Effect of PCBs and other organochlorine compounds on the hatchability of Atlantic salmon (Salmo salar) eggs. Bull. Environm. Contam. Toxicol 21: 125-130. Hansen, L.G., W.B. Wiekhorst, and J. Simon. 1976. Effects of dietary Aroclor 1242 on channel catfish (Ictalurus punctatus) and the selective accumulation of PCB components. J. Fish. Res. Bd. Can. 33:1343-1352. 37. 38. 39. 40. 41. 34 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED BIPHENYLS Chemical Name (Common Synonyms): Aroclor 1248 AROCLOR 1248 CASRN: 12672-29-6 Chemical Characteristics Solubility in Water: 54 g/L at 250C [1] Log Kow: 6.2 [4] Half-Life: No data [2,3] Log Koc: No data [4] Human Health Oral RfD: Inadequate data to calculate [5] Confidence: -- Critical Effect: PCBs have been shown to cause reproductive failure, birth defects, lesions, tumors, liver disorders, and death among sensitive species. Their toxicity is further enhanced by their ability to bioaccumulate and to biomagnify within the food chain due to extremely high lipophilicity [2]. -- Oral Slope Factor: No data [5] Carcinogenic Classification: A2 [5] Wildlife Partitioning Factors: No partitioning factors for Aroclor 1248 were identified for wildlife. Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and USACE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly waterinsoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. A biomagnification factor of 32 was determined for total PCBs from alewife to herring gull eggs in Lake Ontario [11]. No specific food chain multipliers were identified for Aroclor 1248. Aquatic Organisms Partitioning Factors: No partitioning factors for Aroclor 1248 were identified for aquatic organisms. Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify through the food web. Oliver and Niimi [12], studying accumulation of PCBs in various organisms in the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake 35 BIOACCUMULATION SUMMARY AROCLOR 1248 trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [13] reported that each trophic level contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific food chain multipliers were identified for Aroclor 1248. Toxicity/Bioaccumulation Assessment Profile PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in various processes and products because of the extreme stability of many isomers, particularly those with five or more chlorines [14]. A common use of PCBs was as dielectric fluids in capacitors and transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture (e.g., Aroclor 1260 contains biphenyls with approximately 60 percent chlorine). As a result of their stability and their general hydrophobic nature, PCBs released to the environment have dispersed widely throughout the ecosystem [14]. PCBs are among the most stable organic compounds known, and chemical degradation rates in the environment are thought to be slow. As a result of their highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water and at relatively high concentrations in sediment [15]. Individual PCB congeners have different physical and chemical properties based on the degree of chlorination and position of chlorine substitution, although differences with degree of chlorination are more significant [15]. Solubilities and octanol-water partition coefficients for PCB congeners range over several orders of magnitude [16]. Octanol-water partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest for the most chlorinated PCB congeners. Dispersion of PCBs in the aquatic environment is a function of their solubility [15] while PCB mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination [17]. The concentration of PCBs in sediments is a function of the physical characteristics of the sediment, such as grain size [18,19] and total organic carbon content [18,19,20,21]. Fine sediments typically contain higher concentrations of PCBs than coarser sediments because of more surface area [15]. Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [17]. Therefore, it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source [15]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment from reaching the overlying water via diffusion [17]. The persistence of PCBs in the environment is a result of their general resistance to degradation [16]. The rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [22]; other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation to a lesser extent [16]. Photochemical degradation, via reductive dechlorination, is also known to occur in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [21]. Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly than higher chlorinated congeners [23]. PCB congeners with no chlorine substituted in the ortho (2 and 2) positions but with four or more chlorine atoms at the meta (3 and 3) and para (4 and 4) positions can 36 BIOACCUMULATION SUMMARY AROCLOR 1248 assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) [24]. Examples of these more toxic, coplanar congeners are 3,3,4,4-tetrachlorobiphenyl (PCB 77), 3,3,4,4,5-pentachlorobiphenyl (PCB 126), and 3,3,4,4,5,5hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of mixtures is to use toxic equivalency factors (TEFs) [25]. With this method, relative potencies for individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The following TEFs have been recommended [25,26]: Congener Class 3,3,4,4,5-PentaCB 3,3,4,4,5,5-HexaCB 3,34,4-TetraCB Monoortho coplanar PCBs Diortho coplanar PCBs Recommended TEF 0.1 0.05 0.01 0.001 0.00002 Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic organisms have a strong tendency to accumulate PCBs from water and food sources. The bioconcentration factor for fish is approximately 50,000 [27]. This factor represents the ratio of concentration in tissue to the ambient water concentration. Aquatic organisms living in association with PCB-contaminated sediments generally have tissue concentrations equal to or greater than the concentration of PCB in the sediment [27]. Once taken up by an organism, PCBs partition primarily into lipid compartments [15]. Thus, differences in PCB concentration between species and between different tissues within the same species may reflect differences in lipid content [15]. PCB concentrations in polychaetes and fish have been strongly correlated to their lipid content [28]. Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higherchlorinated congeners [29, 30]. In some species, tissue concentrations of PCBs in females can be reduced during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred PCBs are eliminated from the female during spawning [31,32]. Fish and other aquatic organisms biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners [31]. Consequently, fish and other aquatic organisms may accumulate more of the higher chlorinated PCB congeners than is found in the environment [16]. The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate that PCB toxicity is directly related to the duration of exposure [1]. Toxic responses have been noted to occur at concentrations of 0.03 and 0.014 g/L in marine and freshwater environments, respectively [1]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 g/L [1]. Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [33], although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370 g/kg [34]. 37 BIOACCUMULATION SUMMARY AROCLOR 1248 A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic organisms at low tissue concentrations [16]. Field and Dexter [16] suggest that a number of marine and freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0 mg/kg and as low as 0.1 mg/kg. Spies et al. [35] reported an inverse relationship between PCB concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [36] also reported a significant correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with MFO induction by PCBs at tissue concentrations within the range of environmental exposures [16]. 38 Summary of Biological Effects Tissue Concentrations for Aroclor 1248 Species: Taxa Invertebrates Concentration, Units in: Sediment Water Toxicity: Tissue (Sample Type) Effects [NO DATA FOUND] Ability to Accumulate: Log BCF Log BAF BSAF Source: Reference Comments Fishes [NO DATA FOUND] Wildlife [NO DATA FOUND] 39 BIOACCUMULATION SUMMARY References 1. AROCLOR 1248 USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.) Eisler, R. 1986. Polychlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.7). MacKay, D., W.Y. Shiu, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons, chlorobenzenes, and PCBs. Lewis Publishers, Boca Raton, FL. Agency for Toxic Substances and Disease Registry. 1993. Toxicological profile for polychlorinated biphenyls. Prepared by Syracuse Research Corporation. Prepared for U.S. Department of Health and Human Services, Public Health Service. April 1993. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Jones, P.D., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. USACE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food chains. Environ. Sci. Technol. 23:699. Hoffman, D.J., C.P. Rice, and T.J. Kubiak. 1996. PCBs and dioxins in birds. In Environmental contaminants in wildlife, ed. W.N. Beyer, G.H. Heinz, and A.W. Redmon-Horwood, pp. 165-207. Lewis Publishers, Boca Raton, FL. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 40 BIOACCUMULATION SUMMARY 12. AROCLOR 1248 Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Rasmussen, J.B., D.J. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J. Fish. Aquat. Sci. 47:2030-2038. Rand, G.M., P.G. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M. Rand, pp. 3-67. Taylor and Francis, Washington, DC. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments. In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL. Field, L.J. and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments. Unpublished document. January 11, 1988. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ. Pollut. 5B:121-132. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ. Sci. Technol. 13:65-71. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop, pp. 273-287. American Society of Testing and Materials, Philadelphia, PA. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls. In PCBs and the environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc., Boca Raton, FL. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 41 BIOACCUMULATION SUMMARY 23. AROCLOR 1248 Bolger, M. 1993. Overview of PCB toxicology. Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, 1993, pp. 37-53. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, 1993, pp. 3-9. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(1):51-88. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group, Inc., Arlington, MA.) Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution: A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62. Pruell, R.J., J.L. Lake, W.R. Davis, and J.G. Quinn.. 1986. Uptake and depuration of organic contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments. Mar. Biol. 91:497-508. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'Itri and M.A. Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL. Mearns, A.J., M. Matta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G. Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric Administration. Seattle, WA. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 42 BIOACCUMULATION SUMMARY AROCLOR 1248 34. Long, E.R., and L.G. Morgan. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Tech. Memo. NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA. Spies, R.B., D.W. Rice, Jr., P.A. Montagna, and R.R. Ireland. 1985. Reproductive success, xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536. 35. 36. 43 44 BIOACCUMULATION SUMMARY AROCLOR 1254 Chemical Category: POLYCHLORINATED BIPHENYLS Chemical Name (Common Synonyms): Aroclor 1254 Chemical Characteristics Solubility in Water: 12 g/L at 25C[1] Log Kow: -- Half-Life: No data [2,3] Log Koc: -- CASRN: 11097-69-1 Human Health Oral RfD: 2 x 10-5 mg/kg-day [4] Confidence: Medium; uncertainty factor = 300 Critical Effect: Ocular exudate, inflamed and prominent Meibomian glands, distorted growth of fingernails and toenails; decreased antibody (IgG and IgM) response to sheep erythrocyte Oral Slope Factor: No data [4] Carcinogenic Classification: A2 [4] Wildlife Partitioning Factors: No partitioning factors for Aroclor 1254 were identified for wildlife. Food Chain Multipliers: For PCBs as a class, the most toxic congeners have been shown to be selectively accumulated from organisms at one trophic level to the next [5]. At least three studies have concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and predators that feed primarily on aquatic organisms [6,7,8]. The results from Biddinger and Gloss [6] and USACE [8] generally agreed that highly water-insoluble compounds (including PCBs) have the potential to biomagnify in these types of food webs. Thomann's [9] model also indicated that highly waterinsoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. A biomagnification factor of 28 was calculated by [10] for transfer of total PCBs from fish to bald eagle eggs. Similarly, a biomagnification factor of 32 was determined for total PCBs from alewife to herring gull eggs in Lake Ontario [11]. No specific foot chain multipliers were identified for Aroclor 1254. Aquatic Organisms Partitioning Factors: BSAFs for Dover sole were approximately 0.96 for muscle and 1.14 for liver. Invertebrates collected from New Bedford, MA, and Long Island Sound, NY, had BSAFs ranging from 3.2 to 4.8. These data are presented in the attached summary table. Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify through the food web. Oliver and Niimi [12], studying accumulation of PCBs in various organisms in the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and 45 BIOACCUMULATION SUMMARY AROCLOR 1254 several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [13] reported that each trophic level contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific biomagnification data were identified for Aroclor 1254. Toxicity/Bioaccumulation Assessment Profile PCBs are among the most stable organic compounds known, and rates of chemical degradation in the environment are thought to be slow. Highly lipophilic, PCBs are generally found at low concentrations in water and at relatively high concentrations in sediment [14]. PCBs are a class of 209 discrete chemical compounds called congeners, in which one to ten chlorine atoms are attached to biphenyl. PCBs were commonly produced as complex mixtures of congeners for a variety of uses, including dielectric fluids in capacitors and transformers. In the United States, Aroclor is the most familiar requested trademark of commercial PCB formulations. The first two digits in the Aroclor designation (12) indicate that the mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture (e.g., Aroclor 1254 contains biphenyls with approximately 54 percent chlorine). Individual PCB congeners have different physical and chemical properties based on the degree of chlorination and position of chlorine substitution, although differences in the degree of chlorination affect partitioning more significantly, but toxicity is more dependent on position [15]. Octanol-water partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest for PCB congeners with the highest degree of chlorination. Solubilities and octanol-water partition coefficients range over several orders of magnitude. Due to their higher water solubility, lower-chlorinated PCBs might show greater dispersion from a point source, whereas the higher-chlorinated compounds might remain in the sediments closer to the source [15]. The mobility of PCBs in sediment is also a function of the chlorine substitution pattern and degree of chlorination and is generally quite low, particularly for the higher-chlorinated biphenyls [16]. Therefore, high rates of sedimentation could prevent PCBs in the sediment from reaching the overlying water via diffusion [16]. PCB concentrations in sediment are affected by physical characteristics of the sediment such as grain size and total organic carbon content [17,18]. Fine sediments typically contain higher concentrations of PCBs than coarser sediments [15]. Sorption to sediments is a function of total organic carbon content [19,20]. Toxicity of PCB congeners is dependent on the degree of chlorination as well as the isomer. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly than higher chlorinated congeners [21]. PCB congeners with no chlorine substituted in the ortho (2 and 2) positions but with four or more chlorine atoms at the meta (3 and 3) and para (4 and 4) positions can assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) [22]. Examples of these more toxic, coplanar congeners are 3,3,4,4-tetrachlorobiphenyl (PCB 77), 3,3,4,4,5-pentachlorobiphenyl (PCB 126), and 3,3,4,4,5,5hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of mixtures is to use toxic equivalency factors (TEFs) [23]. With this method, relative potencies for individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The following TEFs have been recommended [23,24]: 46 BIOACCUMULATION SUMMARY AROCLOR 1254 Congener Class 3,3,4,4,5-TCB 3,3,4,4,5,5-HCB 3,3,4,4-TeCB Monoortho coplanar PCBs Diortho coplanar PCBs Recommended TEF 0.1 0.05 0.01 0.001 0.00002 Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic organisms have a strong tendency to accumulate PCBs from water and food sources. The bioconcentration factor for fish is approximately 50,000 [25]. This factor represents the ratio of concentration in tissue to the ambient water concentration. PCB concentrations in tissues of aquatic organisms will generally be greater than, or equal to, sediment concentrations [26]. PCB concentrations in fish have been strongly correlated to their lipid content. Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higher-chlorinated congeners [27,28]. Elimination of PCBs from the body can occur during egg production and spawning in females of some species [29,30]. There is a limited capacity for fish and other aquatic organisms to biotransform or metabolize PCBs. Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370 g/kg [31]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 g/L [1]. Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [32], although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons. Toxic responses have been noted to occur at concentrations of 0.03 and 0.014 g/L in marine and freshwater environments, respectively [1]. 47 48 Species: Taxa Nephtys incisa, Polychaete worm Sediment Crassostrea virginica, Oyster Crassostrea virginica, Oyster Summary of Biological Effects Tissue Concentrations for Aroclor 1254 Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF 3.22 n=3 Source: Reference Comments3 [38] F; New Bedford, MA; Long Island Sound, NY AF = Long Island: 40.3-48.3 ng/g (TOC: 2.39-2.62%) [Organism](ng/g lipid [Sediment] (ng/g organ carbo New Bedford: 3,070-7,180 ng/g (TOC: 4.16-4.67%) 4.29 n=3 425 mg/kg (whole body)4 425 mg/kg (whole body)4 101 mg/kg (whole body)4 Cellular, LOED Growth, LOED Cellular, NOED [49] [49] [49] L; atrophy of digestive diverticulata L; reduced growth L; no effect on histopathology of digestive diverticulata L; no effect on growth L; no effect on mortality L; no effect on mortality L; 41% reduction in rate of shell growth L; 19% reduction in rate of shell growth 101 mg/kg (whole body)4 425 mg/kg (whole body)4 101 mg/kg (whole body)4 33 mg/kg (whole body)4 8.1 mg/kg (whole body)4 Growth, NOED Mortality, NOED Mortality, NOED Growth, NA Growth, NA [49] [49] [49] [46] [46] Summary of Biological Effects Tissue Concentrations for Aroclor 1254 Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 33 mg/kg (whole body)4 8.1 mg/kg (whole body)4 Yoldia limatula, Bivalve New Bedford: 3,070-7,180 ng/g (TOC: 4.164.67%) Long Island: 40.3-48.3 ng/g (TOC: 2.392.62%) Macoma nasuta, Clam Concentrations at Stations: Mortality, NOED Mortality, NOED 4.07 n=3 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [46] [46] L; no effect on survival in 96 hours L; no effect on survival in 96 hours F; New Bedford, MA; Long Island Sound, NY [38] 4.79 n=3 [39] L; standard bioassay with field collected sediments with multiple contaminants. 49 50 Species: Taxa Sediment <20 g/kg dw <20 g/kg dw <20 g/kg dw <20 g/kg dw Daphnia magna, Cladoceran Gammarus pseudolimnaeus, Amphipod Gammarus tigrinus, Amphipod Penaeus duorarum, Pink shrimp Palaemonetes kadiakensis, Grass shrimp Summary of Biological Effects Tissue Concentrations for Aroclor 1254 Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 21.4 g/kg, (variance = 9.8, n=5) 100% survival Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Tissue burdens and toxicity were determined in separate aquaria after 20 and 10 days, respectively. 35.2* g/kg, 100% survival (variance = 27.2, n=5) 20 g/kg, (variance = 0, n=5) 100% survival 27.8* g/kg, 100% survival (variance = 20.7, n=5) *statistically significant increase 10.4 mg/kg (whole body)4 7.8 mg/kg (whole body)4 Mortality, NOED Mortality, NOED [52] L; radiolabeled compound L; radiolabeled compound [52] 4.64 mg/kg (whole body)4 3.9 mg/kg (whole body)4 3.2 mg/kg (whole body)4 Behavior, NOED Mortality, ED100 Mortality, NOED [51] L; radiolabeled compound L; 100% mortality after 48 hours L; radiolabeled compound [46] [52] Summary of Biological Effects Tissue Concentrations for Aroclor 1254 Species: Taxa Orconectes nais, Crayfish Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.04 mg/kg (whole body)4 16 mg/kg (whole body)4 33 mg/kg (whole body)4 1.3 mg/kg (whole body)4 33 mg/kg (whole body)4 0.14 mg/kg (whole body)4 Callinectes sapidus, Blue crab Culex tarsalis, Mosquito Chaoborus punctipennis, Midge Corydalus cornutus, Midge Pteronarcys dorsata, Giant black stonefly 51 23 mg/kg (whole body)4 5.4 mg/kg (whole body)4 1.2 mg/kg (whole body)4 1.02 mg/kg (whole body)4 1.4 mg/kg (whole body)4 Mortality, NOED Mortality, NA Behavior, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [52] [46] [46] L; radiolabeled compound L; lethal to 18 of 25 fish in 20 days L; no effect on sense of equilibrium or behavior L; no effect on survival in 48 hours L; no effect on survival in 20 days L; no effect on survival in 48 hours L; no effect on survival in 20 days L; radiolabeled compound L; radiolabeled compound L; radiolabeled compound L; radiolabeled compound [46] [46] [46] [46] [52] [52] [52] [52] 52 Species: Taxa Acheta domesticus, House cricket Sediment Soil: 1,000 ppm 2,000 ppm Fishes Oncorhynchus kisutch, Coho salmon Oncorhynchus mykiss, Rainbow trout Summary of Biological Effects Tissue Concentrations for Aroclor 1254 Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 148.6 ppm 143.9 ppm Signficant mortality (LC50 = 1,200 ppm) Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [37] L; 14-d soil bioassay; despite high mortality no significant differences were seen in growth rate or food consumption between surviving crickets and control crickets. 0.37 mg/kg (liver) Mortality, ED10 Development, LOED Physiological, LOED [48] L; 10% mortality of smolts L; reduced ability of smolts to adapt to seawater L; delayed increase in plasma thyroxine (T4) prior to smoltification by 30 days L; increased ethoxyresorufin odeethylase (EROD) activity 0.15 mg/kg (whole body)4 0.5 mg/kg (liver) [48] [48] 0.2 mg/kg (whole body)4 Physiological, LOED [50] Summary of Biological Effects Tissue Concentrations for Aroclor 1254 Species: Taxa Oncorhynchus mykiss, Rainbow trout Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.2 mg/kg (whole body)4 Physiological, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [50] L; increased ethoxyresorufin odeethylase (EROD) activity L Oncorhynchus mykiss, Rainbow trout Muscle or liver = 300 g/kg Elevated hepatic MFO (EROD) activity after 70 days [40] Pimephales promelas, Fathead minnow 0.82 g/g dw 14-27 g/g dw 5.25-11.6 g/g 13.7-47.2 g/g No effect Reproduction inhibited. Frequency and fecundity 5-30% of control values. [41] L; organism survival and weight unaffected by PCB concentration. Increased lipid concentrations were seen with increased reproductive effects. Measurement endpoints for effects not well-defined. Pleuronectes americanus, Winter flounder Eggs = 7.1 g/kg Reduced growth in length and weight [42] F 53 54 Species: Taxa Microstomus pacificus, Dover sole Sediment 2.3* g/kg, dw (median TOC - 7.6%) Salvelinus fontinalis, Brook trout Cyprinus carpio, Common carp Lagodon rhomboides, Pinfish Ictalurus punctatus, Channel catfish Summary of Biological Effects Tissue Concentrations for Aroclor 1254 Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Muscle = 1.1* g/kg, dw (2.36 %lipids) Liver = 12.0* g/kg, (24.8% lipids) *median concentration 39 mg/kg (fillet) Physiological, LOED [44] L; 7 doses over 18day period; effect at only exposure dose; hepatic enzyme induction L; increased ethoxyresorufin odeethylase (EROD) activity L; no effect on survival in 48 hours L; no effect on survival in 48 hours L; no effect on survival in 48 hours L; no effect on neurotransmitters Ability to Accumulate2: Log BCF Log BAF BSAF 0.96 1.4 Source: Reference Comments3 [43] BSAFs are lipid and TOC normalized values reported in text. 0.1 mg/kg (whole body)4 Physiological, LOED [50] 17 mg/kg (whole body)4 3.8 mg/kg (whole body)4 0.98 mg/kg (whole body)4 100 mg/kg (whole body)4 Mortality, NOED Mortality, NOED Mortality, NOED Physiological, NOED [46] [46] [46] [47] Summary of Biological Effects Tissue Concentrations for Aroclor 1254 Species: Taxa Platycephalus bassensis, Sand flathead Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 10 mg/kg (whole body)4 Physiological, ED50 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [45] L; 50% increase in activity of uridine diphosphoglucuronosyltransferase L; induction (3x) of ethoxyresorufin odeethylase (EROD) activity L; no induction of ethoxyresorufin odeethylase (EROD) activity 100 mg/kg (whole body)4 Physiological, LOED [45] 10 mg/kg (whole body)4 Physiological, NOED [45] 1 2 3 4 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. 55 BIOACCUMULATION SUMMARY AROCLOR 1254 References 1. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/580-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH. February.) Eisler, R. 1986. Polychlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.7). MacKay, D., W.Y. Shiu, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons, chlorobenzenes, and PCBs. Lewis Publishers, Boca Raton, FL. Agency for Toxic Substances and Disease Registry. 1993. Toxicological profile for polychlorinated biphenyls. Prepared by Syracuse Research Corporation. Prepared for U.S. Department of Health and Human Services, Public Health Service. April 1993. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Jones, P.D., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. USACE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food chains. Environ. Sci. Technol. 23:699. Hoffman, D.J., C.P. Rice, and T.J. Kubiak. 1996. PCBs and dioxins in birds. In Environmental contaminants in wildlife, ed. W.N. Beyer, G.H. Heinz, and A.W. Redmon-Horwood, pp. 165-207. Lewis Publishers, Boca Raton, FL. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 56 BIOACCUMULATION SUMMARY AROCLOR 1254 12. Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Rasmussen, J.B., D.J. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J. Fish. Aquat. Sci. 47:2030-2038. Rand, G.M., P.G. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G. M. Rand, pp. 3-67. Taylor and Francis, Washington, DC. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments. In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL. Field, L.J. and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments. Unpublished document. January 11, 1988. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ. Pollut. 5B:121-132. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ. Sci. Technol. 13:65-71. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop, pp. 273-287. American Society of Testing and Materials, Philadelphia, PA. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls. In PCBs and the environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc., Boca Raton, FL. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL. Bolger, M. 1993. Overview of PCB toxicology. Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, 1993, pp. 37-53. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 57 BIOACCUMULATION SUMMARY AROCLOR 1254 24. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, 1993, pp. 3-9. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Critical Reviews in Toxicology 21(1):51-88. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group, Inc., Arlington, MA.) Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136. Shaw, G.R., and D. W. Connell. 1982. Factors influencing concentrations of polychlorinated biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution: A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn.. 1986. Uptake and depuration of organic contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments. Mar. Biol. 91:497-508. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'Itri and M.A. Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the Environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL. Mearns, A.J., M. Matta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G. Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric Administration. Seattle, WA. Long, E.R., and L.G. Morgan. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Tech. Memo. NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success, xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 58 BIOACCUMULATION SUMMARY AROCLOR 1254 36. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536. Paine, J.M., M.J. McKee, and E. Ryan. 1993. Toxicity and bioaccumulation of soil PCBs in crickets: Comparison of laboratory and field studies. Environ. Toxicol. Chem. 12:2097-2103. Lake, J.L., N.I. Rubinstein, H. Lee, C.A. Lake, J. Heltshe, and S. Pavignano. 1990. Equilibrium partitioning and bioaccumulation of sediment-associated contaminants by infaunal organisms. Environ. Toxicol. Chem. 9:1095-1106. Toxscan, Inc. 1990. Technical evaluation of environmental impact potential for proposed ocean disposal of dredged material from Berth 256 Fire Station 111 in Los Angeles Harbor. Toxscan, Inc., Marine Bioassay Laboratories Division, Watsonville, CA. Prepared for the Port of Los Angeles, San Pedro, CA. Melancon, M.J., K.A. Turnquist, and J.J. Lech. 1989. Relation of hepatic monooxygenase activity to tissue PCBs in rainbow trout (Salmo gairdneri) injected with [14C] PCBs. Environ. Toxicol. Chem. 8:777-782. Dillon, T.M., and R.M. Engler. 1988. Relationship between PCB tissue residues and reproductive success of fathead minnows. Environmental effects of Dredging Technical Notes. EEDD-01-13, April 1988. U.S. Army Engineer Waterways Experiment Station. Black, D.E., D.K. Phelps, and R.L. Lapan. 1988. The effect of inherited contamination on eggs in larval winter flounder, Pseudopleuronectes americanus. Mar. Environ. Res. 25:45-62. Young, D.R., A.J. Mearns, and R.W. Gossett. 1991. Bioaccumulation of p,p -DDE and PCB 1254 by a flatfish bioindicator from highly contaminated sediment of southern California. In Organic substances and sediments in water - Biological, ed. R.A. Baker, Vol. 3, pp. 159-169. Lewis Publishers, Inc., Chelsea, MI. Addison, R.F., M.E. Zinck, and D.E. Willis. 1978. Induction of hepatic mixed function oxidase (mfo) enzymes in trout (Salvelinus fontinalis) by feeding Aroclor 1254 or 3-methylcholanthrene. Comp. Biochem. Physiol. 61c:323-325. Brumley, C.M., V.S. Haritos, J.T. Ahokas, and D.A. Holdway. 1995. Validation of biomarkers of marine pollution exposure in sand flathead using aroclor 1254. Aquat. Toxicol. 31:249.262. Duke, T.W., J.I. Lowe, and A.J. Wilson, Jr. 1970. A polychlorinated biphenyl (Aroclor 1254) in the water, sediment, and biota of Escambia Bay, Florida. Bull. Environ. Contam. Toxicol. 5:171180. Fingerman, S., and E.C. Short, Jr. 1983. Changes in neurotransmitter levels in channel catfish after exposure to benzo(a)pyrene, naphthalene, and Aroclor 1254. Bull. Environ. Contam. Toxicol. 30:147-151. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 59 BIOACCUMULATION SUMMARY AROCLOR 1254 48. Folmar, L.C., W.W. Dickhoff, W.S. Zaugg and H.O. Hodgins. 1982. The effects of Aroclor 1254 and No. 2 fuel oil on smoltification and sea-water adaptation of coho salmon (Oncorhynchus kisutch). Aquat. Toxicol. 2:291-299. Lowe, J.I., P.R. Parrish, J.M. Patrick, Jr., and J. Forester. 1972. Effects of the polychlorinated biphenyl Aroclor 1254 on the American oyster Crassostrea virginica. Mar. Biol. 17:209-214. Melancon, M.J., and J.J. Lech. 1983. Dose-effect relationship for induction of hepatic monooxygenase activity in rainbow trout and carp by Aroclor 1254. Aquat. Toxicol. 4:51-61. Pinkney, A.E., G.V. Poje, R.M. Sansur, C.C. Lee, and J.M. O'Connor. 1985. Uptake and retention of 14C-Aroclor 1254 in the amphipod, Gammarus tigrinus, fed contaminated fungus, Fusarium oxysporum. Arch. Environ. Contam. Toxicol. 14: 59-64. Sanders, H.O., and Chandler, J.H. 1972. Biological magnification of a polychlorinated biphenyl (Aroclor 1254) from water by aquatic invertebrates. Bull. Environ. Contam. Toxicol. 49. 50. 51. 52. 60 BIOACCUMULATION SUMMARY AROCLOR 1260 Chemical Category: POLYCHLORINATED BIPHENYLS Chemical Name (Common Synonyms): Aroclor 1260 CASRN: 11096-82-5 Chemical Characteristics Solubility in Water: 0.027 mg/L at 25C [1] Log Kow: 6.8 [4] Half-Life: No data [2,3] Log Koc: No data [4] Human Health Oral RfD: No data [5] Confidence: -- Critical Effect: PCBs have been shown to cause reproductive failure, birth defects, lesions, tumors, liver disorders, and death among sensitive species. Their toxicity is further enhanced by their ability to bioaccumulate and to biomagnify within the food chain due to extremely high lipophilicity [2]. Oral Slope Factor: No data [5] Carcinogenic Classification: A2 [5] Wildlife Partitioning Factors: No partitioning factors for Aroclor 1260 were identified for wildlife. Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and USACE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly waterinsoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. A biomagnification factor of 32 was determined for total PCBs from alewife to herring gull eggs in Lake Ontario [11] No specific food chain multipliers were identified for Aroclor 1260. Aquatic Organisms Partitioning Factors: No partitioning factors for Aroclor 1260 were identified for aquatic organisms. Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify through the food web. Oliver and Niimi [12], studying accumulation of PCBs in various organisms in the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving 61 BIOACCUMULATION SUMMARY AROCLOR 1260 from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [13] reported that each trophic level contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific food chain multipliers were identified for Aroclor 1260. Toxicity/Bioaccumulation Assessment Profile PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in various processes and products because of the extreme stability of many isomers, particularly those with five or more chlorines [14]. A common use of PCBs was as dielectric fluids in capacitors and transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture (e.g., Aroclor 1260 contains biphenyls with approximately 60 percent chlorine). As a result of their stability and their general hydrophobic nature, PCBs released to the environment have dispersed widely throughout the ecosystem [14]. PCBs are among the most stable organic compounds known, and chemical degradation rates in the environment are thought to be slow. As a result of their highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water and at relatively high concentrations in sediment [15]. Individual PCB congeners have different physical and chemical properties based on the degree of chlorination and position of chlorine substitution, although differences with degree of chlorination are more significant [15]. Solubilities and octanol-water partition coefficients for PCB congeners range over several orders of magnitude [16]. Octanol-water partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest for the most chlorinated PCB congeners. Dispersion of PCBs in the aquatic environment is a function of their solubility [15] while PCB mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination [17]. The concentration of PCBs in sediments is a function of the physical characteristics of the sediment, such as grain size [18,19] and total organic carbon content [18,19,20,21]. Fine sediments typically contain higher concentrations of PCBs than coarser sediments because of more surface area [15]. Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [17]. Therefore, it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source [15]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment from reaching the overlying water via diffusion [17]. The persistence of PCBs in the environment is a result of their general resistance to degradation [16]. The rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [22]; other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation to a lesser extent [16]. Photochemical degradation, via reductive dechlorination, is also known to occur in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [21]. Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly 62 BIOACCUMULATION SUMMARY AROCLOR 1260 than higher chlorinated congeners [23]. PCB congeners with no chlorine substituted in the ortho (2 and 2) positions but with four or more chlorine atoms at the meta (3 and 3) and para (4 and 4) positions can assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) [24]. Examples of these more toxic, coplanar congeners are 3,3,4,4-tetrachlorobiphenyl (PCB 77), 3,3,4,4,5-pentachlorobiphenyl (PCB 126), and 3,3,4,4,5,5hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of mixtures is to use toxic equivalency factors (TEFs) [25]. With this method, relative potencies for individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The following TEFs have been recommended [25,26]: Congener Class 3,3,4,4,5-PentaCB 3,3,4,4,5,5-HexaCB 3,3,4,4-TetraCB Monoortho coplanar PCBs Diortho coplanar PCBs Recommended TEF 0.1 0.05 0.01 0.001 0.00002 Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic organisms have a strong tendency to accumulate PCBs from water and food sources. The bioconcentration factor for fish is approximately 50,000 [27]. This factor represents the ratio of concentration in tissue to the ambient water concentration. Aquatic organisms living in association with PCB-contaminated sediments generally have tissue concentrations equal to or greater than the concentration of PCB in the sediment [27]. Once taken up by an organism, PCBs partition primarily into lipid compartments [15]. Thus, differences in PCB concentration between species and between different tissues within the same species may reflect differences in lipid content [15]. PCB concentrations in polychaetes and fish have been strongly correlated to their lipid content [28]. Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higherchlorinated congeners [29, 30]. In some species, tissue concentrations of PCBs in females can be reduced during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred PCBs are eliminated from the female during spawning [31,32]. Fish and other aquatic organisms biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners [31]. Consequently, fish and other aquatic organisms may accumulate more of the higher chlorinated PCB congeners than is found in the environment [16]. The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate that PCB toxicity is directly related to the duration of exposure [1]. Toxic responses have been noted to occur at concentrations of 0.03 and 0.014 g/L in marine and freshwater environments, respectively [1]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 g/L [1]. Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [33], although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low 63 BIOACCUMULATION SUMMARY AROCLOR 1260 concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370 g/kg [34]. A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic organisms at low tissue concentrations [16]. Field and Dexter [16] suggest that a number of marine and freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0 mg/kg and as low as 0.1 mg/kg. Spies et al. [35] reported an inverse relationship between PCB concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [36] also reported a significant correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with MFO induction by PCBs at tissue concentrations within the range of environmental exposures [16]. 64 Summary of Biological Effects Tissue Concentrations for Aroclor 1260 Species: Taxa Invertebrates Clam, Macoma nasuta Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Survival (out of 20): 1.2 mg/kg dw (reference station) 0.9 mg/kg dw 0.976 mg/kg (variance = 4.6x106, n=5) 18.600 mg/kg (variance = na; n=5) 19.8 (variance=0.2, n=5) 5.2 (variance=6.2, n=5) 19.8 (variance=0.2, n=5) Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [37] L; standard bioassay with field collected sediments with multiple contaminants. Tissue burdens and toxicity were determined in separate aquaria after 20 and 10 days, respectively. 3.8 mg/kg dw 9.170 mg/kg (variance = 3.96x108, n=5) 1 2 3 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 65 BIOACCUMULATION SUMMARY AROCLOR 1260 References 1. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.) Eisler, R. 1986. Polychlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.7). MacKay, D., W.Y. Shiu, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons, chlorobenzenes, and PCBs. Lewis Publishers, Boca Raton, FL. Agency for Toxic Substances and Disease Registry. 1993. Toxicological profile for polychlorinated biphenyls. Prepared by Syracuse Research Corporation. Prepared for U.S. Department of Health and Human Services, Public Health Service. April 1993. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Jones, P.D., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. USACE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food chains. Environ. Sci. Technol. 23:699. Hoffman, D.J., C.P. Rice, and T.J. Kubiak. 1996. PCBs and dioxins in birds. In Environmental contaminants in wildlife, ed. W.N. Beyer, G.H. Heinz, and A.W. Redmon-Horwood, pp. 165-207. Lewis Publishers, Boca Raton, FL. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 66 BIOACCUMULATION SUMMARY AROCLOR 1260 12. Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Rasmussen, J.B., D.J. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J. Fish. Aquat. Sci. 47:2030-2038. Rand, G.M., P.G. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M. Rand, pp. 3-67. Taylor and Francis, Washington, DC. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments. In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL. Field, L.J. and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments. Unpublished document. January 11, 1988. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ. Pollut. 5B:121-132. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ. Sci. Technol. 13:65-71. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop, pp. 273-287. American Society of Testing and Materials, Philadelphia, PA. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls. In PCBs and the environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton, Florida. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc. Boca Raton, Florida. Bolger, M. 1993. Overview of PCB toxicology. Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, 1993, pp. 37-53. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 67 BIOACCUMULATION SUMMARY AROCLOR 1260 24. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of Water, Washington, DC, May 10-11, 1993, pp. 3-9. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Critical Reviews in Toxicology 21(1):5188. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group, Inc., Arlington, MA.) Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136. Shaw, G.R., and D. W. Connell. 1982. Factors influencing concentrations of polychlorinated biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution: A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn.. 1986. Uptake and depuration of organic contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments. Mar. Biol. 91:497-508. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'Itri and M.A. Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL. Mearns, A.J., M. Matta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G. Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric Administration. Seattle, WA. Long, E.R., and L.G. Morgan. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Tech. Memo. NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 68 BIOACCUMULATION SUMMARY AROCLOR 1260 35. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success, xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536. Toxscan, Inc. 1990. Technical evaluation of environmental impact potential for proposed ocean disposal of dredged material from Berth 256 Fire Station 111 in Los Angeles Harbor. Toxscan, Inc., Marine Bioassay Laboratories Division, Watsonville, CA. Prepared for the Port of Los Angeles, San Pedro, CA. 36. 37. 69 70 BIOACCUMULATION SUMMARY Chemical Category: METAL Chemical Name (Common Synonyms): ARSENIC ARSENIC CASRN: 7440-38-2 Chemical Characteristics Solubility in Water: Insoluble [1] Log Kow: Half-Life: Not applicable, stable [1] Log Koc: Human Health Oral RfD: 3 x 10-4 mg/kg/day [2] Confidence: Medium, uncertainty factor = 3 Critical Effect: Hyperpigmentation, keratosis, and possible vascular complications Oral Slope Factor: 1.5 x 10+0 per (mg/kg)/day [2] Carcinogenic Classification: A [2] Wildlife Partitioning Factors: Partitioning factors for arsenic in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for arsenic in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Arsenic is a metal that occurs in aquatic systems in a number of chemical forms. The most prevalent form is arsenate, followed by arsenite, which usually is present at lower concentrations. The arsenate ions can be methylated and form alkylated compounds (methylarsenic acid and dimethylarsenic acid). In any aquatic environment only a small portion of the total arsenic (approximately 0.1 percent) exists as methylated species. The arsenic methylation rate is strongly correlated with sediment organic matter content in sediments and amount of sulfate-reducing bacteria. Food Chain Multipliers: The simplified trophic transfer experiment conducted by Lindsay and Sanders [11] effectively ended speculation of food chain transfer to the second trophic level. Arsenic is taken up by aquatic organisms primarily through dietary exposure [3] Toxicity/Bioaccumulation Assessment Profile Arsenic (As) is accumulated by aquatic organisms primarily through dietary exposure [3]. The most toxic form of arsenic in aquatic systems is As III, follow by As V, and the least toxic forms are organic complexes. The bioavailability of arsenic is not dependent on the concentration of acid-volatile sulfides 71 BIOACCUMULATION SUMMARY ARSENIC (AVS). Pore water concentrations of arsenic are two to three orders of magnitude higher than surface water concentrations [4], a factor that can be of considerable toxicological importance to some benthic organisms. It has been demonstrated that sediments are the major source of arsenic to the infaunal organisms and the body burden is related to the concentration of extractable (1N HCL) arsenic normalized for iron [5]. 72 Summary of Biological Effects Tissue Concentrations for Arsenic Species: Taxa Invertebrates, field-collected Concentration, Units in1: Sediment Water Nonfit g/L 1740 158 138 72 31 < 22 Tissue (Sample Type) g/g 34 15 13 27 3 3 6.96 mg/g 4.98 mg/g 7.38 mg/g 2.35 mg/g 5.95 mg/g [7] L Toxicity: Effects Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [8] F Total SEM Filt g/g g/g g/L 404 202 57 102 24 54 68 25 72 46 11 29 11 3 23 4 < 0.5 3 9.78 g/g 1.15 g/g 26 g/g 18 g/g 17 g/g Tubificidae Helisoma campanulata, Snail 4.2 mg/kg (whole body)4 Mortality, ED16 [16] 16 mg/kg (whole body)4 Mortality, NOED [16] 5.8 mg/kg (whole body)4 Mortality, NOED [16] 4 mg/kg (whole body)4 Mortality, NOED [16] L; mixture of 4 arsenic compounds, estimated body burden from graph L; mixture of 4 arsenic compounds, estimated body burden from graph L; mixture of 4 arsenic compounds, estimated body burden from graph L; mixture of 4 arsenic compounds, estimated body burden from graph 73 74 Summary of Biological Effects Tissue Concentrations for Arsenic Species: Taxa Stagnicola emarginata, Snail Concentration, Units in1: Sediment Water Tissue (Sample Type) 3.6 mg/kg (whole body)4 Toxicity: Effects Mortality, NOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [16] L; mixture of 4 arsenic compounds, estimated body burden from graph L; mixture of 4 arsenic compounds, estimated body burden from graph L; mixture of 4 arsenic compounds, estimated body burden from graph L; mixture of 4 arsenic compounds, estimated body burden from graph F 3.6 mg/kg (whole body)4 Mortality, NOED [16] 3.6 mg/kg (whole body)4 Mortality, NOED [16] 3.6 mg/kg (whole body)4 Mortality, NOED [16] Mytilus galloprovincialis, Mussel Ceriodaphnia dubia, 1,120 g/g Cladoceran 2,720 g/g 650 g/g 569 g/g 1295 g/L 3580 g/L 901 g/L 436 g/L 0.44-0.51 mg/kg 0.047 [12] 70% mortality 70% mortality 20% mortality/ no reproduction 0% mortality/ no reproduction [4] L Summary of Biological Effects Tissue Concentrations for Arsenic Species: Taxa Daphnia magna, Cladoceran Concentration, Units in1: Sediment Water Tissue (Sample Type) 3.8 mg/kg (whole body)4 Toxicity: Effects Mortality, NOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [16] L; mixture of 4 arsenic compounds, estimated body burden from graph, tissues exposed 21 d L; mixture of 4 arsenic compounds, estimated body burden from graph, tissues exposed 21 d L; mixture of 4 arsenic compounds, estimated body burden from graph, tissues exposed 21 d L; mixture of 4 arsenic compounds, estimated body burden from graph, tissues exposed 21 d L; lethal body burden after 21 d exposure L; 10% reduction in number of offspring L 9.8 mg/kg (whole body)4 Mortality, NOED [16] 4.4 mg/kg (whole body)4 Mortality, NOED [16] 4 mg/kg (whole body)4 Mortality, NOED [16] 87 mg/kg (whole body)4 33 mg/kg (whole body)4 Hyallela azteca, Amphipod 3580 g/g 1420 g/L Mortality, ED50 Reproduction, ED10 Growth reduction [6] [6] [4] 75 76 Summary of Biological Effects Tissue Concentrations for Arsenic Species: Taxa Hyallela azteca, Amphipod Concentration, Units in1: Sediment Water Tissue (Sample Type) g/g 7 12 4 2 1 0.4 1.15 mg/kg (whole body)4 1.03 mg/kg (whole body)4 1.28 mg/kg (whole body)4 1.14 mg/kg (whole body)4 8.4 mg/kg (whole body)4 Growth, NOED Growth, NOED Growth, NOED Growth, NOED Mortality, NOED [11] [11] [11] [11] L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; mixture of 4 arsenic compounds, estimated body burden from graph L; mixture of 4 arsenic compounds, estimated body burden from graph L; mixture of 4 arsenic compounds, estimated body burden from graph Toxicity: Effects Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [8] F Total SEM Filt Nonfilt g/g g/g g/L g/L 404 202 102 24 68 25 46 11 11 3 4 <0.5 57 54 72 29 23 3 1740 158 138 72 31 <22 Palaemonetes pugio, Grass shrimp Pteronarcys dorsata, Giant black stonefly [16] 6 mg/kg (whole body)4 Mortality, NOED [16] 7 mg/kg (whole body)4 Mortality, NOED [16] Summary of Biological Effects Tissue Concentrations for Arsenic Species: Taxa Concentration, Units in1: Sediment Water Tissue (Sample Type) 8.4 mg/kg (whole body)4 Toxicity: Effects Mortality, NOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [16] L; mixture of 4 arsenic compounds, estimated body burden from graph Fishes Oncorhynchus mykiss, Rainbow trout Oncorhynchus mykiss, Rainbow trout 8.4 mg/L 18.1 mg/L 240 mg/L 1.8 mg/kg 3.5 mg/kg (0.18 mmol/kg) 3 mg/kg (whole body)4 Growth, NOED [10] F [14] 4.7 mg/kg (whole body)4 Mortality, LOED [14] 8.6 mg/kg (whole body)4 13.5 mg/kg (whole body)4 Behavior, ED50 Behavior, ED50 [15] [15] L; exposure to arsenic for 21 d did not affect growth at the longest time interval tested L; pre-exposure to arsenic for 7 d produced significant increase in LC50 (reduced sensitivity to exposure) at shortest time interval tested L; loss of equilibrium, mortality L; loss of equilibrium, mortality 77 78 Summary of Biological Effects Tissue Concentrations for Arsenic Species: Taxa Concentration, Units in1: Sediment Water Tissue (Sample Type) 8.1 mg/kg (whole body)4 8.6 mg/kg (whole body)4 Toxicity: Effects Behavior, ED50 Behavior, ED50 Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [15] L; loss of equilibrium, mortality L; loss of equilibrium, mortality F [15] Lepisosteus osseus, Longnose gar 673 g/g 186 g/L 0.051 mg/kg [9] Esox lucius, Northern pike 673 g/g 186 g/L 0.025 mg/kg [9] F Notemigonus 673 g/g crysoleucas, Golden shiner 186 g/L 0.167 mg/kg [9] F Notropis atherinoides, Emerald shiner 673 g/g 186 g/L 0.036 mg/kg [9] F Notropis hudsonius, 673 g/g Spottail shiner 186 g/L 0.03 mg/kg [9] F Pimephales notatus, 673 g/g Bluntnose minnow 186 g/L 0.0513 mg/kg [9] F Summary of Biological Effects Tissue Concentrations for Arsenic Species: Taxa Pimephales promelas, Fathead minnow Concentration, Units in1: Sediment 9.10 g/g 9.78 g/g 1.25 g/g 26 g/g 15 g/g 18 g/g 17 g/g 17 g/g 11 g/g Water Tissue (Sample Type) 1.39 mg/g 1.14 mg/g 1.58 mg/g 2.40 mg/g 1.76 mg/g 0.66 mg/g 2.33 mg/g 2.22 mg/g 1.82 mg/g Toxicity: Effects Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [7] L Semotilus atromaculatus, Creek chub 673 g/g 186 g/L 2.36 mg/kg [9] F Catostomus commersoni, White sucker 673 g/g 186 g/L 0.132 mg/kg [9] F Fundulus diaphanus, 673 g/g Banded killifish 186 g/L 0.101 mg/kg [9] F Amblolites repestris, 673 g/g Rock bass 186 g/L 0.128 mg/kg [9] F Lepomis gibbosus, Pumpkinseed 79 673 g/g 186 g/L 0.342 mg/kg [9] F 80 Summary of Biological Effects Tissue Concentrations for Arsenic Species: Taxa Lepomis macrochirus, Bluegill Concentration, Units in1: Sediment Water Tissue (Sample Type) 0.52 mg/kg (whole body)4 Toxicity: Effects Mortality, NOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [13] L; no effect on mortality Micropterus salmoides Largemouth bass 673 g/g 186 g/L 0.083 mg/kg [9] F Perca flavescens Yellow perch 673 g/g 186 g/L 0.077 mg/kg [9] F Stizostedion vitreum 673 g/g vitreum, Walleye 1 2 3 4 186 g/L 0.080 mg/kg [9] F Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. BIOACCUMULATION SUMMARY ARSENIC References 1. Weast handbook of chemistry and physics, 68th edition, 1987-1988, B-73. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Woodward, D.F., W.G. Brumbaugh, A.J. DeLonay, E.E. Little, and C.E. Smith. 1994. Effects on rainbow trout fry of a metals-contaminated diet of benthic invertebrates from the Clark Fork River, Montana. Tran. Amer. Fish. Society 123:51-62. Jop, K.M., J. Bleiler, S. Reed, C. George, and A. Putt. 1995. Bioavailability of metals and toxicity identification evaluation of the sediment pore waters from Plow Shop Pond, Fort Devens, Massachusetts. Abstract, 16th Annual Meeting, Society of Environmental Toxicology and Chemistry, Vancouver, British Columbia, Canada, November 5-9, 1995. Bryan, G.W., and W.J. Langston. 1992. Bioavailability, accumulation and effects of heavy metals in sediments with special reference to United Kingdom estuaries: A review. Environ. Pollut. 76:89-131. Enserink, E.L., J.L. Mass-Diepeveen, and C.J. Van Leeuwen. 1991. Combined effects of metals; An ecotoxicological evaluation. Water Res. 25:679-687. Krantzberg, G. 1994. Spatial and temporal variability in metal bioavailability and toxicity of sediment from Hamilton Harbour, Lake Ontario. Environ. Toxicol. Chem. 13:1685-1698. Ingersoll, C.G., W.G. Brumbaugh, F.J. Dwuer, and N.E. Kemble. 1994. Bioaccumulation of metals by Hyalella azteca exposed to contaminated sediments from the Upper Clark Fork River, Montana. Environ. Toxicol. Chem. 13:2013-2020. Azcue, J.M., and D.G. Dixon. 1994. Effects of past mining activities on the arsenic concentration in fish from Moira Lake, Ontario. Internat. Assoc. Great Lakes Res. 20:717-724. 2. 3. 4. 5. 6. 7. 8. 9. 10. McGeachy, S.M., and D.G. Dixon. 1990. Effect of temperature on the chronic toxicity of arsenic to rainbow trout (Oncorhynchus mykiss). Can. J. Fish. Aquat. Sci. 47:2228-2234. 11. Lindsay, D.M., and J.G. Sanders. 1990. Arsenic uptake and transfer in a simplified estuarine food chain. Environ. Toxicol. Chem. 9:391-395. 12. Houkal, D., B. Rummel, and B. Shephard. 1996. Results of an in situ mussel bioassay in the Puget Sound. Abstract, 17th Annual Meeting, Society of Environmental Toxicology and Chemistry, Washington, DC, November 17-21, 1996. 81 BIOACCUMULATION SUMMARY ARSENIC 13. Barrows, M.E., S.R. Petrocelli, K.J. Macek, and J.J. Carroll. 1980. Bioconcentration and elimination of selected water pollutants by bluegill sunfish (Lepomis macrochirus). In Dynamics, exposure and hazard assessment of toxic chemicals, ed. R. Haque, pp. 379-392. 14. Dixon, D.G., and J.B. Sprague. 1981. Acclimation-induced changes in toxicity of arsenic and cyanide to rainbow trout, Salmo gairdneri Richardson. J. Fish Biol. 18: 579-589. 15. Mcgeachy, S.M., and D.G. Dixon. 1992. Whole-body arsenic concentrations in rainbow trout during acute exposure to arsenate. Ecotoxicol. Environ. Saf. 24:301-308. 16. Spehar, R.L., J.T. Fiandt, R.L. Anderson, and D.L. Defoe. 1980. Comparative toxicity of arsenic compounds and their accumulation in invertebrates and fish. Arch. Environm. Contam. Toxicol. 9: 53-63. 82 BIOACCUMULATION SUMMARY BENZO(A)ANTHRACENE Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight) Chemical Name (Common Synonyms): BENZO(A)ANTHRACENE CASRN: 56-55-3 Chemical Characteristics Solubility in Water: 0.014 mg/L at 25C [1] Log Kow: 5.70 [3] Half-Life: No data [2] Log Koc: 5.60 L/kg organic carbon Human Health Oral RfD: No data [4] Critical Effect: -- Oral Slope Factor (Reference): No data [4] Carcinogenic Classification: No data [4] Confidence: -- Wildlife Partitioning Factors: Partitioning factors for benzo(a)anthracene in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for benzo(a)anthracene in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Partitioning factors for benzo(a)anthracene in aquatic organisms were not found in the literature. Food Chain Multipliers: Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were 12.8 (all benthic food web), 1.4 (all pelagic food web), and 8.0 (benthic and pelagic food web). FCMs for trophic level 4 aquatic organisms were 20.2 (all benthic food web), 2.3 (all pelagic food web), and 10.2 (benthic and pelagic food web) [16]. Toxicity/Bioaccumulation Assessment Profile The acute toxicity of hydrocarbons, including benzo(a)anthracene, to both fresh and salt water crustaceans is largely nonselective, i.e., it is not primarily influenced by molecular structure, but is rather controlled by organism-water partitioning which, for nonpolar organic chemicals, is in turn a reflection 83 BIOACCUMULATION SUMMARY BENZO(A)ANTHRACENE of aqueous solubility. The toxic effect is believed to occur at a relatively constant concentration within the organism [5]. Toxicity of benzo(a)anthracene, as well as chrysene and pyrene, to striped bass (Morone saxatilis) decreased as water salinity increased [6]. Bioavailability of sediment-associated polynuclear aromatic hydrocarbons (PAHs), e.g., benzo(a)anthracene, has been observed to decline with increased contact time [7]. The majority of investigations have shown that aquatic organisms are able to release PAHs from their tissues rapidly when they were returned to a clean environment. Mussels exposed to contaminated sediment rapidly accumulated benzo(a)anthracene reaching maximum concentrations at day 20 [8]. The concentration factors for mussels exposed to 675 ng/g of benzo(a)anthracene in sediment ranged from 2,470 to 35,700 [4]. Benzo(a)anthracene was rapidly taken up by the aquatic plant, Fontinalis antipyretica and the uptake kinetics plateaued between 48 and 168 h of exposure [9]. Roy et al. [9] suggested that slow elimination of benzo(a)anthracene from the plant tissue may be due to low aqueous solubility. Sediment-associated benzo(a)anthracene can be accumulated from two sources: interstital water and ingested particles. The accumulation kinetics of benzo(a)anthracene suggest that uptake occurs via the sediment interstitial water and ingested material and is controlled by desorption from sediment particles and dissolved organic matter [10]. Benzo(a)anthracene after 24 h exposure was accumulated by Daphnia pulex mostly from the water, while lower-molecular-weight PAHs like napththalene and phenanthrene were accumulated primarily through algal food [11]. Bioaccumulation of low-molecular-weight PAHs from sediments by Rhepoxynius abronius (amphipod) and Armandia brevis (polychaete) was similar, however, a large difference in tissue concentration between these two species was measured for high-molecular-weight PAHs including benzo(a)anthracene [12]. Meador et al. [12] concluded that the low-molecular-weight PAHs were available to both species from interstitial water, while sediment ingestion was a much more important uptake route for the highmolecular-weight PAHs. The authors also indicated that bioavailability of the high-molecular-weight PAHs to amphipods was significantly reduced due to their partitioning to dissolved organic carbon. 84 Summary of Biological Effects Tissue Concentrations for Benzo(a)anthracene Species: Taxa Invertebrates Corbicula fluminea, 59 g/kg OC Asian clam 3,613 g/kg OC 508 g/kg lipid 1,049 g/kg lipid 8.643 0.290 [15] [15] F; %lipid = 0.61; %sed OC = 1.19 F; %lipid = 0.61; %sed OC = 1.19 Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Macoma nasuta, Clam 4.13 ng/g 6.19 ng/g 39.9 ng/g 39.5 ng/g 138 ng/g 146 ng/g 16.5 ng/g 6.1 ng/g 14 ng/g 11 ng/g 66 ng/g 53 ng/g -0.21 -0.82 -0.62 -0.68 -0.36 -0.32 [13] [13] [13] [13] [13] [13] F F F F F F Daphnia pulex, Cladoceran 5.27 g/L 1.6 ng/g 3.04 [11] L Pontoporeia hoyi, Amphipod 28 ng/g 72 ng/g [10] L 85 86 Summary of Biological Effects Tissue Concentrations for Benzo(a)anthracene Species: Taxa Fishes Leuciscus idus, Golden ide 17.5 mg/kg (whole body) Mortality, NOED [14] L; no effect on survivorship in 3 days Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 1 2 3 4 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. BIOACCUMULATION SUMMARY BENZO(A)ANTHRACENE References 1. USEPA. 1980. Ambient water quality criteria document: Polynuclear aromatic hydrocarbons. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long, 1995. Internal report on summary of measured, calculated, and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January. Abernethy, S., A.M. Bobra, W.Y. Shiu, P.G. Wells and D. Mackay. 1986. Acute lethal toxicity of hydrocarbons and chlorinated hydrocarbons to two planktonic crustaceans: The key role of organism-water partitioning. Aquatic Tox. 8:163-174. Palawski, D., J.B. Hunn, and F.J. Dwyer. 1985. Sensitivity of young striped bass to organic and inorganic contaminants in fresh and saline waters. Trans. Am. Fish. Soc. 114:748-753. Landrum, P.F., B.J. Eadie, and W.R. Faust. 1992. Variation in the bioavailability of polycyclic aromatic hydrocarbons to the amphipod Diporeia (spp.) with sediment aging. Environ. Toxicol. Chem. 11:1197-1208. Pruell, R.J., and J.G. Quinn. 1987. Availability of PCBs and PAHs to Mytilus edulis from artificially resuspended sediments. In Oceanic process in marine pollution, Vol. 1, ed. J.H. Capuzzo and D.R. Kester. Robert E. Kriger Publishing Co., Malabor, FL. Roy, S., J. Pellinen, C.K. Sen, and O. Hanninen. 1994. Benzo(a)anthracene and benzo(a)pyrene exposure in the aquatic plant Fontinalis antipyretica: Uptake, elimination, and the responses of biotransformation and antioxidant enzymes. Chemosphere 29:1301-1311. 2. 3. 4. 5. 6. 7. 8. 9. 10. Landrum, P.F. 1989. Bioavailability and toxicokinetics of polycyclic aromatic hydrocarbons sorbed to sediments for the amphipod Pontoporeia hoyi. Environ. Sci. Technol. 23:588-595. 11. Trucco, R.G., N.R. Engelhardt, and B. Stacey. 1983. Toxicity, accumulation, and clearance of aromatic hydrocarbons in Daphnia pulex. Environ. Pollut. 31:191-202. 87 BIOACCUMULATION SUMMARY BENZO(A)ANTHRACENE 12. Meador, J.P., E. Casillas, C.A. Sloan, and U. Varanasi. 1995. Comparative bioaccumulation of polycyclic aromatic hydrocarbons from sediments by two infaunal invertebrates. Mar. Ecol. Prog. Ser. 123:107-124. 13. Ferraro, S.P., H. Lee II, R.J. Ozretich, and D.T. Specht. 1990. Predicting bioaccumulation potential: A test of a fugacity-based model. Arch. Environ. Contam. Toxicol. 19:386-394. 14. Freitag, D., L. Ballhorn, H. Geyer and F. Korte. 1985. Environmental hazard profile of organic chemicals: An experimental method for the assessment of the behaviour of organic chemicals in the ecosphere by means of laboratory tests with 14C labelled chemicals. Chemosphere 14:1589-1616. 15. Pereira, W.E., J.L. Domagalski, F.D. Hostettler, L.R.Brown, and J.B. Rapp. 1996. Occurrence and accumulation of pesticides and organic contaminants in river sediment, water, and clam tissues from the San Joaquin River and Tributaries, California. Environ. Toxicol. Chem. 15: 172-180. 16. USEPA. 1998. Ambient water quality criteria derivation methodology: Human health. Technical support document. EPA-822-B-98-005. U.S. Environmental Protection Agency. Office of Water, Washington, DC. Final Draft. 88 BIOACCUMULATION SUMMARY BENZO(A)PYRENE Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight) Chemical Name (Common Synonyms): BENZO(A)PYRENE CASRN: 50-32-8 Chemical Characteristics Solubility in Water: 0.0038 mg/L at 25C [1] Half-Life: 5.7 d - 1.45 yrs based on aerobic soil die-away test data at 10-30C [2] Log Koc: 6.01 L/kg organic carbon Log Kow: 6.11 [3] Human Health Oral RfD: No Data [4] Critical Effect: Forestomach cancer in mice Oral Slope Factor: 7.3 x 10+0 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4] Confidence: -- Wildlife Partitioning Factors: Partitioning factors for benzo(a)pyrene in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for benzo(a)pyrene in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Partitioning factors for benzo(a)pyrene in aquatic organisms were not found in the literature. Food Chain Multipliers: Trophic tranfer of benzo(a)pyrene metabolites has been demonstrated between polychaetes and bottom-feeding fish [5]. The diatom Thalassiosira pseudonana cultured in 10 g/L of benzo(a)pyrene and subsequently fed to larvae of the hard clam Mercenaria mercenaria accumulated 42.2 g/g while clams accumulated only 18.6 g/g [6]. The rate of direct uptake by the algae was thus approximately 20 times faster than the rate of trophic transfer. Dobroski and Epifanio [6] concluded that direct uptake and trophic transfer (2 g/g/day) are equally important in accumulation of benzo(a)pyrene. Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were 18.5 (all benthic food web), 1.6 (all pelagic food web), and 11.3 (benthic and pelagic food web). FCMs for trophic level 4 aquatic organisms were 37.4 (all benthic food web), 3.1 (all pelagic food web), and 17.8 (benthic and pelagic food web) [42]. 89 BIOACCUMULATION SUMMARY Toxicity/Bioaccumulation Assessment Profile BENZO(A)PYRENE Bioavailability of sediment-associated polynuclear aromatic hydrocarbon (PAHs), including benzo(a)pyrene has been observed to decline with increased contact time [7]. Oikari and Kukkonene [8] established a relationship between dissolved organic matter including the percentage of hydrophobic acids and accumulation of benz(a)pyrene. They observed that the bioavailability of benzo(a)pyrene decreases in waters with dissolved organic carbon having more high-molecular-weight hydrophobic acids. The reduced bioavailability has been observed for benzo(a)pyrene accumulation from field-collected sediments compared with laboratory spiked sediments [9]. Mean accumulation of benzo(a)pyrene declined by a factor of three in Chironomus riparius exposed to sediment stored one week versus the sediment stored for eight weeks [10]. The concentrations of benzo(a)pyrene in whole sediment and pore water were 0.27-80.9 ng/g and 0.004-0.913 mg/mL, respectively [10]. Short-term exposures (24-h) to 1 mg/L benzo(a)pyrene averaged 8.27 nmol in fish tissue. Of this total, 67 percent was accumulated in the gallbladder or gut, indicating rapid metabolism and excretion [11]. The bioaccumulation of benzo(a)pyrene can be influenced by the lipid reserves [12]. In an experiment conducted by Clements et al. [13], chironomidae larvae rapidly accumulated benzo(a)pyrene from spiked sediment and tissue concentrations were directly proportional to sediment concentrations. However, the level of benzo(a)pyrene in bluegill that were fed contaminated chironomids was generally low, indicating either low uptake or rapid metabolism. According to McCarthy [14], accumulation of hydrophobic chemicals like benzo(a)pyrene in aqueous systems appears to depend on the amount of chemical in solution and on the amount sorbed to particles entering the food chain. Uptake and accumulation of benzo(a)pyrene was reduced by 97 percent due to sorption to organic matter [14]. Studies that report body burdens of the parent compound may, depending on the species, grossly underestimate total bioaccumulation of benzo(a)pyrene and their metabolites [15]. Kane-Driscoll and McElroy [15] concluded that the body burden of the parent compound may represent less than 10 percent of the actual total body burden of parent plus metabolites. The accumulation kinetics of benzo(a)pyrene suggest that uptake occurs largely via the sediment interstitial water and is controlled by desorption from sediment particles and dissolved organic matter [16]. Accumulation of benzo(a)pyrene from water was not affected by the simultaneous presence of naphthalene or PCB [17]. Kolok et al. [18] showed that the concentration of benzo(a)pyrene equivalents in shad (Dorosoma cepedianum) increases when the fish ventilate water turbid with benzo(a)pyrene spiked sediments. Also the turbid water, not sediment ingestion, appears to be a significant source of benzo(a)pyrene for gizzard shad. Bioaccumulation of low-molecular-weight PAHs from sediments by Rhepoxynius abronius (amphipod) and Armandia brevis (polychaete) was similar, however, a large difference in tissue concentration between these two species was measured for high-molecular-weight PAHs including benzo(a)pyrene [19]. Meador et al. [19] concluded that the low-molecular-weight PAHs were available to both species from interstitial water, while sediment ingestion was a much more important uptake route for the highmolecular-weight PAHs. The authors also indicated that bioavailability of the high-molecular-weight PAHs to amphipods was significantly reduced due to their partitioning to dissolved organic carbon. 90 Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene Species: Taxa Invertebrates Nereis diversicolor, Polychaeta worm 236.6 pmol/g 95.2 pmol/g [15] F Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Scolecolepides viridis, Polychaeta worm 184.2 pmol/g 119 pmol/g [15] F Leitoscoloplos fragilis, Polychaeta worm 475.8 pmol/g 3540 pmol/g [15] F Thais haemostoma, Snail BDL 1.45-3.89 g/kg [23] F Physa sp., Snail 3.39 g/L 259.6 g/kg [20] L Dreissena polymorpha, Zebra mussel 3.1 - 4.7 x 106 mg/g [12] L; depending on the lipid content Mytilus edulis, Mussel 91 3.2 mg/kg (whole body)4 Physiological, ED50 [30] L; 50% reduction in feeding, clearance rate, and tolerance to aerial exposure 92 Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.161 mg/kg (whole body)4 3.2 mg/kg (whole body)4 Physiological, LOED Physiological, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [30] L; elevated activity of superoxide dismutase (SOD) L; inhibition of superoxide dismutase (SOD) and catalase activity L, reduced gametogenesis, reproductive success rate [30] 3.2 mg/kg (whole body)4 Reproduction, LOED [30] Macoma nasuta, Clam 9.2 ng/g 50 ng/g -0.07 [12] F Macoma nasuta, Clam 4.7 ng/g 70 ng/g 99 ng/g 228 ng/g 440 ng/g 1.4 ng/g 22 ng/g 45 ng/g 62 ng/g 66 ng/g -1.30 -0.68 -0.48 -0.70 -0.70 [21] [21] [21] [21] [21] F F F F F Macomona liliana, Mollusc 3,533 g/kg OC 189.2 g/kg lipid 0.0536 [40] F, %lipid = 2.95; %sed OC = 0.30 Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene Species: Taxa Concentration, Units in1: Sediment 68,767 g/kg OC 2,864 g/kg OC 2,440 g/kg OC 1,021 g/kg OC Water Toxicity: Tissue (Sample Type) Effects 845.5 g/kg lipid 166.9 g/kg lipid 261.8 g/kg lipid 48.6g/kg lipid Ability to Accumulate2: Log BCF Log BAF BSAF 0.0123 0.0583 0.1073 0.0476 Source: Reference Comments3 [40] [40] [40] [40] F, %lipid = 2.33; %sed OC = 0.73 F, %lipid = 2.57; %sed OC = 0.22 F, %lipid = 2.04; %sed OC = 0.25 F, %lipid = 3.13; %sed OC = 0.48 Austrovenus 3,533 g/kg stutchburyi, Mollusc OC 68,767 g/kg OC 2,864 g/kg OC 2,440 g/kg OC 1,021 g/kg OC 19.2 g/kg lipid 24.6 g/kg lipid 18.8 g/kg lipid 14.5 g/kg lipid 11.0 g/kg lipid 0.0054 0.0004 0.0066 0.0059 0.0108 [40] [40] [40] [40] [40] F, %lipid = 5.62; %sed OC = 0.30 F, %lipid = 5.21; %sed OC = 0.73 F, %lipid = 4.85; %sed OC = 0.22 F, %lipid = 3.87; %sed OC = 0.25 F, %lipid = 4.27; %sed OC = 0.48 Sphaerium corneum, Fingernail Clam 1.25 mg/kg (whole body)4 Mortality, NOED [28] L; no effect on survivorship in 120 hours 93 94 Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 180.3 g/kg lipid 245.9 g/kg lipid Ability to Accumulate2: Log BCF Log BAF BSAF 2.146 0.039 Source: Reference Comments3 [41] [41] F, %lipid =0.61; %sed OC = 1.19 F, %lipid =0.61; %sed OC = 1.19 Corbicula fluminea, 84 g/kg Asian Clam OC 6,387 g/kg OC Mercenaria mercenaria, Quahog Clam, 0.00221 mg/kg (whole body)4 Physiological, LOED [27] L;impaired ability to clear flavobacterium, exp_conc = < 0.001 L; no effect on mortality, exp_conc = <0.001 0.00221 mg/kg (whole body)4 Mortality, NOED [27] Daphnia magna, Cladoceran 3.90 (without organic matter) [14] L Daphnia magna, Cladoceran 3.00 (with organic matter) [14] L Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene Species: Taxa Pontoporeia hoyi, Amphipod Concentration, Units in1: Sediment 15.5 ng/g 410 ng/g 40 ng/g 30 ng/g 3 ng/mL 3.5 ng/mL 2.2 ng/mL Water Toxicity: Tissue (Sample Type) Effects 32 ng/g 600 ng/g 400 ng/g 270 ng/g 4.74 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [16] [22] L L Chironomus riparius, Midge 3,920 g/kg 4,290 g/kg 4,035 g/kg 2,160 ng/L 1,680 ng/L 2,640 ng/L 720 g/kg 252 g/kg 720 g/kg [13] [13] [13] L L L Chironomus riparius, Midge 0.23 mg/kg (whole body)4 0.09 mg/kg (whole body)4 0.04 mg/kg (whole body)4 Behavior, NOED Behavior, NOED Behavior, NOED [38] [38] [38] L; no effect on swimming behavior L; no effect on swimming behavior L; no effect on swimming behavior Chironomus riparius, Midge 1.9 mg/kg (whole body)4 Mortality, NOED [28] L; no effect on survivorship in 120 hours Culex pipiens quinquefasciatus, Mosquito larva 3.39 g/L 73.1 g/kg [21] L 95 96 Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Asterias rubens, Starfish 37.8 mg/kg (pyloric caeca)4 40 mg/kg (whole body)4 2.15 mg/kg (pyloric caeca)4 13.2 mg/kg (pyloric caeca)4 2.5 mg/kg (whole body)4 10 mg/kg (whole body)4 0.5 mg/kg (whole body)4 10 mg/kg (whole body)4 2.5 mg/kg (whole body)4 Physiological, ED100 Physiological, ED100 Physiological, LOED Physiological, LOED Physiological, LOED Physiological, LOED Mortality, NOED Mortality, NOED Mortality, NOED [29] L; 346% induction of benzo(a)pyrene hydroxylase activity L; 346% induction of benzo(a)pyrene hydroxylase activity L; 200% induction of benzo(a)pyrene hydroxylase activity L; 200% induction of benzo(a)pyrene hydroxylase activity L; 200% induction of benzo(a)pyrene hydroxylase activity L; 200% induction of benzo(a)pyrene hydroxylase activity L; no effect on mortality L; no effect on mortality L; no effect on mortality [29] [29] [29] [29] [29] [29] [29] [29] Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 10 mg/kg (whole body)4 40 mg/kg (whole body)4 0.053 mg/kg (pyloric caeca)4 0.5 mg/kg (whole body)4 Mortality, NOED Mortality, NOED Physiological, NOED Physiological, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [29] [29] [29] L; no effect on mortality L; no effect on mortality L; no effect on benzo(a)pyrene hydroxylase activity L; no effect on benzo(a)pyrene hydroxylase activity [29] Fishes Poeciliopsis monoacha, Viviparius 3.96 mol/L 8.27 nmol 48-h LC50 3.75 mg/L [11] L Oncorhynchus mykiss (Salmo gairdneri), Rainbow trout 5 g/egg injection 32,090 cpm (egg) 25,448 cpm (fry) [24] L 14-day 21,839 cpm fry) 35-day 8,922 cpm (fry) 97 98 Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene Species: Taxa Oncorhynchus mykiss, Rainbow trout Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.35 mg/kg (whole body)4 30 mg/kg (whole body)4 12.3 mg/kg (whole body)4 Physiological, LOED Physiological, LOED Development, NA Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [34] [34] L; hepatic enzyme induction L; induction of hepatic mixed function oxidases L; gross abnormalities in alevins noted at all test concentrations 0.08 mg/L and above, significant increase relative to the control L; hatchability not significantly reduced L; hatchability not significantly reduced L; hatchability not significantly reduced L; hatchability not significantly reduced [35] 1.93 mg/kg (whole body)4 7.18 mg/kg (whole body)4 10.2 mg/kg (whole body)4 12.3 mg/kg (whole body)4 Reproduction, NA Reproduction, NA Reproduction, NA Reproduction, NA [35] [35] [35] [35] Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene Species: Taxa Cyprinus carpio, Common carp Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 155 mg/kg (liver)4 Physiological, NA Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [39] L; significant increase in EROD enzyme and P450 1A protein content Gambusia affinis, Mosquito fish 3.39 g/L 14.1 g/kg [20] L Lepomis macrochirus, Bluegill sunfish 1 g/L 39,000 ng/g (gall bladder) 4,600 ng/g (liver) 2,200 ng/g (viscera) 250 ng/g (brain) 370 ng/g (carcass) 4.15 [25] L 1 g/L 1 g/L 1 g/L 1 g/L 3.20 2.89 1.95 2.11 [25] [25] [25] [25] L L L L Dorosoma cepedianum, Gizzard shad 3.62 [18] L 99 100 Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene Species: Taxa Dorosoma cepedianum, Gizzard shad Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 10 mg/kg (whole body)4 Physiological, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [37] L; statistically significant, maximum (11x) induction of ethoxyresorufin-odeethylase (EROD) L; statistically significant induction of ethoxyresorufino-deethylase (EROD) L; statistically significant induction of ethoxyresorufino-deethylase (EROD) L; 10x induction of ethoxyresorufin-odeethylase (EROD) L; statistically significant induction of ethoxyresorufino-deethylase (EROD) 0.0289 mg/kg (whole body)4 Physiological, LOED [37] 0.0283 mg/kg (whole body)4 Physiological, LOED [37] 50 mg/kg (whole body)4 0.0257 mg/kg (whole body)4 Physiological, NA Physiological, NA [37] [37] Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.0265 mg/kg (whole body)4 Physiological, NA Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [37] L; statistically significant induction of ethoxyresorufino-deethylaste (EROD) L; no induction of ethoxyresorufin-odeethylase (EROD) L; no induction of ethoxyresorufin-odeethylase (EROD) L; no induction of ethoxyresorufin-odeethylase (EROD) L; no induction of ethoxyresorufin-odeethylase (EROD) L; no induction of ethoxyresorufin-odeethylase (EROD) L; no induction of ethoxyresorufin-odeethylase (EROD) 0.1 mg/kg (whole body)4 0.0337 mg/kg (whole body)4 0.0201 mg/kg (whole body)4 1 mg/kg (whole body)4 0.0239 mg/kg (whole body)4 0.0196 mg/kg (whole body)4 Physiological, NOED Physiological, NOED Physiological, NOED Physiological, NOED Physiological, NOED Physiological, NOED [37] [37] [37] [37] [37] [37] 101 102 Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene Species: Taxa Ictalurus punctatus, Channel catfish Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 100 mg/kg (whole body)4 Physiological, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [31] L; significant decrease in neurotransmitter levels L; five to six-fold induction of cytochrome P450 0.1 mg/kg (whole body)4 Physiological, LOED [32] Leuciscus idus, Golden ide 24 mg/kg (whole body)4 Mortality, NOED [33] L; no effect on survivorship in 3 days Citharichthys stigmaeus, Sand dab 3 g/L 130 ng/g (liver), 10 ng/g (gut), 400 ng/g (gill), 30 ng/g (flesh), 150 ng/g (heart) [25] L; accumulation within 1 h Psettichthys melanostictus, Sand sole 2.1 mg/kg (whole body)4 2.1 mg/kg (whole body)4 Reproduction, ED50 Development, LOED [36] L; reduced hatching success L; larval abnormalities [36] Summary of Biological Effects Tissue Concentrations for Benzo(a)pyrene Species: Taxa Oligocottus maculosus, Tidepool sculpins Concentration, Units in1: Sediment Water 0.5 g/L Toxicity: Tissue (Sample Type) Effects 120 ng/g (liver), 160 ng/g (gut), 200 ng/g (gill), 130 ng/g (flesh), 70 ng/g (heart) 1 2 3 4 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [25] L; accumulation within 1 h Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. 103 BIOACCUMULATION SUMMARY References 1. BENZO(A)PYRENE MacKay, D., and Shin Wy; J. Chem. Eng. Data 22:399 (1977). Weast handbook of chemistry and physics, 68th edition, 1987-1988, B-73. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual Chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long, 1995. Internal report on summary of measured, calculated, and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January. McElroy, A.E., and J.D. Sisson. 1989. Trophic transfer of benzo[a]pyrene metabolites between benthic marine organisms. Mar. Environ. Res. 28:265-269. Dobroski, C.J., Jr., and Epifanio. 1980. Accumulation of benzo[a]pyrene in a larval bivalve via trophic transfer. Can. J. Fish. Aquat. Sci. 37:2318-2322. Landrum, P.F., B.J. Eadie, and W.R. Faust. 1992. Variation in the bioavailability of polycyclic aromatic hydrocarbons to the amphipod Diporeia (spp.) with sediment aging. Environ. Toxicol. Chem. 11:1197-1208. Kukkonen, J.V.K., and P.F. Landrum. 1998. Effect of particle-xenobiotic contact time on bioavailablility of sediment-associated benzo(a)pyrene by benthic amphipod, Diporeia spp. Aquat. Toxicol. 42:229-242. Varanasi, U., W.L. Reichert, J.E. Stein, D.W. Brown, and H.R. Sanborn. 1985. Bioavailability and biotransformation of aromatic hydrocarbons in benthic organisms exposed to sediment from an urban estuary. Environ. Sci. Technol. 19:836-841. Harkey, G.A., P.F. Landrum, and S.J. Klaine. 1994. Comparison of whole-sediment, elutriate and pore-water exposures for use in assessing sediment-associated organic contaminants in bioassays. Environ. Toxicol. Chem. 13:1315-1329. 2. 3. 4. 5. 6. 7. 8. 9. 10. 104 BIOACCUMULATION SUMMARY 11. BENZO(A)PYRENE Goddard, K.A., R.J. Schultz, and J.J. Stegeman. 1987. Uptake, toxicity, and distribution of benzo[a]pyrene and monooxygenase induction in the topminnows Poeciliopsis monacha and Poeciliopsis lucida. Drug Metab. Disposition 15:449-455. Bruner, K.A., S.W. Fisher, and P.F. Landrum. 1994. The role of the zebra mussel, Dreissena polymorpha, in contaminant cycling: 1. The effect of body size and lipid content on the bioconcentration of PCBs and PAHs. Great Lakes Res. 20:725-734. Clements, W.H., J.T. Oris, and T.E. Wissing. 1993. Accumulation and food chain transfer of fluoranthene and benzo[a]pyrene in Chironomus riparius and Lepomis macrochirus. Arch. Environ. Contam. Toxicol. 26:261-266. McCarthy, J.F. 1983. Role of particulate organic matter in decreasing accumulation of polynuclear aromatic hydrocarbons by Daphnia magna. Arch. Environ. Contam. Toxicol. 12:559-568. Kane-Driscoll, S., and A.E. McElroy. 1996. Bioaccumulation and metabolism of benzo[a]pyrene in three species of polychaete worms. Environ. Toxicol. Chem. 15:1401-1410. Landrum, P.F. 1989. Bioavailability and toxicokinetics of polycyclic aromatic hydrocarbons sorbed to sediments for the amphipod Pontoporeia hoyi. Environ. Sci. Technol. 23:588-595. Fortner, A.R., and L.V. Sick. 1985. Simultaneous accumulations of naphthalene, a PCB mixture and benzo(a)pyrene by the oyster, Crassostrea virginica. Bull. Environ. Contam. Toxicol. 34:256264. Kolok A.S., J.N. Huckins, J.D. Petty, and J.T. Oris. 1996. The role of water ventilation and sediment ingestion in the uptake of benzo(a)pyrene in gizzard shad (Dorsoma cepedianum). Environ. Toxicol. Chem. 15:1752-1759. Meador, J.P., E. Casillas, C.A. Sloan, and U. Varanasi. 1995. Comparative bioaccumulation of polycyclic aromatic hydrocarbons from sediments by two infaunal invertebrates. Mar. Ecol. Prog. Ser. 123: 107-124. Po-Yung, L, R.L. Metcalf, N. Plummer, and D. Mandel. 1977. The environmental fate of three carcinogens: Benzo-(a)-pyrene, benzidine, and vinyl chloride evaluated in laboratory model ecosystems. Arch. Environm. Contam. Toxicol. 6:129-142. Ferraro, S.P., H.Lee II, R.J. Ozretich, and D.T.Specht. 1990. Predicting bioaccumulation potential: A test of a fugacity-based model. Arch. Environ. Contam. Toxicol. 19:386-394. Eadie, B.J., P.F. Landrum, and W.Faust. 1982. Polycyclic aromatic hydrocarbons in sediments, pore water and the amphipod Pontoporeia hoyi from Lake Michigan. Chemosphere 11:847-858. Rostad, C.E., and W.E. Pereira. 1987. Creosote compounds in snails obtained from Pensacola Bay, Florida, near an onshore hazardous-waste site. Chemosphere 16:2397-2404. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 105 BIOACCUMULATION SUMMARY 24. BENZO(A)PYRENE Black, J.J., E. Maccubbin, and C.J. Johnston. 1988. Carcinogenicity of benzo[a]pyrene in rainbow trout resulting from embryo microinjection. Aquatic Tox. 13:297-308. Lee, R.F., and G.H. Dobbs. 1972. Uptake, metabolism and discharge of polycyclic aromatic hydrocarbons by marine fish. Mar. Biol. 17:201-208. Spacie, A., P.F. Landrum, and G.J. Leversee. 1983. Uptake, depuration, and biotransformation of anthracene and benzo[a]pyrene in blugill sunfish. Ecotox. Environ. Saf. 7:330-341. Anderson, R.S., C.S. Giam, L.E. Ray, and M.R. Tripp. 1981. Effects of environmental pollutants on immunological competency of the clam Mercenaria mercenaria: Impaired bacterial clearance. Aquat. Toxicol. 1:187-195. Borchert, J., L. Karbe, and J. Westendorf. 1997. Uptake and metabolism of benzo(a)pyrene absorbed to sediment by the freshwater invertebrate species Chironomus riparius and Sphaerium corneum. Bull. Environ. Contam. Toxicol. 58:158-165. Den Besten, P.J., P. Lemaire, D.R. Livingstone, B. Woodin, J.J. Stegeman, H.J. Herwin, and W. Seinen. 1993. Time-course and dose-response of the apparent induction of the cytochrome P450 monooxygenase system of pyloric caeca microsomes of the female sea star Asterias rubens L. by benzo[a]pyrene and polychlorinated biphenyls. Aquat. Toxicol. 26:23-40. Eertman, R.H.M., C.L. Groenink, B. Sandee, and H. Hummel. 1995. Response of the blue mussel Mytilus edulis L. following exposure to PAHs or contaminated sediment.. Mar. Environ. Res. 39:169-173. Fingerman, S., and E.C. Short, Jr. 1983. Changes in neurotransmitter levels in channel catfish after exposure to benzo(a)pyrene, naphthalene, and Aroclor 1254. Bull. Environ. Contam. Toxicol. 30:147-151. Fingerman, S.W., L.A. Brown, M. Lynn, and E.C. Short, Jr. 1983. Responses of channel catfish to xenobiotics: Induction and partial characterization of a mixed function oxygenase. Arch. Environ. Contam. Toxicol. 12:195-201. Freitag, D., L. Ballhorn, H. Geyer and F. Korte. 1985. Environmental hazard profile of organic chemicals: An experimental method for the assessment of the behaviour of organic chemicals in the ecosphere by means of laboratory tests with 14C labelled chemicals. Chemosphere 14:15891616. Gerhart, E.H., and R.H. Carlson. 1978. Hepatic mixed-function oxidase activity in rainbow trout exposed to several polycyclic aromatic hydrocarbons. Environ. Res. 17:284-295. Hannah, J.B., J.E. Hose, M.L. Landolt, B.S. Miller, S.P. Felton, and W.T. Iwaoka. 1982. Benzo(a)pyrene-induced morphologic and developmental abnormalities in rainbow trout. Arch. Environm. Contam. Toxicol. 11:727-734. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 106 BIOACCUMULATION SUMMARY 36. BENZO(A)PYRENE Hose, J.E., J.B. Hannah, D. Dijulio, M.L. Landolt, B.S. Miller, W.T. Iwaoka, and S.P. Felton. 1982. Effects of benzo(a)pyrene on early development in flatfish. Arch. Environ. Contam. Toxicol. 11:167-171. Levine, S.L., J.T. Oris, and T.E. Wissing. 1994. Comparison of P-450a1 monooxygenase induction in gizzard shad (Dorosoma cepedianum) following intraperitoneal injection or continuous waterborne-exposure with benzo[a]pyrene: Temporal and dose-dependent studies. Aquat. Toxicol. 30:61-75. Lydy, M.J., K.A. Bruner, D.M. Fry, and S.W. Fisher. 1990. Effects of sediment and the route of exposure on the toxicity and accumulation of neutral lipophilic and moderately water soluble metabolizable compounds in the midge, Chironomus riparius. In Aquatic toxicology and risk assessment, Vol. 13, ed. W.G. Landis, et.al., pp. 140-164. American Society for Testing and Materials, Philadelphia, PA. Van Der Weidern, M.E.J., F.H.M. Hanegraaf, M.L. Eggens, M. Celander, W. Seinen, and M. Ven Den Berg. 1994. Temporal induction of cytochrome P450 1a in the mirror carp (Cyprinus carpio) after administration of several polycyclic aromatic hydrocarbons. Environ. Toxicol. Chem. 13: 797802. Hickey, C.W., D.S. Roper, P.T. Holland, and T.M. Trower. 1995. Accumulation of organic contaminants in two sediment-dwelling shellfish with contrasting feeding modes: Deposit (Macomona liliana) and filter-feeding (Austovenus stutchburi). Arch. Environ. Contam. Toxicol. 11:221-231. Pereira, W.E., J.L. Domagalski, F.D. Hostettler, L.R. Brown, and J.B. Rapp. 1996. Occurrence and accumulation of pesticides and organic contaminants in river sediment, water, and clam tissues from the San Joaquin River and tributaries, California. Environ. Toxicol. Chem. 15:172-180. USEPA. 1998. Ambient water quality criteria derivation methodology: Human health. Technical support document. EPA-822-B-98-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. Final Draft. 37. 38. 39. 40. 41. 42. 107 108 BIOACCUMULATION SUMMARY BENZO(B)FLUORANTHENE Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight) Chemical Name (Common Synonyms): BENZO(B)FLUORANTHENE CASRN: 205-99-2 Chemical Characteristics Solubility in Water: 0.0012 mg/L [1] Half-Life: 360 days - 1.67 yrs based on aerobic soil die-away test data [2] Log Koc: 6.09 L/kg organic carbon Log Kow: 6.20 [3] Human Health Oral RfD: No data [4] Critical Effect: -- Oral Slope Factor (Reference): No data [4] Carcinogenic Classification: No data [4] Confidence: -- Wildlife Partitioning Factors: Partitioning factors for benzo(b)fluoranthene in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for benzo(b)fluoranthene in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Partitioning factors for benzo(b)fluoranthene in aquatic organisms were not found in the literature. Food Chain Multipliers: Food chain multipliers for benzo(b)fluoranthene in aquatic organisms were not found in the literature. Toxicity/Bioaccumulation Assessment Profile The acute toxicity of hydrocarbons, including benzo(b)fluoranthene, to both fresh and salt water crustaceans is largely nonselective, i.e., it is not primarily influenced by molecular structure, but is rather controlled by organism-water partitioning which, for nonpolar organic chemicals, is in turn a reflection of aqueous solubility. The toxic effect is believed to occur at a relatively constant concentration within the organism [5]. 109 BIOACCUMULATION SUMMARY BENZO(B)FLUORANTHENE Bioavailability of sediment-associated polynuclear aromatic hydrocarbons (PAHs), e.g., benzo(b)fluoranthene, has been observed to decline with increased contact time [6]. The majority of investigations have shown that aquatic organisms are able to release PAHs from their tissues rapidly when they were returned to a clean environment. The apparent effects threshold concentration of 4,500 ng/g was established for benzo(b)fluoranthene based on effects observed in the marine amphipod Rhepoxynius abronius [7]. Bioaccumulation of low- molecular-weight PAHs from sediments by Rhepoxynius abronius (amphipod) and Armandia brevis (polychaete) was similar, however, a large difference in tissue concentration between these two species was measured for high-molecular-weight PAHs including benzo(b)fluoranthene [8]. Meador et al. [8] concluded that the low-molecular-weight PAHs were available to both species from interstitial water, while sediment ingestion was a much more important uptake route for the high-molecular-weight PAHs. The authors also indicated that bioavailability of the high-molecular-weight PAHs to amphipods was significantly reduced due to their partitioning to dissolved organic carbon. 110 Summary of Biological Effects Tissue Concentrations for Benzo(b)fluoranthene Species: Taxa Invertebrates Crassostrea virginica, Oyster 18 ng/g 2.9 ng/g 9.9 ng/g 18 ng/g 27 ng/g 40 ng/g [9] [9] [9] F F F Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Diporeia spp, Amphipod 1 2 3 27 nmol/g 321 nmol/g [6] L Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 111 BIOACCUMULATION SUMMARY BENZO(B)FLUORANTHENE References 1. Sims, R.C., and M.R. Overcash. Res. Rev. 88:1-68 (1983). (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January. Abernethy, S., A.M. Bobra, W.Y. Shiu, P.G. Wells, and D. MacKay. 1986. Acute lethal toxicity of hydrocarbons and chlorinated hydrocarbons to two planktonic crustaceans: The key role of organism-water partitioning. Aquat. Tox. 8:163-174. Landrum, P.F., B.J. Eadie, and W.R. Faust. 1992. Variation in the bioavailability of polycyclic aromatic hydrocarbons to the amphipod Diporeia (spp.) with sediment aging. Environ. Tox. Chem. 11:1197-1208. Ingersoll, C.G., and M.K. Nelson. 1990. Testing sediment toxicity with Hyalella azteca (Amphipoda) and Chironomus riparius (Diptera). In Aquatic toxicology and risk assessment: ASTM STP 1096, ed. W.G. Landis and W.H. van der Schalie, pp. 93-109. American Society for Testing and Materials, Philadelphia, PA. Meador, J.P., E. Casillas, C.A. Sloan, and U. Varanasi. 1995. Comparative bioaccumulation of polycyclic aromatic hydrocarbons from sediments by two infaunal invertebrates. Mar. Ecol. Prog. Ser. 123:107-124. Sanders, M. 1995. Distribution of polycyclic aromatic hydrocarbons in oyster (Crassostrea virginica) and surface sediment from two estuaries in South Carolina. Arch. Environ. Contam. Toxicol. 28:397-405. 2. 3. 4. 5. 6. 7. 8. 9. 112 BIOACCUMULATION SUMMARY BENZO(G,H,I)PERYLENE Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight) Chemical Name (Common Synonyms): BENZO(G,H,I)PERYLENE CASRN: 191-24-2 Chemical Characteristics Solubility in Water: Insoluble in water [1] Half-Life: 590 d - 650 days based on aerobic soil die-away test data at 30. [2] Log Koc: 6.59 L/kg organic carbon Log Kow: 6.70 [3] Human Health Oral RfD: No data [4] Critical Effect: -- Oral Slope Factor (Reference): No data [4] Carcinogenic Classification: No data [4] Confidence: -- Wildlife Partitioning Factors: Partitioning factors for benzo(g,h,i)perylene in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for benzo(g,h,i)perylene in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Partitioning factors for benzo(g,h,i)perylene in aquatic organisms were not found in the literature. Food Chain Multipliers: An ecotoxicological in situ study conducted at the Baltic Sea, showed that the tissue residue concentration of benzo(g,h,i)perylene decreased with increasing trophic level [5]. The relatively high theoretical flux through the food chain was not possible to detect. 113 BIOACCUMULATION SUMMARY BENZO(G,H,I)PERYLENE Toxicity/Bioaccumulation Assessment Profile The acute toxicity of hydrocarbons, including benzo(g,h,i)perylene, to both fresh and salt water crustaceans is largely nonselective, i.e., it is not primarily influenced by molecular structure, but is rather controlled by organism-water partitioning which, for nonpolar organic chemicals, is in turn a reflection of aqueous solubility. The toxic effect is believed to occur at a relatively constant concentration within the organism [5]. The majority of investigations have shown that aquatic organisms are able to release polynuclear aromatic hydrocarbons (PAHs), e.g., benzo(g,h,i)perylene, from their tissues rapidly when they were returned to clean environment. Tanacredl and Cardenas [6] reported that Mercenaria mercenaria exposed to PAHs accumulated them to high levels in their tissues and failed to release them when returned to clean seawater over the 45-day depuration period. Unlike other marine organisms, this "sequestering" in molluscs may support the apparent inability to metaboilize PAHs to more water soluble and thus easily secreted polar metabolites. Bioaccumulation of low-molecular-weight PAHs from sediments by Rhepoxynius abronius (amphipod) and Armandia brevis (polychaete) was similar; however, a large difference in tissue concentration between these two species was measured for high-molecular-weight PAHs including benzo(g,h,i)perylene [7]. Meador et al. [7] concluded that the low-molecular-weight PAHs were available to both species from interstitial water, while sediment ingestion was a much more important uptake route for the highmolecular-weight PAHs. The authors also indicated that bioavailability of the high-molecular-weight PAHs to amphipods was significantly reduced due to their partitioning to dissolved organic carbon. 114 Summary of Biological Effects Tissue Concentrations for Benzo(g,h,i)perylene Species: Taxa Invertebrates Mytilus edulis, Mussels Crassostrea virginica, Oyster 0.4 ng/g 122.1 ng/g 31.1 ng/g 75.1 ng/g 5.4 ng/g 5.7 ng/g 6.2 ng/g 6.7 ng/g 0.4 ng/g 16.1 ng/g Pontoporeia hoyi, Amphipod Fishes Cyprinus carpio, Common carp 29.6 mg/kg (liver)4 Physiological, NOED [11] L; no significant increase in EROD enzyme and P450 1a protein content 400 ng/g 5 ng/mL 13 ng/g [8] F Concentration, Units in1: Sediment Water Tissue (Sample Type) Toxicity: Effects Ability to Accumulate2: Log BCF Log BAF Source: BSAF Reference Comments3 10 ng/g 16 ng/g 27 ng/g 12 ng/g 14 ng/g 18 ng/g 10 ng/g 10 ng/g 10 ng/g 16 ng/g BDL [10] [10] [10] [10] [10] [10] [10] [10] [10] [10] [9] F F F F F F F F F L 115 116 Species: Taxa Sediment Wildlife Somateria mollissima, Eider duck 1 2 3 4 Summary of Biological Effects Tissue Concentrations for Benzo(g,h,i)perylene Concentration, Units in1: Water Tissue (Sample Type) Toxicity: Effects Ability to Accumulate2: Log BCF Log BAF Source: BSAF Reference Comments3 2 ng/g [8] F Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. BIOACCUMULATION SUMMARY BENZO(G,H,I)PERYLENE References 1. Pearlman, R.S. et al. J. Phys. Chem. Ref. Data 13: 555-562 (1984) as cited in USEPA, Health and Environmental Effects Profile for Benzo(ghi)perylene, p.1 (1987) EPA/600/x-87/395. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Manual chemicals. Draft. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 10. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and recommended log Kow values. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10, draft. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January. Abernethy, S., A.M. Bobra, W.Y. Shiu, P.G.Wells, and D. MacKay. 1986. Acute lethal toxicity of hydrocarbons and chlorinated hydrocarbons to two planktonic crustaceans: The key role of organism-water partitioning. Aquatic Tox. 8:163-174. Tanacredl, J.T., and R.R. Cardenas. 1991. Biodepuration of polynuclear aromatic hydrocarbons from a bivalve mollusc Mercenaria mercenaria L. Environ. Sci. Technol. 25:1453-1461. Meador, J.P., E.Casillas, C.A. Sloan, and U. Varanasi. 1995. Comparative bioaccumulation of polycyclic aromatic hydrocarbons from sediments by two infaunal invertebrates. Mar. Ecol. Prog. Ser. 123:107-124. Broman, D., C. Naf, I. Lundbergh, and Y. Zebuhr. 1990. An in situ study on the distribution, biotransformation and flux of polycyclic aromatic hydrocarbons (PAHs) in an aquatic food chain (seston-Mytilus edulis L - Somateria mollissima L.) from the Baltic: An ecotoxicological perspective. Environ. Tox. Chem. 9:429-442. Eadie, B.J., P.F. Landrum, and W. Faust. 1982. Polycyclic aromatic hydrocarbons in sediments, pore water and the amphipod Pontoporeia hoyi from Lake Michigan. Chemosphere 11:847-858. Sanders, M. 1995. Distribution of polycyclic aromatic hydrocarbons in oyster (Crassostrea virginica) and surface sediment from two estuaries in South Carolina. Arch. Environ. Contam. Toxicol. 28:397-405. 2. 3. 4. 5. 6. 7. 8. 9. 10. 117 BIOACCUMULATION SUMMARY 11. BENZO(G,H,I)PERYLENE Van Der Weidern, M.E.J., F.H.M. Hanegraaf, M.L. Eggens, M. Celander, W. Seinen, and M. Ven Den Berg. 1994. Temporal induction of cytochrome P450 1a in the mirror carp (Cyprinus carpio) after administration of several polycyclic aromatic hydrocarbons. Environ. Toxicol. Chem. 13: 797-802. 118 BIOACCUMULATION SUMMARY BENZO(K)FLUORANTHENE Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight) Chemical Name (Common Synonyms): BENZO(K)FLUORANTHENE CASRN: 207-08-9 Chemical Characteristics Solubility in Water: Insoluble in water [1] Half-Life: 2.49 yrs - 5.86 yrs based on aerobic soil die-away test data [2] Log Koc: 6.09 L/kg organic carbon Log Kow: 6.20 [3] Human Health Oral RfD: No data [4] Critical Effect: -- Oral Slope Factor (Reference): Not available [4] Carcinogenic Classification: B2 [4] Confidence: -- Wildlife Partitioning Factors: Partitioning factors for benzo(k)fluoranthene in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for benzo(k)fluoranthene in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: The only partitioning factors for benzo(k)fluoranthene in aquatic organisms found in the literature were log BAFs of -0.68 to 0.01 for the clam Macoma nasuta [9]. Food Chain Multipliers: An ecotoxicological in situ study conducted at the Baltic Sea [5] showed that the tissue residue concentration of benzo(k)fluoranthene decreased with increasing trophic level. The relatively high theoretical flux through the food chain was not possible to detect. Toxicity/Bioaccumulation Assessment Profile The acute toxicity of hydrocarbons, including benzo(k)fluoranthene, to both fresh and salt water crustaceans is largely nonselective, i.e., it is not primarily influenced by molecular structure, but is rather controlled by organism-water partitioning which, for nonpolar organic chemicals, is in turn a reflection 119 BIOACCUMULATION SUMMARY BENZO(K)FLUORANTHENE of aqueous solubility. The toxic effect is believed to occur at a relatively constant concentration within the organism [6]. The majority of investigations have shown that aquatic organisms are able to release polynuclear aromatic hydrocarbons (PAHs), e.g., benzo(k)fluoranthene, from their tissues rapidly when they were returned to clean environment. The apparent effects threshold concentration of 4500 ng/g for benzo(k)fluoranthene was established based on effects observed in the marine amphipod Rhepoxynius abronius [7]. Bioaccumulation of low-molecular-weight PAHs from sediments by Rhepoxynius abronius (amphipod) and Armandia brevis (polychaete) was similar, however, a large difference in tissue concentration between these two species was measured for high-molecular-weight PAHs including benzo(k)fluoranthene [8]. Meador et al. [8] concluded that the low-molecular-weight PAHs were available to both species from interstitial water, while sediment ingestion was a much more important uptake route for the high-molecular-weight PAHs. The authors also indicated that bioavailability of the high-molecular-weight PAHs to amphipods was significantly reduced due to their partitioning to dissolved organic carbon. 120 121 Species: Taxa Invertebrates Mytilus edulis, Blue mussel Crassostrea virginica, Eastern oyster Sediment 1.5 ng/g 36 ng/g 59.6 ng/g 127.5 ng/g Macoma nasuta, 14.1 ng/g Clam 17 ng/g 121 ng/g 156 ng/g 390 ng/g 610 ng/g Wildlife Somateria mollissima, Eider duck 1 2 3 4 Summary of Biological Effects Tissue Concentrations for Benzo(k)fluoranthene Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 44 ng/g Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference [5] Comments3 F 14 ng/g 85 ng/g 65 ng/g 61 ng/g 92 ng/g 24 ng/g 59 ng/g 87 ng/g 128 ng/g 96 ng/g 0.009 or 0.01 -0.66 -0.48 -0.39 -0.51 -0.68 [10] [10] [10] F F F [9] [9] [9] [9] [9] [9] F F F F F F 4.3 ng/g [5] F Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. BIOACCUMULATION SUMMARY BENZO(K)FLUORANTHENE References 1. Weast handbook of chemistry and physics, 60th edition, 1979, C-180. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January. Broman, D., C. Naf, I. Lundbergh, and Y. Zebuhr. 1990. An in situ study on the distribution, biotransformation and flux of polycyclic aromatic hydrocarbons (PAHs) in an aquatic food chain (seston-Mytilus edulis L - Somateria mollissima L.) from the Baltic: An ecotoxicological perspective. Environ. Toxicol. Chem. 9:429-442. Abernethy, S., A.M. Bobra, W.Y. Shiu, P.G.Wells, and D. MacKay. 1986. Acute lethal toxicity of hydrocarbons and chlorinated hydrocarbons to two planktonic crustaceans: The key role of organism-water partitioning. Aquat. Tox. 8:163-174. Ingersoll, C.G., and M.K. Nelson. 1990. Testing sediment toxicity with Hyalella azteca (Amphipoda) and Chironomus riparius (Diptera). In Aquatic Toxicology and Risk Assessment: ASTM STP 1096, ed. W.G. Landis and W.H. van der Schalie, pp. 93-109. American Society for Testing and Materials, Philadelphia, PA. Meador, J.P., E. Casillas, C.A. Sloan, and U. Varanasi. 1995. Comparative bioaccumulation of polycyclic aromatic hydrocarbons from sediments by two infaunal invertebrates. Mar. Ecol. Prog. Ser. 123:107-124. Ferraro, S.P., H. Lee II, R.J. Ozretich, and D.T. Specht. 1990. Predicting bioaccumulation potential: A test of a fugacity-based model. Arch. Environ. Contam. Toxicol. 19:386-394. Sanders, M. 1995. Distribution of polycyclic aromatic hydrocarbons in oyster (Crassostrea virginica) and surface sediment from two estuaries in South Carolina. Arch. Environ. Contam. Toxicol. 28:397-405. 2. 3. 4. 5. 6. 7. 8. 9. 10. 122 BIOACCUMULATION SUMMARY Chemical Category: METAL (Divalent) Chemical Name (Common Synonyms): CADMIUM CADMIUM CASRN: 7440-43-9 Chemical Characteristics Solubility in Water: Insoluble [1] Log Kow: Half-Life: Not applicable, stable [1] Log Koc: Human Health Oral RfD: 5 x 10-4 mg/kg-day [2] Confidence: High, uncertainty factor = 10 Critical Effect: Significant proteinuria, presence of protein in urine Oral Slope Factor: Not available [2] Carcinogenic Classification: B1 [2] Wildlife Partitioning Factors: Partitioning factors for cadmium in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for cadmium in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Cadmium in the water column can partition to dissolved and particulate organic carbon. The more important issues related to water column concentrations of cadmium are water hardness (i.e., calcium concentration), pH, and metal speciation since the divalent cadmium ion is believed to be responsible for observed biological effects. Cadmium speciation yields primarily the divalent form of the metal, Cd+2, between pH values of 4.0 and 7.0 [3]. In addition, the concentration of acid-volatile sulfides is known to be an important factor controlling the toxicity and bioaccumulation of cadmium in sediments. Food Chain Multipliers: Most studies reviewed contained data which suggest that cadmium is not a highly mobile element in aquatic food webs, and there appears to be little evidence to support the general occurrence of biomagnification of cadmium within marine or freshwater food webs [4,5,6,7]. 123 BIOACCUMULATION SUMMARY Toxicity/Bioaccumulation Assessment Profile CADMIUM Cadmium does not appear to be a highly mobile element under typical conditions in most aquatic habitats [4]. Additional studies reviewed by Kay [4] indicated that no maternal transfer of cadmium was observed in zebrafish and that the cadmium content of bird eggs did not appear to be a good indicator of environmental exposure to cadmium. Tissue residue-toxicity relationships can also be variable because organisms might sequester metal in various forms that can be analytically measurable as tissue residue but might actually be stored in unavailable forms within the organism as a form of detoxification [8]. Whole body residues might also not be indicative of effects concentrations at the organ level because concentrations in target organs, such as the kidneys and liver, may be 20 times higher than whole body residues [9]. The application of "clean" chemical analytical and sample preparation techniques is also critical in the measurement of metal tissue residues. After evaluating the effects of sample preparation techniques on measured concentrations of metals in the edible tissue of fish, Schmitt and Finger [10] concluded that there was little direct value in measuring copper, zinc, iron, or manganese tissue residues in fish because they do not bioaccumulate to any appreciable extent. Cadmium and lead were the only ones found to be of potential concern in edible fish tissue based on the results from Schmitt and Finger's study of "clean" chemical techniques, although Wiener and Stokes [11] suggested that cadmium did not generally accumulate to any appreciable extent in the edible muscle tissue of fish. Rule and Alden [26] studied the relationship between uptake of cadmium and copper from the sediment by the blue mussel (Mytilus edulis), grass shrimp (Palaemonetes pugio), and hard clam (Mercenaria mercenaria). The uptake of cadmium by the blue mussel significantly increased as a function of increasing cadmium concentration in sediment. However, the uptake of cadmium increased when copper was added to the sediments. The uptake of cadmium by the grass shrimp exhibited a pattern similar to that of the mussel, while the uptake of cadmium by the hard clam was low compared to the other two species and related only to the cadmium concentration in sediment. The experiments performed by Meador [28] revealed that the response of the amphipods Rhepoxynius abronius and Eohaustorius estuarius to cadium decreased two- to threefold for animals held in the laboratory for several weeks compared to organisms recently collected from the field. 124 Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Plants Scenedesmus obliquus, Freshwater colonial green algae 2,340 mg/kg (whole body)5 Growth, LOED [31] L; significant inhibition of growth (27% reduction from control) L; 39% reduction in population growth from controls L; no significant inhibition of growth Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference Comments3 658 mg/kg (whole body)5 Growth, LOED [31] 3,030 mg/kg (whole body)5 Growth, NOED [31] Eichhornia crassipes, Water hyacinth 11.4 mg/kg (leaf)5 Growth, LOED Growth, LOED Growth, LOED [47] F; reduced growth rate, chlorosis F; reduced growth rate, chlorosis F; reduced growth rate, chlorosis 262 mg/kg (root)5 [47] 49.6 mg/kg (stem)5 [47] 125 126 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 11.4 mg/kg (leaf)5 Morphology, LOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [47] Comments3 F; chlorosis, browning, necrosis, waterlogging of tissues F; chlorosis, browning, necrosis, waterlogging of tissues F; chlorosis, browning, necrosis, waterlogging of tissues F; reduced growth rate, chlorosis F; reduced growth rate, chlorosis F; reduced growth rate, chlorosis F; reduced growth rate, chlorosis 262 mg/kg (root)5 Morphology, LOED [47] 49.6 mg/kg (stem)5 Morphology, LOED [47] 20.8 mg/kg (leaf)5 Growth, NA [47] 45.8 mg/kg (leaf)5 Growth, NA [47] 578 mg/kg (root)5 Growth, NA [47] 1,300 mg/kg (root)5 Growth, NA [47] Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 84.8 mg/kg (stem)5 Growth, NA Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [47] Comments3 F; reduced growth rate, chlorosis F; reduced growth rate, chlorosis F; chlorosis, browning, necrosis, waterlogging of tissues F; chlorosis, browning, necrosis, waterlogging of tissues F; chlorosis, browning, necrosis, waterlogging of tissues F; chlorosis, browning, necrosis, waterlogging of tissues 159 mg/kg (stem)5 Growth, NA [47] 20.8 mg/kg (leaf)5 Morphology, NA [47] 45.8 mg/kg (leaf)5 Morphology, NA [47] 578 mg/kg (root)5 Morphology, NA [47] 1,300 mg/kg (root)5 Morphology, NA [47] 127 128 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 84.8 mg/kg (stem)5 Morphology, NA Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [47] Comments3 F; chlorosis, browning, necrosis, waterlogging of tissues F; chlorosis, browning, necrosis, waterlogging of tissues F; no effect on growth F; no effect on growth F; no effect on growth F; no effect on plant appearance F; no effect on plant appearance F; no effect on plant appearance 159 mg/kg (stem)5 Morphology, NA [47] 8 mg/kg (leaf)5 142 mg/kg (root)5 27.8 mg/kg (stem)5 8 mg/kg (leaf)5 Growth, NOED Growth, NOED Growth, NOED Morphology, NOED Morphology, NOED Morphology, NOED [47] [47] [47] [47] 142 mg/kg (root)5 [47] 27.8 mg/kg (stem)5 [47] Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Invertebrates Lumbriculus variegatus, Oligochaete 670 mg/kg (whole body)5 310 mg/kg (whole body)5 Mortality, LOED Mortality, NOED [32] L; 40% mortality L; no effect on mortality Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference Comments3 [32] Najas quadulepensis, Southern naiad 10.3 mg/kg (whole body)5 Development, LOED [35] L; reductions in chlorophyll and stolon development Neanthes arenaceodentata, Polychaete 67 mg/kg (whole body)5 67 mg/kg (whole body)5 Reproduction, ED100 Behavior, LOED [46] L; reproductive failure L; reduced tube building, sluggish behavior L; no effect on behavior L; no effect on behavior L; no effect on behavior [46] 4.5 mg/kg (whole body)5 0.22 mg/kg (whole body)5 0.028 mg/kg (whole body)5 129 Behavior, NOED Behavior, NOED Behavior, NOED [46] [46] [46] 130 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.0028 mg/kg (whole body)5 67 mg/kg (whole body5 4.5 mg/kg (whole body)5 0.22 mg/kg (whole body)5 0.028 mg/kg (whole body )5 0.0028 mg/kg (whole body)5 4.5 mg/kg (whole body)5 0.22 mg/kg (whole body)5 0.028 mg/kg (whole body)5 0.0028 mg/kg (whole body)5 Behavior, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [46] [46] [46] [46] [46] [46] [46] [46] [46] [46] Comments3 L; no effect on behavior L; no effect on survival L; no effect on survival L; no effect on survival L; no effect on survival L; no effect on survival L; no effect on reproduction L; no effect on reproduction L; no effect on reproduction L; no effect on reproduction Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Neanthes virens, Polychaete - Sandworm Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 106 mg/kg (whole body)5 78 mg/kg (whole body)5 Behavior, LOED Physiological, LOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [33] Comments3 L; lethargy [33] L; total glycogen reduced, increase in ascorbic acid L; increase in ascorbic acid content [33] 290 mg/kg (whole body)5 Physiological, LOED Helisoma sp., Snail 625 mg/kg (whole body)5 300 mg/kg (whole body)5 460 mg/kg (whole body)5 Mortality, ED50 Mortality, NOED Mortality, NOED [32] [32] [32] L; 50% mortality L; no effect on mortality L; no effect on mortality Dreissena polymorpha, Zebra mussel Day 27: 539-598 g/g 0.96-1.06 mmol/kg 50% mortality [19] L Mytilus edulis, Blue mussel 131 30 mg/kg (whole body)5 Growth, NOED [53] L 132 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 30 mg/kg (whole body)5 6.45 mg/kg (whole body)5 4.22 mg/kg (whole body)5 Mortality, NOED Mortality, NOED Mortality, NA Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [53] [26] [60] Comments3 L; highest body burden reported L; estimated wet weight L; decreased anoxic survival time (Control 10.7 days) L; decreased anoxic survival time (Control 10.7 days) L; decreased anoxic survival time (Control 13 days) L; decreased anoxic survival time (Control 10.7 days) L; no significant changes in adenylate energy charge or glycogen content 8.06 mg/kg (whole body)5 Mortality, NA [60] 3.74 mg/kg (whole body)5 Mortality, NA [60] 8.06 mg/kg (whole body)5 Mortality, NA [60] 8.06 mg/kg (whole body)5 Physiological, NOED [60] Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Mytilus galloprovincialis, Mussel Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.57-0.92 mg/kg Ability to Accumulate2 Log BCF Log BAF BSAF 0.416 Source: Reference [27] Comments3 F Crassostrea virginica, Oyster 18.2 mg/kg (whole body)5 Reproduction, NOED [62] L; no reduced viability of gametes after exposure of adults in 21 ppt seawater L; 24% reduction in viability of gametes after exposure of adults in 21 ppt seawater 54 mg/kg (whole body)5 Reproduction, NOED [62] Daphnia magna, Cladoceran Day 21: 2.36 g/g Week 20: 17.4 g/g Day 21: 2.0 mmol/kg LOEC LOEC 10% mortality [20] [17] [21] F L L 133 134 Species: Taxa Daphnia magna, Cladoceran Sediment Daphnia galeata mendotae, Cladoceran Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 1.7 mg/kg (whole body)5 Reproduction, ED10 Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [21] Comments3 L; 10% reduction in number of offspring L; lethal body burden after 21-day exposure 221 mg/kg (whole body)5 Mortality, ED50 [21] 10.3 mg/kg (whole body) 5 Growth, LOED [48] L; increased weight of individual animals L; reduced longevity, increased prenatal mortality L; reduced longevity, increased prenatal mortality L; reduced longevity, increased prenatal mortality 3.5 mg/kg (whole body) Mortality, LOED [48] 5.7 mg/kg (whole body) 5 Mortality, NA [48] 8.6 mg/kg (whole body)5 Mortality, NA [48] Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 10.3 mg/kg (whole body)5 Mortality, NA Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [48] Comments3 L; reduced longevity, increased prenatal mortality L; no effect on individual weight L; no effect on individual weight L; no effect on individual weight 3.5 mg/kg (whole body)5 5.7 mg/kg (whole body)5 8.6 mg/kg (whole body)5 Growth, NOED Growth, NOED Growth, NOED [48] [48] [48] Folsomia candida, Cladoceran 60 g/g LOEC [22] F Gammarus fossarum, Amphipod Day 14: 60-70 g/g 50% mortality [18] L Moina macrocopa, Cladoceran 16.4 mg/kg (whole body)5 16.4 mg/kg (whole body)5 Reproduction, ED100 Growth, LOED [42] L; no reproduction after 12 days L; reduced growth [42] 135 136 Species: Taxa Sediment Hyallela azteca, Amphipod Pontoporeia affinis, Amphipod (juveniles, 105-460 d) Pontoporeia affinis, Amphipod Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 16.4 mg/kg (whole body)5 10.6 mg/kg (whole body)5 10.6 mg/kg (whole body)5 8 mg/kg (whole body)5 Mortality, LOED Reproduction, LOED Mortality, NOED Reproduction, NOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [42] [42] [42] [42] Comments3 L; reduced survival L; reduced brood size L; no effect on survival L; no effect on brood size Week 6: 15.2 g/g LOAEC [17] L Day 460: 80-90 g/g (0.14 mmol/kg) LOEC [16] L 11 mg/kg (whole body)5 6 mg/kg (whole body)5 6 mg/kg (whole body)5 Mortality, LOED Reproduction, LOED Mortality, NOED [58] [58] L L; percent malformed eggs L [58] Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 3 mg/kg (whole body)5 2 mg/kg (whole body)5 10 mg/kg (whole body)5 Reproduction, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [58] Comments3 L; Percent malformed eggs L; body burden estimated from graph L; body burden estimated from graph [59] [59] Balanus crenatus, Barnacle 52 mg/kg (whole body)5 Behavior, NOED [55] L; regulation of metals endpoint - summer experiment Mysidopsis bahia, Mysid 1.29 mg/kg (whole body)5 Growth, LOED [34] L; reduction in growth, mean dry weight of animals L; altered O:N ratio, shift towards lipid utilization with increasing cadmium concentration 1.29 mg/kg (whole body)5 Physiological, LOED [34] 137 138 Species: Taxa Sediment Oniscus asellus, Isopod Porcellio scaber, Isopod Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 2.38 mg/kg (whole body)5 Growth, NA Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [34] Comments3 L; reduction in growth, mean dry weight of animals L; reduction in growth, mean dry weight of animals L; altered O:N ratio, shift towards lipid utilization with increasing cadmium concentration L; altered O:N ratio, shift towards lipid utilization with increasing cadmium concentration 4.36 mg/kg (whole body)5 Growth, NA [34] 2.38 mg/kg (whole body)5 Physiological, NA [34] 4.36 mg/kg (whole body)5 Physiological, NA [34] Day 91: 8.15 mmol/kg [23] 50% mortality F Day 63: 5.40 mmol/kg 3.77 mmol/kg [23] 50% mortality 50% mortality F Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference Comments3 Palaemonetes pugio, Grass shrimp 0.9 mg/kg (whole body)5 2.6 mg/kg (whole body)5 Mortality, NOED Mortality, NA [26] [61] L; estimated wet weight L; 20% increased mortality over control in 5 ppt water; no statistical analysis L; 22% increased mortality over control in 5 ppt water; no statistical analysis L; 25% increased mortality over control in 5 ppt water; no statistical analysis 5.8 mg/kg (whole body)5 Mortality, NA [61] 7 mg/kg (whole body)5 Mortality, NA [61] Palaemonetes pugio, Grass shrimp 139 Day 21: 4.0 g/g 25% mortality [14] L 140 Species: Taxa Callianassa australiensis, Mole shrimp Sediment Cambarus latimanus, Crayfish Cambarus latimanus, Crayfish Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Day 14: 4.8 g/g 50% mortality Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [15] Comments3 L 14.9 mg/kg (whole body)5 Growth, NOED [13] L; no significant difference from control growth at lowest test concentration L; no significant difference from control mortality L; no significant difference from control temperature sensitivity at lowest test concentration 14.9 mg/kg (whole body)5 Mortality, NOED [13] 14.9 mg/kg (whole body)5 Physiological, NOED [13] Month 5: 4.4 g/g LOEC [13] L Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Orconectes virilis, Crayfish Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Day 14: 5.6 g/g 25% mortality Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [12] Comments3 L Orconectes propinquus, Crayfish 534 mg/kg (whole body)5 Mortality, NOED [39] L; 7% mortality after 190.5 hours, probably not significant Chironomus gr. thummi, Midge 0.156 mg/kg (whole body)5 Morphology, NOED [45] F; 4th instar larvae Glyptotendipes pallens, Midge 20 mg/kg (whole body)5 Behavior, LOED [44] L; modified feeding behavior, reduced net spinning activity L; reduced biomass L; modified feeding behavior, reduced net spinning activity L; lethargy 20 mg/kg (whole body)5 30 mg/kg (whole body)5 Growth, LOED Behavior, NA [44] [44] 50 mg/kg (whole body)5 Behavior, NA [44] 141 142 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 72 mg/kg (whole body)5 138 mg/kg (whole body)5 30 mg/kg (whole body)5 50 mg/kg (whole body)5 72 mg/kg (whole body)5 138 mg/kg (whole body)5 10 mg/kg (whole body)5 Behavior, NA Behavior, NA Growth, NA Growth, NA Growth, NA Growth, NA Behavior, NOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [44] [44] [44] [44] [44] [44] [44] Comments3 L; lethargy L; lethargy L; reduced biomass L; reduced biomass L; reduced biomass L; reduced biomass L; no effect on feeding behavior or activity level L; no effect on feeding behavior or activity level L; no effect on biomass L; no effect on biomass 18 mg/kg (whole body)5 Behavior, NOED [44] 10 mg/kg (whole body)5 18 mg/kg (whole body)5 Growth, NOED Growth, NOED [44] [44] Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 10 mg/kg (whole body)5 18 mg/kg (whole body)5 20 mg/kg (whole body)5 30 mg/kg (whole body)5 50 mg/kg (whole body)5 72 mg/kg (whole body)5 138 mg/kg (whole body)5 Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [44] Comments3 L; no effect on mortality in 96 hours L; no effect on mortality in 96 hours L; no effect on mortality in 96 hours L; no effect on mortality in 96 hours L; no effect on mortality in 96 hours L; no effect on mortality in 96 hours L; no effect on mortality in 96 hours [44] [44] [44] [44] [44] [44] Orchesella cincta, Springtail Day 49: 0.07 mmol/kg 50% mortality [23] F Tomocerus minor, Springtail Day 63: 0.13 mmol/kg 50% mortality [23] F 143 144 Species: Taxa Sediment Platynothrus peltifer, Oribatid mite Classenia sabulosa, Stonefly <0.3 g/g 3.5 g/g 6.6 g/g Hesperoperla pacifica, <0.3 g/g Stonefly 3.5 g/g 6.6 g/g Isogenoides sp., Stonefly <0.3 g/g 3.5 g/g 6.6 g/g Pteronarcys californica, Stonefly <0.3 g/g 3.5 g/g 6.6 g/g Hydropsyche sp., Caddisfly Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference Comments3 Day 63: 0.42 mmol/kg 50% mortality [23] F 0.1 g/g ND 1.4 g/g [24] F 0.2 g/g ND 1.0 g/g [24] F <0.4 g/g 1.4 g/g 1.8 g/g [24] F 0.1 g/g ND 1.0 g/g [24] F 9.8 mg/kg (whole body)5 17.4 mg/kg (whole body)5 29.8 mg/kg (whole body)5 Mortality, LOED Mortality, LOED Mortality, LOED [38] [38] [38] L; mortality in one day L; mortality in two days L; mortality in four days Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.118 mg/kg (whole body)5 0.0934 mg/kg (whole body)5 16 mg/kg (whole body)5 24.8 mg/kg (whole body)5 41.8 mg/kg (whole body)5 0.202 mg/kg (whole body)5 0.284 mg/kg (whole body)5 Mortality, LOED Mortality, LOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [38] [38] [38] Comments3 L; mortality in one day L; mortality in two days L; no effect on mortality in one day L; no effect on mortality in one day L; no effect on mortality in one day L; no effect on mortality in one day L; no effect on mortality in one day [38] [38] [38] [38] Hydropsyche spp., Caddisfly <0.3 g/g 3.5 g/g 6.6 g/g 0.2 g/g 2.2 g/g 2.8 g/g [24] F Arctopsyche grandis, Caddisfly 145 <0.3 g/g 3.5 g/g 6.6 g/g 0.2 g/g ND 4 1.4 g/g [24] F 146 Species: Taxa Asterias rubens, Starfish Sediment Fishes Oncorhynchus mykiss, Rainbow trout Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.03 mg/kg (gonad)5 Development, LOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [37] Comments3 combined, estimated wet weight adult males combined, estimated wet weight adult females 0.14 mg/kg (gonad)5 Development, LOED [37] 16.4 mg/kg (whole body)5 Mortality, ED100 [29] L; complete mortality of alevins within 10 hours L; complete mortality of eggs within 32 hours L; complete mortality of alevins within 320 hours L; erratic swimming L; deformed vertebrae, blood clots in fins 101 mg/kg (whole body)5 Mortality, ED100 [29] 0.84 mg/kg (whole body)5 Mortality, ED100 [29] 0.71 mg/kg (whole body)5 0.21 mg/kg (whole body)5 Behavior, LOED Morphology, LOED [29] [29] Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.21 mg/kg (whole body)5 Mortality, LOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [29] Comments3 L; hatching alevins unable to break free from egg membrane, died L; induction of metallothionein L; no effect on mortality L; hardness: 279 mg/L CaCO3 L; Hardness: 279 Mg/L CaCO3 L; hardness: 70 mg/L CaCO3 L; hardness: 70 mg/L CaCO3 10 mg/kg (whole body)5 0.0599 mg/kg (whole body)5 6.4 mg/kg (whole body)5 3.74 mg/kg (whole body)5 4 mg/kg (whole body)5 2.2 mg/kg (whole body)5 Physiological, LOED Mortality, NOED Mortality, ED50 Mortality, ED50 Mortality, ED50 Mortality, ED50 [30] [41] [51] [51] [51] [51] 147 148 Species: Taxa Salmo salar, Atlantic Salmon Sediment Salvelinus fontinalis, Brook trout Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.26 mg/kg (yolk sac/stomach)5 Growth, LOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [52] Comments3 L; yolk sac/stomach weight - graph and table interpretation L; yolk sac/stomach weight - graph and table interpretation L; yolk sac/stomach weight - graph and table interpretation L; yolk sac/stomach weight - graph and table interpretation 0.26 mg/kg (yolk sac/stomach)5 Mortality, LOED [52] 0.05 mg/kg (yolk sac/stomach)5 Growth, NOED [52] 0.05 mg/kg (yolk sac/stomach)5 Mortality, NOED [52] 3.4 g/g Week 38: 10 g/g, kidney 2 g/g, liver [25] L Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Salvelinus fontinalis, Brook Trout Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.175 mg/kg (liver)5 Mortality, LOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [40] Comments3 L; significant mortality in 10.5 g/L at 15 days and 1.91 g/L at 7 days, but no body burdens measured L; no significant effect on growth L L; significantly reduced survival at lowest test concentration, exp_conc = <3.6 0.232 mg/kg (liver)5 Growth, NA [40] 0.203 mg/kg (liver)5 144 mg/kg (whole body)5 Mortality, NOED Mortality, LOED [40] [40] 149 150 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.742 mg/kg (liver)5 Physiological, LOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [40] Comments3 L; significantly increased metallothionein in whole body tissues at lowest test concentration; no correlation between metallothionein concentration and mortality or whole body tissue residues, exp_conc = < 3.6 L; significantly increased metallothionein in whole body tissues at lowest test concentration; no correlation between metallothionein and mortality or whole body tissue residues, exp_conc = < 3.6 144 mg/kg (whole body)5 Physiological, LOED [40] Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Jordanella floridae, American flagfish Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.4 mg/kg (whole body)5 Mortality, LOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [56] Comments3 L; body burden estimated from graph, fish initially exposed as embryos L; body burden estimated from graph, fish not exposed as embryos L; body burden estimated from graph L; body burden estimated from graph, fish not exposed as embryos L; body burden estimated from graph, fish initially exposed as embryos L; body burden estimated from graph 0.4 mg/kg (whole body)5 Mortality, LOED [56] 6 mg/kg (whole body)5 0.4 mg/kg (whole body)5 Growth, NOED Mortality, NOED [56] [56] 0.09 mg/kg (whole body)5 Mortality, NOED [56] 6 mg/kg (whole body)5 151 Reproduction, NOED [56] 152 Species: Taxa Sediment Poecilia reticulata, Guppy Cyprinodon variegatus, Sheepshead minnow Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 20 mg/kg (whole body)5 10 mg/kg (whole body)5 35 mg/kg (whole body)5 Growth, LOED Growth, NOED Mortality, NOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [57] [57] [57] Comments3 L; total length of females L; total length of females L 8 mg/kg (whole body)5 0.5 mg/kg (whole body)5 1.2 mg/kg (whole body)5 0.8 mg/kg (whole body)5 Mortality, ED50 Growth, LOED Mortality, LOED Growth, NA [43] L; 50% reduction in survival L; reduction in body length within 10 days L; 14% reduction in survival L; reduction in body length within 10 days [43] [43] [43] 0.9 mg/kg (whole body)5 Development, LOED [49] L; decreased time to hatch Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Platichthys flesus, European flounder Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 17.2 mg/kg (kidney)5 Biochemical, LOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [54] Comments3 L; females Cd + estradiol injection: RNA:DNA ratio L; females Cd + estradiol injection: RNA:DNA ratio L; females Cd + estradiol injection: RNA:DNA ratio L; males Cd + estradiol injection: RNA:DNA ratio L; males Cd + estradiol injection: RNA:DNA ratio 21.6 mg/kg (liver)5 Biochemical, LOED [54] 1.82 mg/kg (ovary)5 Biochemical, LOED [54] 33.2 mg/kg (kidney)5 Biochemical, NOED [54] 43.8 mg/kg (liver)5 Biochemical, NOED [54] 153 154 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 4.66 mg/kg (ovary)5 Biochemical, NOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [54] Comments3 L; males Cd + estradiol injection: RNA:DNA ratio L; females Cd + estradiol injection: survival L; males Cd + estradiol injection: survival L; males Cd + estradiol injection: survival L; females Cd + estradiol injection: survival L; males Cd + estradiol injection: survival L; females Cd + estradiol injection: survival 17.2 mg/kg (kidney)5 Mortality, NOED [54] 33.2 mg/kg (kidney)5 Mortality, NOED [54] 43.8 mg/kg (liver)5 Mortality, NOED [54] 21.6 mg/kg (liver)5 Mortality, NOED [54] 4.66 mg/kg (ovary)5 Mortality, NOED [54] 1.82 mg/kg (ovary)5 Mortality, NOED [54] Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Pleuronectes americanus, Winter flounder Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 1 mg/kg (whole body)5 Physiological, LOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [36] Comments3 L; induction of metallothionein Wildlife Ambystoma gracile, Salamander 140 mg/kg (whole body)5 Behavior, LOED [50] L; significant reduction in regurgitation/ food retention L; significant reduction in both length and weight L; significant reduction in both length and weight L; no significant increase in regurgitation/ food retention 6.28 mg/kg (whole body)5 Growth, LOED [50] 4.7 mg/kg (whole body)5 Growth, LOED [50] 71.7 mg/kg (whole body)5 Behavior, NOED [50] 155 156 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Cadmium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 43.5 mg/kg (whole body)5 Growth, NOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [50] Comments3 L; no significant reduction in length or weight at highest test concentration L; no significant reduction in length or weight L; no significant reduction in length or weight at highest test concentration L; no significant reduction in length or weight L; no significant increase in mortality at highest test concentration 3.75 mg/kg (whole body)5 Growth, NOED [50] 145 mg/kg (whole body)5 Growth, NOED [50] 1.62 mg/kg (whole body)5 Growth, NOED [50] 43.5 mg/kg (whole body)5 Mortality, NOED [50] Summary of Biological Effects Tissue Concentrations for Cadmium Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 145 mg/kg (whole body)5 Mortality, NOED Ability to Accumulate2 Log BCF Log BAF BSAF Source: Reference [50] Comments3 L; no significant increase in mortality at highest test concentration L; no significant increase in mortality at highest test concentration 4.13 mg/kg (whole body)5 Mortality, NOED [50] 1 2 3 4 5 Concentration units based on wet weight unless otherwise noted. 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Toxicol. 27:344-348. 162 BIOACCUMULATION SUMMARY Chemical Category: PESTICIDE (ORGANOCHLORINE) Chemical Name (Common Synonyms): CHLORDANE CHLORDANE CASRN: 57-74-9 Chemical Characteristics Solubility in Water: 0.1 mg/L at 20 - 30C [1] Half-Life: 283 days - 3.8 yrs based on unacclimated aerobic river die-away test and reported soil grab sample data [2] Log Koc: 6.21 L/kg organic carbon Log Kow: 6.32 [3] Human Health Oral RfD: 6 x 10-5 mg/kg/day [4] Confidence: Low, uncertainty factor = 1000 Critical Effect: Regional liver hypertrophy in female rats; hepatocellular carcinomas in mice Oral Slope Factor: 1.3 x 10+0 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4] Wildlife Partitioning Factors: Partitioning factors for chlordane in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for chlordane in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: The major components of technical chlordane include gamma chlordane (24 percent), alpha chlordane (19 percent), and trans-nonachlor (7 percent). Alpha chlordane is environmentally more stable and therefore more persistent than gamma chlordane. Oxychlordane is an epoxide metabolite formed in mammalian liver. It is persistent and much more toxic than its parent chemicals [5]. Food Chain Multipliers: In a marine ecosystem the chlordane compounds (nonachlor and oxychlordane) increased significantly with trophic levels from zooplankton to marine mammals [6]. Although the results of the study reported by Kawano et al. [6] indicated a small difference in the chlordane composition in zooplankton from the North Pacific, Bering Sea, and Antarctic, they also revealed a significant difference in chlordane composition between Dall's porpoise and the Weddell seal. Trans-chlordane was present in the seal but not in the porpoise, and the percentage composition of oxychlordane in the seal was larger than that in the porpoise. Furthermore, the compositional percentage 163 164 BIOACCUMULATION SUMMARY CHLORDANE of oxychlordane in the Adelie penguin and thick-billed murre was much higher than that in the other organisms. Marine mammals and seabirds accumulated chlordane via food. Biomagnification of total chlordanes through the food chain is strongly evident in marine mammals. Chlordanes are concentrated gradually from zooplankton, through squid and fish, to porpoises and dolphins [7,8]. Chlordane residues in marine mammals are positively correlated with lipid content and not with the age of the animal [9]. Food chain multipliers (FCMs) for cis- or trans-chlordane for trophic level 3 aquatic organisms were 21.7 (all benthic food web), 1.6 (all pelagic food web), and 13.2 (benthic and pelagic food web). FCMs for trophic level 4 aquatic organisms were 49.5 (all benthic food web), 3.5 (all pelagic food web), and 23.3 (benthic and pelagic food web) [26]. Toxicity/Bioaccumulation Assessment Profile Chlordane adversely affected sensitive species of fish and aquatic invertebrates at concentrations of 0.2 to 2.0 g/L. Specifically, survival of shrimp and crabs was reduced at water concentrations of 0.2 to 2.0 g/L, while survival of freshwater and marine fishes was reduced between 1.7 and 3.0 g/L. Generally, the uptake of chlordane by aquatic organisms is high, ranging from 216.8 g organic carbon cleared per gram organism per hour for Diporeia spp. to 358 g organic carbon cleared per gram organism per hour for Chironomus riparius [10]. Accumulation of chlordane by Diporeia spp., C. riparius, or Lumbriculus variegatus from whole sediment exposures was greater than that from the elutriate or pore water. Neither species was able to metabolize chlordane. A study by Wilcock et al. [11] has shown that the bivalve Macomona liliana can accumulate chlordane bound to sediment at depths below 2 cm. Animals constantly exposed to contaminated sediment accumulated more (5,728 ppb lipid) than those able to feed alternatively on contaminated and uncontaminated sediments (3,617 and 2,756 ppb). An in situ study of the uptake and elimination by adult intertidal benthic infauna of chlordane from contaminated sediment has shown large differences in accumulation between deposit- and suspension-feeding species [12]. In the case of surface feeders, these differences can be attributed to direct exposure to high initial concentration of chlordane in surficial sediments. The extract from the chlordane residues obtained from Lake Michigan lake trout was significantly more toxic (3 to 5 times) than the chlordane used in agricultural applications. Gooch et al. [13] suggested that the increased toxicity of these extracts was due to the presence of the stable metabolite heptachlor epoxide and oxychlordane. Chlordane is persistent in the environment; measurable residues in sediment were found 2.8 years after application to the overlying water column [5]. More than 80 percent of the fish sampled from the Kansas River had detectable chlordanes in their tissue [14]. Residues of cis-chlordane and trans-chlordane were the most abundant and persistent of the chlordane components measured in fish tissues in a U.S. study conducted aproximately 10 years after the termination of the agricultural use of chlordanes [15]. In birds, technical chlordane and its metabolite oxychlordane are frequently elevated in tissues with high lipid content. In northern gannets, the half-time persistence of cis-chlordane, cis-nonachlor, and oxychlordane was estimated at 11, 199, and 35 years [16]. 164 Summary of Biological Effects Tissue Concentrations for Chlordane Species: Taxa Invertebrates Lumbriculus variegatus, Oligochaete worm 125 ng/g 28,197 ng/g [10] F Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 1,406 ng/g BDL4 Crassostrea virginica, Eastern oyster 23,031 ng/g3 0.03 /kg 0.02 mg/kg (whole body)5 2.2 mg/kg (whole body)5 0.3 mg/kg (whole body)5 0.075 mg/kg (whole body)5 0.6 mg/kg (whole body)5 0.78 mg/kg (whole body)5 6.5 mg/kg (whole body)5 Growth, ED18 Growth, ED28 Growth, ED28 Growth, ED30 Growth, ED30 Growth, ED33 Growth, ED33 [22] [17] [22] F L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) [22] [22] [22] [22] 165 166 Species: Taxa Sediment Crassostrea virginica, Eastern oyster Corbicula fluminea, Asian clam 21.7 g/kg OC Summary of Biological Effects Tissue Concentrations for Chlordane Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 1.9 mg/kg (whole body)5 14 mg/kg (whole body)5 5.6 mg/kg (whole body)5 47 mg/kg (whole body)5 0.022 mg/kg (whole body)5 Growth, ED78 Growth, ED78 Growth, ED95 Growth, ED95 Growth, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [22] Comments3 L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; estimated LOED no statistical summary in text L; estimated NOED no statistical summary in text F; trans-chlordane; %lipid not reported; %sed OC = 2.30 [22] [22] [22] [22] 27 mg/kg (whole body)5 11 mg/kg (whole body)5 Growth, LOED Growth, NOED [23] [23] 2,400 g/kg lipid 2.04 [21] Summary of Biological Effects Tissue Concentrations for Chlordane Species: Taxa Gonatopsis borealis, Eight-armed squid Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects cis-chlordane: 15 (11-18) g/kg trans-chlordane: 8.1 (6.3-9.9) g/kg cis-nonachlor: 2.4 (2.2-2.8) g/kg trans-nonachlor: 18 (14-20) g/kg oxychlordane: 1.2 (0.8-1.60) g/kg total chlordanes: 44 (35-52) g/kg 493 ng/g 430 ng/g 23,729 ng/g 40,086 ng/g cis-chlordane: 0.58 g/kg trans-chlordane: 0.51 g/kg cis-nonachlor: 0.22 g/kg trans-nonachlor: 0.8 g/kg oxychlordane: 0.1 g/kg 4.5 mg/kg (whole body)5 Mortality, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [5] Comments3 F; lipid samples Diporeia sp., Amphipod Euphasia superba, Krill [10] F [6] F Palaemonetes pugio, Grass shrimp 167 [23] L; estimated LOED no statistical summary in text 168 Species: Taxa Sediment Penaeus duorarum, Pink shrimp Homarus americanus, American lobster Chironomus riparius, Midge 1,663 ng/g 1,741 ng/g Summary of Biological Effects Tissue Concentrations for Chlordane Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 4.8 mg/kg (whole body)5 Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [23] Comments3 L; estimated NOED no statistical summary in text L; estimated LOED no statistical summary in text L; estimated NOED no statistical summary in text F 1.7 mg/kg (whole body)5 0.71 mg/kg (whole body)5 Mortality, LOED Mortality, NOED [23] [23] cis-chlordane: 80-100 g/kg, hepatopancreas trans-chlordane: 80-100 g/kg, hepatopancreas cis-nonachlor: 30 g/kg, hepatopancreas trans-nonachlor: (380-440) g/kg, hepatopancreas 16,224 ng/g 8,417 ng/g [5] [10] F Summary of Biological Effects Tissue Concentrations for Chlordane Species: Taxa Fishes Oncorhynchus, Salmo, Salvelinus sp., Salmonids 77.8 g/kg OC 0.000034 g/L 19 g/kg 5.75 [20] F; trans-chlordane, % lipid = 11 F; trans-chlordane; %lipid = 11; %sed OC = 2.70 F; trans-chlordane F; cis-chlordane F; median BSAFs calculated in [18] from field data in [20] F; median BSAFs calculated in [18] from field data in [19] F; trans-chlordane; %lipid = 7.8; %sed OC = 0.80 F; trans-chlordane; %lipid = 8.4; %sed OC = 1.79 F; trans-chlordane; %lipid = 9.3; %sed OC = 1.16 Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 172.7 g/kg lipid 2.22 [20] Salmonids 2.00 4.77 2.1 ng/g 34 pg/L 3.6 ng/g 19 ng/g [25] [25] [18,20] Osmerus mordax, Smelt; Oncorhynchus velinus, Coho salmon Cyprinus carpio, Carp 2.5 ng/g 18 ng/g 46.3 33.4 [18,19] Cyprinus carpio, Carp 437.5 g/kg OC 145.3 g/kg OC 112.1 g/kg OC 169 217.9 g/kg lipid 0.498 [24] 110.7 g/kg lipid 0.762 [24] 161.3 g/kg lipid 1.439 [24] 170 Species: Taxa Sediment Cyprinus carpio, Carp 212.5 g/kg OC 128.5 g/kg OC 86.21 g/kg OC Catastomus commersoni, White sucker 437.5 g/kg OC 145.3 g/kg OC 112.1 g/kg OC Catastomus commersoni, White sucker 212.5 g/kg OC 128.5 g/kg OC 86.21 g/kg OC Summary of Biological Effects Tissue Concentrations for Chlordane Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 294.9 g/kg lipid Ability to Accumulate2: Log BCF Log BAF BSAF 1.3878 Source: Reference [24] Comments3 F; cis-chlordane; %lipid = 7.8; %sed OC = 0.80 F; cis-chlordane; %lipid = 8.4; %sed OC = 1.79 F; cis-chlordane; %lipid = 9.3; %sed OC = 1.16 F; trans-chlordane; %lipid = 8.3; %sed OC = 0.8 F; trans-chlordane; %lipid = 7.9; %sed OC = 1.79 F; trans-chlordane; %lipid = 4.5; %sed OC = 1.16 F; cis-chlordane; %lipid = 8.3; %sed OC = 0.8 F; cis-chlordane; %lipid = 7.9; %sed OC = 1.79 F; cis-chlordane; %lipid = 4.5; %sed OC = 1.16 190.5 g/kg lipid 1.4825 [24] 258.1 g/kg lipid 2.9939 [24] 132.5 g/kg lipid 0.301 [24] 189.9 g/kg lipid 1.307 [24] 266.7 g/kg lipid 2.379 [24] 192.8 g/kg lipid 0.9073 [24] 519 g/kg lipid 4.0389 [24] 533.3 g/kg lipid 6.1861 [24] Summary of Biological Effects Tissue Concentrations for Chlordane Species: Taxa Cyprinodon variegatus, Sheepshead minnow Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 909 mg/kg (whole body) 1.2 mg/kg (whole body)5 0.019 mg/kg (whole body)5 0.01 mg/kg (whole body)5 17.5 mg/kg (whole body)5 2 mg/kg (whole body)5 3.9 mg/kg (whole body )5 32 mg/kg (whole body)5 47 mg/kg (whole body)5 6.1 mg/kg (whole body)5 171 Mortality, ED35 Mortality, ED35 Mortality, ED5 Mortality, ED5 Mortality, ED50 Mortality, ED50 Mortality, ED60 Mortality, ED60 Mortality, ED85 Mortality, ED85 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [22] Comments3 L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) [22] [22] [22] [22] [22] [22] [22] [22] [22] 172 Species: Taxa Cyprinodon variegatus, Sheepshead minnow Sediment Lagodon rhomboides, Pinfish Leiostomus xanthurus, Spot Summary of Biological Effects Tissue Concentrations for Chlordane Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 281 mg/kg (whole body)5 3.18 mg/kg (whole body)5 3.18 mg/kg (whole body)5 0.6 mg/kg (whole body)5 87 mg/kg (whole body)5 1.38 mg/kg (whole body)5 1.38 mg/kg (whole body)5 Mortality, LOED Mortality, LOED Reproduction, LOED Mortality, NOED Mortality, NOED Mortality, NOED Reproduction, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [23] Comments3 L; estimated LOED no statistical summary in text L L; hatching success of fry from exposed parents L; estimated NOED no statistical summary in text L; estimated NOED no statistical summary in text L L; hatching success of fry from exposed parents L; estimated LOED no statistical summary in text L; exposure media 65% heptachlor (technical grade) [23] [23] [23] [23] [23] [23] 16.6 mg/kg (whole body)5 Mortality, LOED [23] 0.16 mg/kg (whole body)5 Mortality, ED25 [22] Summary of Biological Effects Tissue Concentrations for Chlordane Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.55 mg/kg (whole body)5 0.89 mg/kg (whole body)5 0.22 mg/kg (whole body)5 3.3 mg/kg (whole body)5 0.94 mg/kg (whole body)5 1.6 mg/kg (whole body)5 7.1 mg/kg (whole body)5 0.7 mg/kg (whole body)5 3.5 mg/kg (whole body)5 0.01 mg/kg (whole body)5 173 Mortality, ED25 Mortality, ED35 Mortality, ED35 Mortality, ED40 Mortality, ED40 Mortality, ED70 Mortality, ED70 Mortality, ED85 Mortality, ED85 Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [22] Comments3 L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) [22] [22] [22] [22] [22] [22] [22] [22] [22] 174 Species: Taxa Sediment Cottus cognatus, Slimy sculpin 2.1 ng/g 77.8 g/kg OC Pimelodus albicans, Oligosarcus jenynsi, Prochilodus platensis 3.4 ng/g Prochilodus platensis, 20 g/kg Curimata OC Pimelodus albicans, Mandi 20 g/kg OC Summary of Biological Effects Tissue Concentrations for Chlordane Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.01 mg/kg (whole body)5 0.01 mg/kg (whole body)5 0.01 mg/kg (whole body)5 Mortality, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [22] Comments3 L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) F; trans-chlordane, % lipid = 8 F; trans-chlordane; %lipid = 8; %sed OC = 2.70 F; median BSAFs calculated in [18] from field data in [21] F; trans-chlordane; %lipid not reported; %sed OC = 1 F; trans-chlordane; %lipid not reported; %sed OC = 1 [22] [22] 34 g/L 30 g/kg 375 g/kg lipid 5.95 2.47 4.821 [18,20] [20] 0.8 ng/L 2.9 g/g 20 [18,21] 4,600 g/kg lipid 230 [21] 1,000 g/kg lipid 50 [21] Summary of Biological Effects Tissue Concentrations for Chlordane Species: Taxa Wildlife Ducks 0.83 19.5 [18,19] F; median BSAFs calculated in [18] from field data in [19] Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 1 2 3 4 5 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. BDL = Below detection limit. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. 175 BIOACCUMULATION SUMMARY References 1. CHLORDANE Merck index, 11th ed., 1989, p. 321. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January. Fish and Wildlife Service. 1990. Chlordane hazards to fish, wildlife, and invertebrates: A synoptic review. Biological Report 85(1.21). Kawano, M., T. Inoue, T. Wada, H. Hidaka, and R. Tatsukawa. 1988. Bioconcentration and residue patterns of chlordane compounds in marine animals: Invertebrates, fish, mammals and seabirds. Environ. Sci. Technol. 22:792-797. Kawano, M., S. Matsushita, T. Inoue, H. Tanaka, and R. Tatsukawa. 1986. Biological accumulation of chlordane compounds in marine organisms from the northern North Pacific and Bering Sea. Mar. Pollut. Bull. 17:512-516. Muir, D.C.G., C.A. Ford, R.E.A. Stewart, T.G. Smith, R.F. Addison, M.E. Zinck, and P. Beland. 1990. Organochlorine contaminants in belugas, Delphinapterus leucas from Canadian waters. Can. Bull. Fish. Aquat. Sci. 224:165-190. Perttila, M., O. Stenman, H. Pyysalo, and K. Wickstrom. 1986. Heavy metals and organochlorine compounds in seals in the Gulf of Finland. Mar. Environ. Res. 18:43-59. Harkey, G.A., P.F. Landrum, and S.J. Klaine. 1994. Comparison of whole-sediment, elutriate, and pore-water exposures for use in assessing sediment-associated organic contaminants in bioassays. Environ. Toxicol. Chem. 13:1315-1329. 2. 3. 4. 5. 6. 7. 8. 9. 10. 176 BIOACCUMULATION SUMMARY 11. CHLORDANE Wilcock, R.J., R.D. Pridmore, G.L. Northcott, J.E. Hewitt, S.F. Thrush, and V.J. Cummings. 1994. Uptake of chlordane by a deposit-feeding bivalve: Does the depth of sediment contamination make a difference. Environ. Toxicol. Chem. 13:1535-1541. Wilcock, R.J., T.J. Smith, R.D. Pridmore, S.F. Thrush, V.J. Cummings, and J.E. Hewitt. 1993. Bioaccumulation and elimination of chlordane by selected intertidal benthic fauna. Environ. Toxicol. Chem. 12:733-742. Gooch, J.W., F. Matsumura, and M.J. Zabik. 1990. Chlordane residues in Great Lakes lake trout: Acute toxicity and interaction at the gaba receptor of rat and lake trout brain. Chemosphere 21:393406. Arruda, J.A., M.S. Cringan, D. Gilliland, S.G. Haslouer, J.E. Fry, R. Broxterman, and K.L. Brunson. 1987. Correspondence between urban areas and the concentrations of chlordane in fish from the Kansas River. Bull. Environ. Contam. Toxicol. 39:563-570. Schmitt, C.J., L. Zajicek, and P.H. Peterman. 1990. National Contaminant Biomonitoring Program: Residues of organochlorine chemicals in U.S. freshwater fish, 1976-1984. Arch. Environ. Contam. Toxicol. 19:748-781. Elliott, J.E., R.J. Norstrom, and J.A. Keith. 1988. Organochlorines and eggshell thinning in northern gannets (Sula bassanus) from eastern Canada, 1968-1984. Environ. Pollut. 52:81-102. Boer, J.D., and P. Wester. 1991. Chlorobiphenyls and organochlorine pesticides in various subantarctic organisms. Mar. Pollut. Bull. 22:441-447. Parkerton, T.F., J.P. Connolly, R.V. Thomann, and C.G. Uchrin. 1993. Do aquatic effects or human health end points govern the development of sediment-quality criteria for nonionic organic chemicals? Environ. Toxicol. Chem. 12:507-523. Smith, V.E., J.M. Spurr, J.C. Filkins, and J.J. Jones. 1985. Organochlorine contaminants of wintering ducks foraging on Detroit River sediments. J. Great Lakes Res. 11:231-246. Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Columbo, J.C., M.F. Khahl, M. Arnac, and A.C. Horth. 1990. Distribution of chlorinated pesticides and individual polychlorinated biphenyls in biotic and abiotic compartments of the Rio de la Plata, Argentina. Environ. Sci. Technol. 24:498-505. Schimmel, S.C., J.M. Patrick, and J. Forester. 1976. Heptachlor: Toxicity to and uptake by several estuarine organisms. J. Toxicol. Environ. Health 1:955-965. Parrish, P.R., S.C. Schimmel, D.J. Hansen, J.M. Patrick, and J. Forester. 1976. Chlordane: Effects on several estuarine organisms. Toxicol. Environ. Health 1:485-494. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 177 BIOACCUMULATION SUMMARY 24. CHLORDANE Tate, C.M., and J.S. Heiny. 1996. Organochlorine compounds in bed sediment and fish tissue in the South Platte River basin, USA, 1992-1993. Arch. Environ. Contam. Toxicol. 30:62-78. USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. USEPA. 1998. Ambient water quality criteria derivation methodology: Human health. Technical Support Document. EPA-822-B-98-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 25. 26. 178 BIOACCUMULATION SUMMARY Chemical Category: PESTICIDE (ORGANOPHOSPHATE) Chemical Name (Common Synonyms): CHLORPYRIFOS CHLORPYRIFOS CASRN: 2921-88-2 Chemical Characteristics Solubility in Water: 0.7 ppm at 20C [1] Log Kow: 5.26 [3] Half-Life: No data [2] Log Koc: 5.17 L/kg organic carbon Human Health Oral RfD: 3 x 10-3 mg/kg/day [4] Confidence: Medium, uncertainty factor =10[4] Critical Effect: Decreased plasma cholinesterase activity after 9 days of 20-day human feeding study Oral Slope Factor): No data [4] Carcinogenic Classification: No data [4], D[5] Wildlife Partitioning Factors: Partitioning factors for chlorpyrifos in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for chlorpyrifos in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: The only partitioning factors for chlorpyrifos in aquatic organisms found in the literature were log BCF of 3.23 for an isopod [14]. Food Chain Multipliers: Food chain multipliers for chlorpyrifos in aquatic organisms were not found in the literature. Toxicity/Bioaccumulation Assessment Profile Chlorpyrifos or Dursban is an organophosphorus insecticide which is used to control both adult and larval mosquitoes [6]. It is more toxic to nontarget organisms like cladocerans, amphipods, and other organisms than to mosquito larvae, however. The increase of chlorpyrifos concentration in water proportionally increased the bioconcentration factor in fish [7]. A low recovery (20 percent or lower) of chlorpyrifos from C-18 columns was attributed to its high binding affinity [8]. Also, acidic or basic conditions were 179 BIOACCUMULATION SUMMARY CHLORPYRIFOS not effective in reducing its concentration in water [9]. Because of the binding capacity and the high Kow, chlorpyrifos does not remain in aqueous solution or suspension but is bound to the organic and clay fractions of sediments. The time for sediment-associated pesticides to degrade and reach nontoxic states is much greater than for aqueous phases [10]. The responses to chlorpyrifos from single-species tests were compared to responses observed in a field mesocosm [11]. The EC50 for seven species in the mesocosms ranged from 0.1 to 3.4 g/L and were within the same order of magnitude as the laboratory data. Toxicity to the most sensitive test species, D. magna , at 1 g/L was representative of sensitive indigenous species. The results of toxicity tests exposing Chironomus tentans to sediments with differing organic carbon content spiked with chlorpyrifos revealed that an organic carbon partitioning model can be reasonably used to predict the toxicity of chlorpyrifos to benthic macroinvertebrates [12]. The TOC-normalized, solid-phase concentration of chlorpyrifos was no better predictor of the toxicity of the pesticide to C. tentans than the sediment dry-weight concentration of chlorpyrifos. The effects based on predicted porewater concentrations were accurate to within a factor of two of expected effects based on water-only toxicity tests with the midge. Distinct pulses of pesticides, including chlorpyrifos, were detected in the San Joaquin River and in the Sacramento River following rainfall events [13]. The results of short-term chronic tests with Ceriodaphnia dubia indicated that Sacramento River water at Rio Vista was acutely toxic for three consecutive days, while San Joaquin River water at Vernalis was toxic for 12 consecutive days. 180 Summary of Biological Effects Tissue Concentrations for Chlorpyrifos Species: Taxa Invertebrates Mytilus galloprovincialis, Mediterranean mussel 42 mg/kg (whole body)4 4 mg/kg (whole body)4 1.9 mg/kg (whole body)4 4 mg/kg (whole body)4 Asellus aquaticus, Isopod Fishes Pimephales promelas, Fathead minnow 0.7 g/L 5.0 g/L 140,000 g/kg 260,000 g/kg Mortality, ED50 Morphology, LOED Morphology, NOED Mortality, NOED [19] L; estimated from table 4 L; presence of functional byssus Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [19] [19] [19] L; estimated from table 4 F 3.23 [14] 2 mg/kg (whole body)4 4.5 mg/kg (whole body)4 Growth, LOED Morphology, LOED [21] [21] 4.5 mg/kg (whole body)4 Mortality, LOED [21] L; significant reduction in growth L; body constriction behind opercula, shortening of caudal peduncle L; significant reduction in survival 181 182 Species: Taxa Summary of Biological Effects Tissue Concentrations for Chlorpyrifos Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.45 mg/kg (whole body)4 Physiological, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [21] Comments3 L; inhibition of acetylcholinester ase (ACHE) activity L; significant reduction in growth L; inhibition of acetylcholinester ase (ACHE) activity L; inhibition of acetylcholinester ase (ACHE) activity L; inhibition of acetylcholinester ase (ACHE) activity L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on appearance or development L; no effect on appearance or development 4.5 mg/kg (whole body)4 4.5 mg/kg (whole body)4 Growth, NA Physiological, NA [21] [21] 2 mg/kg (whole body)4 Physiological, NA [21] 1.1 mg/kg (whole body)4 Physiological, NA [21] 1.1 mg/kg (whole body)4 0.45 mg/kg (whole body)4 0.2 mg/kg (whole body)4 2 mg/kg (whole body)4 1.1 mg/kg (whole body)4 Growth, NOED Growth, NOED Growth, NOED Morphology, NOED Morphology, NOED [21] [21] [21] [21] [21] Summary of Biological Effects Tissue Concentrations for Chlorpyrifos Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.45 mg/kg (whole body)4 0.2 mg/kg (whole body)4 2 mg/kg (whole body)4 1.1 mg/kg (whole body)4 0.45 mg/kg (whole body)4 0.2 mg/kg (whole body)4 0.2 mg/kg (whole body)4 Morphology, NOED Morphology, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Physiological, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [21] Comments3 L; no effect on appearance or development L; no effect on appearance or development L; no effect on survival L; no effect on survival L; no effect on survival L; no effect on survival L; inhibition of acetylcholinester ase (ACHE) activity L; no effect on survivorship after 3 days L [21] [21] [21] [21] [21] [21] Gambusia affinis, Mosquito fish 0.0352 mg/kg (whole body)4 Mortality, NOED [22] Poecilia reticulata, Guppy 0.9 g/L 1.9 g/L 3.9 g/L 10 g/L 19 g/L 37 g/L 6 g/g lipid 33 g/g lipid 66 g/g lipid 350 g/g lipid 710 g/g lipid 2,100 g/g lipid [15] 183 184 Species: Taxa Poecilia reticulata, Guppy Gasterosteus aculeatus, Threespined stickleback Cyprinodon variegatus, Sheepshead minnow Cyprinodon variegatus, Sheepshead minnow Summary of Biological Effects Tissue Concentrations for Chlorpyrifos Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 2,810 mg/kg (whole body)4 0.12 g/L 0.46 g/L 1.0 g/L series 1 0.78g/L 1.7 g/L 3.0 g/L 6.8 g/L series 1 0.78g/L 1.7 g/L 3.0 g/L 6.8 g/L series 1 0.78g/L 1.7 g/L 3.0 g/L 6.8 g/L series 2 3.1 g/L 7.2 g/L 14 g/L 26 g/L 52 g/L 8.1 g/g lipid 31.2 g/g lipid 125 g/g lipid Mortality, ED100 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [18] Comments3 L; lifestage: 2-3 months L [16] [17] 0.033 g/g 0.22 g/g 0.45 g/g 4.8 g/g [17] 0.054 g/g 0.12 g/g 0.78 g/g 2.9 g/g [17] 0.66 g/g 0.19 g/g 2.9 g/g 7.3 g/g [17] 0.67 g/g 1.8 g/g 4.3 g/g 17 g/g 34 g/g L (low feeding: 20 Artemia/fish/ feeding ) L (medium feeding: 110 Artemia/fish/ feeding ) L (high feeding: 550 Artemia/ fish/feeding ) L (low feeding: 20 Artemia/fish/ feeding ) Summary of Biological Effects Tissue Concentrations for Chlorpyrifos Species: Taxa Concentration, Units in1: Sediment Water series 2 3.1 g/L 7.2 g/L 14 g/L 26 g/L 52 g/L series 2 3.1 g/L 7.2 g/L 14 g/L 26 g/L 52 g/L Leuresthes tenuis, California grunion Toxicity: Tissue (Sample Type) Effects 0.82 g/g 2.9 g/g 5.5 g/g 15.9 g/g 52 g/g [17] 2.2 g/g 5.3 g/g 13.9 g/g 37 g/g 95 g/g 0.21 mg/kg (whole body)4 0.038 mg/kg (whole body)4 0.21 mg/kg (whole body)4 0.21 mg/kg (whole body)4 Behavior, LOED Growth, LOED Growth, LOED Morphology, LOED [23] [23] Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [17] Comments3 L (medium feeding: 110 Artemia/fish/ feeding) L (high feeding: 550 Artemia/ fish/feeding) [23] [23] 0.58 mg/kg (whole body)4 0.39 mg/kg (whole body)4 185 Mortality, LOED Mortality, LOED [23] [23] L; reduced activity L; significant reduction in weight of fry L; significant reduction in mean fish weight L; fish appeared darker, abnormal lateral flexure of the back L; nearly 40% reduction in fry survival L; 38% reduction in fry survival 186 Species: Taxa Opsanus beta, Gulf toadfish Summary of Biological Effects Tissue Concentrations for Chlorpyrifos Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.58 mg/kg (whole body)4 0.15 mg/kg (whole body)4 0.015 mg/kg (whole body)4 0.15 mg/kg (whole body)4 0.15 mg/kg (whole body)4 0.015 mg/kg (whole body)4 0.15 mg/kg (whole body)4 0.038 mg/kg (whole body)4 0.21 mg/kg (whole body)4 770 mg/kg (whole body)4 12 mg/kg (whole body)4 175 mg/kg (whole body)4 Growth, NA Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [23] Comments3 L; significant reduction in weight of fry L; no effect on behavior L; no effect on weight of fry L; no effect on growth L; no effect on morphology L; no effect on fry mortality L; no effect on fry survival L; no effect on fry mortality L; no effect on fry survival L; delayed development of 25% of sac fry L; 25% reduction in average weight of fry L; 50% reduction in average weight of fry Behavior, NOED Growth, NOED Growth, NOED Morphology, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Development, ED25 Growth, ED25 Growth, ED50 [23] [23] [23] [23] [23] [23] [23] [23] [20] [20] [20] Summary of Biological Effects Tissue Concentrations for Chlorpyrifos Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 770 mg/kg (whole body)4 0.95 mg/kg (whole body)4 770 mg/kg (whole body)4 2.2 mg/kg (whole body)4 4.7 mg/kg (whole body)4 15 mg/kg (whole body)4 30 mg/kg (whole body)4 9.9 mg/kg (whole body)4 45 mg/kg (whole body)4 770 mg/kg (whole body)4 0.14 mg/kg (whole body)4 12 mg/kg (whole body)4 9.9 mg/kg (whole body)4 Behavior, LOED Growth, LOED Mortality, LOED Growth, NA Growth, NA Growth, NA Growth, NA Growth, NA Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [20] [20] [20] Comments3 L; hyperactivity, hyperventilation L; 9% reduction in fry weight L; significant increase in fry mortality L; 19% reduction in fry weight L; 21% reduction in fry weight L; 37% reduction in fry weight L; 42% reduction in fry weight L; 21% reduction in average weight of fry L; 35% reduction in average weight of fry L; 62% reduction in average weight of fry L; no effect on growth L; no effect on fry mortality L; no effect on fry mortality [20] [20] [20] [20] [20] Growth, NA [20] Growth, NA [20] Growth, NOED Mortality, NOED Mortality, NOED [20] [20] [20] 187 188 Species: Taxa 1 2 3 4 Summary of Biological Effects Tissue Concentrations for Chlorpyrifos Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 45 mg/kg (whole body)4 175 mg/kg (whole body)4 Mortality, NOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [20] [20] Comments3 L; no effect on fry mortality L; no effect on fry mortality Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. BIOACCUMULATION SUMMARY References 1. CHLORPYRIFOS MacKay, D., and Shin Wy; J. Chem Eng Data 22:399 (1977). (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Manual chemicals. Draft. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January. USEPA. 1992. Classification list of chemicals evaluated for carcinogenicity potential - U.S. Environmental Protection Agency, Office of Pesticide Programs, Washington, DC. Mull, M.S., G. Majori, and A.A. Arata. 1979. Impact of biological and chemical mosquito control agents on nontarget biota in aquatic ecosystems. In Mosquito control agents in aquatic ecosystems, pp. 121-173. Springer-Verlag, New York, NY. Weling, W., and J.W. de Vries. 1992. Bioconcentration kinetics of the organophosphorus insecticide chlorpyrifos in guppies (Poecilia reticulata). Ecotoxicol. Environ. Saf. 23:64-75. Racke, K.D. 1993. The environmental fate of chlorpyrifos. In Reviews of environmental contamination and toxicology, ed. G.W. Ware, Vol. 131, pp. 234-276. Springer-Verlag, New York, NY. Bailey, H.C., C. DiGiorgio, K. Kroll, J.L. Miller, D.E. Hinton, and G. Starrett. 1996. Development of procedures for indentifying pesticide toxicity in ambient waters: Carbofutran, diazinon, chlorpyrifos. Environ. Toxicol. Chem. 15:837-845. Green, A.S., G.T. Chandler, and W.W. Piegorsch. 1996. Life-stage-specific toxicity of sedimentassociated chlorpyrifos to a marine, infaunal copepod. Environ. Toxicol. Chem. 15:1182-1185. 2. 3. 4. 5. 6. 7. 8. 9. 10. 189 BIOACCUMULATION SUMMARY 11. CHLORPYRIFOS Wijngaarden van, R.P.A., P.J. van den Brink, S.J.H. Crum, J.H.O. Voshaar, T.C.M. Brock, and P. Leeuwangh. 1996. Effects of the insecticide Dursban 4E (active ingredient chlorpyrifos) in outdoor experimental ditches: I. Comparison of short-term toxicity between the laboratory and the field. Environ. Toxicol. Chem. 15:1133-1142. Ankley, G.T., D.J. Call, J.S. Cox, M.D. Kahl, R.A. Hoke, and P.A. Kosian. 1994. Organic carbon partitioning as a basis for predicting the toxicity of chlorpyrifos in sediments. Environ. Toxicol. Chem. 13:621-626. Kuivila, K.M., and C.G. Foe. 1995. Concentrations, transport and biological effects of dormant spray pesticides in the San Francisco estuary, California. Environ. Toxicol. Chem.14:1141-1150. Montanes, C.J.F., Bert van Hattum, and J. Deneer. 1995. Bioconcentration of chlorpyrifos by the freshwater isopod Asellus aquaticus (L.) in outdoor experimental ditches. Environ. Pollut. 88:137-146. Deneer, J.W. 1993. Uptake and elimination of chlorpyrifos in the guppy at sublethal and lethal aqueous concentrations. Chemosphere 26:1607-1616. Deneer, J.W. 1994. Bioconcentration of chlorpyrifos by the three-spined stickleback under laboratory and field conditions. Chemosphere 29:1561-1575. Cripe, G.M., D.J. Hansen, S.F. Macauley, and J. Forester. 1986. Effects of diet quantity on sheepshead minnows (Cyprinodon variegatus) during early life-stage exposures to chlorpyrifos. In Aquatic toxicology and environmental fate, ASTM STP 921, ed. T.M. Poston and R. Purdy, pp. 450-460. American Society for Testing and Materials, Philadelphia, PA. Ohayo-mitoko, G.J.A., and J.W. Deneer. 1993. Lethal body burdens of four organophosphorus pesticides in the guppy (Poecilia reticulata). Science Total Environ. 559-565. Serrano, R., F. Hernandez, J.B. Pena, V. Dosda, and J. Canales. 1995. Toxicity and bioconcentration of selected organophosphorus pesticides in Mytilus galloprovincialis and Venus gallina. Arch. Environ. Contam. Toxicol. 29: 284-290. Hansen, D.J., L.R. Goodman, G.M. Cripe, and S.F. Macauley. 1986. Early life-stage toxicity test methods for gulf toadfish (Opsanus beta) and results using chlorpyrifos. Ecotoxicol. Environ. Saf. 11:15-22. Jarvinen, A.W., B.R. Nordling, and M.E. Henry. 1983. Chronic toxicity of Dursban (chlorpyrifos) to the fathead minnow (Pimephales promelas) and the resultant acetylcholinesterase inhibition. Ecotoxicol. Environ. Saf. 7:423-434. Metcalf, R.L. 1974. A laboratory model ecosystem to evaluate compounds producing biological magnification. In Essays in Toxicology, ed. W.J. Hayes, Vol. 5, pp. 17-38. Academic Press, New York, NY. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 190 BIOACCUMULATION SUMMARY 23. CHLORPYRIFOS Goodman, L.R., D.J. Hansen, G.M. Cripe, D.P. Middaugh, and J.C. Moore. 1985. A new early lifestage toxicity test using the California grunion (Leuresthes tenuis) and results with chlorpyrifos. Ecotoxicol. Environ. Saf. 10:12-21. 191 192 BIOACCUMULATION SUMMARY CHROMIUM Chemical Category: METAL Chemical Name (Common Synonyms): CHROMIUM (hexavalent) CASRN: 18540-29-9 Chemical Characteristics Solubility in Water: Insoluble [1] Log Kow: Half-Life: Not applicable, stable [1] Log Koc: Human Health Oral RfD: 5 x 10-3 mg/kg/day [2] Confidence: Low, uncertainty factor = 500 Critical Effect: No effects observed (Currently under review by RfD/RfC Work Group) Oral Slope Factor: Not available [2] Carcinogenic Classification: A [2] Wildlife Partitioning Factors: Partitioning factors for chromium in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for chromium in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: In aqueous solutions, within a pH range of 6 to 8, hexavalent chromium is distributed between two species: monovalent hydrochromate anion and divalent chromate anion. Hexavalent chromium may account for 75 to 85 percent of the dissolved chromium while trivalent chromium is generally below detection limits in most oxic surface waters [3]. In some surface waters, as much as 10 to 15 percent of the dissolved chromium may be present in the colloidal/organic form. A log BCF of 2.74 was reported for Daphia magna [9]. Food Chain Multipliers: Little evidence exists for the bioaccumulation/biomagnification of chromium in aquatic food webs, although sediments frequently contain elevated concentrations of trivalent chromium [4]. Toxicity/Bioaccumulation Assessment Profile Chromium appears to have limited mobility under typical conditions in most aquatic habitats because the trivalent form tends to bind to sediments. Plants can, however, bioaccumulate and reduce chromium. 193 BIOACCUMULATION SUMMARY CHROMIUM Tissue residue-toxicity relationships can also be variable because organisms might sequester metal in various forms that might be analytically measurable as tissue residue but are actually stored in unavailable forms within the organism as a form of detoxification [5]. Whole body residues might also not be indicative of effects concentrations at the organ level because concentrations in target organs, such as the kidneys and liver, may be 20 times more than whole body residues [6]. The application of "clean" chemical analytical and sample preparation techniques is critical for the accurate measurement of metal tissue residues [7]. Accumulation of hexavalent chromium in the gills of rainbow trout was significantly higher at pH 6.5 than at 8.1 and is directly coupled with oxygen transfer, irrespective of exposure time or concentration [8]. The authors of that study suggested that chromium uptake might be related to the HCr04 to Cr04 ratio, whereby the monovalent hydrochromate anion is taken up more readily by the gill tissue. 194 Summary of Biological Effects Tissue Concentrations for Chromium Species: Taxa Invertebrates Mytilus galloprovincialis, Mussel Daphnia magna, Cladoceran Xantho hydrophilus, Mud crab 1 g/L Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.73-1.04 mg/kg Ability to Accumulate2: Log Log BCF BAF BSAF 0.018 Source: Reference [13] Comments3 F Day 21: 1.1 mmol/kg 0.2 g/g (whole body) 0.2 g/g (hepatopancreas) 0.4 g/g (gill) 0.05 g/g (muscle) 10% mortality 2.74 [9] F [12] F Fishes Oncorhynchus mykiss (Salmo gairdneri), Rainbow trout 2.5 mg/L Day 22: 171 g/g (skin) 187 g/g (muscle) 132 g/g (gastrointestinal) 49.8 g/g (bone) 75.4 g/g (kidney) 77.2 g/g (blood) 41.4 g/g (gill) 16.9 g/g (fat) 27.3 g/g (liver) 133.6 g/g 16.6 g/g [10] L 10.0 g/L 1.3 g/L [11] L 195 196 Species: Taxa Sediment Oncorhynchus mykiss Salmo gairdneri), Rainbow trout Summary of Biological Effects Tissue Concentrations for Chromium Concentration, Units in1: Water 2.0 mg/L Tissue (Sample Type) 2.0 g/g (whole body) 31.7 g/g (gill) 6.2 g/g (digestive tract) 2.0 g/g (liver) 6.7 g/g (kidney) 0.9 g/g (whole body) 5.1 g/g (gill) 7.4 g/g (digestive tract) 3.4 g/g (liver) 8.5 g/g (kidney) 5.5 g/g (whole body) 51.8 g/g (gill) 9.5 g/g (digestive tract) 3.8 g/g (liver) 10.7 g/g (kidney) 2.3 g/g (whole body) 10.6 g/g (gill) 11.2 g/g (digestive tract) 5.1 g/g (liver) 12.2 g/g (kidney) 8.7 g/g (whole body) 139 g/g (gill) 23.4 g/g (digestive tract) 24.8 g/g (liver) 43.2 g/g (kidney) Toxicity: Effects 100% survival Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference [8] Comments3 L; pH = 6.5 2.0 mg/L 100% survival [8] L; pH = 7.8 5.0 mg/L 100% survival [8] L; pH = 6.5 5.0 mg/L 100% survival [8] L; pH = 7.8 16.5 mg/L 25% survival [8] L; pH = 6.5 Summary of Biological Effects Tissue Concentrations for Chromium Species: Concentration, Units in1: Water 16.5 mg/L Toxicity: Tissue (Sample Type) Effects 8.9 g/g (whole body) 63% survival 35.3 g/g (gill) 22.6 g/g (digestive tract) 25.9 g/g (liver) 24.6 g/g (kidney) 0% survival 10.5 g/g (whole body) 50% survival 37.6 g/g (gill) 45.0 g/g (digestive tract) 84.6 g/g (liver) 70.3 g/g (kidney) 45 mg/kg (digestive tract)4 Mortality, ED50 Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference [8] Comments3 L; pH = 7.8 Taxa Sediment Oncorhynchus mykiss (Salmo gairdneri), Rainbow trout 50 mg/L 50 mg/L [8] [8] L; pH = 6.5 L; pH = 7.8 Oncorhynchus mykiss, Rainbow trout [14] 37.6 mg/kg (gill)4 Mortality, ED50 [14] 70.3 mg/kg (kidney)4 Mortality, ED50 [14] 85.6 mg/kg (liver)4 Mortality, ED50 [14] L; pH 7.8; increased mortality relative to control L; pH 7.8; increased mortality relative to control L; pH 7.8; increased mortality relative to control L; pH 7.8; increased mortality relative to control 197 198 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Chromium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 10.5 mg/kg Mortality, (whole body)4 ED50 Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference [14] Comments3 L; pH 7.8; increased mortality relative to control L; pH 6.5; increased mortality relative to control L; pH 6.5; increased mortality relative to control L; pH 6.5; increased mortality relative to control L; pH 6.5; increased mortality relative to control L; pH 6.5; increased mortality relative to control L; pH 7.8; increased mortality relative to control L; pH 7.8; increased mortality relative to control 23.4 mg/kg (digestive tract)4 Mortality, ED75 [14] 139 mg/kg (gill)4 Mortality, ED75 [14] 43.1 mg/kg (kidney)4 Mortality, ED75 [14] 24.8 mg/kg (liver)4 Mortality, ED75 [14] 8.7 mg/kg (whole body)4 Mortality, ED75 [14] 22.6 mg/kg (digestive tract)4 Mortality, NA [14] 35.3 mg/kg (gill)4 Mortality, NA [14] Summary of Biological Effects Tissue Concentrations for Chromium Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 24.6 mg/kg (kidney)4 Mortality, NA Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference [14] Comments3 L; pH 7.8; increased mortality relative to control L; pH 7.8; increased mortality relative to control L; pH 7.8; increased mortality relative to control L; pH 6.5; no increased mortality relative to control L; pH 7.8; no increased mortality relative to control L; pH 6.5; no increased mortality relative to control L; pH 7.8; no increased mortality relative to control L; pH 6.5; no increased mortality relative to control 25.9 mg/kg (liver)4 Mortality, NA [14] 8.9 mg/kg (whole body)4 Mortality, NA [14] 9.5 mg/kg (digestive tract)4 Mortality, NOED [14] 11.2 mg/kg (digestive tract)4 Mortality, NOED [14] 51.8 mg/kg (gill)4 Mortality, NOED [14] 10.6 mg/kg (gill)4 Mortality, NOED [14] 10.7 mg/kg (kidney)4 Mortality, NOED [14] 199 200 Species: Taxa Sediment 1 2 3 4 Summary of Biological Effects Tissue Concentrations for Chromium Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 12.2 mg/kg (kidney)4 Mortality, NOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference [14] Comments3 L; ph 7.8; no increased mortality relative to control L; pH 6.5; no increased mortality relative to control L; pH 7.8; no increased mortality relative to control L; pH 6.5; no increased mortality relative to control L; pH 7.8; no increased mortality relative to control 3.8 mg/kg (liver)4 Mortality, NOED [14] 5.1 mg/kg (liver)4 Mortality, NOED [14] 5.5 mg/kg (whole body)4 Mortality, NOED [14] 2.3 mg/kg (whole body)4 Mortality, NOED [14] Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed and the reader is strongly urged to consult the publication to confirm the information presented here. BIOACCUMULATION SUMMARY CHROMIUM References 1. Sax. Hawley's condensed chemical dictionary, 11th ed., 1987, p. 280. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Beaubien, S., J. Nriagu, D. Blowes, and G. Lawson. 1994. Chromium speciation and distribution in the Great Lakes. Environ. Sci. Technol. 28:730-736. Weis, J.S., and P. Weis. 1993. Trophic transfer of contaminants from organisms living by chromated-copper-arsenate (CCA)-treated wood to their predators. J. Exp. Mar. Biol. Ecol. 168:25-34. Klerks, P.L., and P.R. Bartholomew. 1991. Cadmium accumulation and detoxification in a Cdresistant population of the oligochaete Limnodrilus hoffmeisteri. Aquatic Toxicol. 19:97-112. McKinney, J. 1993. Metals bioavailability and disposition kinetics research needs workshop. July 18-19, 1990. Toxicol. Environ. Chem. 38:1-71. Schmitt, C.J., and S.E. Finger. 1987. The effects of sample preparation on measured concentrations of eight elements in edible tissues of fish from streams contaminated by lead mining. Arch. Environ. Contam. Toxicol. 16:185-207. Van der Putte, I., and P. Part. 1982. Oxygen and chromium transfer in perfused gills of rainbow trout (Salmo gairdneri) exposed to hexavalent chromium at two different pH levels. Aquat. Toxicol. 2:31-45. Enserink, E.L., J.L. Maas-Diepeveen, and C.J. van Leeuwen. 1991. Combined effects of metals: An ecotoxicological evaluation. Water Res. 25:679-687. Buhler, D.R., R.M. Stokes, and R.S. Caldwell. 1977. Tissue accumulation and enzymatic effects of hexavalent chromium in rainbow trout (Salmo gairdneri). J. Fish. Res. Board Can. 34:9-18. Fromm, P.O., and R.M. Stokes. 1962. Assimilation and metabolism of chromium by trout. J. Water Poll. Control. Fed. 34:1151-1155. Peternac, B., and T. Legovic. 1986. Uptake, distribution and loss of Cr in the crab Xantho hydrophilus. Mar. Biol. 91:467-471. Houkal, D., B. Rummel, and B. Shephard. 1996. Results of an in situ mussel bioassay in the Puget Sound. Abstract, 17th Annual Meeting Society of Environmental Toxicology and Chemistry, Washington, DC, November 17-21, 1996. 201 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. BIOACCUMULATION SUMMARY CHROMIUM 14. Van De Putte, L., J. Lubbers, and Z. Kolar, 1981. Effect of pH on uptake, tissue distribution and retention of hexavelent chromium in rainbow trout (Salmo gairdneri). Aquatic Toxicol. 1: 3-18. 202 BIOACCUMULATION SUMMARY CHRYSENE Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight) Chemical Name (Common Synonyms): CHRYSENE CASRN: 218-01-9 Chemical Characteristics Solubility in Water: 0.0020 mg/L at 25C [1] Half-Life: 1.02 yrs - 2.72 yrs based on aerobic soil die-away test data. [2] Log Koc: 5.60 L/kg organic carbon Log Kow: 5.70 [3] Human Health Oral RfD: No data [4] Critical Effect: -- Oral Slope Factor (Reference): Not available [4] Carcinogenic Classification: B2 [4] Confidence: -- Wildlife Partitioning Factors: Partitioning factors for chrysene in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for chrysene in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Partitioning factors for chrysene in aquatic organisms were not found in the literature. Food Chain Multipliers: Food chain multipliers for chrysene in aquatic organisms were not found in the literature. Log BAF values found in the literature ranged from -0.68 for the clam Macoma nasuta [7] to 4.31 for the amphipod Pontoporeia hoyi [9]. Toxicity/Bioaccumulation Assessment Profile The results from the laboratory experiments performed by Harkey [5] indicated that accumulation of chrysene from elutriates was significantly lower than that from whole sediment, and the elutriate-sediment accumulations followed a downward curve over time. A similar curve was observed for pore water-tosediment accumulation ratios. The concentrations of chrysene in whole sediment and pore water were 34.2 ng/g and 0.305 mg/mL, respectively [5]. Uptake rate coefficients for Diporeia spp. were highest in pore water (244.3 g/goc /h) and lowest in elutriate (55.2 g/g oc /h). The authors concluded that aqueous 203 BIOACCUMULATION SUMMARY CHRYSENE extracts of whole sediment did not accurately represent the exposure observed in whole sediment [5]. The aqueous extracts of whole sediment underexposed organisms, compared to whole sediment, even after adjusting accumulation to the fraction of organic carbon contained in the test media. While the total chrysene concentration in the sediment stayed constant, total concentration decreased appreciably in pore water and elutriate over the course of the exposure, and it is likely that the bioavailability concentrations in these media also decreased. Benthic amphipods, Gammarus pulex, exposed to sediments containing polynuclear aromatic hydrocarbons (PAHs) and water spiked with sediment extract from PAHcontaminated sediment, accumulated chrysene in direct proportion to exposure concentrations [6]. 204 Summary of Biological Effects Tissue Concentrations for Chrysene Species: Taxa Invertebrates Macoma nasuta, Clam 7.4 ng/g 5.9 ng/g 50 ng/g 41 ng/g 174 ng/g 249 ng/g 29 ng/g 8.1 ng/g 29.8 ng/g 30 ng/g 88 ng/g 72 ng/g -0.21 -0.68 -0.40 -0.28 -0.33 -0.41 [7] [7] [7] [7] [7] [7] F F F F F F Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Diporeia spp., Amphipod 15 nmol/g 213 nmol/g [8] L Diporeia spp., Amphipod 2.6 mg/kg (whole body)4 Mortality, NOED [5] L; no increase in mortality in 96 hours Pontoporeia hoyi, Amphipod 50 ng/g 30 ng/g 7 ng/mL 1.5 ng/mL 600 ng/g 180 ng/g 4.31 [9] [9] L L 205 206 Summary of Biological Effects Tissue Concentrations for Chrysene Species: Taxa Fishes Oncorhynchus mykiss, Rainbow trout 30 mg/kg (whole body)4 Physiological, LOED [11] L; induction of hepatic mixed function oxidases Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Cyprinus carpio, Common carp 109 mg/kg (liver)4 Physiological, NA [10] L; significant increase in EROD enzyme and P450 1a protein content 1 2 3 4 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. BIOACCUMULATION SUMMARY References 1. CHRYSENE Mackay, D., and Shin Wy; J. Chem. Eng. Data 22:399 (1977). (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January. Harkey, G.A., P.F. Landrum, and S.J. Klaine. 1994. Comparison of whole-sediment, elutriate and pore-water exposures for use in assessing sediment-associated organic contaminants in bioassays. Environ. Toxicol. Chem. 13:1315-1329. Maltby, L., A.B.A. Boxall, D.M. Forrow, P. Calow, and C.I. Betton. 1995. The effects of motorway runoff on freshwater ecosystems: 2. Identifying major toxicants. Environ. Toxicol. Chem. 14:1093-1101. Ferraro, S.P., H. Lee II, R.J. Ozretich, and D.T. Specht. 1990. Predicting bioaccumulation potential: A test of a fugacity-based model. Arch. Environ. Contam. Toxicol. 19:386-394. Landrum, P.F., B.J. Eadie, and W.R. Faust. 1992. Variation in the bioavailability of polycyclic aromatic hydrocarbons to the amphipod Diporeia (spp.) with sediment aging. Environ. Toxicol. Chem. 11:1197-1208. Eadie, B.J., P.F. Landrum, and W. Faust. 1982. Polycyclic aromatic hydrocarbons in sediments, pore water and the amphipod Pontoporeia hoyi from Lake Michigan. Chemosphere 11:847-858. Van Der Weidern, M.E.J., F.H.M Hanegraaf, M.L Eggens, M. Celander, W. Seinen, and M. Ven Den Berg. 1994. Temporal induction of cytochrome P450 1a in the mirror carp (Cyprinus carpio) after administration of several polycyclic aromatic hydrocarbons. Environ. Toxicol. Chem. 13: 797-802. Gerhart, E.H., and R.H. Carlson. 1978. Hepatic mixed-function oxidase activity in rainbow trout exposed to several polycyclic aromatic hydrocarbons. Environ. Res. 17:284-295. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 207 208 BIOACCUMULATION SUMMARY Chemical Category: METAL Chemical Name (Common Synonyms): COPPER COPPER CASRN: 7440-50-8 Chemical Characteristics Solubility in Water: Insoluble [1] Log Kow: -- Half-Life: Not applicable, stable [1] Log Koc: -- Human Health Oral RfD: Not available [2] Critical Effect: -- Oral Slope Factor: No data [2] Carcinogenic Classification: D [2] Confidence: -- Wildlife Partitioning Factors: Partitioning factors for copper in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for copper in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Up to 29 different species of copper can be present in aqueous solution in the pH range from 6 to 9. Aqueous copper speciation and toxicity depend on the ionic strength of the water. The hydroxide species and free copper ions are mostly responsible for toxicity, while copper complexes consisting of carbonates, phosphates, nitrates, ammonia, and sulfates are weakly toxic or nontoxic. Copper in the aquatic environment can partition to dissolved and particulate organic carbon. The bioavailability of copper also can be influenced to some extent by total water hardness. Bioavailability of copper in sediments is controlled by the acid-volatile sulfide (AVS) concentration [12]. A log BCF of 3.77 was reported for the midge [4]. Food Chain Multipliers: Little evidence exists to support the general occurrence of biomagnification of copper in the aquatic environment [3]. Copper is taken up by aquatic organisms primarily through dietary exposure. 209 BIOACCUMULATION SUMMARY Toxicity/Bioaccumulation Assessment Profile COPPER The free copper ions are the most bioavailable inorganic forms, although they might account for only a minor proportion of the total dissolved metal. The concentration of copper found in interstitial water is usually much lower than that in surface water. The amount of bioavailable copper in sediment is controlled in large part by the concentration of AVS and organic matter. A considerable number of aquatic species are sensitive to dissolved concentrations of copper in the range of 1-10 g/L. Metal metabolism by aquatic biota has significant affects on metal accumulation, distribution in tissues, and toxic effects. Concentration of copper in benthic organisms from contaminated areas can be one to two orders of magnitude higher than normal. Copper is accumulated by aquatic organisms primarily through dietary exposure [3]. However, most organisms retain only a small proportion of the heavy metals ingested with their diet. Rule and Alden [13] studied the relationship between uptake of cadmium and copper from the sediment by blue mussel (Mytilus edulis), grass shrimp (Palaemonetes pugio), and hard clam (Mercenaria mercenaria). The uptake of copper by all organisms was related only to copper concentration in sediment. 210 Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Plants Eichhornia crassipes, Water Hyacinth 11.4 mg/kg (leaf) 549 mg/kg (root) 37.8 mg/kg (stem) 11.4 mg/kg (leaf) Growth, LOED Growth, LOED Growth, LOED Morphology, LOED [22] [22] [22] [22] L; reduced growth rate, chlorosis L; reduced growth rate, chlorosis L; reduced growth rate, chlorosis L; chlorosis, browning, necrosis, waterlogging of tissues L; chlorosis, browning, necrosis, waterlogging of tissues L; chlorosis, browning, necrosis, waterlogging of tissues L; reduced growth rate, chlorosis L; reduced growth rate, chlorosis L; reduced growth rate, chlorosis Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 549 mg/kg (root) Morphology, LOED [22] 37.8 mg/kg (stem) Morphology, LOED [22] 13.8 mg/kg (leaf) 1,750 mg/kg (root) 74.4 mg/kg (stem) 211 Growth, NA Growth, NA Growth, NA [22] [22] [22] 212 Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 13.8 mg/kg (leaf) Morphology, NA Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [22] L; chlorosis, browning, necrosis, waterlogging of tissues L; chlorosis, browning, necrosis, waterlogging of tissues L; chlorosis, browning, necrosis, waterlogging of tissues L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on plant appearance 1,750 mg/kg (root) Morphology, NA [22] 74.4 mg/kg (stem) Morphology, NA [22] 4.6 mg/kg (leaf) 7.8 mg/kg (leaf) 20.8 mg/kg (root) 82.8 mg/kg (root) 10 mg/kg (stem) 15.2 mg/kg (stem) 4.6 mg/kg (leaf) Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Morphology, NOED [22] [22] [22] [22] [22] [22] [22] Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 7.8 mg/kg (leaf) 20.8 mg/kg (root) 82.8 mg/kg (root) 10 mg/kg (stem) 15.2 mg/kg (stem) Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [22] [22] [22] [22] [22] L; no effect on plant appearance L; no effect on plant appearance L; no effect on plant appearance L; no effect on plant appearance L; no effect on plant appearance Invertebrates Invertebrates field-collected Total SEM Filt Nonfilt Body g/g g/g g/L g/L 7,820 6,971 79 11,080 1,382 g/g 583 325 36 698 122 g/g 480 287 16 274 181 g/g 478 251 9 184 266 g/g 128 77 9 58 48 g/g 16 <12 2 35 26 g/g [10] F Tubificidae 172 g/g 185 g/g 175 g/g 125 g/g 130 g/g 17.14 mg/g 10.23 mg/g 16.11 mg/g 20.12 mg/g 14.73 mg/g [9] F 213 214 Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Nereis diversicolor, Polychaete worm Concentration, Units in1: Sediment 41 g/g 44 g/g 52 g/g 73 g/g 436 g/g 591 g/g 3,020 g/g Water Toxicity: Tissue (Sample Type) Effects 28 g/g 22 g/g 33 g/g 31 g/g 106 g/g 257 g/g 1,142 g/g Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [5] L Meretrix casta, Marine clam 201 mg/kg (whole body)4 Mortality, ED50 [25] L; lethal body burden Mytilus edulis, Mussel 67.4 mg/kg (whole body)4 67.4 mg/kg (whole body)4 Mortality, ED50 [21] Behavior, LOED [21] 80 mg/kg (whole body)4 36 mg/kg (whole body)4 23 mg/kg (whole body)4 15 mg/kg (whole body)4 Mortality, ED100 Mortality, ED100 Mortality, ED100 Mortality, ED100 [26] [26] [26] [26] L; lethal body burden after 7 - 8 days L; total valve closure, increased mucus production, reduced byssus production L; lethal body burden L; lethal body burden L; lethal body burden L; lethal body burden Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 12 mg/kg (whole body)4 12 mg/kg (whole body)4 12 mg/kg (whole body)4 56 mg/kg (whole body)4 Mortality, ED100 Mortality, ED100 Mortality, ED100 Mortality, ED100 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [26] [26] [26] [26] L; lethal body burden L; lethal body burden L; lethal body burden L; lethal body burden Mytilus galloprovincialis, Mussel 1.9-3.1 mg/kg 0.04 [14] F Dreissena polymorpha, Zebra mussel 8.1 mg/kg (whole body)4 Physiological; LOED [24] 2.7 mg/kg (whole body)4 Physiological, NOED [24] L; indicative of breakdown of internal Cu regulatory process L; no effect on internal Cu regulatory process 215 216 Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Elliptio complanata, Freshwater mussel Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 5.4 g/g (foot) 2.4 g/g (muscle) 8.5 g/g (visceral) 29.0 g/g (hepatopancreas) 29.5 g/g (gill) 17.6 g/g (mantle) 5.4 g/g (foot) 2.7 g/g (muscle) 10.5 g/g (visceral) 28.8 g/g (hepatopancreas) 27.8 g/g (gill) 11.8 g/g (mantle) 12.7 g/g (foot) 11.7 g/g (muscle) 16.5 g/g (visceral) 44.5 g/g (hepatopancreas) 214 g/g (gill) 94 g/g (mantle) Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [11] F 0.1-23.7 g/g 0.1-40.7 g/g 0.2-106 g/g Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 13.1 g/g (foot) 10.7 g/g (muscle) 16.1 g/g (visceral) 72.9 g/g (hepatopancreas) 132 g/g (gill) 81.7 g/g (mantle) Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Elliptio complanata, 0.3-142 g/g Freshwater mussel Unio pictorum, Freshwater mussel 6.5 mg/kg (digestive gland)4 Physiological; LOED [24] 10 mg/kg (gill)4 Physiological; LOED [24] 4.6 mg/kg (mantle)4 Physiological; LOED [24] 2.7 mg/kg (digestive gland)4 Physiological; NOED [24] L; indicative of breakdown of internal Cu regulatory process L; indicative of breakdown of internal Cu regulatory process L; indicative of breakdown of internal Cu regulatory process L; no effect on internal Cu regulatory process 217 218 Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 1.9 mg/kg (gill)4 Physiological; NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [24] L; no effect on internal Cu regulatory process L; no effect on internal Cu regulatory process L; no effect on internal Cu regulatory process L; no effect on internal Cu regulatory process L; no effect on internal Cu regulatory process L; no effect on internal Cu regulatory process 1.7 mg/kg (gonad)4 Physiological; NOED [24] 4 mg/kg (gonad)4 Physiological; NOED [24] 2 mg/kg (kidney)4 Physiological; NOED [24] 3.7 mg/kg (kidney)4 Physiological; NOED [24] 1.1 mg/kg (mantle)4 Physiological; NOED [24] Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Daphnia magna, Cladoceran Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 5.8 mg/kg (whole body)4 68 mg/kg (whole body)4 Reproduction, ED10 Mortality, ED50 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [7] L; 10% reduction in number of offspring L; lethal body burden after 21 day exposure [7] Hyalella azteca, Amphipod 7.7 g/L 10.7 g/L 16.7 g/L 25.4 g/L 43.8 g/L 81.3 g/L 91 g/g 92 g/g 95 g/g 88 g/g 80 g/g -- 54% survival 50% survival 40% survival 29% survival 6% survival 0% survival [6] L Hyalella azteca, Amphipod Total g/g 583 480 478 128 16 SEM Filt Nonfilt g/g g/L g/L 79 11,080 36 16 9 9 2 698 274 184 58 35 325 287 251 77 <12 Body; 249 g/g 87 g/g 124 g/g 127 g/g 124 g/g 84 g/g [10] F 7,820 6,971 219 220 Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Corophium volutator, Amphipod Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 16.9 mg/kg (whole body)4 NA, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [18] L; 100% dissolved oxygen saturation during test Balanus crenatus, Barnacle 80 mg/kg (whole body)4 Behavior, NOED [29] L; regulation of metals endpointsummer experiment Orconectes rusticus, Crayfish 24 mg/kg (abdomen)4 26 mg/kg (abdomen)4 32 mg/kg (abdomen)4 42 mg/kg (abdomen)4 52 mg/kg (abdomen)4 17.8 mg/kg (claw)4 24 mg/kg (claw)4 24 mg/kg (claw)4 30 mg/kg (claw)4 Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED [19] [19] [19] [19] [19] [19] [19] [19] [19] L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 34 mg/kg (claw)4 42 mg/kg (thorax)4 50 mg/kg (thorax)4 56 mg/kg (thorax)4 60 mg/kg (thorax)4 70 mg/kg (thorax)4 2 mg/kg (whole body)4 9 mg/kg (whole body)4 11.2 mg/kg (whole body)4 19.2 mg/kg (whole body)4 26 mg/kg (whole body)4 Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [19] [19] [19] [19] [19] [19] [19] [19] [19] [19] [19] L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship L; no effect on survivorship 221 222 Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Chironomus riparius, Midge Concentration, Units in1: Sediment Water 0.087 mg/L Toxicity: Tissue (Sample Type) Effects 500 g/g Ability to Accumulate2: Log BCF 3.77 Log BAF BSAF Source: Reference Comments3 [4] F Chironomus thummi, 12.55 mg/kg Midge 35.7 mg/kg 39.7 mg/kg Normal larvae Deformed larvae [8] F Chironomus decorus, Midge 1,000 mg/kg (whole body)4 142 mg/kg (whole body)4 107 mg/kg (whole body)4 126 mg/kg (whole body)4 86.2 mg/kg (whole body)4 130 mg/kg (pupal exuviae)4 Mortality, ED100 Mortality, ED50 Mortality, LOED Mortality, LOED Mortality, NOED Development, LOED [23] [23] [23] [23] [23] [23] L; 100% mortality L; ED50 L; significant mortality L; significant mortality L; no effect on mortality L; increased time to adult emergence by 10 days L; increased time to adult emergence by 10 days L; no effect on time to adult emergence 18 mg/kg (whole body)4 Development, LOED [23] 14.8 mg/kg (pupal exuviae)4 Development, NOED [23] Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 75.6 mg/kg (pupal exuviae)4 2.28 mg/kg (whole body)4 7.2 mg/kg (whole body)4 13 mg/kg (whole body)4 7.14 mg/kg (whole body)4 Development, NOED Development, NOED Development, NOED Development, NOED Morphology, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [23] L; no effect on time to adult emergence L; no effect on time to adult emergence L; no effect on time to adult emergence L; no effect on time to adult emergence L; 4th instar larvae [23] [23] [23] [8] Fishes Oncorhynchus mykiss, Rainbow trout 40 mg/kg (whole body)4 1.6 mg/kg (whole body)4 Physiological; LOED Mortality, ED100 [16] L; induction of metallothionein L; 100% mortality in non-metallothionein-induced fish L; induction of metallothionein L; 50% mortality in 7 hours [17] 6.8 mg/kg (whole body)4 2.22 mg/kg (whole body)4 Physiological, LOED Mortality, LOED [17] [20] 223 224 Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 4.48 mg/kg (whole body)4 3.92 mg/kg (whole body)4 Pimephales promelas, Fathead minnow 78.9 g/g 110 g/g 125 g/g 130 g/g 130 g/g 172 g/g 175 g/g 175 g/g 185 g/g Cyprinus carpio, Common carp 10.28 mg/g 9.32 mg/g 9.13 mg/g 9.70 mg/g 9.86 mg/g 6.92 mg/g 7.28 mg/g 10.96 mg/g 9.37 mg/g 12.1 mg/kg (whole body)4 Morphology, LOED [29] L; larval deformation, pH 6.3, body burden from graph L; larval deformation, pH 7.6, body burden from graph L; larval mortality, pH 6.3, body burden from graph Survival, LOED Not applicable, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [27] [27] L L [9] F 12.1 mg/kg (whole body)4 Morphology, LOED [29] 12.1 mg/kg (whole body)4 Mortality, LOED [29] Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 12.1 mg/kg (whole body)4 Mortality, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [29] L; larval mortality, pH 7.6, body burden from graph L; egg mortality, pH 6.3, body burden from graph L; larval deformation, pH 7.6, body burden from graph L; larval mortality, pH 7.6, body burden from graph L; egg mortality, pH 7.6, body burden from graph L; egg mortality, pH 6.3, body burden from graph L; duration = 22 months or 660 days 24.1 mg/kg (whole body)4 Reproduction, LOED [29] 7.62 mg/kg (whole body)4 Morphology, NOED [29] 7.62 mg/kg (whole body)4 Mortality, NOED [29] 12.1 mg/kg (whole body)4 Reproduction, NOED [29] 12.1 mg/kg (whole body)4 Reproduction, NOED [29] Lepomis macrochirus, Bluegill 225 13 mg/kg (gill)4 Growth, LOED [15] 226 Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 44 mg/kg (kidney)4 Growth, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [15] L; duration = 22 months or 660 days L; duration = 22 months or 660 days L; duration = 22 months or 660 days L; duration = 22 months or 660 days L; duration = 22 months or 660 days L; duration = 22 months or 660 days L; duration = 22 months or 660 days L; duration = 22 months or 660 days L; duration = 22 months or 660 days L; duration = 22 months or 660 days 480 mg/kg (liver)4 Growth, LOED [15] 13 mg/kg (gill)4 Mortality, LOED [15] 44 mg/kg (kidney)4 Mortality, LOED [15] 480 mg/kg (liver)4 Mortality, LOED [15] 13 mg/kg (gill)4 Reproduction, LOED Reproduction, LOED Reproduction, LOED Growth, NOED [15] 44 mg/kg (kidney)4 [15] 480 mg/kg (liver)4 [15] 6 mg/kg (gill)4 [15] 12 mg/kg (kidney)4 Growth, NOED [15] Summary of Biological Effects Tissue Concentrations for Copper Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 57 mg/kg (liver)4 Growth, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [15] L; duration = 22 months or 660 days L; duration = 22 months or 660 days L; duration = 22 months or 660 days L; duration = 22 months or 660 days L; duration = 22 months or 660 days L; duration = 22 months or 660 days L; duration = 22 months or 660 days 6 mg/kg (gill)4 Mortality, NOED [15] 12 mg/kg (kidney)4 Mortality, NOED [15] 57 mg/kg (liver)4 Mortality, NOED [15] 6 mg/kg (gill)4 Reproduction, NOED Reproduction, NOED Reproduction, NOED [15] 12 mg/kg (kidney)4 [15] 57 mg/kg (liver)4 [15] 1 2 3 4 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. 227 BIOACCUMULATION SUMMARY References 1. COPPER Weast handbook of chemistry and physics, 68th edition, 1987-1988, B-88. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Woodward, D.F., W.G. Brumbaugh, A.J. DeLonay, E.E. Little, and C.E. Smith. 1994. Effects on rainbow trout fry of a metals-contaminated diet of benthic invertebrates from the Clark Fork River, Montana. Tran. Amer. Fish. Soc. 123:51-62. Timmermans, K.R., E. Spijkerman, and M. Tonkes. 1992. Cadmium and zinc uptake by two species of aquatic invertebrate predators from dietary and aqueous sources. Can. J. Fish. Aquat. Sci. 49: 655-662. Bryan, G.W., and L.G. Hummerstone. 1971. Adaptation of the polychaete Nereis diversicolor to estuarine sediments containing high concentrations of heavy metals. J. Mar. Biol. Ass. U.K. 51:845863. Borgmann, U., W.P. Norwood, and C. Clarke. 1993. Accumulation, regulation and toxicity of copper, zinc, lead and mercury in Hyalella azteca. Hydrobiologia 259:79-89. Enserink, E.L., J.L. Mass-Diepeveen, and C.J. Van Leeuwen. 1991. Combined effects of metals: An ecotoxicological evaluation. Water Res. 25:679-687. Janssens De Bisthoven, L.G., K.R. Timmermans, and F. Ollevier. 1992. The concentration of cadmium, lead, copper, and zinc in Chironomus gr. tummi larvae (Diptera, Chironomidae) with deformed versus normal antennae. Hydrobiologia 239:141-149. Krantzberg, G. 1994. Spatial and temporal variability in metal bioavailability and toxicity of sediment from Hamilton Harbour, Lake Ontario. Environ. Toxicol. Chem. 13:1685-1698. 2. 3. 4. 5. 6. 7. 8. 9. 10. Ingersoll; C.G., W.G. Brumbaugh, F.J. Dwuer, and N. E. Kemble. 1994. Bioaccumulation of metals by Hyalella azteca exposed to contaminated sediments from the Upper Clark Fork River, Montana. Environ. Toxicol. Chem. 13:2013-2020. 11. Tessier, A., P.G.C. Campbell, J.C. Auclair, and M. Bisson. 1984. Relationships between the partitioning of trace metals in sediments and their accumulation in the tissues of the freshwater mollusc Elliptio complanata in a mining area. Can. J. Fish. Aquat. Sci. 41:1463-1472. 12. Di Toro, D.M., J.D. Mahony, D.J. Hansen, K.J. Scott, M.B. Hicks, S.M. Mayr, and M.S. Redmond. 1990. Toxicity of cadmium in sediments: The role of acid volatile sulfide. Environ. Toxicol. Chem. 9:1487-1502. 228 BIOACCUMULATION SUMMARY COPPER 13. Rule J.H., and R.W. Alden III. 1996. Interactions of Cd and Cu in anaerobic estuarine sediments. II. Bioavailability, body burdens and respiration effects as related to geochemical partitioning. Environ. Toxicol. Chem. 15:466-471. 14. Houkal, D., B. Rummel, and B. Shephard. 1996. Results of an in situ mussel bioassay in the Puget Sound. Abstract, 17th Annual Meeting Society of Environmental Toxicology and Chemistry, Washington, DC, November 17-21, 1996. 15. Benoit, D.A. 1975. Chronic effects of copper on survival; growth, and reproduction of the bluegill (Lepomis macrochirus). Trans. Am. Fish. Soc. 104(2):353-358 16. Bonham, K., M. Zararullah, and L. Gedamu. 1987. The rainbow trout metallothioneins: Molecular cloning and characterization of two distinct cDNA sequences. DNA 6:519-528. 17. Dixon, D.G.,and J.B. Sprague. 1981. Copper bioaccumulation and hepatoprotein synthesis during acclimation to copper by juvenile rainbow trout. Aquat. Toxicol. 1:69-81. 18. Ericksson, S.P., and J.M. Weeks. 1994. Effects of copper and hypoxia on two populations of the benthic amphipod Corophium volutator (Pallas). Aquat. Toxicol. 29:73-81 19. Evans, M.L. 1980. Copper accumulation in the crayfish (Orconectes rusticus). Bull. Environ. Contam. Toxicol. 24:916-920. 20. Handy, R.D. 1992. The assessment of episodic metal pollution. I. Uses and limitations of tissue contaminant analysis in rainbow trout (Oncorhynchus mykiss) after short waterborne exposure to cadmium or copper. Arch. Environ. Contam. Toxicol. 22:74-81. 21. Hvilsom, M.M. 1983. Copper induced differential mortality in the mussel Mytilus edulis. Mar. Biol. 76:291-295. 22. Kay, S.H., W.T. Haller, and L.A. Garrard. 1984. Effects of heavy metals on water hyacinths (Eichhornia crassipes (mart.) Solms). Aquat. Toxicol. 5:117-128. 23. Kosalwat, P., and A.W. Knight. 1987. Acute toxicity of aqueous and substrate bound copper to the midge, Chironomus decorus. Arch. Environ. Contam. Toxicol. 16:275-282. 24. Kraak, M.H.S., M. Toussaint, E.A.J. Bleeker, and D. Lavy. 1993. Metal regulation in two species of freshwater bivalves. In Ecotoxicology of metals in invertebrates, ed., R. Dallinger and P.S. Rainbow, pp. 175-186. Society of Environmental Toxicology and Chemistry Special Pub. Ser., Pensacola, FL. 25. Kumaraguru, A.K., D. Selvi, and V.K. Venugopalan. 1980. Copper toxicity to an estuarine clam (Meretrix casta). Bull. Environ. Contam. Toxicol. 24:853-857. 26. Martin, J.L.M. 1979. Schema of lethal action of copper on mussels. Bull. Environ. Contam. Toxicol. 21:808-814. 229 BIOACCUMULATION SUMMARY COPPER 27. Mount, D.R., A.K. Barth, T.D.Garrison, K.A. Barten, and J.R. Hockett. 1994. Dietary and waterborne exposure of rainbow trout (Oncorhynchus mykiss) to copper, cadmium, lead and zinc using a live diet. Environ. Toxicol. Chem. 13(12):2031-2041. 28. Powell; M.I., K.N. White. 1990. Heavy metal accumulation by barnacles and its implications for their use as biological monitors. Mar. Environ. Res. 30:91-118. 29. Stouthart, J.H.X., J.L.M. Haans, R.A.C. Lock, and S.E.W. Bonga. 1996. Effects of water pH on copper toxicity to early life stages on the common carp (Cyprinus carpio). Environ. Toxicol. Chem. 15(3):376-383. 230 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED DIBENZO-p-DIOXINS Chemical Name (Common Synonyms): 1,2,3,4,6,7,8-HEPTACHLORO DIBENZO-p-DIOXIN 1,2,3,4,6,7,8-HeptaCDD CASRN: 35822-46-9 Chemical Characteristics Solubility in Water: No data [1], 2.4 mg/L [2] Log Kow: No data [4], 8.00 [2] Half-Life: No data [2,3] Log Koc: 7.86 L/kg organic carbon Human Health Oral RfD: No data [5] Critical Effect: -- Oral Slope Factor: No data [5] Carcinogenic Classification: -- Confidence: -- Wildlife Partitioning Factors: Partitioning factors for 1,2,3,4,6,7,8-heptaCDD in wildlife were not found in the studies reviewed. Food Chain Multipliers: Limited information was found on specific biomagnification factors of PCDDs and PCDFs through terrestrial wildlife. Due to the toxicity, high Kow values, and highly persistent nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and biomagnify through the food web. PCDDs and PCDFs have been identified in fish and wildlife throughout the global aquatic and marine environments [6]. Studies conducted in Lake Ontario indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be significant between fish and fisheating birds but not between fish and their food. When calculated for older predaceous fish such as laketrout-eating young smelt, the biomagnification factor (BMF) can equal 3. The log BMF from alewife to herring gulls in Lake Ontario was 1.51 for 2,3,7,8-TCDD [7]. Log BMFs of 1.18 to 1.70 were determined for mink fed 1,2,3,4,6,7,8-Hepta CDD in the diet [18]. EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds. 231 BIOACCUMULATION SUMMARY 1,2,3,4,6,7,8-HeptaCDD Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated Wildlife [8] Sediment Concentration (pg/g dry wt.) Low Risk 50 60 0.7 2.5 6 21 High Risk to Sensitive Species 80 100 7 25 60 210 Water Concentration (pg/L) POC=0.2 0.6 0.008 0.07 1.0 0.08 0.7 POC=1.0 3.1 0.04 0.35 5 0.4 3.5 Organism Fish Mammalian Wildlife Avian Wildlife Fish Mammalian Wildlife Avian Wildlife Fish Concentration (pg/g) Note: POC - Particulate organic carbon Fish lipid of 8% and sediment organic carbon of 3% assumed where needed. For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used. Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and young) in sensitive species. High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and young of sensitive species. Aquatic Organisms Partitioning Factors: In one study, the BSAF for carp collected from a reservoir in central Wisconsin was 0.0048. In a laboratory study, log BCFs for fathead minnow, rainbow trout, and goldfish exposed to 1,2,3,4,6,7,8-HeptaCDD were 2.71, 3.15, and 4.28, respectively. Food Chain Multipliers: No specific food chain multipliers were identified for 1,2,3,4,6,7,8-heptaCDD. Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8TCDD does not appear to be significant between fish and their prey. Limited data for the base of the Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and forage fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the 2,3,7,8-TCDD biotransformation by forage fish. BMFs greater than 1.0 may exist between some zooplankton species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates [8]. Toxicity/Bioaccumulation Assessment Profile The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased with increasing ring chlorination [6]. In general, the PCDDs and PCDFs exhibit relative inertness to acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical 232 BIOACCUMULATION SUMMARY 1,2,3,4,6,7,8-HeptaCDD stability with increasing chlorination [9,6]. Because of their lipophilic nature, the PCDDs and PCDFs have been detected in fish, wildlife, and human adipose tissue, milk, and serum [6]. Each isomer has its own unique chemical and toxicological properties. The most toxic of the PCDD and PCDF isomers is 2,3,7,8-TCDD, one of the 22 possible congeners of tetrachlorodibenzo-p-dioxin [9]. Toxicity equivalency factors (TEFs) have been developed by EPA relating the toxicities of other PCDD and PCDF isomers to that of 2,3,7,8-TCDD [10]. The biochemical mechanisms leading to the toxic response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data suggest that an important role in the development of systemic toxicity resulting from exposure to these chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [10]. Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [10] Isomer Total TetraCDD 2,3,7,8-TCDD Other TCDDs Total PentaCDDs 2,3,7,8-PentaCDDs Other PentaCDDs Total HexaCDDs 2,3,7,8-HexaCDDs Other HexaCDDs Total HeptaCDDs 2,3,7,8-HeptaCDDs Other HeptaCDDs Total TetraCDFs 2,3,7,8-TetraCDF Other TetraCDFs Total PentaCDFs 2,3,7,8-PentaCDFs Other PentaCDFs Total HexaCDFs 2,3,7,8-HexaCDFs Other HexaCDFs Total HeptaCDFs 2,3,7,8-HeptaCDFs Other HeptaCDFs TEF 1 1 0.01 0.5 0.5 0.005 0.04 0.04 0.0004 0.001 0.001 0.00001 0.1 0.1 0.001 0.1 0.1 0.001 0.01 0.01 0.0001 0.001 0.001 0.00001 233 BIOACCUMULATION SUMMARY 1,2,3,4,6,7,8-HeptaCDD In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic carbon fraction of ambient waters [8]. Congener-specific analyses have shown that the 2,3,7,8substituted PCDDs and PCDFs were the major compounds present in most sample extracts [6]. Results from limited epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8TCDD impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus) on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8TCDD concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid-1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [8]. Based on limited information on isomer-specific analysis from animals at different trophic levels, it appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar congeners with the 2,3,7,8-substituted positions [11]. PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined by the habitat and physiology of each species. With log Kow>5, exposure through ingestion of contaminated food becomes an important route for uptake in comparison to respiration of water [8]. The relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake Ontario were examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [8]. There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and single species exposure. Although there is variation in the actual BCF values, in general, the algae and plants have the lowest BCF values, on the order of a few thousand. A log BCF value of 4.38 has been reported for the snail Physa sp. Crustacea and insect larvae appear to have the next highest BCF values, followed by several species of fish, with the highest log BCF value of 4.79 [11]. Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest dose of 0.038 ng/l resulted in significant mortality [12]. A number of biological effects have been reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental effects, and cardiovascular effects [11]. 234 Summary of Biological Effects Tissue Concentrations for 1,2,3,4,6,7,8-HeptaCDD Species: Taxa Fishes Salmonids Oncorhynchus mukiss (Salmo gairderni), Rainbow trout Exposure water 11-55 ng/L 3.15 2.35 0.0031 [20] [16] F L Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Oncorhynchus mukiss (Salmo gairderni), Rainbow trout 0.000035 mg/kg (liver)4 Biochemical, LOED [19] L; significant increase in liver ethoxyresorufin O-deethylase (EROD) Cyprinus carpio, Carp 2,190 pg/g5 27 pg/g5 0.0048 [13] F; Petenwell Reservoir, central Wisconsin; BSAF based on 8% tissue lipid content and 3.1% sediment organic carbon 235 236 Species: Taxa Carassius auratus, Goldfish Pimephales promelas, Fathead minnow Platycephalus caerulopunctatus and Platycephalus bassensis, Flathead Sillago bassensis, School whiting Wildlife Falco peregrinus, Peregrine falcon Summary of Biological Effects Tissue Concentrations for 1,2,3,4,6,7,8-HeptaCDD Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 1.91/2.2 ng/g5 (whole body) Ability to Accumulate2: Log BCF 4.28 Log BAF BSAF Source: Reference Comments3 [15] L; fish were exposed for 120 hr; exposure water contained fly ash extract; concentrations were measured in water, but data were not presented L Exposure water 8-39 ng/L 2.71 2.03 [16] 0.356 pg/g, dw 558 pg/kg [14] 0.356 pg/g, dw 375 pg/kg F; unimpacted coastal site; surface sediment composite; most other dioxin congeners were below detection. 0.7 ng/g (eggs) (n = 6) 11.4% eggshell thinning [17] F; Kola Peninsula, Russia Summary of Biological Effects Tissue Concentrations for 1,2,3,4,6,7,8-HeptaCDD Species: Taxa Mustela vison, Mink Concentration, Units in1: Sediment Diet: 5 pg/g5 Water Toxicity: Tissue (Sample Type) Effects 115 pg/g5 (liver) NOAEL Ability to Accumulate2: Log BCF Log BAF log BMF = 1.18 log BMF = 1.70 BSAF Source: Reference Comments3 [18] L; BMF = lipid-normalized concentration in the liver divided by the lipid-normalized dietary concentration 7 pg/g5 330 pg/g5 (liver) LOAEL; reduced kit body weights followed by reduced survival Reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female 6 pg/g5 290 pg/g5 (liver) log BMF = 1.69 13 pg/g5 380 pg/g5 (liver) log BMF = 1.66 1 2 3 4 5 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. Not clear from reference if concentration is based on wet or dry weight. 237 BIOACCUMULATION SUMMARY References 1. 1,2,3,4,6,7,8-HeptaCDD USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. II, Polynuclear aromatic hydrocarbons, polychlorinated dioxins and dibenzofurans. Lewis Publishers, Boca Raton, FL. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxicity equivalency factors (TEF). Crit. Rev. Toxicol. 21:51-88. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957-968. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8-tetrachlorodibenzop-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055. U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wildl. Ser. Biol. Rep. 85 (1.8). 37 pp. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of chlorinated dibenzo-p-dioxins and -dibenzofurans (CDDs and CDFs) and 1989 update. EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum, Washington, DC. 2. 3. 4. 5. 6. 7. 8. 9. 10. 238 BIOACCUMULATION SUMMARY 1,2,3,4,6,7,8-HeptaCDD 11. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242. 12. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.H. Peterman, D.L. Stalling, G.M. DeGraeve, J.J. Coyle, and W.J. Adams. 1988. Toxicity and bioconcentration of 2,3,7,8tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout. Environ. Toxicol. Chem. 7:47-62. Kuehl, D.W., P.M. Cook, A.R. Batterman, D. Lothenbach, and B.C. Butterworth. 1987. Bioavailability of polychlorinated dibenzo-p-dioxins and dibenzofurans from contaminated Wisconsin River sediment to carp. Chemosphere 16(4):667-679. Mosse, P.R.L., and D. Haynes. 1993. Dioxin and furan concentrations in uncontaminated waters, sediments and biota of the Ninety Mile Beach, Bass Strait, Australia. Marine Pollut. Bull. 26(8):465-468. Sijm, D.T.H.M., H. Wever, and A. Opperhuizen. 1993. Congener-specific biotransformation and bioaccumulation of PCDDs and PCDFs from fly ash in fish. Environ. Tox. Chem. 12:1895-1907. Muir, D.C.G., W.K. Marshall, and G.R.B. Webster. 1985. Bioconcentration of PCDDs by fish: Effects of molecular structure and water chemistry. Chemosphere 14(6/7):829-833. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J/P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. Parrott, J.L., P.V. Hodson, M.R. Servos, S.L. Huestis, and G.D. Dixon. 1995. Relative potency of polychlorinated dibenzo-p-dioxins and dibenzofurans for inducing mixed-function oxygenase activity in rainbow trout. Environ. Toxicol. Chem. 14(6):1041-1050. USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 13. 14. 15. 16. 17. 18. 19. 20. 239 240 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED DIBENZO-p-DIOXINS Chemical Name (Common Synonyms): 1,2,3,4,7,8-HEXACHLORODIBENZO-p-DIOXIN 1,2,3,4,7,8-HexaCDD CASRN: 39227-28-6 Chemical Characteristics Solubility in Water: No data [1], 8.25 x 10-6 mg/L [1,2] Log Kow: No data [4], 7.70 [2] Half-Life: No data [2,3] Log Koc: 7.57 L/kg organic carbon Human Health Oral RfD: No data [5] Critical Effect: -- Oral Slope Factor (Reference): No data [5] Carcinogenic Classification: -- Confidence: -- Wildlife Partitioning Factors: Partitioning factors for 1,2,3,4,7,8-hexaCDD in wildlife were not found in the studies reviewed. Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors of PCDDs and PCDFs through terrestrial wildlife. Due to the toxicity, high Kow values, and highly persistent nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and biomagnify through the food web. PCDDs and PCDFs have been identified in fish and wildlife throughout the global aquatic and marine environments [6]. Studies conducted in Lake Ontario indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be significant between fish and fish-eating birds but not between fish and their food. When calculated for older predaceous fish such as lake-trout-eating young smelt, the biomagnification factor (BMF) can equal 3. The BMF from alewife to herring gulls in Lake Ontario was 32 for 2,3,7,8-TCDD [7]. A log BMF of 0.97 was reported for mink exposed to 1,2,3,4,7,8-hexaCDD in the diet. [14]. EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds. 241 BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDD Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated Wildlife [8] Fish Concentration (pg/g) Sediment Concentration (pg/g dry wt.) Low Risk 50 60 0.7 2.5 6 21 High Risk to Sensitive Species 80 100 7 25 60 210 Water Concentration (pg/L) POC=0.2 0.6 0.008 0.07 1.0 0.08 0.7 POC=1.0 3.1 0.04 0.35 5 0.4 3.5 Organism Fish Mammalian Wildlife Avian Wildlife Fish Mammalian Wildlife Avian Wildlife Note: POC - Particulate organic carbon Fish lipid of 8% and sediment organic carbon of 3% assumed where needed. For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used. Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and young) in sensitive species. High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and young of sensitive species. Aquatic Organisms Partitioning Factors: In a laboratory study, log BCFs for rainbow trout and fathead minnow exposed to 1,2,3,4,7,8-HexaCDD were 3.73 and 4.00, respectively. Food Chain Multipliers: No specific food chain multipliers were identified for 1,2,3,4,7,8-hexaCDD. Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8TCDD does not appear to be significant between fish and their prey. Limited data for the base of the Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and forage fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the 2,3,7,8-TCDD biotransformation by forage fish. BMFs greater than 1.0 may exist between some zooplankton species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates [8]. Toxicity/Bioaccumulation Assessment Profile The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased with increasing ring chlorination [6]. In general, the PCDDs and PCDFs exhibit relative inertness to acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical 242 BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDD stability with increasing chlorination [9,6]. Because of their lipophilic nature, the PCDDs and PCDFs have been detected in fish, wildlife, and human adipose tissue, milk, and serum [6]. Each isomer has its own unique chemical and toxicological properties. The most toxic of the PCDD and PCDF isomers is 2,3,7,8-TCDD, one of the 22 possible congeners of tetrachlorodibenzo-p-dioxin [10]. Toxicity equivalency factors (TEFs) have been developed by EPA relating the toxicities of other PCDD and PCDF isomers to that of 2,3,7,8-TCDD [9]. The biochemical mechanisms leading to the toxic response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data suggest that an important role in the development of systemic toxicity resulting from exposure to these chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [10]. Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [10] Isomer Total TetraCDD 2,3,7,8-TCDD Other TCDDs Total PentaCDDs 2,3,7,8-PentaCDDs Other PentaCDDs Total HexaCDDs 2,3,7,8-HexaCDDs Other HexaCDDs Total HeptaCDDs 2,3,7,8-HeptaCDDs Other HeptaCDDs Total TetraCDFs 2,3,7,8-TetraCDF Other TetraCDFs Total PentaCDFs 2,3,7,8-PentaCDFs Other PentaCDFs Total HexaCDFs 2,3,7,8-HexaCDFs Other HexaCDFs Total HeptaCDFs 2,3,7,8-HeptaCDFs Other HeptaCDFs TEF 1 1 0.01 0.5 0.5 0.005 0.04 0.04 0.0004 0.001 0.001 0.00001 0.1 0.1 0.001 0.1 0.1 0.001 0.01 0.01 0.0001 0.001 0.001 0.00001 243 BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDD In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8-substituted PCDDs and PCDFs were the major compounds present in most sample extracts [6]. Results from limited epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-TCDD impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus) on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8-TCDD concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [8]. Based on limited information on isomer-specific analysis from animals at different trophic levels, it appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar congeners with the 2,3,7,8-substituted positions [11]. PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined by the habitat and physiology of each species. With log Kow>5, exposure through ingestion of contaminated food becomes an important route for uptake in comparison to respiration of water [8]. The relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake Ontario were examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [8]. There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and single species exposure. Although there is variation in the actual BCF values, in general, the algae and plants have the lowest BCF values, on the order of a few thousand. A log BCF value of 4.38 has been reported for the snail Physa sp. Crustacea and insect larvae appear to have the next highest BCF values, followed by several species of fish, with the highest log BCF value of 4.79 [11]. Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest dose of 0.038 ng/l resulted in significant mortality [12]. A number of biological effects have been reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental effects, and cardiovascular effects [11]. 244 Summary of Biological Effects Tissue Concentrations for 1,2,3,4,7,8-HexaCDD Species: Taxa Fishes Oncorhynchus mukiss (Salmo gairderni), Rainbow trout Exposure water 10-47 ng/L 3.73 [11] L Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Oncorhynchus mukiss, Rainbow trout 0.0000395 mg/kg (liver)4 Biochemical, LOED [15] L; significant increase in liver ethoxyresorufin O-deethylase (EROD) Pimephales promelas, Fathead minnow Exposure water 10-47 ng/L 4.00 [11] L Wildlife Falco peregrinus, Peregrine falcon 3.3 ng/g (eggs) (n = 6) 11.4% eggshell thinning [13] F; Kola Peninsula, Russia 245 246 Species: Taxa Mustela vison, Mink Diet: 2 pg/g5 1 pg/g5 3 pg/g5 1 2 3 4 5 Summary of Biological Effects Tissue Concentrations for 1,2,3,4,7,8-HexaCDD Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 6 pg/g5 (liver) LOAEL; reduced kit body weights followed by reduced survival Reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female Ability to Accumulate2: Log BCF Log BAF No BMF reported BSAF Source: Reference Comments3 [14] L; BMF = biomagnification factor = vl/vd vl = lipidnormalized tissue concentration, vd = lipidnormalized dietary concentration. 77 pg/g5 (liver) No BMF reported Log BMF = 0.97 15 pg/g5 (liver) Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. Not clear from reference if concentration is based on wet or dry weight. BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDD References 1. USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH. February. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. II, Polynuclear aromatic hydrocarbons, polychlorinated dioxins and dibenzofurans. Lewis Publishers, Boca Raton, FL. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxicity equivalency factors (TEF). Crit. Rev. Toxicol. 21:51-88. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957968. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8-tetrachlorodibenzop-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055. U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.8). 37pp. 2. 3. 4. 5. 6. 7. 8. 9. 10. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of chlorinated dibenzo-p-dioxins and dibenzofurans (CDDs and CDFs) and 1989 update. EPA/625/389/016. U.S. Environmental Protection Agency, Risk Assessment Forum, Washington, DC. 11. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242. 247 BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDD 12. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.H. Peterman, D.L. Stalling, G.M. DeGraeve, J.J. Coyle, and W.J. Adams. 1988. Toxicity and bioconcentration of 2,3,7,8tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout. Environ. Toxicol. Chem. 7:47-62. 13. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739749. WWGPB/The Pica Press. 14. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J/P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. 15. Parrott, J.L., P.V. Hodson, M.R. Servos, S.L. Huestis, and G.D. Dixon. 1995. Relative potency of polychlorinated dibenzo-p-dioxins and dibenzofurans for inducing mixed-function oxygenase activity in rainbow trout. Environ. Toxicol. Chem. 14(6):1041-1050. 16. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 248 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED DIBENZO-p-DIOXINS Chemical Name (Common Synonyms): 1,2,3,6,7,8-HEXACHLORODIBENZO-p-DIOXIN 1,2,3,6,7,8-HexaCDD CASRN: 57653-85-7 Chemical Characteristics Solubility in Water: No data [1,2] Log Kow: No data [2,4] Half-Life: No data [2,3] Log Koc: -- Human Health Oral RfD: No data [5] Critical Effect: Hepatic tumors in mice and rats Oral Slope Factor: 6.2 x 10+3 per (mg/kg)/day [5] Carcinogenic Classification: B2 [5] Confidence: -- Wildlife Partitioning Factors: Partitioning factors for 1,2,3,6,7,8-hexaCDD in wildlife were not found in the studies reviewed. Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors of PCDDs and PCDFs through terrestrial wildlife. Due to the toxicity, high Kow values, and highly persistent nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and biomagnify through the food web. PCDDs and PCDFs have been identified in fish and wildlife throughout the global aquatic and marine environments [6]. Studies conducted in Lake Ontario indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be significant between fish and fish-eating birds but not between fish and their food. When calculated for older predaceous fish such as lake-trout-eating young smelt, the biomagnification factor (BMF) can equal 3. The BMF from alewife to herring gulls in Lake Ontario was 32 for 2,3,7,8-TCDD [7]. Log BMFs of 1.42 and 1.43 were reported for mink exposed to 1,2,3,6,7,8-hexaCDD in the diet [18]. EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds. 249 BIOACCUMULATION SUMMARY 1,2,3,6,7,8-HexaCDD Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated Wildlife [8] Sediment Concentration (pg/g dry wt.) Low Risk 50 60 0.7 2.5 6 21 High Risk to Sensitive Species 80 100 7 25 60 210 Water Concentration (pg/L) POC=0.2 0.6 0.008 0.07 1.0 0.08 0.7 POC=1.0 3.1 0.04 0.35 5 0.4 3.5 Organism Fish Mammalian Wildlife Avian Wildlife Fish Mammalian Wildlife Avian Wildlife Fish Concentration (pg/g) Note: POC - Particulate organic carbon Fish lipid of 8% and sediment organic carbon of 3% assumed where needed. For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used. Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and young) in sensitive species. High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and young of sensitive species. Aquatic Organisms Partitioning Factors: In one study, the BSAF for carp collected from a reservoir in central Wisconsin was 0.035. The log BCF for goldfish during a laboratory exposure for 120 hours was 4.61. Food Chain Multipliers: No specific food chain multipliers were identified for 1,2,3,6,7,8-hexaCDD. Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8TCDD does not appear to be significant between fish and their prey. Limited data for the base of the Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and forage fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the 2,3,7,8-TCDD biotansformation by forage fish. BMFs greater than 1.0 may exist between some zooplankton species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates[8]. Toxicity/Bioaccumulation Assessment Profile The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased with increasing ring chlorination [6]. In general, the PCDDs and PCDFs exhibit relative inertness to acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical 250 BIOACCUMULATION SUMMARY 1,2,3,6,7,8-HexaCDD stability with increasing chlorination [9,6]. Because of their lipophilic nature, the PCDDs and PCDFs have been detected in fish, wildlife, and human adipose tissue, milk, and serum [6]. Each isomer has its own unique chemical and toxicological properties. The most toxic of the PCDD and PCDF isomers is 2,3,7,8 TCDD, one of the 22 possible congeners of tetrachlorodibenzo-p-dioxin [9]. Toxicity equivalency factors (TEFs) have been developed by EPA relating the toxicities of other PCDD and PCDF isomers to that of 2,3,7,8-TCDD [10]. The biochemical mechanisms leading to the toxic response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data suggest that an important role in the development of systemic toxicity resulting from exposure to these chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [10]. Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [10] Isomer Total TetraCDD 2,3,7,8-TCDD Other TCDDs Total PentaCDDs 2,3,7,8-PentaCDDs Other PentaCDDs Total HexaCDDs 2,3,7,8-HexaCDDs Other HexaCDDs Total HeptaCDDs 2,3,7,8-HeptaCDDs Other HeptaCDDs Total TetraCDFs 2,3,7,8-TetraCDF Other TetraCDFs Total PentaCDFs 2,3,7,8-PentaCDFs Other PentaCDFs Total HexaCDFs 2,3,7,8-HexaCDFs Other HexaCDFs Total HeptaCDFs 2,3,7,8-HeptaCDFs Other HeptaCDFs TEF 1 1 0.01 0.5 0.5 0.005 0.04 0.04 0.0004 0.001 0.001 0.00001 0.1 0.1 0.001 0.1 0.1 0.001 0.01 0.01 0.0001 0.001 0.001 0.00001 251 BIOACCUMULATION SUMMARY 1,2,3,6,7,8-HexaCDD In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8substituted PCDDs and PCDFs were the major compounds present in most sample extracts [6]. Results from limited epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8TCDD impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus) on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8TCDD concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid-1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [8]. Based on limited information on isomer-specific analysis from animals at different trophic levels, it appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar congeners with the 2,3,7,8-substituted positions [11]. PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined by the habitat and physiology of each species. With log Kow>5, exposure through ingestion of contaminated food becomes an important route for uptake in comparison to respiration of water [8]. The relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake Ontario were examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [8]. There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and single species exposure. Although there is variation in the actual BCF values, in general, the algae and plants have the lowest BCF values, on the order of a few thousand. A log value of 4.38 has been reported for the snail Physa sp. Crustacea and insect larvae appear to have the next highest BCF values, followed by several species of fish, with the highest log BCF value of 4.79 [11]. Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest dose of 0.038 ng/l resulted in significant mortality [12]. A number of biological effects have been reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental effects, and cardiovascular effects [11]. 252 Summary of Biological Effects Tissue Concentrations for 1,2,3,6,7,8-HexaCDD Species: Taxa Fishes Carassius auratus, Goldfish 0.79 ng/g4 (whole body) 4.61 [14] L; fish were exposed for 120 hr; exposure water contained fly ash extract; concentrations were measured in water, but data were not presented Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Cyprinus carpio, Carp 180 pg/g4 16 pg/g4 0.035 [13] F; Petenwell Reservoir, central Wisconsin; BSAF based on 8% tissue lipid content and 3.1% sediment organic carbon Salmonids 0.0073 [19] F 253 254 Species: Taxa Wildlife Sediment Falco peregrinus, Peregrine falcon Haliaeetus leucocephalus, Bald eagle chicks Summary of Biological Effects Tissue Concentrations for 1,2,3,6,7,8-HexaCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 7.2 ng/g (eggs) (n = 6) 11.4% eggshell thinning [17] F; Kola Peninsula, Russia Powell River site: A hepatic ~9,000 ng/kg lipid cytochrome weight basis (yolk sac) P4501A crossreactive protein Reference site: ~500 (CYP1A) was ng/kg lipid weight induced nearly basis (yolk sac) 6-fold in chicks from Powell River site compared to the reference (p < 0.05). No significant concentrationrelated effects were found for morphological, physiological, or histological parameters. [15] F; southern coast of British Columbia; eggs were collected from nests and hatched in the lab; ~ indicates value was taken from a figure Summary of Biological Effects Tissue Concentrations for 1,2,3,6,7,8-HexaCDD Species: Taxa Ardea herodias, Great blue heron chicks Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Nicomekl site: 103.4 ng/kg (egg) (n=11) Vancouver site: 8945.4 ng/kg (egg) (n=12) Depression of growth compared to Nicomekl site. Presence of edema. Depression of growth compared to Nicomekl site. Presence of edema. Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [16] L; eggs were collected from three British Columbia colonies with different levels of contamination and incubated in the laboratory Crofton site: 430105.9 ng/kg (egg) (n=6) 255 256 Species: Taxa Mustela vison, Mink Sediment Diet: 1 pg/g4 3 pg/g4 6 pg/g4 1 2 Summary of Biological Effects Tissue Concentrations for 1,2,3,6,7,8-HexaCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 54 pg/g4 (liver) LOAEL; reduced kit body weights followed by reduced survival Reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female Ability to Accumulate2: Log BCF Log BAF No BMF reported BSAF Source: Reference Comments3 [18] L; BMF = biomagnification factor = vl/vd, vl = lipidnormalized tissue concentration, vd = lipidnormalized dietary concentration. 77 pg/g4 (liver) log BMF = 1.42 130 pg/g4 (liver) log BMF = 1.53 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 Not clear from reference if concentration is based on wet or dry weight. BIOACCUMULATION SUMMARY References 1. 1,2,3,6,7,8-HexaCDD USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH. February. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. II, Polynuclear aromatic hydrocarbons, polychlorinated dioxins and dibenzofurans. Lewis Publishers, Boca Raton, FL. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxicity equivalency factors (TEF). Crit. Rev. Toxicol. 21:51-88. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957-968. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8-tetrachlorodibenzop-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055. U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85 (1.8). p. 37. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of chlorinated dibenzo-p-dioxins and -dibenzofurans (CDDs and CDFs) and 1989 update. EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum, Washington, DC. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242. 257 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. BIOACCUMULATION SUMMARY 12. 1,2,3,6,7,8-HexaCDD Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.H. Peterman, D.L. Stalling, G.M. DeGraeve, J.J. Coyle, and W.J. Adams. 1988. Toxicity and bioconcentration of 2,3,7,8tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout. Environ. Toxicol. Chem. 7:47-62. Kuehl, D.W., P.M. Cook, A.R. Batterman, D. Lothenbach, and B.C. Butterworth. 1987. Bioavailability of polychlorinated dibenzo-p-dioxins and dibenzofurans from contaminated Wisconsin River sediment to carp. Chemosphere 16(4):667-679. Sijm, D.T.H.M., H. Wever, and A. Opperhuizen. 1993. Congener-specific biotransformation and bioaccumulation of PCDDs and PCDFs from fly ash in fish. Environ. Toxicol. Chem. 12:1895-1907. Elliott, J.E., R.J. Norstrom, A. Lorenzen, L.E. Hart, H. Philibert, S.W. Kennedy, J.J. Stegeman, G.D. Bellward, and K.M. Cheng. 1996. Biological effects of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls in bald eagle (Haliaeetus leucocephalus) chicks. Environ. Toxicol. Chem. 15(5): 782-793. Hart, L.E., K.M. Cheng, P.E. Whitehead, R.M. Shah, R.J. Lewis, S.R. Ruschkowski, R.W. Blair, D.C. Bennett, S.M. Bandiera, R.J.Norstrom, and G.D. Bellward. 1991. Dioxin contamination and growth and development in great blue heron embryos. J. Toxicol. Environ. Health 32:331344. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 13. 14. 15. 16. 17. 18. 19. 258 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED DIBENZO-p-DIOXINS Chemical Name (Common Synonyms): 1,2,3,7,8-PENTACHLORODIBENOZ-p-DIOXIN 1,2,3,7,8-PentaCDD CASRN: 40321-76-4 Chemical Characteristics Solubility in Water: No data [1,3] Log Kow: No data [3,4] Half-Life: No data [2,3] Log Koc: -- Human Health Oral RfD: No data [5] Critical Effect: -- Oral Slope Factor: No data [5] Carcinogenic Classification: -- Confidence: -- Wildlife Partitioning Factors: Partitioning factors for 1,2,3,7,8-pentaCDD in wildlife were not found in the studies reviewed. Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors of PCDDs and PCDFs through terrestrial wildlife; no information was available for 1,2,3,7,8-pentaCDD, specifically. Due to the toxicity, high Kow values, and highly persistent nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and biomagnify through the food web. PCDDs and PCDFs have been identified in fish and wildlife throughout the global aquatic and marine environments [6]. Studies conducted in Lake Ontario indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be significant between fish and fish-eating birds but not between fish and their food. When calculated for older predaceous fish such as lake-trout-eating young smelt, the log biomagnification factor (BMF) can equal 0.48. The log BMF from alewife to herring gulls in Lake Ontario was 1.51 for 2,3,7,8-TCDD [7]. EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds. 259 BIOACCUMULATION SUMMARY 1,2,3,7,8-PentaCDD Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated Wildlife [8] Sediment Concentration (pg/g dry wt.) Low Risk 50 60 0.7 2.5 6 21 High Risk to Sensitive Species 80 100 7 25 60 210 Water Concentration (pg/L) POC=0.2 0.6 0.008 0.07 1.0 0.08 0.7 POC=1.0 3.1 0.04 0.35 5 0.4 3.5 Organism Fish Mammalian Wildlife Avian Wildlife Fish Mammalian Wildlife Avian Wildlife Fish Concentration (pg/g) Note: POC - Particulate organic carbon Fish lipid of 8% and sediment organic carbon of 3% assumed where needed. For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used. Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and young) in sensitive species. High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and young of sensitive species. Aquatic Organisms Partitioning Factors: Partitioning factors for 1,2,3,7,8-pentaCDF in aquatic organisms were not found in the studies reviewed. Food Chain Multipliers: No specific food chain multipliers were identified for 1,2,3,7,8-pentaCDD. Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8TCDD does not appear to be significant between fish and their prey. Limited data for the base of the Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and forage fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the 2,3,7,8-TCDD biotransformation by forage fish. BMFs greater than 1.0 might exist between some zooplankton species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates[8]. Toxicity/Bioaccumulation Assessment Profile The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased with increasing ring chlorination [6]. In general, the PCDDs and PCDFs exhibit relative inertness to acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical stability with increasing chlorination [6,9]. Because of their lipophilic nature, the PCDDs and PCDFs have been detected in fish, wildlife, and human adipose tissue, milk, and serum [6]. 260 BIOACCUMULATION SUMMARY 1,2,3,7,8-PentaCDD Each isomer has its own unique chemical and toxicological properties. The most toxic of the PCDD and PCDF isomers is 2,3,7,8-TCDD, one of the 22 possible congeners of tetrachlorodibenzo-p-dioxin [9]. Toxicity equivalency factors (TEFs) have been developed by the U.S. EPA relating the toxicities of other PCDD and PCDF isomers to that of 2,3,7,8-TCDD [10]. The biochemical mechanisms leading to the toxic response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data suggest that an important role in the development of systemic toxicity resulting from exposure to these chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [10]. Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [10] Isomer Total TetraCDD 2,3,7,8-TCDD Other TCDDs Total PentaCDDs 2,3,7,8-PentaCDDs Other PentaCDDs Total HexaCDDs 2,3,7,8-HexaCDDs Other HexaCDDs Total HeptaCDDs 2,3,7,8-HeptaCDDs Other HeptaCDDs Total TetraCDFs 2,3,7,8-TetraCDF Other TetraCDFs Total PentaCDFs 2,3,7,8-PentaCDFs Other PentaCDFs Total HexaCDFs 2,3,7,8-HexaCDFs Other HexaCDFs Total HeptaCDFs 2,3,7,8-HeptaCDFs Other HeptaCDFs TEF 1 1 0.01 0.5 0.5 0.005 0.04 0.04 0.0004 0.001 0.001 0.00001 0.1 0.1 0.001 0.1 0.1 0.001 0.01 0.01 0.0001 0.001 0.001 0.00001 In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic carbon fraction of ambient waters [8]. Congener-specific analyses have shown that the 2,3,7,8substituted PCDDs and PCDFs were the major compounds present in most sample extracts [6]. Results 261 BIOACCUMULATION SUMMARY 1,2,3,7,8-PentaCDD from limited epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8TCDD impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus) on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8TCDD concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid-1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [8]. Based on limited information on isomer-specific analysis from animals at different trophic levels, it appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar congeners with the 2,3,7,8-substituted positions [11]. PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined by the habitat and physiology of each species. With log Kow>5, exposure through ingestion of contaminated food becomes an important route for uptake in comparison to respiration of water [8]. The relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake Ontario were examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [8]. There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and single species exposure. Although there is variation in the actual log BCF values, in general, the algae and plants have the lowest BCF values, on the order of a few thousand. A log BCF value of 4.38 has been reported for the snail Physa sp. Crustacea and insect larvae appear to have the next highest BCF values, followed by several species of fish, with the highest log BCF value of 4.78 [11]. Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest dose of 0.038 ng/l resulted in significant mortality [12]. A number of biological effects have been reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental effects, and cardiovascular effects [11]. 262 Summary of Biological Effects Tissue Concentrations for 1,2,3,7,8-PentaCDD Species: Taxa Fishes Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Carassius auratus, Goldfish 1.59/2.61 ng/g4 (whole body) 16,982 [14] L; fish were exposed for 120 hr; exposure water contained fly ash extract; concentrations were measured in water, but data were not presented Cyprinus carpio, Carp 31 pg/g4 4.8 pg/g4 0.06 [13] F; Petenwell Reservoir, central Wisconsin; BSAF based on 8% tissue lipid content and 3.1% sediment organic carbon Salmonids 0.054 [18] F Wildlife Falco peregrinus, Peregrine falcon 263 11 ng/g (eggs) (n = 6) 11.4% eggshell thinning [17] F; Kola Peninsula, Russia 264 Species: Taxa Sediment Haliaeetus leucocephalus, Bald eagle chicks Summary of Biological Effects Tissue Concentrations for 1,2,3,7,8-PentaCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Powell River site: A hepatic ~2,800 ng/kg lipid cytochrome weight basis (yolk sac) P4501A crossreactive protein Reference site: (CYP1A) was ~500 ng/kg lipid induced nearly weight basis (yolk sac) six-fold in chicks from Powell River site compared to the reference (p < 0.05). No significant concentrationrelated effects were found for morphological, physiological, or histological parameters. [15] F; southern coast of British Columbia; eggs were collected from nests and hatched in the lab; ~ indicates value was taken from a figure. Summary of Biological Effects Tissue Concentrations for 1,2,3,7,8-PentaCDD Species: Taxa Ardea herodias, Great blue heron chicks Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Nicomekl site: 62.2 ng/kg (egg) (n = 11) Vancouver site: 5725.8 ng/kg (egg) (n = 12) Depression of growth compared to Nicomekl site. Presence of edema. Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [16] L; eggs were collected from three British Columbia colonies with different levels of contamination and incubated in the laboratory Crofton site: Depression of 26369.9 ng/kg (egg) growth (n = 6) compared to Nicomekl site. Presence of edema. 1 2 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 Not clear from reference if concentration is based on wet or dry weight. 265 BIOACCUMULATION SUMMARY References 1. 1,2,3,7,8-PentaCDD USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. II, Polynuclear aromatic hydrocarbons, polychlorinated dioxins and dibenzofurans. Lewis Publishers, Boca Raton, FL. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxicity equivalency factors (TEF). Crit. Rev. Toxicol. 21:51-88. Braune, B.M. And R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957-968. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8tetrachlorodibenzo-p-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055. U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.8). 37 pp. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of chlorinated dibenzo-p-dioxins and -dibenzofurans (CDDs and CDFs) and 1989 update. EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum, Washington, DC. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 266 BIOACCUMULATION SUMMARY 12. 1,2,3,7,8-PentaCDD Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.H. Peterman, D.L. Stalling, G.M. DeGraeve, J.J. Coyle, and W.J. Adams. 1988. Toxicity and bioconcentration of 2,3,7,8tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout. Environ. Toxicol. Chem. 7:47-62. Kuehl, D.W., P.M. Cook, A.R. Batterman, D. Lothenbach, and B.C. Butterworth. 1987. Bioavailability of polychlorinated dibenzo-p-dioxins and dibenzofurans from contaminated Wisconsin River sediment to carp. Chemosphere 16(4):667-679. Sijm, D.T.H.M., H. Wever, and A. Opperhuizen. 1993. Congener-specific biotransformation and bioaccumulation of PCDDs and PCDFs from fly ash in fish. Environ. Toxicol. Chem. 12: 1895-1907. Elliott, J.E., R.J. Norstrom, A. Lorenzen, L.E. Hart, H. Philibert, S.W. Kennedy, J.J. Stegeman, G.D. Bellward, and K.M. Cheng. 1996. Biological effects of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls in bald eagle (Haliaeetus leucocephalus) chicks. Environ. Toxicol. Chem. 15(5):782-793. Hart, L.E., K.M. Cheng, P.E. Whitehead, R.M. Shah, R.J. Lewis, S.R. Ruschkowski, R.W. Blair, D.C. Bennett, S.M. Bandiera, R.J.Norstrom, and G.D. Bellward. 1991. Dioxin contamination and growth and development in great blue heron embryos. J. Toxicol. Environ. Health 32:331344. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in Peregrine Falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor Conservation Today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749, WWGPB/The Pica Press. USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 13. 14. 15. 16. 17. 18. 267 268 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED DIBENZO-p-DIOXINS Chemical Name (Common Synonyms): 2,3,7,8-TETRACHLORODIBENZO-p-DIOXIN 2,3,7,8-TCDD CASRN: 1746-01-6 Chemical Characteristics Solubility in Water: 19.3 ng/L [1] Half-Life: 1.1.15 - 1.62 years based on soil die-away test and lake water and sediment die-away test [2] Log Koc: 6.42 L/kg organic carbon Log Kow: 6.53 [3] Human Health Oral RfD: No data [4] Critical Effect: -- Oral Slope Factor: 1.5 x 10+5 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4] Confidence: -- Wildlife Partitioning Factors: Partitioning factors for 2,3,7,8-TCDD in wildlife were not found in the literature. Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors of PCDDs and PCDFs through terrestrial wildlife. Due to the toxicity, high Kow values, and highly persistent nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and biomagnify through the food web. PCDDs and PCDFs have been identified in fish and wildlife throughout the global aquatic and marine environments [5]. Studies conducted in Lake Ontario indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be significant between fish and fish-eating birds but not between fish and their food. When calculated for older predaceous fish such as lake-trout-eating young smelt, the biomagnification factor (BMF) can equal 3. The BMF from alewife to herring gulls in Lake Ontario was 32 for 2,3,7,8-TCDD [6]. EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds. 269 BIOACCUMULATION SUMMARY 2,3,7,8-TCDD Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated Wildlife [7] Sediment Concentration (pg/g dry wt.) Low Risk 50 60 0.7 2.5 6 21 High Risk to Sensitive Species 80 100 7 25 60 210 Water Concentration (pg/L) POC=0.2 0.6 0.008 0.07 1.0 0.08 0.7 POC=1.0 3.1 0.04 0.35 5 0.4 3.5 Organism Fish Mammalian Wildlife Avian Wildlife Fish Mammalian Wildlife Avian Wildlife Fish Concentration (pg/g) Note: POC - Particulate organic carbon Fish lipid of 8% and sediment organic carbon of 3% assumed where needed. For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used. Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and young) in sensitive species. High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and young of sensitive species. Aquatic Organisms Partitioning Factors: Steady-state BSAFs for invertebrates exposed to 2,3,7,8-TCDD in the laboratory ranged from about 0.5 to 0.9 [8]. The BSAF for carp collected from a reservoir in central Wisconsin was 0.27 [9]. Food Chain Multipliers: Biomagnification of 2,3,7,8-TCDD does not appear to be significant between fish and their prey. Limited data for the base of the Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and forage fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the 2,3,7,8-TCDD biotansformation by forage fish. BMFs greater than 1.0 may exist between some zooplankton species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates [7]. Toxicity/Bioaccumulation Assessment Profile The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased with increasing ring chlorination [5]. In general, the PCDDs and PCDFs exhibit relative inertness to acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical stability with increasing chlorination [10,5]. Because of their lipophilic nature, the PCDDs and PCDFs have been detected in fish, wildlife, and human adipose tissue, milk, and serum [5]. 270 BIOACCUMULATION SUMMARY 2,3,7,8-TCDD Each isomer has its own unique chemical and toxicological properties. The most toxic of the PCDD and PCDF isomers is 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD), one of the 22 possible congeners of tetrachlorodibenzo-p-dioxin [10]. Toxicity equivalency factors (TEFs) have been developed by the EPA relating the toxicities of other PCDD and PCDF isomers to that of 2,3,7,8-TCDD [11]. The biochemical mechanisms leading to the toxic response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data suggest that an important role in the development of systemic toxicity resulting from exposure to these chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [11]. Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [11] Isomer Total TetraCDD 2,3,7,8-TCDD Other TCDDs Total PentaCDDs 2,3,7,8-PentaCDDs Other PentaCDDs Total HexaCDDs 2,3,7,8-HexaCDDs Other HexaCDDs Total HeptaCDDs 2,3,7,8-HeptaCDDs Other HeptaCDDs Total TetraCDFs 2,3,7,8-TetraCDF Other TetraCDFs Total PentaCDFs 2,3,7,8-PentaCDFs Other PentaCDFs Total HexaCDFs 2,3,7,8-HexaCDFs Other HexaCDFs Total HeptaCDFs 2,3,7,8-HeptaCDFs Other HeptaCDFs TEF 1 1 0.01 0.5 0.5 0.005 0.04 0.04 0.0004 0.001 0.001 0.00001 0.1 0.1 0.001 0.1 0.1 0.001 0.01 0.01 0.0001 0.001 0.001 0.00001 In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8271 BIOACCUMULATION SUMMARY 2,3,7,8-TCDD substituted PCDDs and PCDFs were the major compounds present in most sample extracts [5]. Results from limited epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8TCDD impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus) on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8TCDD concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid-1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [7]. Based on limited information on isomer-specific analysis from animals at different trophic levels, it appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar congeners with the 2,3,7,8-substituted positions [12]. PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined by the habitat and physiology of each species. With log Kow>5, exposure through ingestion of contaminated food becomes an important route for uptake in comparison to respiration of water [7]. The relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake Ontario were examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [7]. There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and single species exposure. Although there is variation in the actual BCF values, in general, the algae and plants have the lowest BCF values, on the order of a few thousand. A log BCF value of 4.38 has been reported for the snail Physa sp. Crustacea and insect larvae appear to have the next highest BCF values, followed by several species of fish, with the highest log BCF value of 4.79 [12]. Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest dose of 0.038 ng/l resulted in significant mortality [13]. A number of biological effects have been reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental effects, and cardiovascular effects [12]. 272 Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Plants Oedogonium cardiacum, Green algae 1.34 mg/kg (whole body)4 Growth, NOED [35] L; no effect on growth Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Lemna minor, Duckweed 0.00614 mg/kg (whole body)4 Growth, NOED [35] L; no observed effect Invertebrates Nereis virens, Sandworm 65697 pg/g dw; (n = 6) 422103 pg/g dw (whole body) ~0.5 [8,14] L; 180-day exposure; sediment TOC was 57 mg/kg; ~ indicates approximate value, as numbers were estimated from bar graphs. Physa sp., Snail 0.364 mg/kg (whole body)4 Mortality, NOED [35] L; no effect on survival 273 274 Species: Taxa Macoma nasuta, Clam Sediment 65697 pg/g dw; (n = 6) Daphnia magna, Cladaceran Palaemonetes pugio, Grass shrimp 65697 pg/g dw; (n = 6) Pacifastacus leniusculus, Crayfish Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 142 20 pg/g dw Ability to Accumulate2: Log BCF Log BAF BSAF ~0.9 Source: Reference Comments3 [8,14] L; 120-day exposure; sediment TOC was 57 mg/kg; ~ indicates approximate value, as numbers were estimated from bar graphs. 2.08 mg/kg (whole body)4 Mortality, NOED [35] L; no effect on survival 138 20 pg/g dw ~0.7 [8,14] L; 28-day exposure; sediment TOC was 57 mg/kg ~ indicates approximate value, as numbers were estimated from bar graphs. 0.003 mg/kg (whole body)4 0.03 mg/kg (whole body)4 Mortality, ED25 Mortality, ED50 [31] L; 25% mortality after 40 days L; lethargy, 50% to 66% increase in mortality [31] Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.003 mg/kg (whole body)4 0.003 mg/kg (whole body)4 0.003 mg/kg (whole body)4 Behavior, LOED Physiological, LOED Physiological, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [31] [31] L; lack of avoidance response L; significant induction of cytochrome P450 L; significant induction of liver enzymes (cytochrome P450) L; no significant pathology at highest dose L; no effect on mortality L; no significant induction of liver enzymes (cytochrome P450) [31] 0.1 mg/kg (whole body)4 Morphology, NOED [31] 0.0003 mg/kg (whole Mortality, body)4 NOED 0.0003 mg/kg (whole Physiological, body)4 NOED [31] [31] Callinectes sapidus, 32.2 ppt5 Blue crab (TOC = 3.2%) 52.8 ppt5 (TOC = 3.9%) 8.2 ppt5 (hepatopancreas) (% lipid = 7.6) -0.72 0.089 [15] F; northeastern Florida; bleachkraft paper mill receiving stream; BAF and BSAF calculated using mean of two sediment concentrations. 275 276 Species: Taxa Chironomus tentans, Midge Sediment Fishes Oncorhynchus mykiss (Salmo gairdneri), Rainbow trout Oncorhynchus mykiss, Rainbow trout Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.47 mg/kg (whole body) Growth, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [44] L; concentrations are lipid water exposure 0.038 ng/L water exposure 0.382 ng/L 1.0 g/kg5 28-day LOEC (survival, growth) 4.41 [13] L 10.95 ng/g5 (whole body) 4.46 L; 6-hour exposure period 0.00388 mg/kg (extractable lipid)4 Growth, LOED [32] L; reduced growth, exposed fish weighed 50 g vs. 130 g for controls L; reduced growth, exposed fish weighed 50 g vs. 130 g for controls L; reduced growth, exposed fish weighed 50 g vs. 130 g for controls 0.00371 mg/kg (liver)4 Growth, LOED [32] 0.00026 mg/kg (muscle)4 Growth, LOED [32] Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.00065 mg/kg (whole body)4 Growth, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [32] L; reduced growth, exposed fish weighed 50 g vs. 130 g for controls L; livers enlarged to nearly twice the size of control fish livers, fin rot L; livers enlarged to nearly twice the size of control fish livers, fin rot L; livers enlarged to nearly twice the size of control fish livers, fin rot L; livers enlarged to nearly twice the size of control fish livers, fin rot L; lethal to 7 of 90 fish over 139 days L; lethal to 7 of 90 fish over 139 days L; lethal to 7 of 90 fish over 139 days 0.00388 mg/kg (etractable lipid)4 Morphology, LOED [32] 0.00371 mg/kg (liver)4 Morphology, LOED [32] 0.00026 mg/kg (muscle)4 Morphology, LOED [32] 0.00065 mg/kg (whole body)4 Morphology, LOED [32] 0.00388 mg/kg (extractable lipid)4 0.00371 mg/kg (liver)4 0.00026 mg/kg (muscle)4 277 Mortality, LOED Mortality, LOED Mortality, LOED [32] [32] [32] 278 Species: Taxa Sediment Oncorhynchus mykiss, Rainbow trout Oncorhynchus mykiss, Rainbow trout Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.00065 mg/kg (whole body)4 Mortality, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [32] L; lethal to 7 of 90 fish over 139 days 0.01 mg/kg (whole body)4 0.001 mg/kg (whole body)4 0.025 mg/kg (whole body)4 Mortality, ED50 Growth, LOED Morphology, LOED [36] [36] [36] L; 80-day LD50 for mortality L; reduction in body weight L; fin necrosis, hyperpigmentation 0.000315 mg/kg (carcass)4 Growth, NOED [38] [38] [38] [38] [38] [38] [38] L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth 0.000102 mg/kg Growth, NOED (gastrointestinal tract)4 0.000244 mg/kg (gill)4 0.00007 mg/kg (heart)4 0.000092 mg/kg (kidney)4 0.000072 mg/kg (liver)4 0.000355 mg/kg (pyloric caeca)4 Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.000029 mg/kg (skeletal muscle)4 0.000201 mg/kg (skin)4 0.000085 mg/kg (spleen)4 0.00327 mg/kg (visceral fat)4 0.00025 mg/kg (whole body)4 0.000315 mg/kg (carcass)4 Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Morphology, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] [38] [38] [38] [38] [38] L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage 0.000102 mg/kg Morphology, (gastrointestinal tract)4 NOED 0.000244 mg/kg (gill)4 0.00007 mg/kg (heart)4 0.000092 mg/kg (kidney)4 279 Morphology, NOED Morphology, NOED Morphology, NOED [38] [38] [38] [38] 280 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.000072 mg/kg (liver)4 0.000355 mg/kg (pyloric caeca)4 0.000029 mg/kg (skeletal muscle)4 0.000201 mg/kg (skin)4 0.000085 mg/kg (spleen)4 0.00327 mg/kg (visceral fat)4 0.00025 mg/kg (whole body)4 0.000315 mg/kg (carcass)4 Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on mortality L; no effect on mortality [38] [38] [38] [38] [38] [38] [38] [38] 0.000102 mg/kg Mortality, (gastrointestinal tract)4 NOED Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.000244 mg/kg (gill)4 0.00007 mg/kg (heart)4 0.000092 mg/kg (kidney)4 0.000072 mg/kg (liver)4 0.000355 mg/kg (pyloric caeca)4 0.000029 mg/kg (skeletal muscle)4 0.000201 mg/kg (skin)4 0.000085 mg/kg (spleen)4 0.00327 mg/kg (visceral fat)4 0.00025 mg/kg (whole body)4 0.00452 mg/kg (whole body)4 Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Survival, ED50 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [13] L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; exposure concentration is the mean of measured TCDD concentration 281 282 Species: Taxa Sediment Oncorhynchus mykiss, Rainbow trout Oncorhynchus mykiss, Rainbow trout Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 0.0000047 mg/kg (liver)4 Biochemical, LOED [40] L; significant increase in liver ethoxyresorufin Odeethylase (EROD) L; significant increase in liver ethoxyresorufin Odeethylase (EROD) L; significant increase in liver ethoxyresorufin Odeethylase (EROD) 0.000038 mg/kg (liver)4 Biochemical, LOED [40] 0.000016 mg/kg (liver)4 Biochemical, LOED [40] 0.000439 mg/kg (whole body)4 Mortality, ED50 [42] L; mortality from fertilization to swim-up; exposure dose calculated from text; residue measured in egg at 5-days post exposure; dosed for 48 hours and endpoint measured after approximately 24 days Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.000421 mg/kg (whole body)4 Mortality, ED50 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [42] L; mortality from fertilization to swim-up; liposome used to carry dose; 93% of dose retained in egg and assumed to be in swim-up fry, flow rate = 8-12 L; significant increase in mortality from hatch to swim-up at lowest exposure concentration tested; exposure dose calculated from text; residue measured in egg at 5-days post exposure; dosed for 48 hours and endpoint measured after approximately 24 days 0.000279 mg/kg (whole body)4 Mortality, LOED [42] 283 284 Species: Taxa Sediment Oncorhynchus mykiss, Rainbow trout Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.000437 mg/kg (whole body)4 Mortality, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [42] L; significant increase in mortality from hatch to swim-up; liposome used to carry dose; 93% of dose retained in egg and assumed to be in swim-up fry, flow rate = 8-12 L; no significant increase in mortality from hatch to swim-up; liposome used to carry dose; 93% of dose retained in egg and assumed to be in swim-up fry, flow rate = 8 to 12 0.000291 mg/kg (whole body)4 Mortality, NOED [42] 0.00017 mg/kg (whole body)4 Mortality, ED50 [43] L; estimated LD50s for 6 strains of rainbow trout, orig_con_wet ranged from 170 to 488; used low value; exposure concentration = 170 to 488 Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Salmo trutta, Brown trout 5.2 pg/g5 (fillet) 4.25-4.45 [22] F; locations throughout Maine; a range of mean BAFs is presented; the values are means for locations throughout Maine, and the range is for BAFs calculated using river concentrations from years prior to the sampling date to account for declines in paper mill discharges Salvelinus fontinalis, Brook trout 0.0006 mg/kg (whole body)4 Physiological [33] L; induction of hepatic EROD 285 286 Species: Taxa Salvelinus fontinalis, Brook trout Sediment Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.0012 mg/kg (whole body)4 Growth, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [41] L; no significant growth effect at highest target body burden; TCDDspiked diet to produce desired body burden; abstract with minimal information L; no significant mortality at highest target body burden; TCDD-spiked diet to produce desired body burden; abstract with minimal information L; significant delay in spawning; TCDD-spiked diet to produce desired body burden; abstract with minimal information 0.0012 mg/kg (whole body)4 Mortality, NOED [41] 0.0012 mg/kg (whole body)4 Reproduction, LOED [41] Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.0006 mg/kg (whole body)4 Reproduction, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [41] L; no delay in spawning; TCDDspiked diet to produce desired body burden; abstract with minimal information Salvelinus fontinalis, Brook trout 0.0002 mg/kg (whole body)4 Mortality, ED50 [43] L; estimated LD50 Amia calva, Bowfin 11.2 ppt5 (liver) (n = 1) 18.6 ppt5 (liver) (n = 1) 46.1 ppt5 (ovary) (n=1) -0.59 0.180 [15] -0.36 0.255 0.03 0.281 F; northeastern Florida; bleachedkraft paper mill receiving stream; BAF and BSAF calculated using mean of two sediment concentrations. BAF = (pg TCDD/g tissue) (pg TCDD / g sediment); BSAF = (pg TCDD/g lipid) (pg TCDD / g TOC). 287 288 Species: Taxa Sediment Oncorhynchus kisutch, Coho salmon Carp, (scientific name unknown) Salvelinus namaycush, Lake trout, (early life stage) Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 0.000478 mg/kg (whole body)4 0.000478 mg/kg (whole body)4 0.00217 mg/kg (whole body)4 0.00217 mg/kg (whole body)4 0.000125 mg/kg (whole body)4 0.000125 mg/kg (whole body)4 Growth, LOED [39] L; reduced growth Mortality, LOED Growth, NA Mortality, NA Behavior, NOED Growth, NOED [39] [39] [39] [39] L; reduced survival L; reduced growth L; reduced survival L; no effect on food consumption or feeding L; no effect on growth [39] water exposure 62 pg/L 2.2 g/kg5 Death (71 days) [16] L water exposure 20 ng/L 0.055 g/kg5 (egg) 48-hour LOEC (mortality) [21] L Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Concentration, Units in1: Sediment Water water exposure 10 ng/L water exposure 62 ng/L Toxicity: Tissue (Sample Type) Effects 0.034 g/kg5 (egg) 48-hour NOEC (mortality) 48-hour LOEC (hatchability) Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [21] L 0.226 g/kg5 (egg) [21] L Salvelinus namaycush, Lake trout 0.000065 mg/kg (whole body)4 0.000055 mg/kg (whole body)4 Mortality, ED50 Mortality, LOED [15] L; lethal to 50% of sac fry L; lowest statistically significant increase in mortality of sac fry L; reduced hatchability of eggs L; no effect on mortality of sac fry L; LD50 for sac fry mortality [15] 0.000226 mg/kg (whole body)4 0.000035 mg/kg (whole body)4 Salvelinus namaycush, Lake trout 0.000044 mg/kg (whole body)4 Reproduction, L Mortality, NOED Mortality, ED50 [15] [15] [34] 289 290 Species: Taxa Salvelinus namaycush, Lake trout Sediment Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.000065 mg/kg (whole body)4 Mortality, ED50 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [42] L; mortality from fertilization to swim-up; exposure dose calculated from text; residue measured in egg at 5-days post exposure; dosed for 48 hours and endpoint measured after approximately 24 days L; significant increase in mortality from hatch to swim-up; exposure dose calculated from text; residue measured in egg at 5-days post exposure; dosed for 48 hours and endpoint measured after approximately 24 days 0.000055 mg/kg (whole body)4 Mortality, LOED [42] Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.000058 mg/kg (whole body)4 Mortality, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [42] L; significant increase in mortality from hatch to swim-up; high control mortality; liposome used to carry dose; 93% of dose retained in egg and assumed to be in swim-up fry, flow rate = 8-12 L; no significant increase in mortality from hatch to swim-up; exposure dose calculated from text; residue measured in egg at 5-days post exposure; dosed for 48 hours and endpoint measured after approximately 24 days 0.000034 mg/kg (whole body)4 Mortality, NOED [42] 291 292 Species: Taxa Sediment Salvelinus namaycush, Lake trout Carassius auratus, Goldfish Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.000044 mg/kg (whole body)4 Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [42] L; no significant increase in mortality from hatch to swim-up; high control mortality; liposome used to carry dose; 93% of dose retained in egg and assumed to be in swim-up fry, flow rate = 8 to 12 0.000065 mg/kg (whole body)4 Mortality, ED50 [43] L; estimated LD50 0.58-0.63 ng/g5 (whole body) 4.39 [18] L; fish were exposed for 120 hr; exposure water contained fly ash extract; concentrations were measured in water, but data were not presented Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Cyprinus carpio, Carp Concentration, Units in1: Sediment 170 pg/g5 Water Toxicity: Tissue (Sample Type) Effects 120 pg/g5 Ability to Accumulate2: Log BCF Log BAF BSAF 0.27 Source: Reference Comments3 [9] F; Petenwell Reservoir, central Wisconsin; BSAF based on 8% tissue lipid content and 3.1% sediment organic carbon Cyprinus carpio, Carp 0.0022 mg/kg (whole body)4 0.0022 mg/kg (whole body) 4 0.0022 mg/kg (whole body)4 Behavior, LOED Cellular, LOED Morphology, LOED [15] [15] [15] L; difficulty swimming L; edema, body wall ulcers L; fin erosion, hemorrhage, morphologically resembling Blue Sac Disease Cyprinus carpio, Carp 0.003 mg/kg (whole body)4 Mortality, ED50 [36] L; 80-day LD50 for mortality Cyprinus carpio, Carp 0.0022 mg/kg (whole body)4 Mortality, LOED [15] L; increased mortality 293 294 Species: Taxa Danio rerio, Zebrafish Sediment Bracydanio rerio, Zebrafish Pimephales promelas, Fathead minnow Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 2.16 ng/g (egg) ED50 (pericardial edema) ED50 (yolk sac edema) LD50 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [23] L; newly fertilized eggs were exposed for 1 hr to water containing graded concentrations of TCDD 2.43 ng/g (egg) 2.45 ng/g (egg) 8.3 g/kg5 8.3 g/kg5 LOEC (reproduction) LOEC (oogenesis) [24] [24] L; food exposure L; food exposure 17-2,042 g/kg5 LD100 [17] L; food exposure Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Catostomus commerson, White sucker Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 9.6 pg/g5 (whole body) Ability to Accumulate2: Log BCF Log BAF 4.89-5.03 BSAF Source: Reference Comments3 [22] F; locations throughout Maine; a range of mean BAFs is presented; the values are means for locations throughout Maine, and the range is for BAFs calculated using river concentrations from years prior to the sampling date to account for declines in paper mill discharges 295 296 Species: Taxa Sediment Ictalurus nebulosus, 32.2 -52.8 Brown bullhead ppt5 catfish (TOC = 3.23.9%) Ictalurus melas, Black bullhead Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 1.8 ppt5 (liver) (% lipid = 3.5) 2.6 ppt5 (liver) (% lipid = 2.9) 2.8 ppt5 (liver) (% lipid = 3.2) Ability to Accumulate2: Log BCF Log BAF -1.40 BSAF 0.043 Source: Reference Comments3 [15] F; northeastern Florida; bleachedkraft paper mill receiving stream; BAF and BSAF calculated using mean of two sediment concentrations. BAF = (pg TCDD/g tissue) (pg TCDD/ g sediment); BSAF = (pg TCDD/g lipid) (pg TCDD / g TOC). -1.22 0.074 -1.15 0.073 0.005 mg/kg (whole body)4 0.025 mg/kg (whole body)4 Mortality, ED50 Morphology, LOED [36] [36] L; 80 day LD50 for mortality L; fin necrosis, hyperpigmentation Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Ictalurus punctatus, Channel catfish Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.0044 mg/kg (whole body)4 Mortality, ED10 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [45] L; radiolabelled compounds in sediment, compound leached into water for exposure; all fish died between days 14 and 15; body residues from dead fish Gambusia affinis, Mosquito fish 0.0072 mg/kg (whole body)4 Mortality, ED10 [45] L; radiolabelled compounds in sediment, compound leached into water for exposure; all fish died between days 14 and 15; body residues from dead fish Oryzias latipes, Japanese medaka Water exposure 2.2 ng/L 0.24 g/kg5 (embryo) Lesions in embryos [19] L 297 298 Species: Taxa Oryzias latipes, Japanese medaka (juveniles) Sediment Oryzias latipes, Japanese medaka Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water water exposure 101 26 pg/L (n = 23) Toxicity: Tissue (Sample Type) Effects 2,408 241 pg/g Obvious signs of TCDD toxicity such as generalized edema, fin erosion, and discoloration in many of the exposed fish Ability to Accumulate2: Log BCF 4.38 nonsteady state 5.71 predicted steady state Log BAF BSAF Source: Reference Comments3 [20] L; 12-day exposure period; lipid content 7.5% 0.24 mg/kg (whole body)4 0.3 mg/kg (whole body)4 Lesions, ED50 Lesions, LOED [19] [19] L; ten replicates per treatment L; 50% of embryos with lesions but no statistical significance analyzed; ten replicates per treatment L; no significant incidence of lesions at lowest doseage tested; 10 replicates per treatment, resd_conc_wet value > 0.1 0.1 mg/kg (whole body)4 Lesions, NOED [19] Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Morone americana, White perch Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 1.2 pg/g5 Ability to Accumulate2: Log BCF Log BAF 3.48-3.88 BSAF Source: Reference Comments3 [22] F; locations throughout Maine; a range of mean BAFs is presented; the values are means for locations throughout Maine, and the range is for BAFs calculated using river concentrations from years prior to the sampling date to account for declines in paper mill discharges Lepomis macrochirus, Bluegill 0.016 mg/kg (whole body)4 0.005 mg/kg (whole body)4 0.025 mg/kg (whole body)4 Mortality, ED50 Growth, LOED Morphology, LOED [36] [36] [36] L; 80-day LD50 for mortality L; reduction in body weight L; fin necrosis, hyperpigmentation 299 300 Species: Taxa Microperus dolomieu, Smallmouth bass Sediment Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 3.4 pg/g5 (fillet) Ability to Accumulate2: Log BCF Log BAF 4.06-4.39 BSAF Source: Reference Comments3 [22] F; locations throughout Maine; a range of mean BAFs is presented; the values are means for locations throughout Maine, and the range is for BAFs calculated using river concentrations from years prior to the sampling date to account for declines in paper mill discharges Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Micropterus samoides, Largemouth bass Concentration, Units in1: Sediment 32.2 ppt5 (TOC=3.2%) 52.8 ppt5 (TOC=3.9%) Water Toxicity: Tissue (Sample Type) Effects 1.8 ppt5 (liver) (% lipid =3.9) 2.9 ppt5 (liver) (% lipid =2.4) 8.8 ppt5 (ovary) (% lipid =7.6) Ability to Accumulate2: Log BCF Log BAF -1.40 BSAF 0.038 Source: Reference Comments3 [15] F; northeastern Florida; bleached kraft paper mill receiving stream; BAF and BSAF calculated using mean of two sediment concentrations. BAF = (pg TCDD / g tissue) (pg TCDD/ g sediment); BSAF = (pg TCDD/g lipid) (pg TCDD/ g TOC). L; 80-day LD50 For Mortality L; Fin Necrosis, Hyperpigmentation -1.15 0.100 -0.68 0.096 Micropterus salmoides, Largemouth bass 0.011 mg/kg (whole body)4 0.025 mg/kg (whole body)4 Mortality, ED50 Morphology, LOED [36] [36] Perca flavescens, Yellow perch 0.003 mg/kg (whole body)4 0.005 mg/kg (whole body)4 Mortality, ED50 Growth, LOED [36] [36] L; 80-day LD50 for mortality L; reduction in body weight 301 302 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.025 mg/kg (whole body)4 0.000129 mg/kg (carcass)4 Morphology, LOED Growth, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [36] [37] [37] [37] [37] [37] [37] [37] [37] [37] [37] [37] L; fin necrosis, hyperpigmentation L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth 0.000148 mg/kg Growth, NOED (gastrointestinal tract)4 0.000155 mg/kg (gill)4 0.000077 mg/kg (heart)4 0.000119 mg/kg (kidney)4 0.000466 mg/kg (liver)4 0.000143 mg/kg (pyloric caeca)4 0.000009 mg/kg (skeletal muscle)4 0.000041 mg/kg (skin)4 0.000166 mg/kg (spleen)4 0.00277 mg/kg (visceral fat)4 Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.000143 mg/kg (whole body)4 0.000129 mg/kg (carcass)4 Growth, NOED Morphology, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [37] [37] L; no effect on growth L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage 0.000148 mg/kg Morphology, (gastrointestinal tract)4 NOED 0.000155 mg/kg (gill)4 0.000077 mg/kg (heart)4 0.000119 mg/kg (kidney)4 0.000466 mg/kg (liver)4 0.000143 mg/kg (pyloric caeca)4 0.000009 mg/kg (skeletal muscle)4 303 Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED [37] [37] [37] [37] [37] [37] [37] 304 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.000041 mg/kg (skin)4 0.000166 mg/kg (spleen)4 0.00277 mg/kg (visceral fat)4 0.000143 mg/kg (whole body)4 0.000129 mg/kg (carcass)4 Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [37] L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on fin necrosis or hemorrhage L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality [37] [37] [37] [37] [37] [37] [37] [37] [37] 0.000148 mg/kg Mortality, (gastrointestinal tract)4 NOED 0.000155 mg/kg (gill)4 0.000077 mg/kg (heart)4 0.000119 mg/kg (kidney)4 0.000466 mg/kg (liver)4 Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.000143 mg/kg (pyoric ceca)4 0.000009 mg/kg (skeletal muscle)4 0.000041 mg/kg (skin)4 0.000166 mg/kg (spleen)4 0.00277 mg/kg (visceral fat)4 0.000143 mg/kg (whole body)4 Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [37] [37] [37] [37] [37] [37] L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L., no effect on mortality Salmonids 0.059 [46] F 305 306 Species: Taxa Wildlife Aix sponsa, Wood duck Sediment Aix sponsa, Wood duck Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 pg/g (eggs): Site 1 geometric mean: 36 (1.6 to 482) Site 2 geometric mean: 14 (0.8-74) Site 3 geometric mean: 4.2 (<1 to 19) % eggs hatched: 47% (9.7 SE) [29] 62% (10.1 SE) 79% (3.8 SE) Site 4 geometric 93% (3.4 SE) mean: 0.01 (<1 to 0.5) F; central Arkansas; egg TEFs and hatching success and duckling production were negatively correlated; clutch size was similar among wetland Sites 1-3 which were 9, 17, and 58 km downstream from point source of contamination. respectively, and Site 4 which was 111 km away on a separate drainage; duckling abnormalities were also noted Threshold range of reduced productivity was > 20-50 ppt TEF. Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Falco peregrinus, Peregrine falcon Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 11 ng/g (eggs) (n= 6) 11.4% eggshell thinning Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [26] F; Kola Peninsula, Russia Haliaeetus leucocephalus, Bald eagle chicks Powell River site: 2,200 ng/kg lipid weight basis (yolk sac) Reference site: 300 ng/kg lipid weight basis (yolk sac) A nearly 6-fold greater incidence of an hepatic cytochrome P4501A crossreactive protein was induced in chicks from Powell River site as compared to the reference (p < 0.05). No significant concentrationrelated effects were found for morphological, physiological, or histological parameters. [25] F; southern coast of British Columbia; eggs were collected from nests and hatched in the lab; ~ indicates value was taken from a figure. 307 308 Species: Taxa Sterna forsteri, Forster's tern Sediment Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Lake Poygan site: 8.0 pg/g; (egg) (n = 6) Green Bay site: 37.3 pg/g; (egg) (n = 6) Birds from Green Bay had increased incubation period, reduced hatchability, lower body weight, increased liver to body weight ratio, and occurrence of edema when compared to birds from Lake Poygan. There was a significantly higher incidence of congenital abnormalities in dead embryos and chicks from Green Bay. Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [27] F; Green Bay, Lake Michigan, and Lake Poygan, Wisconsin Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Species: Taxa Ardea herodias, Great blue heron chicks Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Nicomekl site: 100.9 ng/kg; (egg) (n = 11) Vancouver site: 13549.6 ng/kg (egg) (n = 12) Depression of growth compared to Nicomekl site. Presence of edema. Depression of growth compared to Nicomekl site. Presence of edema. Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [28] L; eggs were collected from three British Columbia colonies with different levels of contamination and incubated in the laboratory Crofton site: 2 1133.7 ng/kg (egg) (n = 6) 309 310 Species: Taxa Mustela vison, Mink Sediment Diet: 2 pg/g5 Diet: 3 pg/g5 Diet: 7 pg/g5 1 2 3 4 5 Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 21 pg/g5 (liver) LOAEL; reduced kit body weights followed by reduced survival Reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female Ability to Accumulate2: Log BCF Log BAF log BMF= 1.05 BSAF Source: Reference Comments3 [30] L; BMF = biomagnification factor = v l /vd, vl = lipidnormalized concentration in tissue; vd = lipidnormalized dietary concentration 34 pg/g5 (liver) log BMF = 1.06 50 pg/g5 (liver) log BMF = 1.04 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed and the reader is strongly urged to consult the publication to confirm the information presented here. Not clear from reference if concentration is based on wet or dry weight. BIOACCUMULATION SUMMARY References 1. 2,3,7,8-TCDD Podoll, R.T., et al., 1986, Environ. Sci. Technol. 20:490-492 (cited in: USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH. February). USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1995. Health Effects Assessment Summary Tables: FY-1995 Annual. EPA/540/R95/036. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, DC. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxicity equivalency factors (TEF). Crit. Rev. Toxicol. 21:51-88. Braune, B.M. and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957-968. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8tetrachlorodibenzo-p-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055. U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC. Pruell, R.J., N.I. Rubinstein, B.K. Taplin, J.A. LiVolsi, and R.D. Bowen. 1993. Accumulation of polychlorinated organic contaminants from sediment by three benthic marine species. Arch. Environ. Contam. Toxicol. 24:290-297. Kuehl, D.W., P.M. Cook, A.R. Batterman, D. Lothenbach, and B.C. Butterworth. 1987. Bioavailability of polychlorinated dibenzo-p-dioxins and dibenzofurans from contaminated Wisconsin River sediment to carp. Chemosphere 16(4):667-679. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85 (1.8):37. 2. 3. 4. 5. 6. 7. 8. 9. 10. 311 BIOACCUMULATION SUMMARY 11. 2,3,7,8-TCDD USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of chlorinated dibenzo-p-dioxins and dibenzofurans (CDDs and CDFs) and 1989 update. EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum, Washington, DC. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.H. Peterman, D.L. Stalling, G.M. DeGraeve, J.J. Coyle, and W.J. Adams. 1988. Toxicity and bioconcentration of 2,3,7,8tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout. Environ. Toxicol. Chem. 7:47-62. Rubinstein, N.I., R.J. Pruell, B.K. Taplin, J.A. LiVolsi, and C.B. Norwood. 1990. Bioavailability of 2,3,7,8-TCDD, 2,3,7,8-TCDF and PCBs to marine benthos from Passaic River sediments. Chemosphere 20(7-9):1097-1102. Schell, J.D. Jr., D.M. Campbell, and E. Lowe. 1993. Bioaccumulation of 2,3,7,8tetrachlorodibenzo-p-dioxin in feral fish collected from a bleach-kraft paper mill receiving stream. Environ. Toxicol. Chem. 12:2077-2082. Cook, P.M., D.W. Kuehl, M.K. Walker, and R.E. Peterson. 1991. Bioaccumulation and toxicity of TCDD and related compounds in aquatic ecosystems. Abstract, in Dioxin '92. Adams, W.J., G.M. DeGraeve, T.D. Sabourin, J.D. Cooney, and G.M. Mosher. 1986. Toxicity and bioconcentration of 2,3,7,8-TCDD to fathead minnow (Pimephales promelas). Chemosphere 15:1503-1511. Sijm, D.T.H.M., H. Wever, and A. Opperhuizen. 1993. Congener-specific biotransformation and bioaccumulation of PCDDs and PCDFs from fly ash in fish. Environ. Toxicol. Chem. 12: 1895-1907. Wisk, J.D., and K.R. Cooper. 1990. The stage specificity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in embryos of the Japanese medaka (Oryzias latipes). Environ. Toxicol. Chem. 9:1159-1169. Schmieder, P., D. Lothenbach, J. Tietge, R. Erickson, and R. Johnson. 1995. [3H]-2,3,7,8TCDD uptake and elimination kinetics of medaka (Oryzias latipes). Environ. Toxicol. Chem. 14(10):1735-1743. Walker, M.K., J.M. Spitsbergen, J.R. Olson, and R.E. Peterson. 1991. 2,3,7,8Tetrachorodibenzo-p-dioxin (TCDD) toxicity during early life stage development of lake trout (Salvelinus namaycush). Can. J. Fish. Aquat. Sci. 48:875-883. Frakes, R.A., C.Q. T. Zeeman, and B. Mower. 1993. Bioaccumulation of 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) by fish downstream of pulp and paper mills in Maine. Ecotoxicol. Environ. Saf. 25:244-252. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 312 BIOACCUMULATION SUMMARY 23. 2,3,7,8-TCDD Henry, T.R., M.W. Hornung, C.C. Abnet, and R.E. Peterson. 1995. Early life stage toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in zebrafish (Danio rerio). Poster presentation at the 16th Annual Meeting of the Society of Environmental Toxicology and Chemistry (SETAR), Second SETAC World Congress, November 5-9, 1995, Vancouver, British Columbia, Canada. Wannamacher, R., A. Rebstock, E. Kulzer, D. Schrenk, and K.W. Bock. 1992. Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on reproduction and oogenesis in zebrafish (Brachydanio rerio). Chemosphere 24:1361-1368. Elliott, J.E., R.J. Norstrom, A. Lorenzen, L.E. Hart, H. Philibert, S.W. Kennedy, J.J. Stegeman, G.D. Bellward, and K.M. Cheng. 1995. Biological effects of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls in bald eagle (Haliaeetus leucocephalus) chicks. Environ. Toxicol. Chem. 15(5):782-793. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor Conservation Today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. Kubiak, T.J., H.J. Harris, L.M. Smith, T.R. Schwartz, D.L. Stalling, J.A. Trick, L. Sileo, D.E. Docherty, and T.C. Erdman. 1989. Microcontaminants and reproductive impairment of the Forster's tern on Green Bay, Lake Michigan1983. Arch. Environ. Contam. Toxicol. 18:706727. Hart, L.E., K.M. Cheng, P.E. Whitehead, R.M. Shah, R.J. Lewis, S.R. Ruschkowski, R.W. Blair, D.C. Bennett, S.M. Bandiera, R.J. Norstrom, and G.D. Bellward. 1991. Dioxin contamination and growth and development in great blue heron embryos. J. Toxicol. Environ. Health 32:331344. White, D.H., and J.T. Seginak. 1994. Dioxins and furans linked to reproductive impairment in wood duck. J.Wildl. Manage. 58(1):100-106. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. Ashley, C.M., M.G. Simpson, D.M. Holdich, and D.R. Bell. 1996. 2,3,7,8-tetrachloro-dibenzo-pdioxin is a potent toxin and induces cytochrome P450 in the crayfish, Pacifastacus leniusculus. Aquat. Toxicol. 35:157-169. Branson, D.R., L.T. Takahashi, W.M. Parker, and G.E. Blau. 1985. Bioconcentration kinetics of 2,3,7,8-tetrachlorodibenzo-p-dioxin in rainbow trout. Environ. Toxicol. Chem. 4:779-788. Daniel, F.B., S. Cormier, B. Subramanian, D. Williams, J. Torsella, and J. Lech. 1994. Six month EROD response pattern of dioxin fed brook trout. Abstract, 15th Annual Meeting, Society of Environmental Toxicology and Chemistry, 30 October-3 November, 1994, Denver, CO. 313 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. BIOACCUMULATION SUMMARY 34. 2,3,7,8-TCDD Guiney, P., E. Zabel, R. Peterson, P. Cook, J. Casselman, J. Fitzsimons, and H. Simonin. 1993. Assessment of Lake Ontario lake trout for 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents (TEQS) induced sac fry mortality in 1991. Presentation 519, 14th Annual Meeting, Society of Environmental Toxicology and Chemistry, Houston, TX. Isensee, A.R., and G.E. Jones. 1975. Distribution of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in an aquatic model ecosystem. Environ. Sci. Technol. 9:668-672. Kleeman, J.M., J.R. Olson, and R.E. Peterson. 1988. Species differences in 2,3,7,8tetrachlorodibenzo-p-dioxin toxicity and biotransformation in fish. Fund. Appl. Toxicol. 10:206213. Kleeman, J.M., J.R. Olson, S.M. Chen, and R.E. Peterson. 1986. 2,3,7,8-tetrachlorodibenzo-pdioxin metabolism and disposition in yellow perch. Toxicol. Appl. Pharmacol. 83:402-411. Kleeman, J.M., J.R. Olson, S.M. Chen, and R.E. Peterson. 1986. Metabolism and disposition of 2,3,7,8-tetrachlorodibenzo-p-dioxin in rainbow trout. Toxicol. Appl. Pharmacol. 83:391-401. Miller, R.A., L.A. Norris, and B.R. Loper. 1979. The response of coho salmon and guppies to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in water. Trans. Amer. Fish. Soc. 108:401-407. Parrott, J.L., P.V. Hodson, M.R. Servos, S.L. Huestis, and G.D. Dixon. 1995. Relative potency of polychlorinated dibenzo-p-dioxins and dibenzofurans for inducing mixed-function oxygenase activity in rainbow trout. Environ. Toxicol. Chem. 14(6):1041-1050. Tietge, J.E. 1994. Reproductive and toxicological effects in brook trout following a dietary exposure to 2,3,7,8-TCDD. Abstract, 15th Annual Meeting, Society of Environmental Toxicology and Chemistry, Denver, CO, October 30-November 3, 1994. Walker, M.K., L.C. Hufnagle, Jr., M.K. Clayton, and R.E. Peterson. 1992. An egg injection method for assessing early life stage mortality of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls in rainbow trout (Oncorhynchus mykiss). Aquat. Toxicol. 22:15-38. Walker, M.K., E.W. Zabel, and R.E Peterson. 1993. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced toxicity during salmonid early life stage development: Cross species and strain comparisons. Abstract, Society of Environmental Toxicology and Chemistry, 14th Annual Meeting, Houston, TX, November 14-18, 1993. West, C.W., G.T. Ankley, J.W. Nichols, G.E. Elonen, and D.E. Nessa. 1997. Toxicity and bioaccumulation of 2,3,7,8-tetrachlorodibenzo-p-dioxin in long-term tests with the freshwater benthic invertebrates Chironomus tentans and Lumbriculus variegatus. Environ. Toxicol. Chem. 16(6):1287-1294. Yockim, R.S., A.R. Isensee, and G.E. Jones. 1978. Distribution and toxicity of TCDD and 2,4,5-T in an aquatic model ecosystem. Chemosphere 7: 215-220. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 314 BIOACCUMULATION SUMMARY 46. 2,3,7,8-TCDD USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 315 316 BIOACCUMULATION SUMMARY Chemical Category: PESTICIDE (ORGANOCHLORINE) Chemical Name (Common Synonyms): 1,1-(2,2-DICHLOROETHYLIDENE)BIS(4-CHLOROBENZENE), p,p-DICHLORODIPHENYLDICHLOROETHANE 4,4-DICHLORODIPHENYLDICHLOROETHANE p,p-DDD CASRN: 72-54-8 Chemical Characteristics Solubility in Water: 0.16 mg/L at 24C [1] Half-Life: 2.0-15.6 years based on biodegradation of DDD in aerobic soils under field conditions [2] Log Koc: 6.0 L/kg organic carbon Log Kow: 6.10 [3] Human Health Oral RfD: Not available [4] Confidence: -- Critical Effect: Lung tumors in male and female mice, liver tumors in male mice, thyroid tumors in male rats Oral Slope Factor: 2.4 x 10-1 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4] Wildlife Partitioning Factors: Partitioning factors for DDD in wildlife were not calculated in the studies reviewed. However, based on the data presented in one study reviewed, log BCFs for birds from the lower Detroit River ranged from 4.97 to 5.22. Concentrations of DDD in birds were 3.5 to 6.1 times higher than those in sediment. Food Chain Multipliers: Biomagnification factors of 3.2 and 85 were determined for DDT and DDE, respectively, from alewife to herring gulls in Lake Ontario [5]. A study of arctic marine food chains measured biomagnification factors for DDE that ranged from 17.6 to 62.2 for fish to seal, 0.3 to 0.7 for seal to bear, and 10.7 for fish to bear [6]. Aquatic Organisms Partitioning Factors: Partitioning factors for DDD in aquatic organisms were not calculated in the studies reviewed. However, the data from one study reviewed showed BCFs of 17,600 for oligochaetes and 565,000 for carp. Ratios of DDD in tissue to sediment were 0.65 for oligochaetes and 21 for carp. BSAFs for clams ranged from 0.120 to 2.745 [22,25]. BSAFs for fish ranged from 0.079 to 2.379 [21,23,24,25]. 317 BIOACCUMULATION SUMMARY p,p-DDD Food Chain Multipliers: Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were 18.5 (all benthic food web), 1.6 (all pelagic food web), and 11.3 (benthic and pelagic food web). FCMs for trophic level 4 aquatic organisms were 37.4 (all benthic food web), 3.1 (all pelagic food web), and 17.8 (benthic and pelagic food web) [28]. Toxicity/Bioaccumulation Assessment Profile DDT is very persistent in the environment due to its low vapor pressure, high fat solubility, and resistance to degradation and photooxidation. DDT is degraded to DDE under aerobic conditions and to DDD in anoxic systems [7]. These metabolites, DDD and DDE, are similar to DDT in both their stability and toxicity. Chronic effects of DDT and its metabolites on ecological receptors include changes in enzyme production, hormonal balance, and calcium metabolism, which may cause changes in behavior and reproduction. The high octanol-water partition coefficient of DDT indicates that it is easily accumulated in tissues of aquatic organisms. Laboratory studies have shown that these compounds are readily bioconcentrated in aquatic organisms, with reported log BCFs for DDT ranging from 3.08 to 7.65 and for DDE ranging from 4.80 to 5.26 [8]. Invertebrate species are generally more susceptible than fish species to effects associated with exposure to DDT in the water column [8]. In general, the low solubility of DDT and its metabolites in water suggests that water column exposures are likely to be lower than exposures from ingestion of food or sediment. Sediments contaminated with pesticides, including DDT, have been shown to affect benthic communities at low concentrations. Results of laboratory and field investigations suggest that chronic effects generally occur at total DDT concentrations in sediment exceeding 2 g/kg [9]. Equilibrium partitioning methods predict that chronic effects occur at DDT concentrations in sediment of 0.6 to 1.7 g/kg [10]. For fish, the primary route of uptake is via prey items, but both DDT and its metabolites can be accumulated through the skin or gills upon exposure to water. Short-term exposure to DDT concentrations of less than 1 g/L have been reported to elicit toxic responses in both freshwater and marine fish [8]. DDT may also be transfered to embryos from contaminated adults. DDT concentrations of 1.1 to 2.4 mg/kg in fish embryos have been associated with fry mortality [11,12]. Eggshell thinning, embryo mortality, and decreased hatchling survival have been linked to chronic exposure to DDT and its metabolites in the diet of birds. Of the three compounds, evidence strongly indicates that DDE is responsible for most reproductive toxicity in avian species [13]. Measurements of residues in eggs of birds are a reliable indicator of adverse effects. There is a large amount of variability in sensitivity to DDT and its metabolites among bird species, with waterfowl and raptor species showing the greatest sensitivities. Studies have shown the brown pelican to be most susceptible to adverse effects, with eggshell thinning and depressed productivity occurring at 3.0 g/g of DDE in the egg and total reproductive failure when residues exceed 3.7 g/g [13]. 318 Summary of Biological Effects Tissue Concentrations for p,p-DDD Species: Taxa Invertebrates Tubifex sp., Oligochaetes water = 0.023 mg/kg 0.85 ng/L n=1 n=1 [14] 0.015 mg/kg n=1 F; lower Detroit River Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Macomona liliana, Mollusk 66.7 g/kg OC 1,096.0 g/kg OC 286.4 g/kg OC 20.0 g/kg OC 25.0 g/kg OC 76.3 g/kg lipid 765.2 g/kg lipid 75.1 g/kg lipid 54.9 g/kg lipid 22.4 g/kg lipid 1.144 0.698 0.262 2.745 0.894 [22] [22] [22] [22] [22] F; %lipid = 2.95; %sed OC = 0.30 F; %lipid = 2.33; %sed OC = 0.73 F; %lipid = 2.57; %sed OC = 0.22 F; %lipid = 2.04; %sed OC = 0.25 F; %lipid = 3.13; %sed OC = 0.48 Austrovnus 66.7 g/kg stutchburyi, Mollusk OC 286.4 g/kg OC 20 g/kg OC 25 g/kg OC 319 42.4 g/kg lipid 34.4 g/kg lipid 27.7 g/kg lipid 25.1 g/kg lipid 0.635 0.120 1.383 1.002 [22] [22] [22] [22] F; %lipid = 5.62; %sed OC = 0.30 F; %lipid = 4.85; %sed OC = 0.22 F; %lipid = 3.87; %sed OC = 0.25 F; %lipid = 4.27; %sed OC = 0.48 320 Species: Taxa Sediment Corbicula fluminea, 58.8 g/kg Asian clam OC 159.7 g/kg OC Fish Anguilla anguilla, Eel 126 g/kg OC Corogonus autumnalis, Omul (endemic whitefish ) Oncorhynchus, Salmo, Salvelinus sp., Salmonids 2,667 g/kg OC Salvelinus fontinalis, Brook trout Summary of Biological Effects Tissue Concentrations for p,p-DDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 82 g/kg lipid 82 g/kg lipid Ability to Accumulate2: Log BCF Log BAF BSAF 1.394 0.513 Source: Reference Comments3 [25] [25] F; %lipid = 0.61; %sed OC = 1.19 F; %lipid = 0.61; %sed OC = 1.19 10 g/kg lipid 0.079 [26] F; %lipid = 13; %sed OC = 32 particulate: 1.0 pg/L 1.0 n=7 dissolved: 17 pg/L 7.3 n=7 0.0086-0.15 mg/kg lipid (whole body) n=1 754.5 g/kg lipid 0.283 [24] F; %lipid = 11; %sed OC = 2.7 F; %lipid = 11 L; temperature selection after 24 h exposure to chemical 0.000093 g/L 83 g/kg 4.79 mg/kg (whole body)4 Behavior, NOED 5.93 [24] [18] Summary of Biological Effects Tissue Concentrations for p,p-DDD Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Salvelinus namaycush, Lake trout 0.9 mg/kg (whole body)4 Mortality, LOED [20] L; survival of fry reduced Leuciscus cephalus cabeda, Chub 478 g/kg OC 378 g/kg lipid 0.790 [21,27] F; %lipid = 1.27; %sed OC = 2.76 Alburnus alburnus alborella, Bleak 478 g/kg OC 769 g/kg lipid 1.608 [21,27] F; %lipid = 1.95; %sed OC = 2.76 Cyprinus carpio, Carp water = 0.023 mg/kg 0.85 ng/L n=1 n=1 [14] 0.48 0.26 mg/kg n=9 F; lower Detroit River; value is mean SD Pimephales promelas, Fathead minnow 0.6 mg/kg (whole body)4 Reproduction, LOED [17] L; significantly different from control (p = 0.05) Gambusia affinis, Mosquito fish Catastoma macrocheilus, Largescale sucker 321 530 g/kg OC 5.3 mg/kg (whole body)4 1,261 g/kg lipid Mortality, NOED 2.379 [19] L; no effect on survivorship after 3 days F; %lipid = 11.1; %sed OC = 1.0 [23] 322 Species: Taxa Cottus cognatus, Slimy sculpin Sediment 2667 g/kg OC Comephorus dybowskii, Pelagic sculpin Wildlife Aythya affinis, Lesser scaup Aythya marila, Greater scaup Summary of Biological Effects Tissue Concentrations for p,p-DDD Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 587.5 g/kg lipid 0.000093 g/L 47 g g/kg 5.70 Ability to Accumulate2: Log BCF Log BAF BSAF 0.220 Source: Reference Comments3 [24] [24] F; %lipid = 8; %sed OC = 2.7 F; %lipid = 8 particulate: 1.0 pg/L 1.0 n=7 dissolved: 17 pg/L 7.3 n=7 0.12-0.16 mg/kg lipid (whole body) n=1 [15] F; Lake Baikal, Siberia Bucephala clangula, water = Goldeneye 0.023 mg/kg 0.85 ng/L n=1 n=1 [14] 0.080 0.024 mg/kg n=3 F; lower Detroit River; value is mean SD water = 0.023 mg/kg 0.85 ng/L n=1 n=1 [14] 0.093 0.027 mg/kg n=7 F; lower Detroit River; value is mean SD water = 0.023 mg/kg 0.85 ng/L n=1 n=1 [14] 0.140.045 mg/kg n=3 F; lower Detroit River; value is mean SD Summary of Biological Effects Tissue Concentrations for p,p-DDD Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Falco peregrinus, Peregrine falcon (eggs) 9 ng/g (eggs) n=6 11.4% eggshell thinning [16] F; Kola Penninsula, Russia; n = number of clutches sampled Phoca siberica, Baikal seal particulate: 1.0 pg/L 1.0 n=7 dissolved: 17 pg/L 7.3 n=7 2.0-2.2 mg/kg5 lipid (blubber) n=1 [15] F; Lake Baikal, Siberia 1 2 3 4 5 Concentration units based on wet weight, unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. Not clear from reference if concentration is based on wet or dry weight. 323 BIOACCUMULATION SUMMARY References 1. p,p-DDD Verschueren. Hdbk. Environ. Data Org. Chem., 1983, p. 433. (Cited in: USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol. Chem. 8:957-968. Muir, D.C.G., R.J. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related compounds. Environ. Sci. Technol. 22:1071-1079. Charles, M.J., and R.A. Hites. 1987. Sediments as archives. In Sources and fates of aquatic pollutants, ed. R.A. Hites and S.J. Eisenreich, Advances In Chemistry Series, Vol. 216, pp. 365389. American Chemical Society, Washington, DC. USEPA. 1980. Ambient water quality criteria for DDT. EPA440/5-80-038. U.S. Environmental Protection Agency, Office of Water Regulations and Standards, Criteria and Standards Division, Washington, DC. Long, E.R., D.D. MacDonald, S.L. Smith, and F.D. Calder. 1995. Incidence of adverse biological effects within ranges of chemical concentrations in marine and estuarine sediments. Environ. Manage. 19(1):81-97. Pavlou, S., R. Kadeg, A. Turner, and M. Marchlik. 1987. Sediment quality criteria methodology validation: Uncertainty analysis of sediment normalization theory for nonpolar organic contaminants. Work Assignment 45, Task 3. Battelle, Washington, DC. 2. 3. 4. 5. 6. 7. 8. 9. 10. 324 BIOACCUMULATION SUMMARY 11. p,p-DDD Johnson, H.E., and C. Pecor. 1969. Coho salmon mortality and DDT in Lake Michigan. Transactions of the 34th North American Wildlife Conference. Smith, R.M., and C.F. Cole. 1973. Effects of egg concentrations of DDT and dieldrin on reproduction in winter flounder (Pseudopleuronectes americanus). J. Fish. Res. Board Can. 30:1894-1898. Blus, L.J. 1996. DDT, DDD, and DDE in birds. In Environmental contaminants in wildlife, ed. W. N. Beyer, G.H. Heinz, and A.W. Redmon-Norwood, pp. 49-71. Lewis Publishers, Boca Raton, FL. Smith., E.V., J.M. Spurr, J.C. Filkins, and J.J. Jones. 1985. Organochlorine contaminants of wintering ducks foraging on Detroit River sediments. J. Great Lakes Res. 11(3):231-246. Kucklick, J.R., T.F. Bidleman, L.L. McConnell, M.D. Walla, and G.P. Ivanov. 1994. Organochlorines in the water and biota of Lake Baikal, Siberia. Environ. Sci. Technol. 28:31-37. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. Jarvinen, A.W., M.J. Hoffman, and T.W. Thorslund. 1977. Long-term toxic effects of DDT food and water exposure on fathead minnows (Pimephales promelas). J. Fish. Res. Board. Can. 34:2089-2103. Peterson, R.H. 1973. Temperature selection of Atlantic salmon (Salmo salar) and brook trout (Salvelinus fontinalis) as influenced by various chlorinated hydrocarbons. J. Fish. Res. Bd. Can. 30(8). Metcalf, R.L. 1974. A laboratory model ecosystem to evaluate compounds producing biological magnification. In Essays in toxicology, ed. W.J. Hayes, Vol. 5, pp. 17-38. Academic Press, New York, NY. Burdick, G.E., E.J. Harris, H.J. Dean, T.M. Walker J. Skea, and D. Colby. 1964. The accumulation of DDT in lake trout and the effect on reproduction. Trans. Amer. Fish. Soc. 93:127-136. Galassi, S., G. Gandolfi, and G. Pacchetti. 1981. Chlorinated hydrocarbons in fish from the River Po (Italy). Sci. Total Environ. 20:231-240. Hickey, C.W., D.S. Roper, P.T. Holland, and T.M. Trower. 1995. Accumulation of organic contaminants in two sediment-dwelling shellfish with contrasting feeding modes: Deposit(Macomona liliana) and filter-feeding (Austovenus stutchburi). Arch. Environ. Contam. Toxicol. 11:21-231. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 325 BIOACCUMULATION SUMMARY 23. p,p-DDD Johnson, A., D. Norton, and B. Yake. 1988. Persistence of DDT in the Yakima River drainage, Washington. Arch. Environ. Contam. Toxi. 17:291-297. Oliver, G.G., and A.J. Niimi. 1988. Chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22(4):388-397. Pereira, W.E., J.L. Domagalski, F.D. Hostettler, L.R. Brown, and J.B. Rapp. 1996. Occurrence and accumulation of pesticides and organic contaminants in river sediment, water, and clam tissues from the San Jaoquin River and tributaries, California. Environ. Toxicol. Chem. 15:172180. Van der Oost, R. A. Opperhuizen, K. Satumalay, H. Heida, and P.E. Vermulen. 1996. Biomonitoring aquatic pollution with feral eel (Anguilla anguilla) I. Bioaccumulation: Biotasediment ratios of PCBs, OCPs, PCDDs and PCDFs. Aquat. Toxicol. 35:21-46. Galassi, S., and M. Migliavacca. 1986. Organochlorine residues in River Po sediment: testing the equilibrium condition with fish. Ecotoxicol. Environ. Safe. 12:120-126. USEPA. 1998. Ambient water quality criteria derivation methodology human health: Technical support document. Final draft. EPA-822-B-98-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 24. 25. 26. 27. 28. 326 BIOACCUMULATION SUMMARY Chemical Category: PESTICIDE (ORGANOCHLORINE) Chemical Name (Common Synonyms): 1,1-(DICHLOROETHYLIDENE)BIS(4-CHLOROBENZENE), p,p-DICHLORODIPHENYLDICHLOROETHYLENE 4,4-DICHLORODIPHENYLDICHLOROETHYLENE p,p-DDE CASRN: 72-55-9 Chemical Characteristics Solubility in Water: 0.065 mg/L at 24C [1] Half-Life: 2.0 - 15.6 years based on biodegradation of DDD in aerobic soils under field conditions [2] Log Koc: 6.65 L/kg organic carbon Log Kow: 6.76 [3] Human Health Oral RfD: No data [4] Confidence: -- Critical Effect: Liver tumors in mice and hamsters, thyroid tumors in female rats Oral Slope Factor: 3.4 x 10-1 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4] Wildlife Partitioning Factors: Based on the data presented in one study, log BCFs for birds collected from the lower Detroit River ranged from 5.92 to 6.36. Concentrations of DDE in birds were 40 to 108 times higher than in sediment. BSAFs were calculated for red-winged blackbird eggs and tree swallow eggs during a study in the Great Lakes area, with values ranging from 13 to 870 as reported in the attached summary table. BSAFs for tree swallow nestlings were 5 and 49. Food Chain Multipliers: Biomagnification factors of 3.2 and 85 were determined for DDT and DDE, respectively, from alewife to herring gulls in Lake Ontario [5]. A study of arctic marine food chains measured biomagnification factors for DDE that ranged from 17.6 to 62.2 for fish to seal, 0.3 to 0.7 for seal to bear, and 10.7 for fish to bear [6]. Aquatic Organisms Partitioning Factors: Partitioning factors for DDE in aquatic organisms were not calculated in the studies reviewed. However, the data showed ratios of DDT in tissue to sediment of 0.49 for oligochaetes and 32 for fish from the lower Detroit River. Ratios of DDT in lipid to sediment for three fish species from Rio de la Plata, Argentina ranged from 87 to 26,000. BSAFs for clams ranged from 1.2313 to 327 BIOACCUMULATION SUMMARY p,p-DDE 107.7 [15,41,36]. BSAFs for dover sole collected in southern California ranged from 1.7 to 3.4. BSAFs for other species ranged from 1.274 to 140. Food Chain Multipliers: Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were 23.7 (all benthic food web), 1.7 (all pelagic food web), and 14.4 (benthic and pelagic food web). FCMs for trophic level 4 aquatic organisms were 57.5 (all benthic food web), 3.7 (all pelagic food web), and 26.7 (benthic and pelagic food web) [46]. Toxicity/Bioaccumulation Assessment Profile DDT is very persistent in the environment due to its low vapor pressure, high fat solubility, and resistance to degradation and photooxidation. DDT is degraded to DDE under aerobic conditions and to DDD in anoxic systems [7]. These metabolites, DDD and DDE, are similar to DDT in both their stability and toxicity. Chronic effects of DDT and its metabolites on ecological receptors include changes in enzyme production, hormonal balance, and calcium metabolism, which may cause changes in behavior and reproduction. The high octanol-water partition coefficient of DDT indicates that it is easily accumulated in tissues of aquatic organisms. Laboratory studies have shown that these compounds are readily bioconcentrated in aquatic organisms, with reported log BCFs for DDT ranging from 3.08 to 6.65 and for DDE ranging from 4.80 to 5.26 [8]. Invertebrate species are generally more susceptible than fish species to effects associated with exposure to DDT in the water column [8]. In general, the low solubility of DDT and its metabolites in water suggests that water column exposures are likely to be lower than exposures from ingestion of food or sediment. Sediments contaminated with pesticides, including DDT, have been shown to impact benthic communities at low concentrations. Results of laboratory and field investigations suggest that chronic effects generally occur at total DDT concentrations in sediment exceeding 2 g/kg [9]. Equilibrium partitioning methods predict that chronic effects occur at DDT concentrations in sediment of 0.6 to 1.7 g/kg [10]. For fish, the primary route of uptake is via prey items, but both DDT and its metabolites can be accumulated through the skin or gills upon exposure to water. Short-term exposure to DDT concentrations of less than 1 g/L have been reported to elicit toxic responses in both freshwater and marine fish [8]. DDT may also be transferred to embryos from contaminated adults. DDT concentrations of 1.1 to 2.4 mg/kg in fish embryos have been associated with fry mortality [11,12]. Eggshell thinning, embryo mortality, and decreased hatchling survival have been linked to chronic exposure to DDT and its metabolites in the diet of birds. Of the three compounds, evidence strongly indicates that DDE is responsible for most reproductive toxicity in avian species [13]. Measurements of residues in eggs of birds are a reliable indicator of adverse effects. There is a large amount of variability in sensitivity to DDT and its metabolites among bird species, with waterfowl and raptor species showing the greatest sensitivities. Studies have shown the brown pelican to be most susceptible to adverse effects, with eggshell thinning and depressed productivity occurring at 3.0 g/g of DDE in the egg and total reproductive failure when residues exceed 3.7 g/g [13]. 328 Summary of Biological Effects Tissue Concentrations for p,p-DDE Species: Taxa Invertebrates Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Tubifex sp., Oligochaetes Surface 0.012 mg/kg water (n = 1) 0.57 ng/L (n = 1) [14] 0.0059 mg/kg (n = 1) F; lower Detroit River; value is mean SD Viviparus conectus, Gastropod mollusk 294 g/kg OC 368 g/kg lipid 1.2517 [36] F; %lipid = 7.06; %sed OC = 1.02 Unio elongatulus, Bivalve mollusk 294 g/kg OC 362 g/kg lipid 1.2313 [36] F; %lipid = 10.49; %sed OC = 1.02 Mollusks (unspecified) 99.67 g/kg OC 229 g/kg lipid 2.298 [37] F; %lipid = 1.1; %sed OC = 2.8 Macomona liliana, Mollusk 36.67 g/kg OC 35.62 g/kg OC 36.36 g/kg OC 20 g/kg OC 522.20 g/kg lipid 573.39 g/kg lipid 278.21 g/kg lipid 328.92 g/kg lipid 14.241 16.097 7.652 16.446 [38] [38] [38] [38] F; %lipid = 2.95; %sed OC = 0.30 F; %lipid = 2.33; %sed OC = 0.73 F; %lipid = 2.57; %sed OC = 0.22 F; %lipid = 2.04; %sed OC = 0.25 329 330 Species: Taxa Sediment 6.25 g/kg OC Austrovenus 36.67 g/kg stutchburyi, Mollusk OC 35.62 g/kg OC 36.36 g/kg OC 20 g/kg OC 6.25 g/kg OC Corbicula fluminea, 13 g/kg Asian clam OC Corbicula fluminea, (0-5 cm) Asian clam 0.3 ng/g dw 0.6 ng/g dw Corbicula fluminea, 9,664 g/kg Asian clam OC 168 g/kg OC Summary of Biological Effects Tissue Concentrations for p,p-DDE Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 61.34 g/kg lipid Ability to Accumulate2: Log BCF Log BAF BSAF 9.814 Source: Reference Comments3 [38] F; %lipid = 3.13; %sed OC = 0.48 141.64 g/kg lipid 148.75 g/kg lipid 57.94 g/kg lipid 59.95 g/kg lipid 10.54 g/kg lipid 3.863 4.176 1.594 2.998 1.686 [38] [38] [38] [38] [38] F; %lipid = 5.62; %sed OC = 0.30 F; %lipid = 5.21; %sed OC = 0.73 F; %lipid = 4.85; %sed OC = 0.22 F; %lipid = 3.87; %sed OC = 0.25 F; %lipid = 4.27; %sed OC = 0.48 1,400 g/kg lipid 107.7 [15] F; %lipid not reported; %sed OC = 2.3 F; Rio de La Plata, Argentina; lipid content 2.4-3.8% Surface water 1.8 ng/L [15] 1.4 g/g lipid (whole tissue) 1.4 g/g lipid (whole tissue) 540,984 g/kg lipid 4,098 g/kg lipid 55.979 24.393 [41] [41] F; %lipid = 0.61; %sed OC = 0.19 F; %lipid = 0.61; %sed OC = 0.19 Summary of Biological Effects Tissue Concentrations for p,p-DDE Species: Taxa Concentration, Units in1: Sediment 210 g/kg OC Water Toxicity: Tissue (Sample Type) Effects 2,131 g/kg lipid Ability to Accumulate2: Log BCF Log BAF BSAF 10.148 Source: Reference Comments3 [41] F; %lipid = 0.61; %sed OC = 0.19 Astacidae, Crayfish 99.67 g/kg OC 177 g/kg lipid 1.776 [37] F; %lipid = 1.3; %sed OC = 2.8 Chironomus riparius, Midge 1.6 mg/kg (whole body)4 0.27 mg/kg (whole body)4 0.1 mg/kg (whole body)4 Behavior, NOED Behavior, NOED Behavior, NOED Development, LOED [31] [31] [31] [34] L; no effect on swimming behavior L; no effect on swimming behavior L; no effect on swimming behavior L; development time from egg to 4th instar decreased from 2225 days to 19-21 days L; no effect on developmental period of larvae Chironomus riparius, Midge 7.35 mg/kg (whole body)4 3.75 mg/kg (whole body)4 Development, NOED [34] Fishes Anguilla anguilla, Eel 5 g/kg OC 156 g/kg lipid 31.200 [43] F; %lipid = 7; %sed OC = 7 331 332 Species: Taxa Sediment 5 g/kg OC 32 g/kg OC 76 g/kg OC 23 g/kg OC 72 g/kg OC Oncorhynchus mykiss, Rainbow trout Summary of Biological Effects Tissue Concentrations for p,p-DDE Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 213 g/kg lipid 2117 g/kg lipid 849 g/kg lipid 658 g/kg lipid 2,176 g/kg lipid Ability to Accumulate2: Log BCF Log BAF BSAF 42.600 66.156 11.171 28.609 30.222 Source: Reference Comments3 [43] [43] [43] [43] [43] F; %lipid = 7; %sed OC = 14 F; %lipid = 6; %sed OC = 18 F; %lipid = 10; %sed OC = 12 F; %lipid = 10; %sed OC = 12 F; %lipid = 13; %sed OC = 32 0.15 mg/kg (fat)4 Growth, ED40 [29] L; 40% decrease in growth relative to control L; 30% decrease in hemoglobin content relative to control L; 30% increase in liver size relative to control L; 35% increase in kidney size relative to control 0.15 mg/kg (fat)4 Physiological, ED30 [29] 0.15 mg/kg (fat)4 Physiological, ED30 Physiological, ED35 [29] 0.08 mg/kg (fat)4 [29] Summary of Biological Effects Tissue Concentrations for p,p-DDE Species: Taxa Oncorhynchus, Salmo, Salvelinus spp., Salmonids Concentration, Units in1: Sediment 1,889 g/kg OC 0.000076 g/L Water Toxicity: Tissue (Sample Type) Effects 7,817 g/kg lipid Ability to Accumulate2: Log BCF Log BAF BSAF 4.139 Source: Reference Comments3 [40] F; %lipid = 11; %sed OC =2.7 F; %lipid = 11 860 g/kg 7.05 [40] Oncorhynchus sp., Salmon 99.67 g/kg OC 925 g/kg lipid 9.281 [37] F; %lipid = 13.1; %sed OC = 2.8 Prosopium williamsoni, Mountain whitefish 544.4 g/kg OC 3,500 g/kg OC 2,333 g/kg lipid 4.285 [39] F; %lipid = 12.0, %sed OC = 0.9 F; %lipid = 12.25 %sed OC = 0.3 4,460 g/kg lipid (arithmetic mean of two samples) 1.274 [39] Coregonus autumnalis, Omul (endemic whitefish) particulate: <14 pg/L n=7 dissolved: 177.1 pg/L n=7 0.31-0.50 mg/kg lipid n=2 333 334 Species: Taxa Salvelinus fontinalis, Brook trout Sediment Salvelinus namaycush, Lake trout Alburnus alburnus 294 g/kg alborella, Bleak fish OC Alburnus alburnus 358 g/kg alborella, Bleak fish OC Chondrostoma soetta 294 g/kg OC Cyprinus carpio, Common carp Cyprinus carpio, Common carp 99.67 g/kg OC 174 g/kg OC Summary of Biological Effects Tissue Concentrations for p,p-DDE Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 44.9 mg/kg (whole body)4 Behavior, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [30] L; temperature selection after 24 h exposure to chemical 1.09 mg/kg (whole body)4 Mortality, LOED [33] L; survival of fry reduced 1,092 g/kg lipid 2,113 g/kg lipid 3.7143 5.9022 [36] [35, 45] F; %lipid = 21.43; %sed OC = 1.02 F; %lipid = 1.95; %sed OC = 2.76 1,179 g/kg lipid 4.0102 [36] F; %lipid = 9.75; %sed OC = 1.02 4,209 g/kg lipid 1,905 g/kg lipid 42.229 10.948 [37] [42] F, %lipid = 13.9; %sed OC = 2.8 F, %lipid = 8.4; %sed OC = 2.13 Summary of Biological Effects Tissue Concentrations for p,p-DDE Species: Taxa Cyprinus carpio, Carp Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.38 0.15 mg/kg (n = 9) Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [14] F; lower Detroit River; value is mean SD Surface 0.012 mg/kg water 0.57 (n = 1) ng/L (n = 1) Scardinius erythrophalmus, Rudd 294 g/kg OC 1,473 g/kg lipid 6.546 [36] F; %lipid = 11.66; %sed OC = 1.02 Leuciscus cephalus, Chub 294 g/kg OC 1,473 g/kg lipid 5.0102 [36] F; %lipid = 9.98; %sed OC = 1.02 Leuciscus cephalus cabeda, Chub 358 g/kg OC 1,953 g/kg lipid 5.4553 [35, 45] F; %lipid = 1.27; %sed OC = 2.76 Rutilus pigus 294 g/kg OC 728 g/kg lipid 2.4762 [36] F; %lipid = 12.63; %sed OC = 1.02 Rutilus rubilio 294 g/kg OC 1,167 g/kg lipid 3.9694 [36] F; %lipid = 11.05; %sed OC = 1.02 Catostomus commersoni, White sucker 208 g/kg OC 1,519 g/kg lipid 7.303 [42] F; %lipid = 7.9; %sed OC = 1.44 335 336 Species: Taxa mixed Catastoma sp., Suckers Sediment 3,500 g/kg OC Catastoma macrocheilus, Largescale sucker 3,010 g/kg OC Barbus barbus, Barbel 294 g/kg OC Siluris glanis, Wels fish, juveniles Siluris glanis, Wels fish, adults 294 g/kg OC 294 g/kg OC Pimelodus albicans, 0.2 ng/g dw Mandi Pimelodus albicans, 20 g/kg Mandi OC Gambusia affinis, Mosquito fish Summary of Biological Effects Tissue Concentrations for p,p-DDE Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 3,253 g/kg lipid (arithmetic mean of two samples) Ability to Accumulate2: Log BCF Log BAF BSAF 0.929 Source: Reference Comments3 [39] F; %lipid = 9.2; %sed OC = 0.3 7,477 g/kg lipid 2.484 [39] F; %lipid = 11.1; %sed OC = 1.0 1,333 g/kg lipid 4.5340 [36] F; %lipid = 16.43; %sed OC = 1.02 731 g/kg lipid 1,613 g/kg lipid 2.4864 5.4864 [36] [36] F; %lipid = 3.83; %sed OC = 1.02 F; %lipid = 5.38; %sed OC = 1.02 0.6 g/g lipid (n = 2) (muscle) 600 g/kg lipid 30.0 [15] F; Rio de La Plata, Argentina; lipid content 4% F; %lipid not reported; %sed OC = 1.0 [15] 29.2 mg/kg (whole body)4 Mortality, NOED [32] L; no effect on survivorship after 3 days Summary of Biological Effects Tissue Concentrations for p,p-DDE Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Ambloplites 99.67 g/kg rupestris, Rock bass OC 365 g/kg lipid 3.662 [37] F; %lipid = 0.7; %sed OC = 2.8 Sunfish (unspecified) 99.67 g/kg OC 254 g/kg lipid 2.548 [37] F; %lipid = 3.7; %sed OC = 2.8 Roccus chrysops, White bass 99.67 g/kg OC 1,586 g/kg lipid 15.913 [37] F; %lipid = 1.8; %sed OC = 2.8 Micropterus salmoides, Smallmouth bass 99.67 g/kg OC 1,352 g/kg lipid 13.565 [37] F; %lipid = 0.6; %sed OC = 2.8 Dorosoma cepedianum, Gizzard shad 99.67 g/kg OC 382 g/kg lipid 3.833 [37] F; %lipid = 6.8; %sed OC = 2.8 Perca fluviatilis, Perch 294 g/kg OC 3,390 g/kg lipid 11.5306 [36] F; %lipid = 5.84; %sed OC = 1.02 Stizostedion vitreum, Walleye 99.67 g/kg OC 2,593 g/kg lipid 26.016 [37] F; %lipid = 1.2; %sed OC = 2.8 337 338 Species: Taxa Microstomus pacificus, Dover sole Sediment 27 g/g dw (n = 5) 0.09 g/g dw (n = 10) Oligosarcus jenynsi, 5.7 ng/g dw Common name not available Prochilodus platensis, Curimata Prochilodus platensis, Curimata 20 g/kg OC 0.2 ng/g dw Summary of Biological Effects Tissue Concentrations for p,p-DDE Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF log MBAF -0.26 0.79 BSAF Source: Reference Comments3 [16] 1.7 2.0 F; Southern California Bight; modified bioaccumulation factor (MBAF) = Corg ww/ Csed dw; water content of tissue was not measured 16.0 g/g (n = 5) (muscle) 210 g/g (n = 3) (liver) 0.24 g/g (n = 10) (muscle) 0.80 g/g (n = 6) (liver) log MBAF 0.43 1.79 1.8 3.4 0.5 g/g lipid (n = 7) (muscle) [15] F; Rio de La Plata, Argentina; lipid content 0.32% 2,800 g/kg lipid 140 [15] F, %lipid not reported; %sed OC = 1.0 F; Rio de La Plata, Argentina; lipid content 1-12.7% Three composite samples: 1.2 (n = 4), 5.2 (n = 4) and 2 (n = 5) g/g lipid (muscle) [15] Summary of Biological Effects Tissue Concentrations for p,p-DDE Species: Taxa Gar pike (unspecified) Concentration, Units in1: Sediment 99.67 g/kg OC Water Toxicity: Tissue (Sample Type) Effects 11,986 g/kg lipid Ability to Accumulate2: Log BCF Log BAF BSAF 120.257 Source: Reference Comments3 [37] F; %lipid = 0.8; %sed OC = 2.8 Comephorus bybowskii, Pelagic sculpin, particulate: <14 pg/L n=7 dissolved: 17 pg/L 7.1 n=7 [17] 0.74-0.76 mg/kg lipid n=1 F; Lake Baikal, Siberia Cottus cognatus, Slimy sculpin 1,889 g/kg OC 0.000076 g/L 2,375 g/kg lipid 190 g/kg 6.40 1.257 [40] [40] F; %lipid = 8; %sed OC = 2.7 F; %lipid =8; %sed OC = 2.7 Wildlife Bucephala clangula, Goldeneye Surface water 0.012 mg/kg 0.57 ng/L (n = 1) (n = 1) seston = 0.10 mg/kg [14] 0.48 0.18 mg/kg (whole body) (n = 3) F; lower Detroit River; value is mean SD 339 340 Species: Taxa Sediment Aythya affinis, Lesser scaup Aythya marila, Greater scaup Falco peregrinus, Peregrine falcon Summary of Biological Effects Tissue Concentrations for p,p-DDE Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Surface water 0.012 mg/kg 0.57 ng/L (n = 1) (n = 1) [14] 0.80 0.33 mg/kg (whole body) (n = 7) F; lower Detroit River; value is mean SD Surface water 0.012 mg/kg 0.57 ng/L (n = 1) (n = 1) [14] 1.3 0.25 mg/kg (whole body) (n = 3) F; lower Detroit River; value is mean SD g/g (egg): 15 15-30 >30 Young produced per active nest: 1.8 2.0 1.0 [26] F; Alaska; young produced not adjusted for sample egg collected Summary of Biological Effects Tissue Concentrations for p,p-DDE Species: Taxa Aquila chrysaetos, Golden eagle g/g (egg): 0.1 0.1 0.2 0.3 0.3 Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Mean % eggshell thinning = 7% 1% 3% 4% 5% Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [24] F; Great Britain; percentage of thinning based on thickness index [24] Haliaeetus leucocephalus, Bald eagle 10 g/g (egg) Mean percent eggshell thinning= 10% Young produced per active nest: 1.0 1.0 0.5 0.3 0.2 [22] F; Oregon and Washington [23] F g/g (egg): <2.2 2.2-3.5 3.6-6.2 6.3-11.9 12 Ardea herodias, Great blue heron 4 g/g (egg) 5 g/g (egg) Mean percent eggshell thinning = 10% 13% [18] F; Washington 341 342 Species: Taxa Plegadis chihi, White-faced ibis Sediment Egretta thula, Snowy egret Summary of Biological Effects Tissue Concentrations for p,p-DDE Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Mean percent eggshell thinning= 12% 8% Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [20] F; Nevada 2 g/g (egg) 1 g/g (egg) g/g (egg): 1 1-4 4-8 8-16 >16 Young produced per active nest: 1.8 1.8 1.3 0.8 0.6 [21] F; Nevada; young produced not adjusted for sample egg collected 1 g/g (egg) 2 g/g (egg) Mean percent eggshell thinning= 3% 12% Young produced per active nest: 2.2 2.4 1.0 1.0 [20] F; Nevada; young produced not adjusted for sample egg collected g/g (egg): 1 1-5 5-10 10-20 Summary of Biological Effects Tissue Concentrations for p,p-DDE Species: Taxa Sula bassanus, Northern gannet g/g (egg) 19 Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Mean % eggshell thinning = 17% Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [19] F; Quebec Larus californicus, California gull 430 mg/kg (brain)4 175 mg/kg (breast)4 3,100 mg/kg (liver)4 220 mg/kg (brain)4 490 mg/kg (breast)4 800 mg/kg (liver)4 750 mg/kg (liver)4 Mortality, not available (NA) Mortality, NA Mortality, NA NA, NA NA, NA NA NA Mortality, NA Mortality, NA Mortality, NA [28] [28] [28] [28] [28] [28] [28] [28] [28] [28] L L L L L L L L L L Pelecanus occidentalis, Brown pelican 4.4 mg/kg (brain)4 59.5 mg/kg (breast)4 7.15 mg/kg (liver)4 343 344 Species: Taxa Agelaius phoeniceus, Redwinged blackbird (eggs) Sediment 40.5 ng/g TOC = 2.5% 7.9 ng/g TOC = 21.0% 373.1 ng/g TOC = 7.5% 1,160.7 ng/g TOC = 12% 10.4 ng/g TOC-18.5% 65.4 ng/g TOC = 11.5% 1.6 ng/g TOC = 10.5% 0.8 ng/g TOC = 13.8% 1.3 ng/g TOC = 11.1% 3.0 ng/g TOC = 23.9% Summary of Biological Effects Tissue Concentrations for p,p-DDE Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 3,088.1 ng/g 777.7 ng/g Ability to Accumulate2: Log BCF Log BAF BSAF 41.4 Source: Reference Comments3 [25] F; Great Lakes/St. Lawrence River basin; 12 wetlands sites; sediment concentration reported as wet weight concentration which may be a typographical error 372.7 648.7 ng/g 1,299.6 ng/g 305.7 ng/g 12.9 13.2 113.3 826.2 ng/g 30.3 416.1 ng/g 582.4 145.1 ng/g 522 326.4 183.5 ng/g 203.7 117.6 ng/g Summary of Biological Effects Tissue Concentrations for p,p-DDE Species: Taxa Tachycineta bicolor, Tree swallow Nestlings 65.4 ng/g TOC = 11.5% 0.8 ng/g TOC = 13.8% Eggs 65.4 ng/g TOC = 11.5% 0.8 ng/g TOC = 13.8% Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects (whole body minus feet, beak, wings, and feathers) 288.2 ng/g Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [25] F; Great Lakes/St. Lawrence River basin; 12 wetlands sites; sediment concentration reported as wet weight concentration which may be a typographical error 548.9 22.4 ng/g 794.7 ng/g 16.2 458.2 ng/g 868.6 3.5 g/g (egg) (n = 6) 11.4% eggshell thinning [27] F; Kola Penninsula, Russia; n = number of clutches sampled 345 346 Species: Taxa Phoca siberica, Baikal seal Sediment 1 2 3 4 Summary of Biological Effects Tissue Concentrations for p,p-DDE Concentration, Units in1: Water particulate: <14 pg/L n=7 dissolved: 17 pg/L 7.1 n=7 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from The Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. Toxicity: Tissue (Sample Type) Effects 43-44 mg/kg lipid n=1 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [17] F; Lake Baikal, Siberia BIOACCUMULATION SUMMARY References 1. p,p-DDE Verschueren. Hdbk. Environ. Data Org. Chem., 1983, p. 433. (Cited in: USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957-968. Muir, D.C.G., R.J. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related compounds. Environ. Sci. Technol. 22:1071-1079. Charles, M.J., and R.A. Hites. 1987. Sediments as archives. In Sources and fates of aquatic pollutants, eds. R.A. Hites and S.J. Eisenreich, Advances In Chemistry Series, Vol. 216, pp. 365389. American Chemical Society, Washington, DC. USEPA. 1980. Ambient water quality criteria for DDT. EPA440/5-80-038. U.S. Environmental Protection Agency, Office of Water Regulations and Standards, Criteria and Standards Division, Washington, DC. Long, E.R., D.D. MacDonald, S.L. Smith, and F.D. Calder. 1995. Incidence of adverse biological effects within ranges of chemical concentrations in marine and estuarine sediments. Environ. Manage. 19(1):81-97. Pavlou, S., R. Kadeg, A. Turner, and M. Marchlik. 1987. Sediment quality criteria methodology validation: Uncertainty analysis of sediment normalization theory for nonpolar organic contaminants. Work Assignment 56, Task 3. Battelle, Washington, DC. 2. 3. 4. 5. 6. 7. 8. 9. 10. 347 BIOACCUMULATION SUMMARY 11. p,p-DDE Johnson, H.E., and C. Pecor. 1969. Coho salmon mortality and DDT in Lake Michigan. Transactions of the 34th North American Wildlife Conference. Smith, R.M., and C.F. Cole. 1973. Effects of egg concentrations of DDT and dieldrin on reproduction in winter flounder (Pseudopleuronectes americanus). J. Fish. Res. Board Can. 30:1894-1898. Blus, L.J. 1996. DDT, DDD, and DDE in birds. In Environmental contaminants in wildlife, ed. W. N. Beyer, G.H. Heinz, and A.W. Redmon-Norwood, pp. 49-71. Lewis Publishers, Boca Raton, FL. Smith., E.V. , J.M. Spurr, J.C. Filkins, and J.J. Jones. 1985. Organochlorine contaminants of wintering ducks foraging on Detroit River sediments. J. Great Lakes Res. 11(3):231-246. Columbo, J.C., M.F. Khalil, M. Arnac, and A.C. Horth. 1990. Distribution of chlorinated pesticides and individually polychlorinated biphenyls in biotic and abiotic compartments of the Rio de la Plata, Argentina. Environ. Sci. Technol. 24:498-505. Young, D.R., A.J. Mearns, and R.W. Gossett. 1991. Bioaccumulation of p,p-DDE and PCB 1254 by a flatfish bioindicator from highly contaminated marine sediments of Southern California. In Organic substances and sediments in water, ed. R.A. Baker, Vol. 3, pp. 159-169. Lewis Publishers, Boca Raton, FL. Kucklick, J.R., T.F. Bidleman, L.L. McConnell, M.D. Walla, and G.P. Ivanov. 1994. Organochlorines in the water and biota of Lake Baikal, Siberia. Environ. Sci. Technol. 28:31-37. Fitzner, R.E., L.J. Blus, C.J. Henny, and D.W. Carlile. 1988. Organochlorine residues in great blue herons from the northwestern United States. Colon. Waterbirds 11:293-300. Elliott, J.E., R.J. Norstrom, and J.A. Keith. 1988. Organochlorines and eggshell thinnning in northern gannets (Sula bassanus) from eastern Canada, 1968-1984. Environ. Pollut. 52:81-102. Henny, C.J., L.J. Blus, and C.S. Hulse. 1985. Trends and effects of organochlorine residues on Oregon and Nevada wading birds, 1979-1983. Colon. Waterbirds. 8:117-128. Henny, C.J., and G.B. Herron. 1989. DDE, selenium, mercury, and white-faced ibis reproduction at Carson Lake, Nevada. J. Wildl. Manage. 53:1032-1045. Anthony, R.G., M.G. Garrett, and C.A. Schuler. 1993. Environmental contaminants in bald eagles in the Columbia River estuary. J. Wildl. Manage. 57:10-19. Wiemeyer, S.N., C.M Bunck, and C.J. Stafford. 1993. Environmental contaminants in bald eagle eggs--1980-84--and further interpretations of relationships to productivity and shell thickness. Arch. Environ. Contam. Toxicol. 24:213-227. Ratcliffe, D.A. 1967. Decrease in eggshell weight in certain birds of prey. Nature. 215:208210. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 348 BIOACCUMULATION SUMMARY 25. p,p-DDE Bishop, C.A., M.D. Koster, A.A. Chek, D.J.T. Hussell, and K. Jock. 1995. Chlorinated hydrocarbons and mercury in sediments, red-winged blackbirds (Agelaius phoeniceus) and tree swallows (Tachycineta bicolor) from wetlands in the Great Lakes-St. Lawrence river basin, Environ. Toxicol. Chem. 14:491-501. Ambrose, R.E., C.J., Henny, R.E. Hunter, and J.A. Crawford. 1988. Organochlorines in Alaskan peregrine falcon eggs and their current impact on productivity. In Peregrine falcon populations: Their management and recovery, ed. T. J. Cade, J.H. Enderson, C.G. Thelander, and C.M. White, pp. 385-393. Peregrine Fund, Boise, ID. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. Young, D.R., and T.C. Heeson. 1977. Marine bird deaths at the Los Angeles zoo. Coastal Water Research Program Annual Report. Southern California Coastal. Poels, C.L.M., M.A. van Der Gaag, and J.F.J. van de Kerkhoff. 1980. An investigation into the long-term effect of Rhine water on rainbow trout. Water Res. 14:1029-1033. Peterson, R.H. 1973. Temperature selection of Atlantic salmon (Salmo salar) and brook trout (Salvelinus fontinalis) as influenced by various chlorinated hydrocarbons. J. Fish. Res. B. Can. 30(8). Lydy, M.J., K.A. Bruner, D.M. Fry, and S.W. Fisher. 1990. Effects of sediment and the route of exposure on the toxicity and accumulation of neutral lipophilic and moderately water soluble metabolizable compounds in the midge, Chironomus riparius. ASTM STP-1096. Aquatic toxicology and risk assessment, ed. W.G. Landis, et.al. pp. 140-164, American Society for Testing and Materials, Philadelphia, PA. Metcalf, R.L. 1974. A laboratory model ecosystem to evaluate compounds producing biological magnification. In Essays in toxicology, ed. W.J. Hayes, Vol. 5, pp. 17-38, Academic Press, New York, NY. Burdick, G.E., E.J. Harris, H.J. Dean, T.M. Walker, J. Skea, and D. Colby. 1964. The accumulation of DDT in lake trout and the effect on reproduction. Trans. Amer. Fish. Soc. 93:127-136. Derr, S.K., and M.J. Zabik. 1972. Biologically active compounds in the aquatic environment: The uptake and distribution of [1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene], DDE by Chironomus tentans Fabricius (Diptera: Chironomidae). Trans. Amer. Fish. Soc. 101:323-329. Galassi, S., G. Gandolfi, and G. Pacchetti. 1981. Chlorinated hydrocarbons in fish from the River Po (Italy). Sci. Total Environ. 20:231-240. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 349 BIOACCUMULATION SUMMARY 36. p,p-DDE Galassi, S., L. Guzzella, M. Battegazzore, and A. Carrieri. 1994. Biomagnification of PCBs, p,p-DDE, and HCB in the River Po ecosystem (northern Italy). Ecotoxicol. Environ. Safe. 29:174-186. Haffner, G.D., M. Tomczak, and R. Lazar. 1994. Organic contaminant exposure in the Lake St. Clair food web. Hydrobiologia 281:19-27. Hickey, C.W., D.S. Roper, P.T. Holland, and T.M. Trower. 1995. Accumulation of organic contaminants in two sediment-dwelling shellfish with contrasting feeding modes: Deposit(Macomona liliana) and filter-feeding (Austovenus stutchburi). Arch. Environ. Contam. Toxicol. 11:21-231. Johnson, A., D. Norton, and B. Yake. 1988. Persistence of DDT in the Yakima River drainage, Washington. Arch. Environ. Contam. Toxicol. 17:291-297. Oliver, G.G., and A.J. Niimi. 1988. Chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22(4):388-397. Pereira, W.E., J.L. Domagalski, F.D. Hostettler, L.R. Brown, and J.B. Rapp. 1996. Occurrence and accumulation of pesticides and organic contaminants in river sediment, water, and clam tissues from the San Jaoquin River and tributaries, California. Environ. Toxicol. Chem. 15:172180. Tate, C.M., and J.S. Heiny. 1996. Organochlorine compounds in bed sediment and fish tissue in the South Platte River basin, USA, 1992-1993. Arch. Environ. Contam. Toxicol. 11:221-231. Van der Oost, R. A. Opperhuizen, K. Satumalay, H. Heida, and P.E. Vermulen. 1996. Biomonitoring aquatic pollution with feral eel (Anguilla anguilla) I. Bioaccumulation: Biotasediment ratios of PCBs, OCPs, PCDDs and PCDFs. Aqua. Toxicol. 35:21-46. USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. Galassi, S., and M. Migliavacca. 1986. Organochlorine residues in River Po sediment: Testing the equilibrium condition with fish. Ecotoxicol. Environ. Safe. 12:120-126. USEPA. 1998. Ambient water quality criteria derivation methodology human health: Technical support document. Final draft. EPA-822-B-98-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 350 BIOACCUMULATION SUMMARY Chemical Category: PESTICIDE (ORGANOCHLORINE) Chemical Name (Common Synonyms): 1,1-(2,2,2-TRICHLOROETHYLIDENE)BIS(4-CHLOROBENZENE), p,p-DICHLORODIPHENYLTRICHLOROETHANE, 4,4-DICHLORODIPHENYLTRICHLOROETHANE p,p-DDT CASRN: 50-29-3 Chemical Characteristics Solubility in Water: 0.0031 - 0.0034 mg/L at 25C [1] Half-Life: 2.0 - 15.6 years based on biodegradation of DDD in aerobic soils under field conditions [2] Log Koc: 6.71 L/kg organic carbon Log Kow: 6.83 [3] Human Health Oral RfD: 5 x 10-4 mg/kg/day [4] Confidence: Medium, uncertainty factor = 100 Critical Effect: Liver lesions in rats, liver tumors in mice and rats Oral Slope Factor: 3.4 x 10-1 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4] Wildlife Partitioning Factors: Partitioning factors for DDT in wildlife were not calculated in the studies reviewed. However, based on the data in one study, log BCFs for birds from the lower Detroit River ranged from 4.81 to 5.01. Concentrations of DDT in birds were 2.1 to 3.3 times higher than in sediment. Food Chain Multipliers: Biomagnification factors of 3.2 and 85 were determined for DDT and DDE, respectively, from alewife to herring gulls in Lake Ontario [5]. A study of arctic marine food chains measured biomagnification factors for DDE that ranged from 17.6 to 62.2 for fish to seal, 0.3 to 0.7 for seal to bear, and 10.7 for fish to bear [6]. Aquatic Organisms Partitioning Factors: Based on the results from one study reviewed, the log BCF for carp collected from the lower Detroit River was 4.77. Ratios of DDT in lipids to sediment were 450 in clams and 1,250 to 11,000 in fish from the Rio de la Plata, Argentina. BSAFs for clams ranged from 0.060 to 302.326 [14,33,36]. BSAFs for fish ranged from 0.120 to 88.07. 351 BIOACCUMULATION SUMMARY p,p-DDT Food Chain Multipliers: Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were 22.5 (all benthic food web), 1.7 (all pelagic food web), and 13.7 (benthic and pelagic food web). FCMs for trophic level 4 aquatic organisms were 52.5 (all benthic food web), 3.6 (all pelagic food web), and 24.6 (benthic and pelagic food web) [39]. Toxicity/Bioaccumulation Assessment Profile DDT is very persistent in the environment due to its low vapor pressure, high fat solubility, and resistance to degradation and photooxidation. DDT is degraded to DDE under aerobic conditions and to DDD in anoxic systems [7]. These metabolites, DDD and DDE, are similar to DDT in both their stability and toxicity. Chronic effects of DDT and its metabolites on ecological receptors include changes in enzyme production, hormonal balance, and calcium metabolism, which may cause changes in behavior and reproduction. The high octanol-water partition coefficient of DDT indicates that it is easily accumulated in tissues of aquatic organisms. Laboratory studies have shown that these compounds are readily bioconcentrated in aquatic organisms, with reported log BCFs for DDT ranging from 3.08 to 6.65 and for DDE ranging from 4.80to 5.26 [8]. Invertebrate species are generally more susceptible than fish species to effects associated with exposure to DDT in the water column [8]. In general, the low solubility of DDT and its metabolites in water suggests that water column exposures are likely to be lower than exposures from ingestion of food or sediment. Sediments contaminated with pesticides, including DDT, have been shown to affect benthic communities at low concentrations. Results of laboratory and field investigations suggest that chronic effects generally occur at total DDT concentrations in sediment exceeding 2 g/kg [9]. Equilibrium partitioning methods predict that chronic effects occur at DDT concentrations in sediment of 0.6 to 1.7 g/kg [10]. For fish, the primary route of uptake is via prey items, but both DDT and its metabolites can be accumulated through the skin or gills upon exposure to water. Short-term exposure to DDT concentrations of less than 1 g/L have been reported to elicit toxic responses in both freshwater and marine fish [8]. DDT may also be transfered to embryos from contaminated adults. DDT concentrations of 1.1 to 2.4 mg/kg in fish embryos have been associated with fry mortality [11,12]. Eggshell thinning, embryo mortality, and decreased hatchling survival have been linked to chronic exposure to DDT and its metabolites in the diet of birds. Of the three compounds, evidence strongly indicates that DDE is responsible for most reproductive toxicity in avian species [13]. Measurements of residues in eggs of birds are a reliable indicator of adverse effects. There is a large amount of variability in sensitivity to DDT and its metabolites among bird species, with waterfowl and raptor species showing the greatest sensitivities. Studies have shown the brown pelican to be most susceptible to adverse effects, with eggshell thinning and depressed productivity occurring at 3.0 g/g of DDE in the egg and total reproductive failure when residues exceed 3.7 g/g [13]. 352 Summary of Biological Effects Tissue Concentrations for p,p-DDT Species: Taxa Invertebrates Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Macomona liliana, Mollusk 63.33 g/kg OC 76.71 g/kg OC 127.27 g/kg OC 20.83 g/kg OC 13.22 g/kg lipid 33.91 g/kg lipid 24.12 g/kg lipid 0.209 0.442 0.190 [33] [33] [33] F; %lipid = 2.95; %sed OC = 0.30 F; %lipid = 2.33; %sed OC = 0.73 F; %lipid = 2.57; %sed OC = 0.22 F; %lipid = 3.13; %sed OC = 0.48 7.35 g/kg lipid 0.353 [33] Austrovenus stutchburyi, Mollusk 63.33 g/kg OC 76.71 g/kg OC 127.71 g/kg OC 8.01 g/kg lipid 0.126 [33] F; %lipid = 5.62; %sed OC = 0.30 F; %lipid = 5.21; %sed OC = 0.73 F; %lipid = 4.85; %sed OC = 0.22 7.29 g/kg lipid 7.63 g/kg lipid 0.095 0.060 [33] [33] Corbicula fluminea, 4.3 g/kg Asian clam OC Corbicula fluminea, 3277 g/kg Asian clam OC 353 1,300 g/kg lipid 302.326 [14] F; %lipid = not reported; %sed OC = 2.3 F; %lipid = 0.61; %sed OC = 1.19 108,197 g/kg lipid 33.017 [36] 354 Species: Taxa Sediment 67 g/kg OC 92 g/kg OC Corbicula fluminea, (0-5 cm) Asian clam 2.9 ng/g dw Mercenaria mercenaria, Quahog clam Mya arenaria, Soft shell clam Daphnia magna, Cladoceran Diporeia spp., Amphipod Summary of Biological Effects Tissue Concentrations for p,p-DDT Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 508 g/kg lipid 164 g/kg lipid Ability to Accumulate2: Log BCF Log BAF BSAF 7.563 1.774 Source: Reference Comments3 [36] [36] F; %lipid = 0.61; %sed OC = 1.19 F; %lipid = 0.61; %sed OC = 1.19 1.3 g/g lipid (whole tissue) [14] F; Rio de La Plata, Argentina; lipid content 2.4-3.8% 0.126 mg/kg (whole body)4 Behavior, NOED [29] L; No effect on feeding activity NOED [29] L; no effect on feeding activity 1.83 mg/kg (whole body)4 Mortality, NOED [23] L; no effect on survivorship in 3 days 19.7 mg/kg (whole body)4 Mortality, NOED [22] L; no increase in mortality in 96 hours Summary of Biological Effects Tissue Concentrations for p,p-DDT Species: Taxa Gammarus fasciatus, Amphipod Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.336 mg/kg (whole body)4 Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [23] L; no effect on survivorship in 3 days Palaemonetes kadiakensis, Grass shrimp 0.1 mg/kg (whole body)4 Mortality, NOED [23] L; no effect on survivorship in 3 days Orconectes nais, Crayfish 0.0466 mg/kg (whole body)4 Mortality, NOED [23] L; no effect on survivorship in 3 days Ephemera danica, Mayfly 6 mg/kg (whole body)4 6 mg/kg (whole body)4 Growth, NOED Mortality, NOED [20] L L Hexagenia bilineata, Mayfly 0.336 mg/kg (whole body)4 Mortality, NOED [23] L; no effect on survivorship after 3 days Siphlonurus sp., Mayfly 0.216 mg/kg (whole body)4 Mortality, NOED [23] L; no effect on survivorship after 3 days 355 356 Species: Taxa Libellula sp., Dragonfly Sediment Ischnura verticalis, Damselfly Chironomus sp., Midge Chironomus riparius, Midge Fishes Squalus acanthias, Spiny dogfish Summary of Biological Effects Tissue Concentrations for p,p-DDT Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 0.0144 mg/kg (whole body)4 Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [23] L; no effect on survivorship after 2 days 0.075 mg/kg (whole body)4 Mortality, NOED [23] L; no effect on survivorship after 2 days 0.44 mg/kg (whole body)4 Mortality, NOED [23] L; no effect on survivorship in 3 days 0.83 mg/kg (whole body)4 0.18 mg/kg (whole body)4 0.08 mg/kg (whole body)4 Behavior, LOED Behavior, NOED Behavior, NOED [24] [24] [24] L; reduced swimming ability L; no effect on swimming behavior L; no effect on swimming behavior 0.1 mg/kg (whole body)4 Mortality, NOED [32] L; no effect on mortality in 24 hours Summary of Biological Effects Tissue Concentrations for p,p-DDT Species: Taxa Anguilla anguilla, Eel Concentration, Units in1: Sediment 23 g/kg OC 8 g/kg OC 14 g/kg OC 25 g/kg OC 34 g/kg OC 144 g/kg OC Water Toxicity: Tissue (Sample Type) Effects 158 g/kg lipid 135 g/kg lipid 1233 g/kg lipid 221 g/kg lipid 287 g/kg lipid 1064 g/kg lipid Ability to Accumulate2: Log BCF Log BAF BSAF 6.87 16.88 88.07 8.84 8.44 7.39 Source: Reference Comments3 [37] [37] [37] [37] [37] [37] F; %lipid = 7; %sed OC = 7 F; %lipid = 7; %sed OC = 14 F; %lipid = 6; %sed OC = 18 F; %lipid = 10; %sed OC = 12 F; %lipid = 10; %sed OC = 12 F; %lipid = 13; %sed OC = 32 Oncorhynchus, Salmo, Salvelinus sp., Salmonids 667 g/kg OC 0.000019 g/L 727 g/kg lipid 1.091 [35] F; %lipid = 11; %sed OC = 2.7 F; %lipid = 11 F 80 g/kg lipid 6.62 1.67 [35] [38] Salmonids Oncorhynchus kisutch, Coho salmon 95 mg/kg (whole body)4 Mortality, ED50 [27] L; 50% mortality in 31 days 357 358 Species: Taxa Prosopium williamsoni, Mountain whitefish Sediment 244 g/kg OC 6,433 g/kg OC Corogonus autumnalis, Omul (endemic whitefish) Salmo salar, Atlantic salmon Salvelinus namaycush, Lake trout Summary of Biological Effects Tissue Concentrations for p,p-DDT Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 417 g/kg lipid Ability to Accumulate2: Log BCF Log BAF BSAF 1.706 Source: Reference Comments3 [34] F; %lipid = 12.0; %sed OC = 0.9 F; %lipid = 12.25; %sed OC = 0.30 772 g/kg lipid 0.120 [34] particulate: 5.1pg/L 2.3 n=7 dissolved: 50 pg/L 23 n=7 0.16-0.27 mg/kg5 lipid (whole body) n=2 [16] F; Lake Baikal, Siberia 3 mg/kg (whole body)4 Morphology, NOED [26] L; no effect on metabolic rate or growth, resd_conc_wet value range 3.0-5.0 3.9 mg/kg (whole body)4 Behavior, LOED [21] L; temperature selection after 24hour exposure to chemical Summary of Biological Effects Tissue Concentrations for p,p-DDT Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 27.8 mg/kg (whole body)4 Behavior, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [21] L; temperature selection after 24hour exposure to chemical L; survival of fry reduced L; survival of fry reduced Salvelinus namaycush, Lake trout 3.66 mg/kg (whole body)4 2 mg/kg (whole body)4 Mortality, LOED Mortality, LOED [28] [28] Carassius auratus, Goldfish 5.1 mg/kg (whole body)4 Behavior, LOED [31] L; behavioral changes, loss of equilibrium, convulsions Pimephales promelas, Fathead minnow 3.8 mg/kg (whole body)4 24 mg/kg (whole body)4 Reproduction, LOED Reproduction, LOED [19] L; significantly different from control (p = 0.05) L; significantly different from control (p = 0.05) [19] Cyprinus carpio, Carp 359 Surface 0.012 mg/kg water (n = 1) 0.39 ng/L (n = 1) [15] 0.023 0.012 mg/kg (n = 9) F; lower Detroit River; value is mean SD 360 Species: Taxa Sediment Mixed Catastoma sp., Suckers 6433 g/kg OC Catastoma macrocheilus, Largescale sucker 340 g/kg OC Pimelodus albicans, 0.4 ng/g dw (Marine catfish) Pimelodus albicans, 40.0 g/kg Mandi OC Gambusia affinis, Mosquito fish Leuciscus idus, Golden ide Summary of Biological Effects Tissue Concentrations for p,p-DDT Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 869 g/kg lipid 0.135 [34] F; %lipid = 9.2; %sed OC = 0.30 811 g/kg lipid 2.385 [34] F; %lipid = 11.1; %sed OC = 1.0 0.5 g/g lipid (n = 7) (muscle) [14] F; Rio de La Plata, Argentina; lipid content 4% 500 g/kg lipid [14] F; %lipid = not reported; %sed OC = 1.0 18.6 mg/kg (whole body)4 Mortality, NOED [25] L; no effect on survivorship after 3 days 95 mg/kg (whole body)4 Mortality, NOED [30] L; no effect on survivorship in 3 days Summary of Biological Effects Tissue Concentrations for p,p-DDT Species: Taxa Lepomis macrochirus, Bluegill Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 4.2 mg/kg (whole body)4 Behavior, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [31] L; behavioral changes, loss of equilibrium, convulsions Comephorus dybowskii, Pelagic sculpin particulate: 5.1pg/L 2.3 n=7 dissolved: 50 pg/L 23 n=7 0.52-0.64 mg/kg lipid (whole body) n=1 [16] F; Lake Baikal, Siberia Cottus cognatus, Slimy sculpin 667 g/kg OC 0.000019 g/L 362 g/kg lipid 29 g/kg lipid 6.18 0.544 [35] [35] F; %lipid = 8; %sed OC = 2.7 F; %lipid = 8 Prochilodus platensis, common name not available 0.4 ng/g dw Three composite samples (g/g lipid): 2.4 (n = 4) (muscle) 9.3 (n = 4) (muscle) 4.3 (n = 5) (muscle) [14] F; Rio de La Plata, Argentina; lipid content 1-12.7% Prochilodus platensis, Curimata 361 40.0 g/kg OC 5,333.33 g/kg lipid [14] F; %lipid = not reported; %sed OC = 1.0 362 Species: Taxa Wildlife Sediment Aythya affinis, Lesser scaup Aythya marila, Greater scaup Falco peregrinus, Peregrine falcon (eggs) Larus californicus, California gull Summary of Biological Effects Tissue Concentrations for p,p-DDT Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Bucephala clangula, 0.012 mg/kg water = Goldeneye (n = 1) 0.39 ng/L (n = 1) 0.040 mg/kg (whole body) (n = 3) [15] F; lower Detroit River; value is mean SD 0.012 mg/kg surface (n = 1) water 0.39 ng/L (n = 1) 0.025 mg/kg (whole body) (n = 7) [15] F; lower Detroit River; value is mean SD 0.012 mg/kg surface (n = 1) water 0.39 ng/L (n = 1) 0.040 0.0094 mg/kg (whole body) (n = 3) [15] F; lower Detroit River; value is mean SD 22 ng/g (eggs) (n = 6) 11.4% eggshell thinning [17] F; Kola Penninsula, Russia; n = number of clutches sampled 440 mg/kg (brain)4 183 mg/kg (breast)4 3200 mg/kg (liver)4 Mortality, NA Mortality, NA Mortality, NA [18] [18] [18] L L L Summary of Biological Effects Tissue Concentrations for p,p-DDT Species: Taxa Pelecanus occidentalis, Brown pelican Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 4.55 mg/kg (brain)4 66 mg/kg (breast)4 7.8 mg/kg (liver)4 Mortality, NA Mortality, NA Mortality, NA Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [18] [18] [18] L L L Phalacrocorax penicillatus, Brandts cormorant 230 mg/kg (brain)4 500 mg/kg (breast)4 840 mg/kg (liver)4 810 mg/kg (Liver)4 Mortality, NA Mortality, NA Mortality, NA Mortality, NA [18] [18] [18] [18] L L L L Phoca siberica, Baikal seal particulate: 5.1pg/L 2.3 n=1 dissolved: 50 pg/L 23 n=1 17-21 mg/kg5 lipid (blubber) n=1 [16] F; Lake Baikal, Siberia 1 2 3 4 5 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. Not clear from reference if concentration is based on wet or dry weight. 363 BIOACCUMULATION SUMMARY References 1. p,p-DDT Verschueren. Hdbk. Environ. Data Org. Chem.,1983, p. 437 (cited in: USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February). USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Braune, B.M. and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957-968. Muir, D.C.G., R.J. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related compounds. Environ. Sci. Technol. 22:1071-1079. Charles, M.J., and R.A. Hites. 1987. Sediments as archives. In Sources and fates of aquatic pollutants, ed. R.A. Hites and S.J. Eisenreich, Advances In Chemistry Series, Vol. 216, pp. 365389. American Chemical Society, Washington, DC. USEPA. 1980. Ambient water quality criteria for DDT. EPA440/5-80-038. U.S. Environmental Protection Agency, Office of Water Regulations and Standards, Criteria and Standards Division, Washington, DC. Long, E.R., D.D. MacDonald, S.L. Smith, and F.D. Calder. 1995. Incidence of adverse biological effects within ranges of chemical concentrations in marine and estuarine sediments. Environ. Manage. 19(1):81-97. Pavlou, S., R. Kadeg, A. Turner, and M. Marchlik. 1987. Sediment quality criteria methodology validation: Uncertainty analysis of sediment normalization theory for nonpolar organic contaminants. Work Assignment 56, Task 3. Battelle, Washington, DC. 2. 3. 4. 5. 6. 7. 8. 9. 10. 364 BIOACCUMULATION SUMMARY 11. p,p-DDT Johnson, H.E., and C. Pecor. 1969. Coho salmon mortality and DDT in Lake Michigan. Transactions of the 34th North American Wildlife Conference. Smith, R.M., and C.F. Cole. 1973. Effects of egg concentrations of DDT and dieldrin on reproduction in winter flounder (Pseudopleuronectes americanus). J. Fish. Res. Board Can. 30:1894-1898. Blus, L.J. 1996. DDT, DDD, and DDE in birds. In Environmental contaminants in wildlife, ed. W. N. Beyer, G.H. Heinz, and A.W. Redmon-Norwood, pp. 49-71. Lewis Publishers, Boca Raton, FL. Columbo, J.C., M.F. Khalil, M. Arnac, and A.C. Horth. 1990. Distribution of chlorinated pesticides and individually polychlorinated biphenyls in biotic and abiotic compartments of the Rio de la Plata, Argentina. Environ. Sci. Technol. 24:498-505. Smith., E.V., J.M. Spurr, J.C. Filkins, and J.J. Jones. 1985. Organochlorine contaminants of wintering ducks foraging on Detroit River sediments. J. Great Lakes Res. 11(3):231-246. Kucklick, J.R., T.F. Bidleman, L.L. McConnell, M.D. Walla, and G.P. Ivanov. 1994. Organochlorines in the water and biota of Lake Baikal, Siberia. Environ. Sci. Technol. 28:31-37. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. Young, D.R., and T.C. Heeson. 1977. Marine bird deaths at the Los Angeles zoo. Coastal Water Research Program Annual Report. Southern California Coastal. Jarvinen, A.W., M.J. Hoffman, and T.W. Thorslund. 1977. Long-term toxic effects of DDT food and water exposure on fathead minnows (Pimephales promelas). J. Fish. Res. Board. Can. 34:2089-2103. Sodergren, A., and B. Svensson. 1973. Uptake and accumulation of DDT and PCB by Ephemera danica (Ephemeroptera) in continuous-flow systems. Bull. Environ. Contam. Toxicol. 9(6). Peterson, R.H. 1973. Temperature selection of Atlantic salmon (Salmo salar) and brook trout (Salvelinus fontinalis) as influenced by various chlorinated hydrocarbons. J. Fish. Res. B. Can. 30(8). Harkey, G.A., P.F. Landrum, and S.J. Klaine. 1994. Comparison of whole-sediment, elutriate and pore-water exposures for use in assessing sediment-associated organic contaminants in bioassays. Environ. Toxicol. Chem. 13:1315-1329. Johnson, B.T., C.R. Saunders, H.O. Sanders, and R.S. Campbell. 1971. Biological magnification and degradation of DDT and aldrin by freshwater invertebrates. J. Fish. Res. Bd. Can. 28:705-709. 365 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. BIOACCUMULATION SUMMARY 24. p,p-DDT Lydy, M.J., K.A. Bruner, D.M. Fry, and S.W. Fisher. 1990. Effects of sediment and the route of exposure on the toxicity and accumulation of neutral lipophilic and moderately water soluble metabolizable compounds in the midge, Chironomus riparius. ASTM STP-1096. Aquatic toxicology and risk assessment, ed. W.G. Landis, et.al. pp. 140-164. American Society for Testing and Materials, Philadelphia, PA. Metcalf, R.L. 1974. A laboratory model ecosystem to evaluate compounds producing biological magnification. In Essays in toxicology, ed. W.J. Hayes, Vol. 5, pp. 17-38. Academic Press, New York, NY. Addison, R.F., M.E. Zinck, and J.R. Leahy. 1976. Metabolism of single and combined doses of 14C-aldrin and 3H-p,pDDT by Atlantic salmon (Salmo salar) fry. J. Fish. Res. B. Can. 33:2073-2076. Buhler, D.R., and W.E. Shanks. 1970. Influence of body weight on chronic oral DDT toxicity in coho salmon. J. Fish. Res. B. Can. 27:347-358. Burdick, G.E., E.J. Harris, H.J. Dean, T.M. Walker, J. Skea, and D. Colby. 1964. The accumulation of DDT in lake trout and the effect on reproduction. Trans. Amer. Fish. Soc. 93:127-136. Butler, P.A. 1971. Influence of pesticides on marine ecosystems. Proc. Royal Soc. London, Ser. B 177:321-329. Freitag, D., L. Ballhorn, H. Geyer, and F. Korte. 1985. Environmental hazard profile of organic chemicals: An experimental method for the assessment of the behaviour of organic chemicals in the ecosphere by means of laboratory tests with 14C labelled chemicals. Chemosphere 14:1589-1616. Gakstatter, J.H., and C.M. Weiss. 1967. The elimination of DDT-C14, dieldrin-C14, and lindane-C14 from fish following a single sublethal exposure in aquaria. Trans. Amer. Fish. Soc. 96:301-307. Guarino, A.M., and S.T. Arnold. 1979. Xenobiotic transport mechanisms and pharmacokinetics in the dogfish shark. In Pesticide and xenobiotic metabolism in aquatic organisms, ed. M.A.Q. Khan et al., pp. 233-258. Hickey, C.W., D.S. Roper, P.T. Holland, and T.M. Trower. 1995. Accumulation of organic contaminants in two sediment-dwelling shellfish with contrasting feeding modes: Deposit(Macomona liliana) and filter-feeding (Austovenus stutchburi). Arch. Environ. Contam. Toxicol. 11:21-231. Johnson, A., D. Norton, and B. Yake. 1988. Persistence of DDT in the Yakima River drainage, Washington. Arch. Environ. Contam. Toxi. 17:291-297. Oliver, G.G., and A.J. Niimi. 1988. Chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22(4):388-397. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 366 BIOACCUMULATION SUMMARY 36. p,p-DDT Pereira, W.E., J.L. Domagalski, F.D. Hostettler, L.R. Brown, and J.B. Rapp. 1996. Occurrence and accumulation of pesticides and organic contaminants in river sediment, water, and clam tissues from the San Jaoquin River and tributaries, California. Environ. Toxicol. Chem. 15:172180. Van der Oost, R. A. Opperhuizen, K. Satumalay, H. Heida, and P.E. Vermulen. 1996. Biomonitoring aquatic pollution with feral eel (Anguilla anguilla) I. Bioaccumulation: Biotasediment ratios of PCBs, OCPs, PCDDs and PCDFs. Aquat. Toxicol. 35:21-46. USEPA. 1995. Great Lakes Water Quality Initiative Technical Support Document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. USEPA. 1998. Ambient water quality criteria derivation methodology human health: Technical support document. Final draft. EPA-822-B-98-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 37. 38. 39. 367 368 BIOACCUMULATION SUMMARY Chemical Category: PESTICIDE (ORGANOPHOSPHATE) Chemical Name (Common Synonyms): DIAZINON DIAZINON CASRN: 333-41-5 Chemical Characteristics Solubility in Water: 0.004% at 20C [1] Log Kow: 3.70 [3] Half-Life: No data [2] Log Koc: 3.64 L/kg organic carbon Human Health Oral RfD: 9 x 10-4 mg/kg/day [4] Critical Effect: Decreased cholinesterase activity Oral Slope Factor: No data [4,5] Carcinogenic Classification: No data [4,5] Confidence: -- Wildlife Partitioning Factors: Partitioning factors for diazinon in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for diazinon in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Partitioning factors for diazinon in aquatic organisms were not found in the literature. Log BCFs ranged from 0.69 to 1.23 (invertebrates) and from 1.59 to 2.90 (fishes). Food Chain Multipliers: Food chain multipliers for diazinon in aquatic organisms were not found in the literature. Toxicity/Bioaccumulation Assessment Profile Diazinon is relatively toxic to aquatic organisms. The acute toxicity for aquatic invertebrates ranged from 0.9 g/L (48-h LC50) for Daphnia pulex [6] to 200g/L (96-h LC50) for Gammarus lacustris [7], while chronic toxicity ranged from 0.27 g/L (30-d LC50) for Gammarus pseudolimneaus to 4.6 g/L (30-d LC50) for Acroneuria lycorias [8]. The maximum acceptable concentration (MATC) for diazinon based on the exposure with sheepshead minnows, was 0.47 g/L [5], and 3.2 g/L based on the exposure with fathead minnows [9]. 369 BIOACCUMULATION SUMMARY DIAZINON The mode of toxic action of organophosphorus compounds is related to the inhibition of acetylcholinesterase in tissue of animals [10]. A representative of organophosphorus insecticides, diazinon shows species-selective toxicity in fish [11]. For example, diazinon was about 10 times more toxic to the guppy than to the zebra fish [12] and 22 times more potent to loach than killifish [10]. Both the guppy and zebra fish metabolized diazinon to 2-isopropyl-6-methyl-4-pyrimidinol (pyrimidinol). The species-specific oxidative transformation of diazinon or inhibition of acetylcholinesterase are responsible for the differences in diazinon toxicity. During the exposure of pretreated fish (guppies and zebra fish) to diazinon [13], the tissue concentration of pyrimidinol initially increased, then declined to very low levels. Keizer et al. [13] hypothesized that the toxicity of diazinon to guppy is due to its metabolism to a highly toxic metabolite, e.g., diazoxon whereas toxicity to zebra fish is related to bioaccumulation of the parent compound. Fish reached an apparent steady state after 48 hours [12] or 96 hours [14]. Diazinon was most rapidly excreted from the gallbladder followed by liver, muscle, and kidney [11]. The slow excretion rate from kidney was probably because diazinon was transported from all parts of the fish to the kidney before excretion [15]. The log BCFs for eels exposed to 56 g/L of diazinon were 2.90 in liver, 3.20 in muscle, and 3.36 in gill tissue [16]. Diazinon elimination from the selected tissues was rapid; it was not detected in any tissue after 24-hour exposure in clean water [16]. The results of the study by Kanazawa [17] showed that the concentration of diazinon in tissue of the freshwater fish reached a maximum after 4 days and then decreased gradually. The uptake of diazinon by killifish was not influenced if the fish were exposed to the individual pesticide, or to a pesticide mixture [18]. Diazinon was identified as a major toxicant in municipal effluents [19], indicating persistence of this pesticide in the environment. According to Lee et al. [20 ], the toxicity of diazinon can be induced by dissolved organic materials. 370 Summary of Biological Effects Tissue Concentrations for Diazinon Species: Taxa Invertebrates Cipangopoludina malleata, Pond snail Procambarus clarkii, Crayfish Concentration, Units in1: Sediment Water Tissue (Sample Type) Toxicity: Effects Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 10 g/L 0.77 [21] L 10 g/L 0.69 [21] L Indoplanorbis exustus, Red snail 10 g/L 1.23 [21] L Fishes Pseudorasbora parva, Topmouth gudgeon Anguilla anguilla, Eel Anguilla anguilla, Eel Gnathopogon caerulescens, Willow shiner 371 50 g/L 11.3 ng/g 2.32 [22] L 10 g/L 80 ng/g (liver) 2.90 [16] L 10 g/L 160 ng/g (muscle) 2.90 [16] L 2.39 [23] F 372 Species: Taxa Pseudorasbora parva, Topmouth gudgeon Pseudorasbora parva, Motsugo Brachydanio rerio, Zebra fish Zacco slatypus, Pale chub Plecoglossus altivelis, Ayu sweetfish Cyprinodon variegatus, Sheepshead minnow Ingestion Sediment Cyprinodon variegatus, Sheepshead minnow Summary of Biological Effects Tissue Concentrations for Diazinon Concentration, Units in1: Water Tissue (Sample Type) Toxicity: Effects Ability to Accumulate2: Log Log BCF BAF BSAF 2.18 Source: Reference Comments3 [23] F 0.7 mg/kg 211 mg/kg (4-day) 17 mg/kg (30 day) Bleeding, abnormal swimming Mortality, ED100 1.81 [17] L 1,550 mg/kg (whole body)4 [13] L; Lethal body burden 2.18 [23] F 1.79 [23] F 1.8 g/L 3.5 g/L 6.5 g/L 0.26 mg/kg in 4d, 0.11 mg/kg in 7d, 0.31 mg/kg in 14d 0.38 mg/kg in 4d, 0.21 mg/kg in 7d, 0.49 mg/kg in 14d 1.3 mg/kg in 4d, 0.5 mg/kg in 7d, 1.4 mg/kg in 14d 0.3 mg/kg (whole body)4 Morphology, LOED 2.17 [14] L 2.17 [14] L 2.33 [14] L [14] L; body darkened, lateral curvature of body Summary of Biological Effects Tissue Concentrations for Diazinon Species: Taxa Concentration, Units in1: Sediment Water Tissue (Sample Type) 1.4 mg/kg (whole body)4 0.5 mg/kg (whole body)4 0.05 mg/kg (whole body)4 1.4 mg/kg (whole body)4 0.5 mg/kg (whole body)4 0.3 mg/kg (whole body)4 0.05 mg/kg (whole body)4 0.05 mg/kg (whole body)4 1.4 mg/kg (whole body)4 0.5 mg/kg (whole body)4 0.3 mg/kg (whole body)4 1.4 mg/kg (whole body)4 373 Toxicity: Effects Morphology, not applicable Morphology, not applicable Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Physiological, LOED Physiological, NA Physiological, NA Physiological, NA Reproduction, ED50 Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [14] L; body darkened, lateral curvature of body [14] L; body darkened, lateral curvature of body [14] L; no effect on morphology or appearance [14] L; no effect on mortality [14] L; no effect on mortality [14] L; no effect on mortality [14] L; no effect on mortality [14] L; inhibition of acetylcholinesterase activity [14] L; 71% inhibition of acetylcholinesterase activity [14] L; inhibition of acetylcholinesterase activity [14] L; inhibition of acetylcholinesterase activity [14] L; 45-55% reduction in average number of eggs produced 374 Species: Taxa Sediment Poecilia reticulata, Guppy Poecilia reticulata, Guppy 1 2 3 4 Summary of Biological Effects Tissue Concentrations for Diazinon Concentration, Units in1: Water Tissue (Sample Type) 0.5 mg/kg (whole body)4 0.3 mg/kg (whole body)4 0.05 mg/kg (whole body)4 Toxicity: Effects Reproduction, ED50 Reproduction, ED50 Reproduction, LOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [14] L; 45-55% reduction in average number of eggs produced [14] L; 45-55% reduction in average number of eggs produced [14] L; statistically significant reduction in number of eggs produced [13] L; lethal body burden 0.8 mg/L 25.8 g/g in 24h, 90.3 g/g in 48h, 167.7 g/g in 96h, 109 mg/kg (whole body)4 2,430 mg/kg (whole body)4 2,430 mg/kg (whole body)4 Mortality, ED100 Mortality, ED100 Mortality, ED100 [24] [24] L; lifestage: 2-3 months L; lifestage: 2-3 months Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. BIOACCUMULATION SUMMARY References 1. DIAZINON Budavari, Merck index, 11th ed., 1989, p. 472. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1995. Health effects assessment summary tables: FY-1995 Annual. EPA/540/R-95/036. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, DC. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January. Sanders, H.O., and O.B. Cope. 1966. Toxicities of several pesticides to two species of cladocerans. Trans. Amer. Fish. Soc. 95:165-169. Sanders, H.O. 1970. Toxicities of some herbicides to six species of freshwater crustaceans. J. Wat. Pollut. Contr. Fed. 42:1544-1550. Bell, H.L. 1971. Unpublished data. National Water Quality Laboratory, Duluth, Minnesota. Allison, D.T., and R.O. Hermanutz. 1977. Toxicity of diazinon to brook trout and fathead minnows. EPA-600/3-77-060. U.S. Environmental Protection Agency, Office of Research and Development, Duluth, MN. 2. 3. 4. 5. 6. 7. 8. 9. 10. Oh, H.S., S.K. Lee, Y.H. Kim, and J.K. Roah. 1991. Mechanism of selective toxicity of diazinon to killifish (Oryzias latipes) and loach (Misgurnus anguillicaudatus). ASTM STP 1124. Aquatic toxicology and risk assessment, ed. M.A. Mayes and M.G. Barron, pp. 343-353. American Society for Testing and Materials, Philadelphia, PA. 11. Vittozzi, L., and G. De Angelis. 1991. A critical review of comparative acute toxicity data on freshwater fish. Aquat. Toxicol. 19:167-204. 375 BIOACCUMULATION SUMMARY DIAZINON 12. Keizer, J., G. D'Agostino, and L. Vittozzi. 1991. The importance of biotransformation in the toxicity of xenobiotics to fish. I. Toxicity and bioaccumulation of diazinon in guppy (Poecilia reticulata) and zebra fish (Brachydanio rerio). Aquat. Toxicol. 21:239-254. 13. Keizer, J., G. D'Agostino, R. Nagel, F. Gramenzi, and L.Vittozzi. 1993. Comparative diazinon toxicity in guppy and zebra fish: Different role of oxidative metabolism. Environ. Tox. Chem. 12:1243-1250. 14. Goodman, L.R., D.J. Hansen, D.L. Coppage, J.C. Moore, and E. Matthews. 1979. Diazinon, chronic toxicity to, and brain acetylcholinesterase inhibition in, the sheepshead minnow, Cyprinodon variegatus. Trans. Am. Fish. Soc.108:479-488. 15. Tsuda, T., S. Aoki, M. Kojima, and H. Harada. 1990. Bioconcentration and excretion of diazinon, IBP, malathion and fenitrothion by carp. Comp. Biochem. Physiol. 1:23-26. 16. Sancho, E., M.D. Ferrando, E. Andreu, and M. Gamon. 1993. Bioconcentration and excretion of diazinon by eel. Bull. Environ. Contam. Toxicol. 50:578-585. 17. Kanazawa, J. 1975. Uptake and excretion of organophosphorus and carbamate insecticides by freshwater fish, motsugo, Pseudorasbora parva. Bull. Environ. Contam. Toxicol. 14:346-352. 18. Tsuda, T., S. Aoki, T. Inoue, and M. Kojima. 1995. Accumulation and excretion of diazinon, fenthion and fenitrothion by killifish: Comparison of individual and mixed pesticides. Wat. Res. 29:455-458. 19. Amato, J.R., D.I. Mount, E.J. Durhan, M.T. Lukasewych, G.T. Ankley, and E.D. Robert. 1992. An example of the identification of diazinon as a primary toxicant in an effluent. Environ. Toxicol. Chem. 11:209-216. 20. Lee, S.K., D. Freitag, C. Steinberg, A. Kettrup, and Y.H. Kim. 1993. Effects of dissolved humic materials on acute toxicity of some organic chemicals to aquatic organisms. Water Res. 27:199-204. 21. Tsuda, T., S. Auki, M. Kojima, and T. Fujita. 1992. Pesticides in water and fish from rivers flowing into Lake Biwa. Chemosphere 24:1523-1531. 22. Kanazawa, J. 1978. Bioconcentration ratio of diazinon by freshwater fish and snail. Bull. Environ. Contam. Toxicol. 20:613-617. 23. Kanazawa, J. 1983. A method of predicting the bioconcentration potential of pesticides by using fish. Japan Agricult. Res. Quart. 17:173-179. 24. Ohayo-mitoko, G.J.A., and J.W. Deneer. 1993. Lethal body burdens of four organophosphorus pesticides in the guppy (Poecilia reticulata). Sci. Tot. Environ., Supp.:559-565. 376 BIOACCUMULATION SUMMARY DICOFOL Chemical Category: PESTICIDE (ORGANOCHLORINE) Chemical Name (Common Synonyms): DICOFOL CASRN: 115-32-2 Chemical Characteristics Solubility in Water: 1.2 mg/L at 20 C (99% purity) [1] Log Kow: No data [3] Half-Life: No data [2] Log Koc: -- Human Health Oral RfD: 1 x 10-3 mg/kg/day [4] Confidence: -- Critical Effect: Increase in liver to body weight ratios in rats Oral Slope Factor: No data [5] Carcinogenic Classification: C [6] Wildlife Partitioning Factors: Partitioning factors for dicofol in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for dicofol in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Log BCFs ranging from 4.02-4.16 were reported in a study exposing fathead minnows to dicofol [10]. Food Chain Multipliers: Food chain multipliers for dicofol in aquatic organisms were not found in the literature. Toxicity/Bioaccumulation Assessment Profile Dicofol is an organochlorine compound used as a miticide. The principal commercial dicofol product, Kelthane, is made from DDT [7]. Clark et al. [7] reported reduction in eggshell weight and thickness of American kestrels due to dicofol. They also observed that 10 g/g of dicofol reduced hatchability of eggs. They suggested that dicofol concentrations above 3 g/g in food may affect bird reproduction. The 48-h and 100-h LC50s for grass shrimp (Crangon franciscorum) exposed to dicofol (Kelthane) were 590 and 100 g/L, respectively [8]. 377 BIOACCUMULATION SUMMARY DICOFOL The major metabolite of dicofol is 1,1-bis(4-chlorophenol)2,2dichloroethanol (pp-DCD) [9]. Because dicofol is more lipophilic than its metabolites, it was abundant in every tissue except for liver and brain. The dicofol metabolites are less toxic than dicofol and they have less impact on the formation of normal eggshells by doves [9]. The bioconcentration of dicofol in fathead minnows was reduced by 35 percent by clay particles (65 mg/L) indicating that more than 30 percent of the dicofol sorbed onto clay and was biologically unavailable to the fish [10]. Bioconcentration factors at the two dicofol concentrations were not significantly different and steady-state concentrations occured with 40 to 60 days of exposure at 10,500 to 13,900 times water levels. 378 Summary of Biological Effects Tissue Concentrations for Dicofol Species: Taxa Fishes Pimephales promelas, Fathead minnow 12.38 g/L 4.02-4.16 [10] L Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 1.15 g/L Wildlife Streptopelia risoria, 32 mg/kg Ring neck dove (diet) 116.5g/g in fat 1.07g/g in liver 4.55g/g in heart 0.37g/g in brain 4.12-4.14 [10] L [9] L 1 2 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 379 BIOACCUMULATION SUMMARY References 1. DICOFOL Verschueren. HDBK Environ. Data Org. Chem. 1983, p.786. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September). USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1993. Reference dose tracking report. U.S. Environmental Protection Agency, Office of Pesticide programs, Health Effects Division, Washington, DC. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January. USEPA. 1992. Classification list of chemicals evaluated for carcinogenicity potential. U.S. Environmental Protection Agency, Office of Pesticide Programs, Washington, DC. Clark, D.R. Jr., J.W. Spann, and C.M. Bunck. 1990. Dicofol (Kelthane)-induced eggshell thinning in captive American kestrels. Environ. Toxicol. Chem. 9:1063-1069. Khorram, S., and A.W. Knight. 1977. The toxicity of Kelthane to the grass shrimp (Crangon franciscorum). Bull. Environ. Contam. Toxicol. 15:398-401. Schwarzbach, S.E. 1991. The role of dicofol metabolites in the eggshell thinning response of ring neck doves. Arch. Environ. Contam. Toxicol. 20:200-205. Eaton, J.G., V.R. Mattson, L.H. Mueller, and D.K. Tanner. 1983. Effects of suspended clay on bioconcentration of Kelthane in fathead minnows. Arch. Environ. Contam. Toxicol. 12:439-445. 2. 3. 4. 5. 6. 7. 8. 9. 10. 380 BIOACCUMULATION SUMMARY Chemical Category: PESTICIDE (ORGANOCHLORINE) Chemical Name (Common Synonyms): DIELDRIN DIELDRIN CASRN: 60-57-1 Chemical Characteristics Solubility in Water: 186 g/L at 25C [1] Half-Life: 175 days to 3 years, based on unacclimated aerobic soil grab sample data and reported half-life in soil based on field data [2] Log Koc: 5.28 L/kg organic carbon Log Kow: 5.37 [3] Human Health Oral RfD: 5 x 10-5 mg/kg/day [4] Confidence: Medium, uncertainty factor = 100 Critical Effect: Liver lesions (focal proliferation and focal hyperplasia) in rats, liver carcinomas in mice Oral Slope Factor: 1.6 x 10+1 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4] Wildlife Partitioning Factors: Log BCFs for tadpole and juvenile frogs have been measured at 2.20 to 3.33, whereas log BCFs for adult frogs were 1.57 to 2.58. Dieldrin appears to bioconcentrate to a lesser extent in frogs than in fish. Mallard ducklings exposed to dieldrin-contaminated water for drinking and swimming had log BCFs ranging from 1.69 to 2.21 in liver, 0.98 to 1.97 in muscle, 2.25 to 2.84 in skin, and 2.85 to 3.30 in lipid. Mallard ducklings exposed for longer periods had log BCFs up to 9.30. BSAFs were calculated for red-winged blackbirds and tree swallow eggs during a study in the Great Lakes area, with values ranging from 7.5 to 448, as reported in the attached summary table. The BSAF for tree swallow nestings was 341. Food Chain Multipliers: A biomagnification factor of 16 has been reported for dieldrin for herring gulls feeding on alewife in Lake Ontario [5]. A study of arctic marine food chains measured biomagnification factors for dieldrin that ranged from 2.2 to 2.4 for fish to seal, 4.9 to 5.5 for seal to bear, and 11.4 for fish to bear [6]. Aquatic Organisms Partitioning Factors: In older studies, the following log BCFs have been reported for dieldrin: 4.51 in freshwater alga [7]; from 3.38 to 4.83 in fish [8]; and log 3.20 in a saltwater mussel [9]. A log BCF of 5.36 was found for rainbow trout [34]. BSAFs ranging from 1.120 to 7.134 were reported to bivalves [33]. 381 BIOACCUMULATION SUMMARY DIELDRIN Food Chain Multipliers: Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were 8.6 (all benthic food web), 1.2 (all pelagic food web), and 5.5 (benthic and pelagic food web). FCMs for trophic level 4 aquatic organisms were 10.8 (all benthic food web), 1.9 (all pelagic food web), and 5.8 (benthic and pelagic food web) [36]. Toxicity/Bioaccumulation Assessment Profile Dieldrin is the name of an insecticide that was used in the United States for locust and mosquito control until production and importation were banned. In addition to man-made production, dieldrin is derived from the oxidation of aldrin, which is also an insecticide. Aldrin is readily converted to dieldrin under normal environmental conditions [10]. In addition, aldrin is readily metabolized to dieldrin, so the effects seen in animals exposed to aldrin may be caused by dieldrin [11]. Dieldrin is one of the most persistent of the chlorinated hydrocarbons, and is highly resistant to biodegradation and abiotic degradation. In water, volatilization of dieldrin to the atmosphere is probably an important process, but transformation processes in soils and sediment are slow. Dieldrin sorbs tightly to soil and sediment, particularly if substantial amounts of organic carbon are present. Dieldrin is toxic to aquatic organisms, birds, and mammals and is capable of producing carcinogenic, teratogenic, and reproductive effects [10]. Teratogenic effects include cleft palate, webbed foot, and skeletal anomalies. Reproductive effects include decreased fertility, increased fetal death, and effects on gestation [10]. In aquatic organisms, the acute toxicity of dieldrin ranges from 0.5 to 740 g/L for freshwater and 0.7 to >100 g/L for saltwater organisms [12]. Differences between dieldrin concentrations causing acute lethality and chronic toxicity in species acutely sensitive to this insecticide are small; acute-chronic ratios ranged from 2.4 to 12.8 for three species [12]. Dieldrin is generally an order of magnitude more toxic to fish than is aldrin [11]. LC50s for freshwater and saltwater aquatic invertebrates exposed to sediment spiked with dieldrin in the laboratory have been shown to range from 0.0041 to 386 g/g dw [12]. Bioconcentration factors for dieldrin in various aquatic organisms range from 400 to 68,000 [8], indicating that dieldrin will show moderate to significant bioaccumulation in various aquatic species. Mammals appear to be more sensitive to dieldrin poisoning than birds. Brain concentrations associated with lethality in mammals are 5 mg/kg and in birds are 10 mg/kg [11]. Concentrations as low as 1 mg/kg in the brain might trigger irreversible starvation in sensitive individuals of birds [13]. Major effects on reproduction in wildlife are not expected to occur at dieldrin concentrations of less than one half those causing mortality [11]. Dieldrin is commonly found in the brain, tissues, and eggs of fish-eating birds that also have residues of organochlorines such as DDE and PCBs. Based on a number of literature studies, the State of New York proposed a dietary fish flesh criterion of 0.12 mg/kg to protect piscivorous wildlife [14]. There are limited studies relating aldrin concentrations to toxicity because of the rapid conversion of aldrin into dieldrin. 382 Summary of Biological Effects Tissue Concentrations for Dieldrin Species: Taxa Invertebrates Crassostrea virginica, Eastern oyster 107 mg/kg (whole body)4 11 mg/kg (whole body)4 1.03 mg/kg (whole body)4 Cellular, NOED [23] L; no histological effects on structure of gill, gut or mantle Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Cellular, NOED Cellular, NOED [23] [23] Crassostrea virginica, Eastern oyster 1.44 mg/kg (whole body)4 18.6 mg/kg (whole body)4 1.44 mg/kg (whole body)4 18.6 mg/kg (whole body)4 Behavior, LOED [29] Behavior, NA Mortality, NOED Mortality, NOED [29] [29] [29] L; erratic shell movements, extended shell closure indicated irritation L; no effect on mortality within 168 hours Crassostrea virginica, Eastern oyster 13.9 mg/kg (whole body)4 Growth, NOED [31] L; estimated NOED no statistical summary in text 383 384 Species: Taxa Macomona liliana, Mollusk Sediment 73.3 g/kg OC 52.1 g/kg OC 72.7 g/kg OC 60.0 g/kg OC 20.8 g/kg OC Austrovenus 73.3 g/kg stutchburyi, Mollusk OC 52.1 g/kg OC 72.7 g/kg OC 60.0 g/kg OC 20.8 g/kg OC Mercenaria mercenaria, Quahog clam Summary of Biological Effects Tissue Concentrations for Dieldrin Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 201.7 g/kg lipid 371.7 g/kg lipid 172.0 g/kg lipid 76.0 g/kg lipid 80.2 g/kg lipid Ability to Accumulate2: Log BCF Log BAF BSAF 2.752 7.134 2.366 1.267 3.856 Source: Reference Comments3 [33] [33] [33] [33] [33] F, %lipid = 2.95; %sed OC = 0.30 F, %lipid = 2.33; %sed OC = 0.73 F, %lipid = 2.57; %sed OC = 0.22 F, %lipid = 2.04; %sed OC = 0.25 F, %lipid = 3.13; %sed OC = 0.48 102.7 g/kg lipid 127.6 g/kg lipid 105.2 g/kg lipid 67.2 g/kg lipid 58.6 g/kg lipid 1.401 2.449 1.447 1.120 2.817 [33] [33] [33] [33] [33] F, %lipid = 5.62; %sed OC = 0.30 F, %lipid = 5.21; %sed OC = 0.73 F, %lipid = 4.85; %sed OC = 0.22 F, %lipid = 3.87; %sed OC = 0.25 F, %lipid = 4.27; %sed OC = 0.48 0.38 mg/kg (whole body)4 Behavior, NOED [22] L; no effect on feeding activity Summary of Biological Effects Tissue Concentrations for Dieldrin Species: Taxa Mya arenaria, Soft shell clam Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.87 mg/kg (whole body)4 Behavior, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [22] L; no effect on feeding activity Chlamydotheca arcuata, Ostracod 1 mg/kg (whole body)4 Mortality, LOED [28] L; immobility, mortality, resd_conc_wet value > 1.0 Palaemonetes pugio, Grass shrimp 2.1 mg/kg (whole body)4 0.09 mg/kg (whole body)4 Mortality, LOED Mortality, NOED [31] L; estimated loed - no statistical summary in text L; estimated noed - no statistical summary in text [31] Penaeus duorarum, Pink shrimp 0.23 mg/kg (whole body)4 0.08 mg/kg (whole body)4 0.01 mg/kg (whole body)4 Mortality, ED50 Mortality, LOED Mortality, NOED [31] [31] L; ED50 via Spearman Karber 1.5 (msl) L; estimated LOED no statistical summary in text L; estimated NOED no statistical summary in text [31] Chironomus riparius, Midge 1.9 mg/kg (whole body)4 Mortality, ED10 [24] L; all larvae moribund in 2 hours 385 386 Species: Taxa Sediment Fishes Squalus acanthias, Spiny dogfish Oncorhynchus mykiss, Rainbow trout Summary of Biological Effects Tissue Concentrations for Dieldrin Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 1.1 mg/kg (whole body)4 1.1 mg/kg (whole body)4 1.1 mg/kg (whole body)4 1.1 mg/kg (whole body)4 Behavior, ED50 Mortality, ED50 Behavior, ED50 Mortality, ED50 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [24] L; 50 - 75% mortality, lethargy within 2 hours [24] [24] [24] L; 50 - 75% mortality, lethargy within 2 hours 1 mg/kg (whole body)4 0.14 mg/kg (fat)4 Mortality, NOED Physiological, ED30 Physiological, ED30 Physiological, ED35 Growth, ED40 [27] L; no effect on mortality in 24 hours L; 30% decrease in hemoglobin content relative to control L; 30% increase in liver size relative to control L; 35% increase in kidney size relative to control L; 40% decrease in growth relative to control [32] 0.14 mg/kg (fat)4 [32] 0.05 mg/kg (fat)4 [32] 0.14 mg/kg (fat)4 [32] Summary of Biological Effects Tissue Concentrations for Dieldrin Species: Taxa Oncorhynchus mykiss, Rainbow trout (juveniles) Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF 5.36 Log BAF BSAF Source: Reference Comments3 [34] L Salmonids 6.65 [35] F Carassius auratus, Goldfish 3.8 mg/kg (whole body)4 Behavior, LOED [26] L; hyperexcit-ability Leuciscus idus, Golden ide 151 mg/kg (whole body)4 Mortality, NOED [25] L; no effect on survivorship in 3 days Cyprinodon variegatus, Sheepshead minnow 52.9 mg/kg (whole body)4 34 mg/kg (whole body)4 12.8 mg/kg (whole body)4 Mortality, ED50 Mortality, LOED Mortality, NOED [31] [31] [31] L; ED50 via Spearman Karber 1.5 (msl) L; estimated NOED no statistical summary in text Gambusia affinis, Mosquito fish 28 mg/kg (whole body)4 Mortality, NOED [30] L; no effect on survivorship after 3 days 387 388 Species: Taxa Poecilia reticulata, Guppy Sediment Lepomis macrochirus, Bluegill Wildlife Xenopus laevis, African clawed frog (tadpole stage) Summary of Biological Effects Tissue Concentrations for Dieldrin Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 10.7 mg/kg (whole body)4 Growth, NA Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [21] L; decreased biomass of guppy population in laboratory ecosystem 3.7 mg/kg (whole body)4 Behavior, LOED [26] L; behavioral changes, loss of equilibrium, convulsions water 0.7 mg/kg5 exposure (whole body) 2.30.2 g/L water 1.81.2 mg/kg5 exposure (whole body) 1.10.1 g/L (water exposure) g/L 2.00.0 4.20.1 9.30.2 20.50.4 g/L (water exposure): 0.90.1 1.80.2 3.80.3 9.70.4 mg/kg5 (whole body): 0.8 20.00 3.00.6 7.0 mg/kg5 (whole body) 0.40 0.80.2 1.50.5 3.01.0 2.48 [15] L; 28-day exposure; insufficient tissue for replicates; values are mean SE L; 28-day exposure 3.213.04 [15] [15] 2.60 2.680 2.510.07 2.53 [15] 2.670 2.621.92 2.592.11 2.492.01 L; 28-day exposure; insufficient tissue for replicates for all exposures; values are mean SE L; 24-day exposure; values are mean SE; effects based on mortality NOAEL LOAEL Summary of Biological Effects Tissue Concentrations for Dieldrin Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Xenopus laevis, African clawed frog (tadpole stage) water exposure 5.5 g/L [15] 1.8 mg/kg5 (whole body) LC50 L; 24-day exposure; LC50 tissue dieldrin estimated by graphical extrapolation Xenopus laevis, African clawed frog (juvenile stage) water exposure 4.50.3 mg/kg5 2.10.2 g/L (whole body) [15] 3.332.38 L; 28-day exposure; values are mean SE Rana pipiens, Leopard frog (tadpole stage) water exposure 0.60.2 mg/kg5 0.80.1 g/L (whole body) water exposure 0.80.1 mg/kg5 2.10.1 g/L (whole body) water exposure (g/L) 0.80.1 1.90.2 4.10.3 10.00.3 whole body5 (mg/kg ) 0.40.1 0.40 0.60.1 2.00.1 [15] 2.842.28 [15] 2.591.60 [15] NOAEL LOAEL 2.641.18 2.320 2.201.08 2.300 L; 28-day exposure; values are mean SE L; 28-day exposure; values are mean SE L; 28-day exposure; values are mean SE; effects based on mortality Rana pipiens, Leopard frog (tadpole stage) 389 water 1.7 mg/kg5 exposure 8.3 (whole body) g/L LC50 [15] L; 24-day exposure; LC50 tissue dieldrin estimated by graphical extrapolation 390 Species: Taxa Sediment Rana pipiens, Leopard frog (adult stage) Anas platyrhynchos, Mallard (ducklings) Summary of Biological Effects Tissue Concentrations for Dieldrin Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 water exposure 10.71.3 g/L water exposure 56.24.1 g/L water exposure 53.4 g/L 0.40.4 mg/kg5 (skin) 0.90.1 mg/kg5 (muscle) 1.50.5 mg/kg5 (liver) 7.32.8 mg/kg (skin) 17.87.8 mg/kg5 (muscle) 21.53.3 mg/kg5 (liver) 5.5 mg/kg5 (skin) 10.0 mg/kg5 (muscle) 13.0 mg/kg5 (liver) LC50 LC50 LC50 5 1.571.57 1.920.95 2.151.67 2.111.69 2.512.15 2.581.64 [15] L; 28-day exposure; values are mean SE [15] L; 28-day exposure; values are mean SE [15] L; 28-day exposure; LC50 tissue dieldrin estimated by graphical extrapolation 0.0141 mg/L 24.5 mg/kg (lipid) 2.3 mg/kg (liver) 1.3 mg/kg (muscle) No mortality or effects on behavior or survival observed No mortality or effects on behavior or survival observed 3.24 [18] 0.0524 mg/L 68.9 mg/kg (lipid) 3.4 mg/kg (liver) 1.15 mg/kg (muscle) 3.12 L; 34-day exposure; 1-day-old birds had access to dieldrincontaminated water for drinking and swimming Summary of Biological Effects Tissue Concentrations for Dieldrin Species: Taxa Concentration, Units in1: Sediment Water 0.11811 mg/L Toxicity: Tissue (Sample Type) Effects 128 mg/kg (lipid) 7.4 mg/kg (liver) 1.1 mg/kg (muscle) No mortality or effects on behavior or survival observed Ability to Accumulate2: Log BCF 3.04 Log BAF BSAF Source: Reference Comments3 Anas platyrhynchos, Mallard (ducklings) 0.0192 mg/L 37.9 mg/kg (lipid) 13 mg/kg (skin) 1.9 mg/kg (liver) No mortality or effects on behavior or survival observed No mortality or effects on behavior or survival observed No mortality or effects on behavior or survival observed 3.30 [18] 0.0751 mg/L 107 mg/kg (lipid) 39.5 mg/kg (skin) 4.8 mg/kg (liver) 3.15 L; 24-day exposure; 1-day old birds had access to dieldrincontaminated water for drinking and swimming 0.1938 mg/L 217 mg/kg (lipid) 75 mg/kg (skin) 11.3 mg/kg (liver) 3.05 0.17711 mg/L 125 mg/kg (lipid) 31.5 mg/kg (skin) 8.6 mg/kg (liver) 2.3 mg/kg (brain) 0.97 mg/kg muscle) 0.97 mg/kg (blood) 2.84 2.25 1.69 1.11 0.74 0.51 [18] L; 8-day exposure; 14-day old birds had access to dieldrincontaminated water for drinking and swimming 391 392 Species: Taxa Sediment Falco peregrinus, Peregrine falcon (eggs) Falco tinnunculus, European kestrel Summary of Biological Effects Tissue Concentrations for Dieldrin Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 915 mg/kg (lipid) 305 mg/kg (skin) 52 mg/kg (liver) 395 mg/kg (lipid) 193 mg/kg (skin) 12 mg/kg (liver) 5 mg/kg (brain) 2 mg/kg (muscle) 180 mg/kg (lipid) 102 mg/kg (skin) 7 mg/kg (liver) 2.5 mg/kg (brain) <1 mg/kg (muscle) 4 mg/kg (lipid) 2 mg/kg (skin) <1 mg/kg (liver) <1 mg/kg (brain) <1 mg/kg (muscle) 96-Hour LC50 Ability to Accumulate2: Log BCF 0.74 0.26 0.52 1.13 0.81 0.40 0.70 1.00 Log BAF BSAF Source: Reference Comments3 [18] L; 24-day exposure; birds were dosed with food spiked with dieldrin at measured concentrations of 0.3 to 165 mg/kg. 24-Day LC50 24-Day LOAEL 1.05 0.81 0.40 0.70 24-Day NOAEL 1.12 0.83 59 ng/g (eggs) (n = 6) 11.4% eggshell thinning [19] F; Kola Peninsula, Russia; n = number of clutches sampled 6-30 mg/kg (liver) mortality [16] F Summary of Biological Effects Tissue Concentrations for Dieldrin Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 16.6 ng/g Ability to Accumulate2: Log BCF Log BAF BSAF 7.5 Source: Reference Comments3 [20] F; Great Lakes/St. Lawrence River basin; 12 wetlands sites; sediment concentration reported as wet weight concentration which may be a typographical error. 203.7 117.6 ng/g ww Agelaius phoeniceus, 1.2 ng/g Red-winged TOC=21.0% blackbird (eggs) 11.0 ng/g TOC=7.5% 127.8 ng/g TOC=12% 0.6 ng/g TOC=18.5% 0.7 ng/g TOC=11.5% 0.1 ng/g TOC=10.5% 31.0 ng/g 21 84.6 ng/g 7.8 8.9 ng/g 57.2 9.1 ng/g 31.1 20.0 ng/g 448 Tachycineta bicolor, Tree swallow (whole body minus feet, beak, wings, and feathers) 0.7 ng/g TOC=11.5% 0.7 ng/g TOC=11.5% 211.4 ng/g 340.5 [20] (nestlings) (eggs) 19.3 ng/g 36.9 F; Great Lakes/ St. Lawrence River basin; 12 wetlands sites; sediment concentration reported as wet weight concentration which may be a typographical error. 393 394 Species: Taxa Tyto alba, Barn owl 1 2 3 4 Summary of Biological Effects Tissue Concentrations for Dieldrin Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 6-44 mg/kg (liver) mortality Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [17] F 5 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. Not clear from reference if concentration is based on wet or dry weight. BIOACCUMULATION SUMMARY DIELDRIN References 1. USEPA, Hazard Profile, Dieldrin, 1980, p. 1. (Cited in: USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1995. 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Diagnostic brain residues of dieldrin: Some new insights. In ASTM STP 757, Avian and mammalian wildlife toxicology: Second Conference, ed. D. Lamb and G. Kenaga, pp. 72-92. American Society of Testing and Materials, Philadelphia, PA. Newell, A.J., D.W. Johnson, and L.K. Allen. 1987. Niagara River biota contamination project: Fish flesh criteria for piscivorous wildlife. Tech. Rep. 87-3. New York Department of Environmental Conservation, Bureau of Environmental Protection. Schuytema, G.S., A.V. Nebecker, W.L. Griffis, and K.N. Wilson. 1991. Teratogenesis, toxicity, and bioconcentration in frogs exposed to dieldrin. Arch. Environ. Contam. Toxicol. 21:332-350. Newton, I., I. Wyllie, and A. Asher. 1992. Mortality from the pesticides aldrin and dieldrin in British sparrowhawks and kestrels. Ecotoxicology 1:31-44. Newton, I., I. Wyllie, and A. Asher. 1991. Mortality causes in British barn owls, Tyto alba, with a discussion of aldrin-dieldrin poisoning. Ibis 133:162-169. Nebeker, A.V., W.L. Griffis, T.W. Stutzman, G.S. Schuytema, L.A. Carey, and S.M. Scherer. 1992. Effects of aqueous and dietary exposure of dieldrin on survival, growth and bioconcentration in mallard ducklings. Environ. Toxicol. Chem. 11:687-699. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. Bishop, C.A., M.D. Koster, A.A. Chek, D.J.T. Hussell, and K. Jock. 1995. Chlorinated hydrocarbons and mercury in sediments, red-winged blackbirds (Agelaius phoeniceus) and tree swallows (Tachycineta bicolor) from wetlands in the Great Lakes-St. Lawrence river basin, Environ. Toxicol. Chem. 14:491-501. Burnett, K.M., and W.J. Liss. 1990. Multi-steady-state toxicant fate and effect in laboratory aquatic ecosystems. Environ. Toxicol. Chem. 9:637-647. Butler, P.A. 1971. Influence of pesticides on marine ecosystems. Proc. Royal Soc. London, Series B 177:321-329. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 396 BIOACCUMULATION SUMMARY DIELDRIN 23. Emanuelsen, N., J.L. Lincer, and K. Rifkin. 1978. The residue uptake and histology of American oysters (Crassostrea virginica Gmelin) exposed to dieldrin. Bull. Environ. Contam. Toxicol. 19:121-129. Estenik, J.F., and W.J. Collins. 1979. In vivo and in vitro studies of mixed-function oxidase in an aquatic insect, Chironomus riparius. In Pesticide and xenobiotic metabolism in aquatic organisms, ed. M.A.Q. Khan, J.J. Lech, and J.J. Menn, pp. 349-370. American Chemical Society, Washington, DC. Freitag, D., L. Ballhorn, H. Geyer, and F. Korte. 1985. Environmental hazard profile of organic chemicals: An experimental method for the assessment of the behaviour of organic chemicals in the ecosphere by means of laboratory tests with 14C-labelled chemicals. Chemosphere 14:15891616. Gakstatter, J.H., and C.M. Weiss. 1967. The elimination of DDT-C14, dieldrin-C14, and lindaneC14 from fish following a single sublethal exposure in aquaria. Trans. Amer. Fish. Soc. 96:301307. Guarino, A.M., and S.T. Arnold. 1979. Xenobiotic transport mechanisms and pharmacokinetics in the dogfish shark. In Pesticide and xenobiotic metabolism in aquatic organisms, ed. M.A.Q. Khan, J.J. Lech, and J.J. Menn, pp.233-258. American Chemical Society, Washington, DC. Kawatski, J.A., and J.C. Schmulbach. 1971. Accumulation of insecticide in freshwater ostracods exposed continuously to sublethal concentrations of aldrin or dieldrin. Trans. Amer. Fish. Soc. 100:565-567. Mason, J.W., and D.R. Rowe. 1976. The accumulation and loss of dieldrin and endrin in the eastern oyster. Arch. Environ. Contam. Toxicol. 4:349-360. Metcalf, R.L. 1974. A laboratory model ecosystem to evaluate compounds producing biological magnification. In Essays in toxicology, ed. W.J. Hayes, Vol. 5, pp. 17-38. Academic Press. New York, NY. Parrish, P.P., J.A. Couch, J. Forester, J.M. Patrick, and G.H. Cook. NS. Dieldrin: Effects on several estuarine organisms. Contribution No. 178, Gulf Breeze Environmental Research Laboratory, Sabine Island, Gulf Breeze, FL. Poels, C.L.M., M.A. van Der Gaag, and J.F.J. van de Kerkhoff. 1980. An investigation into the long-term effect of Rhine water on rainbow trout. Water Research (14):1029-1033. Hickey, C.W., D.S. Roper, P.T. Holland, and T.M. Trower. 1995. Accumulation of organic contaminants in two sediment-dwelling shellfish with contrasting feeding modes: Deposit(Macomona liliana) and filter-feeding (Austovenus stutchburi). Arch. Environ. Contam. Toxicol. 11:221-231. Shubat and Curtis. 1986. Environ. Toxicol. Chem. 5:69-77. 397 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. BIOACCUMULATION SUMMARY DIELDRIN 35. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 398 BIOACCUMULATION SUMMARY DISULFOTON Chemical Category: PESTICIDE (ORGANOPHOSPHATE) Chemical Name (Common Synonyms): DISULFOTON CASRN: 298-04-4 Chemical Characteristics Solubility in Water: 25 ppm at 23C [1] Half-Life: 3 days - 21 days based on aerobic soil field data [2] Log Kow: 3.98 [3] Log Koc: 3.91 L/kg organic carbon Human Health Oral RfD: 4 X 10-5 mg/kg/day [4] Confidence: Medium, uncertainty factor = 1000 [4] Critical Effect: Cholinesterase inhibition and optic nerve degeneration in dogs Oral Slope Factor: No data [4] Carcinogenic Classification: D [6] Wildlife Partitioning Factors: Partitioning factors for disulfoton in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for disulfoton in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Partitioning factors for disulfoton in aquatic organisms were not found in the literature. Food Chain Multipliers: Food chain multipliers for disulfoton in aquatic organisms were not found in the literature. Toxicity/Bioaccumulation Assessment Profile The toxicity of insecticidally active organophosphorus compounds like disulfoton to animals is attributed to their ability to inhibit acetylcholinesterase, which is a class of enzymes that catalyzes the hydrolysis of the neurotransmitting agent acetylcholine [7]. 399 BIOACCUMULATION SUMMARY DISULFOTON Disulfoton is relatively toxic to aquatic organisms. The acute toxicity for aquatic invertebrates ranged from 5 g/L (96-h LC50) for Pteronarcys californica [8] to 52 g/L (96-h LC50) for Gammarus lacustris [9], while chronic toxicity ranged from 1.4 g/L (30-d LC50) for Acroneuria pacifica to 1.9 g/L (30-d LC50) for Pteronarcys californica [10]. Fish are less sensitive to disulfoton. The 96-h LC50 based on the exposure with fathead minnows was 3700 g/L [11]. The toxicity of disulfoton and its most important degradation products were measured using Daphnia magna [12]. The toxicity of disulfoton (24-h LC50 of 55 g/L) was similar to two of its degradation products (disulfoton-sulfoxide and disulfoton). The remaining degradation products were much less toxic than the parent compound. 400 Summary of Biological Effects Tissue Concentrations for Disulfoton Species: Taxa Invertebrates Concentration, Units in: Sediment Toxicity: Ability to Accumulate: BCF BAF BSAF Source: Reference Comments Pore Water Tissue (Sample Type) Effects [NO DATA FOUND] Fishes [NO DATA FOUND] Wildlife [NO DATA FOUND] 401 BIOACCUMULATION SUMMARY DISULFOTON References 1. NRC. Drinking Water and Health. 1977. p. 615. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1992. Reference dose tracking report. U.S. Environmental Protection Agency, Office of Pesticide Programs, Health Effects Division, Washington, DC. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January. USEPA. 1992. Classification list of chemicals evaluated for carcinogenicity potential. U.S. Environmental Protection Agency, Office of Pesticide Programs, Washington, DC. Fukuto, T.R. 1990. Mechanism of action of organophosphorus and carbamate insecticides. Environ. Health Perspect. 87:245-254. Sanders, H.O., and O.B. Cope. 1968. The relative toxicities of several pesticides to naiads of three species of stoneflies. Limnol. Oceanogr. 13:112-117. Sanders, H.O. 1969. Toxicity of pesticides to the crustacean, Gammarus lacustris. Bureau of Sport Fisheries and Wildlife Technical Paper 25. U.S. Government Printing Office, Washington, DC. Jensen, L.D., and A.R. Gaufin. 1964. Long-term effects of organic insecticides on two species of stonefly naiads. Tran. Amer. Fish. Soc. 93:357-363. Pickering, Q.H., C. Henderson, and A.E. Lemke. 1962. The toxicity of organic phosphorus insecticides to different species of warmwater fishes. Trans. Amer. Fish. Soc. 91:175-184. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 402 BIOACCUMULATION SUMMARY 12. DISULFOTON Galli, R., H.W. Rich, and R. Scholtz. 1994. Toxicity of organophosphate insecticides and their metabolites to the water flea Daphnia magna, the Microtox test and an acetylcholinesterase inhibition test. Aquat. Toxicol. 30:259-269. 403 BIOACCUMULATION SUMMARY DISULFOTON 404 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED DIBENZOFURANS Chemical Name (Common Synonyms): 1,2,3,4,7,8-HEXACHLORODIBENZOFURAN 1,2,3,4,7,8-HexaCDF CASRN: 70648-26-9 Chemical Characteristics Solubility in Water: No data [1] Log Kow: No data [3] Half-Life: No data [2] Log Koc: -- Human Health Oral RfD: No data [4] Critical Effect: -- Oral Slope Factor: No data [4] Carcinogenic Classification: -- Confidence: -- Wildlife Partitioning Factors: Partitioning factors for 1,2,3,4,7,8-hexaCDF in wildlife were not found in the studies reviewed. Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors of PCDDs and PCDFs through terrestrial wildlife. Due to the toxicity, high Kow values, and highly persistent nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and biomagnify through the food web. PCDDs and PCDFs have been identified in fish and wildlife throughout the global aquatic and marine environments [5]. Studies conducted in Lake Ontario indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be significant between fish and fish-eating birds but not between fish and their food. When calculated for older predaceous fish such as lake-trout-eating young smelt, the biomagnification factor (BMF) can equal 3. The BMF from alewife to herring gulls in Lake Ontario was 32 for 2,3,7,8-TCDD [6]. Log BMFs of 1.70 to 1.81 were reported for mink from 1,2,3,4,7,8-hexaCDF-contaminated diet exposures. EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds. 405 BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDF Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated Wildlife [7] Sediment Concentration (pg/g dry wt.) Low Risk 50 60 0.7 2.5 6 21 High Risk to Sensitive Species 80 100 7 25 60 210 Water Concentration (pg/L) POC=0.2 0.6 0.008 0.07 1 0.08 0.7 POC=1.0 3.1 0.04 0.35 5 0.4 3.5 Organism Fish Mammalian Wildlife Avian Wildlife Fish Mammalian Wildlife Avian Wildlife Fish Concentration (pg/g) Note: POC - Particulate organic carbon Fish lipid of 8% and sediment organic carbon of 3% assumed where needed. For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used. Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and young) in sensitive species. High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and young of sensitive species. Aquatic Organisms Partitioning Factors: Partitioning factors for 1,2,3,4,7,8-hexaCDF in aquatic organisms were not found in the studies reviewed. Food Chain Multipliers: No specific food chain multipliers were identified for 1,2,3,7,8-hexaCDF. Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8TCDD does not appear to be significant between fish and their prey. Limited data for the base of the Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and forage fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the 2,3,7,8TCDD biotansformation by forage fish. BMFs greater than 1.0 might exist between some zooplankton species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates [7]. Log BMFs of 1.70 to 1.81 were determined for mink [13]. Toxicity/Bioaccumulation Assessment Profile The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased with increasing ring chlorination [5]. In general, the PCDDs and PCDFs exhibit relative inertness to acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical stability 406 BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDF with increasing chlorination [8,5]. Because of their lipophilic nature, the PCDDs and PCDFs have been detected in fish, wildlife, and human adipose tissue, milk, and serum [5]. Each isomer has its own unique chemical and toxicological properties. The most toxic of the PCDD and PCDF isomers is 2,3,7,8-TCDD, one of the 22 possible congeners of tetrachlorodibenzo-p-dioxin [9]. Toxicity equivalency factors (TEFs) have been developed by EPA relating the toxicities of other PCDD and PCDF isomers to that of 2,3,7,8-TCDD [9]. The biochemical mechanisms leading to the toxic response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data suggest that an important role in the development of systemic toxicity resulting from exposure to these chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [9]. Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [9] Isomer Total TetraCDD 2,3,7,8-TCDD Other TCDDs Total PentaCDDs 2,3,7,8-PentaCDDs Other PentaCDDs Total HexaCDDs 2,3,7,8-HexaCDDs Other HexaCDDs Total HeptaCDDs 2,3,7,8-HeptaCDDs Other HeptaCDDs Total TetraCDFs 2,3,7,8-TetraCDF Other TetraCDFs Total PentaCDFs 2,3,7,8-PentaCDFs Other PentaCDFs Total HexaCDFs 2,3,7,8-HexaCDFs Other HexaCDFs Total HeptaCDFs 2,3,7,8-HeptaCDFs Other HeptaCDFs TEF 1 1 0.01 0.5 0.5 0.005 0.04 0.04 0.0004 0.001 0.001 0.00001 0.1 0.1 0.001 0.1 0.1 0.001 0.01 0.01 0.0001 0.001 0.001 0.00001 407 BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDF In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8-substituted PCDDs and PCDFs were the major compounds present in most sample extracts [5]. Results from limited epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-TCDD impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus) on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8-TCDD concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid-1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [7]. Based on limited information on isomer-specific analysis from animals at different trophic levels, it appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar congeners with the 2,3,7,8substituted positions [10]. PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined by the habitat and physiology of each species. With log Kow>5, exposure through ingestion of contaminated food becomes an important route for uptake in comparison to respiration of water [7]. The relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake Ontario was examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [7]. There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and single species exposure. Although there is variation in the actual log BCF values, in general, the algae and plants have the lowest BCF values, on the order of a few thousand. A value of 4.38 has been reported for the snail Physa sp. Crustacea and insect larva appear to have the next highest log BCF values, followed by several species of fish, with the highest log BCF value of 4.79 [10]. Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and 2,3,7,8-TCDF in water for 28 days resulted in adverse effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest dose of 0.038 ng/L resulted in significant mortality [11]. A number of biological effects have been reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental effects, and cardiovascular effects [10]. 408 Summary of Biological Effects Tissue Concentrations for 1,2,3,4,7,8-HexaCDF Species: Taxa Fishes Salmonids Wildlife Falco peregrinus, Peregrine falcon 3.2 ng/g (eggs) (n = 6) 11.4% eggshell thinning [12] F; Kola Peninsula, Russia 0.0045 [14] F Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Mustela vison, Mink Diet: 1 pg/g4 33 pg/g4 (liver) LOAEL; reduced kit body weights followed by reduced survival Reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female No BMF reported [13] 2 pg/g4 73 pg/g4 (liver) Log BMF = 1.70 L; BMF = lipidnormalized concentration in the liver divided by the lipidnormalized dietary concentration 3 pg/g4 130 pg/g4 (liver) Log BMF = 1.81 1 2 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 Not clear from reference if concentration is based on wet or dry weight. 409 BIOACCUMULATION SUMMARY References 1. 1,2,3,4,7,8-HexaCDF USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxicity equivalency factors (TEF). Crit. Rev. Toxicol. 21:51-88. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957-968. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8tetrachlorodibenzo-p-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055. U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: a synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85 (1.8). 37 pp. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of chlorinated dibenzo-p-dioxins and dibenzofurans (CDDs and CDFs) and 1989 update. EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum, Washington, DC. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.H. Peterman, D.L. Stalling, G.M. DeGraeve, J.J. Coyle, and W.J. Adams. 1988. Toxicity and bioconcentration of 2,3,7,8- 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 410 BIOACCUMULATION SUMMARY 1,2,3,4,7,8-HexaCDF tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout. Environ. Toxicol. Chem. 7:47-62. 12. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J/P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 13. 14. 411 412 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED DIBENZOFURANS Chemical Name (Common Synonyms): 1,2,3,7,8-PENTACHLORODIBENZOFURAN 1,2,3,7,8-PentaCDF CASRN: 57117-41-6 Chemical Characteristics Solubility in Water: No data [1] Log Kow: No data [3] Half-Life: No data [2] Log Koc: -- Human Health Oral RfD: No data [4] Critical Effect: -- Oral Slope Factor: No data [4] Carcinogenic Classification: -- Confidence: -- Wildlife Partitioning Factors: Partitioning factors for 1,2,3,7,8-pentaCDF in wildlife were not found in the studies reviewed. Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors of PCDDs and PCDFs through terrestrial wildlife; no information was available for 1,2,3,7,8-pentaCDF, specifically. Due to the toxicity, high Kow values, and highly persistent nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and biomagnify through the food web. PCDDs and PCDFs have been identified in fish and wildlife throughout the global aquatic and marine environments [5]. Studies conducted in Lake Ontario indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be significant between fish and fish-eating birds but not between fish and their food. When calculated for older predaceous fish such as lake-trout-eating young smelt, the log biomagnification factor (BMF) can equal 0.48. The log BMF from alewife to herring gulls in Lake Ontario was 1.51 for 2,3,7,8-TCDD [6]. EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds. 413 BIOACCUMULATION SUMMARY 1,2,3,7,8-PentaCDF Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and associated Wildlife [7] Sediment Concentration (pg/g dry wt.) Low Risk 50 60 0.7 2.5 6 21 High Risk to Sensitive Species 80 100 7 25 60 210 Water Concentration (pg/L) POC=0.2 0.6 0.008 0.07 1 0.08 0.7 POC=1.0 3.1 0.04 0.35 5 0.4 3.5 Organism Fish Mammalian Wildlife Avian Wildlife Fish Mammalian Wildlife Avian Wildlife Fish Concentration (pg/g) Note: POC - Particulate organic carbon Fish lipid of 8% and sediment organic carbon of 3% assumed where needed. For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used. Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and young) in sensitive species. High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and young of sensitive species. Aquatic Organisms Partitioning Factors: Partitioning factors for 1,2,3,7,8-pentaCDF in aquatic organisms were not found in the studies reviewed. Food Chain Multipliers: No specific food chain multipliers were identified for 1,2,3,7,8-pentaCDF. Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8TCDD does not appear to be significant between fish and their prey. Limited data for the base of the Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and forage fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the 2,3,7,8TCDD biotransformation by forage fish. BMFs greater than 1.0 might exist between some zooplankton species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates [7]. Toxicity/Bioaccumulation Assessment Profile The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased with increasing ring chlorination [5]. In general, the PCDDs and PCDFs exhibit relative inertness to acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical stability with increasing chlorination [8,5]. Because of their lipophilic nature, the PCDDs and PCDFs have been detected in fish, wildlife, and human adipose tissue, milk, and serum [5]. 414 BIOACCUMULATION SUMMARY 1,2,3,7,8-PentaCDF Each isomer has its own unique chemical and toxicological properties. The most toxic of the PCDD and PCDF isomers is 2,3,7,8-TCDD, one of the 22 possible congeners of tetrachlorodibenzo-p-dioxin [8]. Toxicity equivalency factors (TEFs) have been developed by the U.S. EPA relating the toxicities of other PCDD and PCDF isomers to that of 2,3,7,8-TCDD [9]. The biochemical mechanisms leading to the toxic response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data suggest that an important role in the development of systemic toxicity resulting from exposure to these chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects on body weight gain, thymic involution, and chloracnegenic response has been correlated with their binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [9]. Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [9] Isomer Total TetraCDD 2,3,7,8-TCDD Other TCDDs Total PentaCDDs 2,3,7,8-PentaCDDs Other PentaCDDs Total HexaCDDs 2,3,7,8-HexaCDDs Other HexaCDDs Total HeptaCDDs 2,3,7,8-HeptaCDDs Other HeptaCDDs Total TetraCDFs 2,3,7,8-TetraCDF Other TetraCDFs Total PentaCDFs 2,3,7,8-PentaCDFs Other PentaCDFs Total HexaCDFs 2,3,7,8-HexaCDFs Other HexaCDFs Total HeptaCDFs 2,3,7,8-HeptaCDFs Other HeptaCDFs TEF 1 1 0.01 0.5 0.5 0.005 0.04 0.04 0.0004 0.001 0.001 0.00001 0.1 0.1 0.001 0.1 0.1 0.001 0.01 0.01 0.0001 0.001 0.001 0.00001 In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8-substituted PCDDs and PCDFs were the major compounds present in most sample extracts [5]. Results from limited 415 BIOACCUMULATION SUMMARY 1,2,3,7,8-PentaCDF epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-TCDD impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus) on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8-TCDD concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid-1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [7]. Based on limited information on isomer-specific analysis from animals at different trophic levels, it appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar congeners with the 2,3,7,8substituted positions [10]. PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined by the habitat and physiology of each species. With log Kow>5, exposure through ingestion of contaminated food becomes an important route for uptake in comparison to respiration of water [7]. The relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake Ontario was examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [7]. There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and single species exposure. Although there is variation in the actual log BCF values, in general, the algae and plants have the lowest BCF values, on the order of a few thousand. A value of 4.38 has been reported for the snail Physa sp. Crustacea and insect larva appear to have the next highest BCF values, followed by several species of fish, with the highest log BCF value of 4.78 [10]. Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest dose of 0.038 ng/l resulted in significant mortality [11]. A number of biological effects have been reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental effects, and cardiovascular effects [10]. 416 Summary of Biological Effects Tissue Concentrations for 1,2,3,7,8-PentaCDF Species: Taxa Fishes Salmonids 0.013 [15] F Concentration, Units in1: Sediment Water Tissue (Sample Type) Toxicity: Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Wildlife Falco peregrinus, Peregrine falcon 4.0 ng/g (eggs) (n = 6) 11.4% eggshell thinning [13] F; Kola Peninsula, Russia Haliaeetus leucocephalus, Bald eagle chicks Powell River site: ~160 A hepatic cytochrome ng/kg lipid weight basis P4501A crossreactive (yolk sac) protein (CYP1A) was induced nearly six-fold Reference site: ~30 in chicks from Powell ng/kg lipid weight basis River site compared to (yolk sac) the reference (p<0.05). No significant concentration-related effects were found for morphological, physiological, or histological parameters. [12] F; southern coast of British Columbia; eggs were collected from nests and hatched in the lab; ~ indicates value was taken from a figure. 417 418 Species: Taxa Mustela vison, Mink Sediment Diet: 1 pg/g4 2 pg/g4 4 pg/g4 1 2 Summary of Biological Effects Tissue Concentrations for 1,2,3,7,8-PentaCDF Concentration, Units in1: Water Tissue (Sample Type) 1 pg/g4 (liver) Toxicity: Effects LOAEL; reduced kit body weights followed by reduced survival Reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [14] Comments3 L 2 pg/g4 (liver) 2 pg/g4 (liver) Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 Not clear from reference if concentration is based on wet or dry weight. BIOACCUMULATION SUMMARY References 1. 1,2,3,7,8-PentaCDF USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxicity equivalency factors (TEF). Cri. Rev. Toxicol. 21:51-88. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957-968. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8tetrachlorodibenzo-p-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055. U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85 (1.8). 37 pp. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of chlorinated dibenzo-p-dioxins and dibenzofurans (CDDs and CDFs) and 1989 update. EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum, Washington, DC. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.H. Peterman, D.L. Stalling, G.M. DeGraeve, J.J. Coyle, and W.J. Adams. 1988. Toxicity and bioconcentration of 2,3,7,8- 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 419 BIOACCUMULATION SUMMARY 1,2,3,7,8-PentaCDF tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout. Environ. Toxicol. Chem. 7:47-62. 12. Elliott, J.E., R.J. Norstrom, A. Lorenzen, L.E. Hart, H. Philibert, S.W. Kennedy, J.J. Stegeman, G.D. Bellward, and K.M. Cheng. 1995. Biological effects of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls in bald eagle (Haliaeetus leucocephalus) chicks. Environ. Toxicol. Chem. 15(5):782-793. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 13. 14. 15. 420 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED DIBENZOFURANS Chemical Name (Common Synonyms): 2,3,4,7,8-PENTACHLORODIBENZOFURAN 2,3,4,7,8-PentaCDF CASRN: 57117-31-4 Chemical Characteristics Solubility in Water: 0.24 g/L [1] Log Kow: No data [4], 6.92 [2] Half-Life: No data [2,3] Log Koc: 6.80 L/kg organic carbon Human Health Oral RfD: No data [5] Critical Effect: -- Oral Slope Factor: No data [5] Carcinogenic Classification: -- Confidence: -- Wildlife Partitioning Factors: Partitioning factors for 2,3,4,7,8-pentaCDF in wildlife were not found in the studies reviewed. Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors of PCDDs and PCDFs through terrestrial wildlife; no information was available for 2,3,4,7,8-pentaCDF, specifically. Due to the toxicity, high Kow values, and highly persistent nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and biomagnify through the food web. PCDDs and PCDFs have been identified in fish and wildlife throughout the global aquatic and marine environments [6]. Studies conducted in Lake Ontario indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be significant between fish and fish-eating birds but not between fish and their food. When calculated for older predaceous fish such as lake-trout-eating young smelt, the biomagnification factor (BMF) can equal 3. The BMF from alewife to herring gulls in Lake Ontario was 32 for 2,3,7,8-TCDD [7]. Log BMFs of 1.73 to 1.74 were determined for mink [18]. EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds. 421 BIOACCUMULATION SUMMARY 2,3,4,7,8-PentaCDF Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated Wildlife [8] Fish Concentration (pg/g) Sediment Concentration Low Risk 50 60 0.7 2.5 6 21 High Risk to Sensitive Species 80 100 7 25 60 210 Water Concentration (pg/L) POC=0.2 POC=1.0 0.6 0.008 0.07 1 0.08 0.7 3.1 0.04 0.35 5 0.4 3.5 Organism Fish Mammalian Wildlife Avian Wildlife Fish Mammalian Wildlife Avian Wildlife Note: POC - Particulate organic carbon Fish lipid of 8% and sediment organic carbon of 3% assumed where needed. For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used. Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and young) in sensitive species. High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and young of sensitive species. Aquatic Organisms Partitioning Factors: In one study, the BSAF for carp collected from a reservoir in central Wisconsin was 0.28. The log BCF for goldfish measured during a laboratory exposure of 120 hours was 4.48 Food Chain Multipliers: No specific food chain multipliers were identified for 2,3,4,7,8-pentaCDF. Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8TCDD does not appear to be significant between fish and their prey. Limited data for the base of the Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and forage fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the 2,3,7,8TCDD biotransformation by forage fish. BMFs greater than 1.0 might exist between some zooplankton species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates [8]. Toxicity/Bioaccumulation Assessment Profile The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased with increasing ring chlorination [6]. In general, the PCDDs and PCDFs exhibit relative inertness to acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical stability with increasing chlorination [6,9]. Because of their lipophilic nature, the PCDDs and PCDFs have been detected in fish, wildlife, and human adipose tissue, milk, and serum [6]. 422 BIOACCUMULATION SUMMARY 2,3,4,7,8-PentaCDF Each isomer has its own unique chemical and toxicological properties. The most toxic of the PCDD and PCDF isomers is 2,3,7,8-TCDD, one of the 22 possible congeners of tetrachlorodibenzo-p-dioxin [8]. Toxicity equivalency factors (TEFs) have been developed by the EPA relating the toxicities of other PCDD and PCDF isomers to that of 2,3,7,8-TCDD [10]. The biochemical mechanisms leading to the toxic response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data suggest that an important role in the development of systemic toxicity resulting from exposure to these chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression of toxicity of 2,3,7,8-TCDD-related compounds, including cleft palate formation, liver damage, effects on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [10]. Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [10] Isomer Total TetraCDD 2,3,7,8-TCDD Other TCDDs Total PentaCDDs 2,3,7,8-PentaCDDs Other PentaCDDs Total HexaCDDs 2,3,7,8-HexaCDDs Other HexaCDDs Total HeptaCDDs 2,3,7,8-HeptaCDDs Other HeptaCDDs Total TetraCDFs 2,3,7,8-TetraCDF Other TetraCDFs Total PentaCDFs 2,3,7,8-PentaCDFs Other PentaCDFs Total HexaCDFs 2,3,7,8-HexaCDFs Other HexaCDFs Total HeptaCDFs 2,3,7,8-HeptaCDFs Other HeptaCDFs TEF 1 1 0.01 0.5 0.5 0.005 0.04 0.04 0.0004 0.001 0.001 0.00001 0.1 0.1 0.001 0.1 0.1 0.001 0.01 0.01 0.0001 0.001 0.001 0.00001 In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8-substituted PCDDs and PCDFs were the major compounds present in most sample extracts [6]. Results from limited 423 BIOACCUMULATION SUMMARY 2,3,4,7,8-PentaCDF epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-TCDD impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus) on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8-TCDD concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid-1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [8]. Based on limited information on isomer-specific analysis from animals at different trophic levels, it appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar congeners with the 2,3,7,8substituted positions [11]. PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined by the habitat and physiology of each species. With log Kow>5, exposure through ingestion of contaminated food becomes an important route for uptake in comparison to respiration of water [8]. The relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake Ontario was examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [8]. There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and single species exposure. Although there is variation in the actual log BCF values, in general, the algae and plants have the lowest BCF values, on the order of a few thousand. A value of 4.38 has been reported for the snail Physa sp. Crustacea and insect larva appear to have the next highest BCF values, followed by several species of fish, with the highest log BCF value of 4.79 [11]. Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest dose of 0.038 ng/L resulted in significant mortality [12]. A number of biological effects have been reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental effects, and cardiovascular effects [11]. 424 Summary of Biological Effects Tissue Concentrations for 2,3,4,7,8-PentaCDF Species: Taxa Fishes Carassius auratus, Goldfish 2.69/2.5 ng/g4 (whole body) 4.48 [14] L; fish were exposed for 120 hr; exposure water contained fly ash extract; concentrations were measured in water, but data were not presented Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Reference Comments3 Source: Cyprinus carpio, Carp 8 pg/g4 4.4 pg/g4 0.28 [13] F; Petenwell Reservoir, central Wisconsin; BSAF based on 8% tissue lipid content and 3.1% sediment organic carbon Salmonids 0.095 [19] F Wildlife Falco peregrinus, Peregrine falcon 27 ng/g (eggs) (n = 6) 11.4% eggshell thinning [17] F; Kola Peninsula, Russia 425 426 Species: Taxa Haliaeetus leucocephalus, Bald eagle chicks Sediment Summary of Biological Effects Tissue Concentrations for 2,3,4,7,8-PentaCDF Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Powell River site: ~800 ng/kg lipid weight basis (yolk sac) Reference site: ~100 ng/kg lipid weight basis (yolk sac) A nearly 6-fold increase in hepatic cytochrome P4501A crossreactive protein (CYP1A) was induced in chicks from Powell River site compared to the reference (p<0.05). No significant concentrationrelated effects were found for morphological, physiological, or histological parameters. Ability to Accumulate2: Log BCF Log BAF BSAF Reference [15] Comments3 F; southern coast of British Columbia; eggs were collected from nests and hatched in the lab; ~ indicates value was taken from a figure. Source: Summary of Biological Effects Tissue Concentrations for 2,3,4,7,8-PentaCDF Species: Taxa Ardea herodias, Great blue heron chicks Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Nicomekl site: <2 ng/kg (egg) (n = 11) Vancouver site: 3318.5 ng/kg (egg) (n = 12) Depression of growth compared to Nicomekl site. Presence of edema. Depression of growth compared to Nicomekl site. Presence of edema. Ability to Accumulate2: Log BCF Log BAF BSAF Reference [16] Comments3 L; eggs were collected from three British Columbia colonies with different levels of contamination and incubated in the laboratory Source: Crofton site: 337.6 ng/kg (egg) (n = 6) 427 428 Species: Taxa Mustela vison, Mink Sediment Diet: 4 pg/g4 6 pg/g4 14 pg/g4 1 2 Summary of Biological Effects Tissue Concentrations for 2,3,4,7,8-PentaCDF Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 170 pg/g4 (liver) LOAEL; reduced kit body weights followed by reduced survival Reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female No BMF reported Ability to Accumulate2: Log BCF Log BAF BSAF Reference [18] Comments3 L; BMF = lipidnormalized concentration in the liver divided by the lipid-normalized dietary concentration Source: 320 pg/g4 (liver) Log BMF = 1.74 490 pg/g4 (liver) Log BMF = 1.73 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 Not clear from reference if concentration is based on wet or dry weight. BIOACCUMULATION SUMMARY References 1. 2,3,4,7,8-PentaCDF USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals Vol. II, Polynuclear aromatic hydrocarbons, polychlorinated dioxins and dibenzofurans. Lewis Publishers, Boca Raton, FL. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxicity equivalency factors (TEF). Cri. Rev. Toxicol. 21:51-88. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957-968. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8-tetrachlorodibenzop-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055. U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: a synoptic review. U.S. Fish and Wildl. Serv. Biol. Rep. 85 (1.8). 37 pp. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of chlorinated dibenzo-p-dioxins and dibenzofurans (CDDs and CDFs) and 1989 update. EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum, Washington, DC. 2. 3. 4. 5. 6. 7. 8. 9. 10. 429 BIOACCUMULATION SUMMARY 11. 2,3,4,7,8-PentaCDF Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.H. Peterman, D.L. Stalling, G.M. DeGraeve, J.J. Coyle, and W.J. Adams. 1988. Toxicity and bioconcentration of 2,3,7,8tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout. Environ. Toxicol. Chem. 7:47-62. Kuehl, D.W., P.M. Cook, A.R. Batterman, D. Lothenbach, and B.C. Butterworth. 1987. Bioavailability of polychlorinated dibenzo-p-dioxins and dibenzofurans from contaminated Wisconsin River sediment to carp. Chemosphere 16(4):667-679. Sijm, D.T.H.M., H. Wever, and A. Opperhuizen. 1993. Congener-specific biotransformation and bioaccumulation of PCDDs and PCDFs from fly ash in fish. Environ. Toxicol. Chem. 12:18951907. Elliott, J.E., R.J. Norstrom, A. Lorenzen, L.E. Hart, H. Philibert, S.W. Kennedy, J.J. Stegeman, G.D. Bellward, and K.M. Cheng. 1995. Biological effects of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls in bald eagle (Haliaeetus leucocephalus) chicks. Environ. Toxicol. Chem. 15(5):782-793. Hart, L.E., K.M. Cheng, P.E. Whitehead, R.M. Shah, R.J. Lewis, S.R. Ruschkowski, R.W. Blair, D.C. Bennett, S.M. Bandiera, R.J.Norstrom, and G.D. Bellward. 1991. Dioxin contamination and growth and development in great blue heron embryos. J. Toxicol. Environ. Health 32:331344. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J/P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 12. 13. 14. 15. 16. 17. 18. 19. 430 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED DIBENZOFURANS Chemical Name (Common Synonyms): 2,3,7,8-TETRACHLORODIBENZOFURAN 2,3,7,8-TCDF CASRN: 51207-31-9 Chemical Characteristics Solubility in Water: No data [1], 0.42 g/L [2] Log Kow: No data [4], 6.53 [2] Half-Life: No data [3] Log Koc: -- Human Health Oral RfD: No data [5] Critical Effect: -- Oral Slope Factor: No data [5] Carcinogenic Classification: -- Confidence: -- Wildlife Partitioning Factors: Partitioning factors for 2,3,7,8-TCDF in wildlife were not found in the studies reviewed. Food Chain Multipliers: Limited information was found reporting on specific biomagnification factors of PCDDs and PCDFs through terrestrial wildlife; no information was available for 2,3,7,8-TCDF, specifically. Due to the toxicity, high Kow values, and highly persistent nature of the PCDDs and PCDFs, they possess a high potential to bioaccumulate and biomagnify through the food web. PCDDs and PCDFs have been identified in fish and wildlife throughout the global aquatic and marine environments [6]. Studies conducted in Lake Ontario indicated that biomagnification of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) appears to be significant between fish and fish-eating birds but not between fish and their food. When calculated for older predaceous fish such as lake-trout-eating young smelt, the biomagnification factor (BMF) can equal 3. The BMF from alewife to herring gulls in Lake Ontario was 32 for 2,3,7,8-TCDD [7]. A log BMF of -0.40 was determined for mink [2]. EPA has developed risk-based concentrations of 2,3,7,8-TCDD in different media that present low and high risk to fish, mammalian, and avian wildlife. These concentrations were developed based on toxic effects of 2,3,7,8-TCDD and its propensity to bioaccumulate in fish, mammals, and birds. 431 BIOACCUMULATION SUMMARY 2,3,7,8-TCDF Environmental Concentrations Associated With 2,3,7,8-TCDD Risk to Aquatic Life and Associated Wildlife [8] Sediment Concentration (pg/g dry wt.) Low Risk 50 60 0.7 2.5 6 21 High Risk to Sensitive Species 80 100 7 25 60 210 Water Concentration (pg/L) POC=0.2 0.6 0.008 0.07 1 0.08 0.7 POC=1.0 3.1 0.04 0.35 5 0.4 3.5 Organism Fish Mammalian Wildlife Avian Wildlife Fish Mammalian Wildlife Avian Wildlife Fish Concentration (pg/g) Note: POC - Particulate organic carbon Fish lipid of 8% and sediment organic carbon of 3% assumed where needed. For risk to fish, BSAF of 0.3 used; for risk to wildlife, BSAF of 0.1 used. Low risk concentrations are derived from no-effects thresholds for reproductive effects (mortality in embryos and young) in sensitive species. High risk concentrations are derived from TCDD doses expected to cause 50 to 100% mortality in embryos and young of sensitive species. Aquatic Organisms Partitioning Factors: In one study, steady-state BSAFs for invertebrates exposed to 2,3,7,8-TCDF in the laboratory ranged from about 0.3 to 0.7. The BSAF for carp collected from a reservoir in central Wisconsin was 0.06. Food Chain Multipliers: No specific food chain multipliers were identified for 2,3,7,8-TCDF. Food chain multiplier information was only available for 2,3,7,8-TCDD. Biomagnification of 2,3,7,8-TCDD does not appear to be significant between fish and their prey. Limited data for the base of the Lake Ontario lake trout food chain indicated little or no biomagnification between zooplankton and forage fish. BMFs based on fish consuming invertebrate species are probably close to 1.0 because of the 2,3,7,8TCDD biotansformation by forage fish. BMFs greater than 1.0 might exist between some zooplankton species and their prey due to the lack of 2,3,7,8-TCDD biotransformation in invertebrates [8]. Toxicity/Bioaccumulation Assessment Profile The polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) each consist of 75 isomers that differ in the number and position of attached chlorine atoms. The PCDDs and PCDFs are polyhalogenated aromatic compounds and exhibit several properties common to this group of compounds. These compounds tend to be highly lipophilic and the degree of lipophilicity is increased with increasing ring chlorination [6]. In general, the PCDDs and PCDFs exhibit relative inertness to acids, bases, oxidation, reduction, and heat, increasing in environmental persistence and chemical stability 432 BIOACCUMULATION SUMMARY 2,3,7,8-TCDF with increasing chlorination [9,6]. Because of their lipophilic nature, the PCDDs and PCDFs have been detected in fish, wildlife, and human adipose tissue, milk, and serum [6]. Each isomer has its own unique chemical and toxicological properties. The most toxic of the PCDD and PCDF isomers is one of the 22 possible congeners of tetrachlorodibenzo-p-dioxin [9]. Toxicity equivalency factors (TEFs) have been developed by EPA relating the toxicities of other PCDD and PCDF isomers to that of 2,3,7,8-TCDD [10]. The biochemical mechanisms leading to the toxic response resulting from exposure to PCDDs and PCDFs are not known in detail, but experimental data suggest that an important role in the development of systemic toxicity resulting from exposure to these chemicals is played by an intracellular protein, the Ah receptor. This receptor binds halogenated polycyclic aromatic molecules, including PCDDs and PCDFs. In several mouse strains, the expression of toxicity of 2,3,7,8TCDD-related compounds, including cleft palate formation, liver damage, effects on body weight gain, thymic involution, and chloracnegenic response, has been correlated with their binding affinity for the Ah receptor, and with their ability to induce several enzyme systems [10]. Toxicity Equivalency Factors (TEF) for PCDD and PCDF Isomers [10] Isomer Total TetraCDD 2,3,7,8-TCDD Other TCDDs Total PentaCDDs 2,3,7,8-PentaCDDs Other PentaCDDs Total HexaCDDs 2,3,7,8-HexaCDDs Other HexaCDDs Total HeptaCDDs 2,3,7,8-HeptaCDDs Other HeptaCDDs Total TetraCDFs 2,3,7,8-TetraCDF Other TetraCDFs Total PentaCDFs 2,3,7,8-PentaCDFs Other PentaCDFs Total HexaCDFs 2,3,7,8-HexaCDFs Other HexaCDFs Total HeptaCDFs 2,3,7,8-HeptaCDFs Other HeptaCDFs TEF 1 1 0.01 0.5 0.5 0.005 0.04 0.04 0.0004 0.001 0.001 0.00001 0.1 0.1 0.001 0.1 0.1 0.001 0.01 0.01 0.0001 0.001 0.001 0.00001 433 BIOACCUMULATION SUMMARY 2,3,7,8-TCDF In natural systems, PCDDs and PCDFs are typically associated with sediments, biota, and the organic carbon fraction of ambient waters [7]. Congener-specific analyses have shown that the 2,3,7,8-substituted PCDDs and PCDFs were the major compounds present in most sample extracts [6]. Results from limited epidemiology studies are consistent with laboratory-derived threshold levels to 2,3,7,8-TCDD impairment of reproduction in avian wildlife. Population declines in herring gulls (Larus argentatus) on Lake Ontario during the early 1970s coincided with egg concentrations of 2,3,7,8-TCDD and related chemicals expected to cause reproductive failure based on laboratory experiments (2,3,7,8-TCDD concentrations in excess of 1,000 pg/g). Improvements in herring gull reproduction through the mid-1980s were correlated with declining 2,3,7,8-TCDD concentrations in eggs and lake sediments [8]. Based on limited information on isomer-specific analysis from animals at different trophic levels, it appears that at higher trophic levels, i.e., fish-eating birds and fish, there is a selection of the planar congeners with the 2,3,7,8substituted positions [11]. PCDDs and PCDFs are accumulated by aquatic organisms through exposure routes that are determined by the habitat and physiology of each species. With log Kow>5, exposure through ingestion of contaminated food becomes an important route for uptake in comparison to respiration of water [8]. The relative contributions of water, sediment, and food to uptake of 2,3,7,8-TCDD by lake trout in Lake Ontario was examined by exposing yearling lake trout to Lake Ontario smelt and sediment from Lake Ontario along with water at a 2,3,7,8-TCDD concentration simulated to be at equilibrium with the sediments. Food ingestion was found to contribute approximately 75 percent of total 2,3,7,8-TCDD [8]. There have been a number of bioconcentration studies of 2,3,7,8-TCDD using model ecosystem and single species exposure. Although there is variation in the actual log BCF values, in general, the algae and plants have the lowest BCF values, on the order of a few thousand. A value of 4.38 has been reported for the snail Physa sp. Crustacea and insect larva appear to have the next highest BCF values, followed by several species of fish, with the highest log BCF value of 4.79 [11]. Exposure of juvenile rainbow trout to 2,3,7,8-TCDD and -TCDF in water for 28 days resulted in adverse effects on survival, growth, and behavior at extremely low concentrations. A no-observed-effects concentration (NOEC) for 2,3,7,8-TCDD could not be determined because the exposure to the lowest dose of 0.038 ng/L resulted in significant mortality [12]. A number of biological effects have been reported in fish following exposure to 2,3,7,8-TCDD including enzyme induction, immunological effects, wasting syndrome, dermatological effects, hepatic effects, hematological effects, developmental effects, and cardiovascular effects [11]. 434 Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDF Species: Taxa Invertebrates Nereis virens, Sandworm 3346 pg/g dw n=6 11251 pg/g dw (whole body) ~0.25 [13,14] L; 180-day exposure; sediment TOC was 57 mg/kg; ~ indicates approximate value, as numbers were estimated from bar graphs Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Macoma nasuta, Clam 3346 pg/g dw n=6 51.46.8 pg/g dw ~0.7 [13,14] L; 120-day exposure; sediment TOC was 57 mg/kg; ~ indicates approximate value, as numbers were estimated from bar graphs Palaemonetes pugio, 3346 pg/g Grass shrimp dw n=6 58.87.7 pg/g dw ~0.6 [13,14] L; 28-day exposure; sediment TOC was 57 mg/kg; ~ indicates approximate value, as numbers were estimated from bar graphs 435 436 Species: Taxa Fishes Oncorhynchus mykiss (Salmo gairdneri), Rainbow trout Sediment Oncorhynchus mykiss, Rainbow trout Salmonids Cyprinus carpio, Carp 182 pg/g4 Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDF Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Water exposure 0.41 ng/L Water exposure 1.79 ng/L 2.5 g/kg4 28-Day NOEC (growth) [15] L 7.6 g/kg4 28-Day NOEC (survival) [15] 0.00009 mg/kg (whole Growth, NOED body)4 [15] L 0.047 [22] F 28 pg/g4 0.06 [16] F; Petenwell Reservoir, central Wisconsin; BSAF based on 8% tissue lipid content and 3.1% sediment organic carbon Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDF Species: Taxa Wildlife Falco peregrinus, Peregrine falcon 30 ng/g (eggs) (n=6) 11.4% eggshell thinning [19] F; Kola Peninsula, Russia Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Haliaeetus leucocephalus, Bald eagle chicks Powell River site: A hepatic 8,000 ng/kg lipid cytochrome weight basis (yolk sac) P4501A crossreactive protein Reference site: 500 (CYP1A) was ng/kg lipid weight basis induced nearly (yolk sac) 6-fold in chicks from Powell River site compared to the reference (p<0.05). No significant concentrationrelated effects were found for morphological, physiological, or histological parameters. [17] F; southern coast of British Columbia; eggs were collected from nests and hatched in the laboratory. 437 438 Species: Taxa Ardea herodias, Great blue heron chicks Sediment Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDF Concentration, Units in1: Water Nicomekl site: <1 ng/kg (egg) n = 11 Vancouver site: 114.3 Depression of ng/kg (egg) n = 12 growth compared to Nicomekl site. Presence of edema. Crofton site: 82.3 ng/kg (egg) n = 6 Depression of growth compared to Nicomekl site. Presence of edema. Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [18] Comments3 L; eggs were collected from three British Columbia colonies with different levels of contamination and incubated in the laboratory Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDF Species: Taxa Aix sponsa, Wood duck Concentration, Units in1: Sediment Water pg/g (eggs): % eggs hatched: Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference [20] Comments3 F; central Arkansas; egg TEFs, hatching success, and duckling production were negatively correlated; clutch size was similar among wetland Sites 1-3, 9, 17, and 58 km downstream from point source of contamination, respectively, and Site 4, which was 111 km away on a separate drainage; duckling abnormalities were also noted; threshold range of reduced productivity was >20-50 ppt TEF Site 1 geometric mean: 47 (9.7 SE) 26 (2.4-244) Site 2 geometric mean: 62 (10.1 SE) 11 (1.4-60) Site 3 geometric mean: 79 (3.8 SE) 5.4 (<1-22) Site 4 geometric mean: 93 (3.4 SE) 0.3 (<1-3.2) 439 440 Species: Taxa Mustela vison, Mink Sediment Diet: 2 pg/g5 4 pg/g5 12 pg/g5 1 2 3 4 5 Summary of Biological Effects Tissue Concentrations for 2,3,7,8-TCDF Concentration, Units in1: Water 2 pg/g5 (liver) LOAEL; reduced kit body weights followed by reduced survival Reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF No BMF reported BSAF Source: Reference [21] Comments3 L; BMF= lipidnormalized concentration in the liver divided by the lipidnormalized dietary concentration 2 pg/g5 (liver) Log BMF= -0.4 3 pg/g5 (liver) Log BMF= -0.4 Concentration units based on wet weight, unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations. noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. Not clear from reference if concentration is based on wet or dry weight. 440 BIOACCUMULATION SUMMARY References 1. 2,3,7,8-TCDF USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. II, Polynuclear aromatic hydrocarbons, polychlorinated dioxins and dibenzofurans. Lewis Publishers, Boca Raton, FL. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxicity equivalency factors (TEF). Crit. Rev. Toxicol. 21:51-88. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957-968. USEPA. 1993. Interim report on data and methods for assessment of 2,3,7,8tetrachlorodibenzo-p-dioxin risks to aquatic life and associated wildlife. EPA/600/R-93/055. U.S. Environmental Protection Agency, Office of Research and Development, Washington, DC. Eisler, R. 1986. Dioxin hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85 (1.8). 37 pp. USEPA. 1989. Interim procedures for estimating risks associated with exposure to mixtures of chlorinated dibenzo-p-dioxins and dibenzofurans (CDDs and CDFs) and 1989 update. EPA/625/3-89/016. U.S. Environmental Protection Agency, Risk Assessment Forum, Washington, DC. Cooper, K.R. 1989. Effects of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans on aquatic organisms. Rev. Aquat. Sci. 1:227-242. 441 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. BIOACCUMULATION SUMMARY 12. 2,3,7,8-TCDF Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.H. Peterman, D.L. Stalling, G.M. DeGraeve, J.J. Coyle, and W.J. Adams. 1988. Toxicity and bioconcentration of 2,3,7,8tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout. Environ. Toxicol. Chem. 7:47-62. Pruell, R.J., N.I. Rubinstein, B.K. Taplin, J.A. LiVolsi, and R.D. Bowen. 1993. Accumulation of polychlorinated organic contaminants from sediment by three benthic marine species. Arch. Environ. Contam. Toxicol. 24:290-297. Rubinstein, N.I., R.J. Pruell, B.K. Taplin, J.A. LiVolsi, and C.B. Norwood. 1990. Bioavailability of 2,3,7,8-TCDD, 2,3,7,8-TCDF and PCBs to marine benthos from Passaic River sediments. Chemosphere 20(7-9):1097-1102. Mehrle, P.M., D.R. Buckler, E.E. Little, L.M. Smith, J.D. Petty, P.H. Peterman, D.L. Stalling, G.M. DeGraeve, J.J. Coyle, and W.J. Adams. 1988. Toxicity and bioconcentration of 2,3,7,8tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout. Environ. Toxicol. Chem. 7:47-62. Kuehl, D.W., P.M. Cook, A.R. Batterman, D. Lothenbach, and B.C. Butterworth. 1987. Bioavailability of polychlorinated dibenzo-p-dioxins and dibenzofurans from contaminated Wisconsin River sediment to carp. Chemosphere 16(4):667-679. Elliott, J.E., R.J. Norstrom, A. Lorenzen, L.E. Hart, H. Philibert, S.W. Kennedy, J.J. Stegeman, G.D. Bellward, and K.M. Cheng. 1995. Biological effects of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls in bald eagle (Haliaeetus leucocephalus) chicks. Environ. Toxicol. Chem. 15(5):782-793. Hart, L.E., K.M. Cheng, P.E. Whitehead, R.M. Shah, R.J. Lewis, S.R. Ruschkowski, R.W. Blair, D.C. Bennett, S.M. Bandiera, R.J. Norstrom, and G.D. Bellward. 1991. Dioxin contamination and growth and development in great blue heron embryos. J. Toxicol. Environ. Health 32:331344. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. White, D.H., and J.T. Seginak. 1994. Dioxins and furans linked to reproductive impairment in wood duck. J.Wildl. Manage. 58(1):100-106. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 442 BIOACCUMULATION SUMMARY FLUORANTHENE Chemical Category: POLYNUCLEAR AROMATIC HYDROCARBON (high molecular weight) Chemical Name (Common Synonyms): FLUORANTHENE Chemical Characteristics Solubility in Water: 0.20-0.26 mg/L [1] Half-Life: 140-440 days, aerobic soil die-away test [2] Log Koc: 5.03 L/kg organic carbon CASRN: 206-44-0 Log Kow: 5.12 [3] Human Health Oral RfD: 4 x 10-2 mg/kg-day [4] Confidence: Low, uncertainty factor = 3000 Critical Effect: Nephropathy, increased liver weights, hematological alterations, and clinical effects Oral Slope Factor: No data [4] Carcinogenic Classification: D [4] Wildlife Partitioning Factors: Partitioning factors for fluoranthene in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for fluoranthene in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: The water quality criterion tissue level (WQCTL) for fluoranthene, which is calculated by multiplying the water quality chronic value (16 g/L) by the BCF (1741.8), is 27,869 g/kg [5]. Salinity and particle size of the sediment had no or very little effect on survival of three amphipod species during exposure to fluoranthene [6]. Log BCFs ranged from -0.92 for Lumbriculues variegatus [16] to 0.63 for Hyallela azteca [9]. Log BAFs of 0.36 to 0.56 were calculated for the midges Chironomus tentans [24]. Food Chain Multipliers: Food chain multipliers for fluoranthene in aquatic organisms were not found in the literature. Toxicity/Bioaccumulation Assessment Profile Polynuclear aromatic hydrocarbons, (PAHs) are readily metabolized and excreted by fish and invertebrates [7], affecting bioaccumulation kinetics and equilibrium tissue residues. According to McCarty et al. [8], the toxic body residue of individual PAHs in tissues ranged from 513 to 4,248 mg/kg. 443 BIOACCUMULATION SUMMARY FLUORANTHENE The concentration of 382 ppb produced biological effects in environmental samples (Puget Sound). The LC50 values for fluoranthene using freshwater amphipods ranged from 11.7 to 150.3 nmol/g dry weight [9]. Fluoranthene is relatively toxic to aquatic species (10-day EC50 = 2.3 to 7.4 g/L for H. azteca, 10-day EC50 = 3.0 to 8.7 g/L C. tentans). Its toxicity increased 6- to 17-fold under UV light [10]. H. azteca accumulated up to 1,131 g/g of fluoranthene during 10 days of exposure to the LC50 concentration. Below the toxic level, the concentration of fluoranthene in amphipod tissue reached 200 to 400 g/g within the first 48 hours and then dropped to 100 g/g [9]. During 30-day bioaccumulation exposures, fed H. azteca accumulated significantly more fluoranthene than unfed organisms [11]. Furthermore, in exposures in which food was added, organisms gained weight and reproduced, even when sediment was dosed with concentrations approximately 20 to 90 times the 10-day LC50 value, with sediment containing levels of organic carbon comparable to the Suedel et al. [12] experiments. These data suggest that animals in fed exposures preferentially consumed the food, given the relatively high accumulation of compound in animal tissue. Mortality due to narcosis, the mechanism thought to be responsible for PAH toxicity, ranged from 2 to 8 mol/g for acute responses and 0.2 to 0.8 mol/g for chronic exposures in fish [13]. In the study by Harkey et al. [11], animals accumulated up to 1.4 mol/g after 30 days in the highest (1,004 nmol/g) sediment concentration. Previous water-only exposures [14] predicted that a body burden of 5.6 mol/g in H. azteca needs to be attained to produce 50 percent mortality. The body burden of fluoranthene associated with 50 percent mortality of Leptocheirus plumulosus was 0.69 mol/g wet wt, which is lower than the predicted critical body residue for nonpolar narcotic compounds [15]. 444 Summary of Biological Effects Tissue Concentrations for Fluoranthene Species: Taxa Invertebrates Lumbriculus variegatus, Oligochaete worm Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF -0.92 Log BAF BSAF Source: Reference Comments3 [16] F Nereis succinea, Polychaete worm 0.218 g/g OC 0.436 g/g OC 0.48 g/g OC 1.4 g/g OC 4.55 g/g OC 10.2 g/g OC 19.5 g/g OC 30.1 g/g OC 9.20 g/g lipid [17] F 2.55 g/g lipid 35.6 g/g lipid 4.80 g/g lipid 3.79 g/g lipid 14.1 g/g lipid 24.0 g/g lipid Nereis virens, Sand worm -0.096 or -0.10 -0.02 0.52 0.36 [18] F Modiolus demissus, Northern horse mussel [19] F Mytilus edulis, Blue mussel -0.44 [19] F 445 446 Species: Taxa Mytilus edulis, Mussel Sediment Crassostrea virginica, Eastern oyster Crassostrea virginica, Eastern oyster Summary of Biological Effects Tissue Concentrations for Fluoranthene Concentration, Units in1: Water Tissue (Sample Type) 627 mg/kg (whole body)4 1.9 mg/kg (whole body)4 Toxicity: Effects Physiological, ED50 Physiological, ED50 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [27] L; 50% reduction in feeding rate [28] L; 50% reduction in feeding, clearance rate and tolerance to aerial exposure [28] L; elevated activity of superoxide dimutase (SOD) [28] L; inhibition of superoxide dimutase (SOD) and catalase activity [28] L; reduced gametogenesis, reproductive success rate [30] L; thickness of digestive epithelium 0.112 mg/kg (whole body) 1.5 mg/kg (whole body)4 Physiological, LOED Physiological, LOED 1.5 mg/kg (whole body)4 62 mg/kg (whole body)4 Reproduction, LOED Morphology, LOED -0.15 -0.28 [19] F Summary of Biological Effects Tissue Concentrations for Fluoranthene Species: Taxa Macoma balthica, Baltic macoma Concentration, Units in1: Sediment Water 0.218 g/g OC 0.436 g/g OC 0.48 g/g OC 1.4 g/g OC 4.55 g/g OC 10.2 g/g OC 19.5 g/g OC 30.1 g/g OC Toxicity: Tissue (Sample Type) Effects 7.62 g/g lipid 5.12 g/g lipid Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [17] F 96.2 g/g lipid 7.48 g/g lipid 5.73 g/g lipid 17.2 g/g lipid Macoma nasuta, Clam 0.58 0.39 -0.26 -0.05 [18] F Mercenaria mercenaria, Northern quahog Mya arenaria, Softshell [19] F -0.08 [19] F Daphnia magna, Cladoceran 9 g/L 77 nM/g 0.51 [20] L 447 448 Species: Taxa Hyalella azteca, Amphipod Sediment Hyalella azteca, Amphipod Summary of Biological Effects Tissue Concentrations for Fluoranthene Concentration, Units in1: Water 14.2 g/L Toxicity: Tissue (Sample Type) Effects 25.6 g/g 44.0 g/g 44.8 g/g 65.7 g/g 78.4 g/g 169 g/g 320 g/g 458 g/g 751 g/g 350 g/g 531 g/g 714 g/g 800 g/g 1,192 g/g 644 g/g 898 g/g 1,074 g/g 1,199 g/g 1,248 g/g 307 g/g 363 g/g 515 g/g 517 g/g 763 g/g 815 g/g 852 g/g 566 g/g 825 g/g 829 g/g 1,035 g/g 1,171 g/g 1,213 g/g 1,310 g/g Ability to Accumulate2: Log BCF 0.51 0.54 0.54 0.56 0.57 0.59 0.55 0.57 0.54 0.60 0.59 0.58 0.62 0.61 0.61 0.59 0.60 0.56 0.58 0.58 0.59 0.60 0.63 0.63 0.60 0.61 0.61 0.61 0.61 0.63 0.60 0.61 0.58 Log BAF BSAF Source: Reference Comments3 [9] L 56.7 g/L [9] L 86.2 g/L [9] L 100.8 g/L 41.5 g/L 98.3 g/L Summary of Biological Effects Tissue Concentrations for Fluoranthene Species: Taxa Hyalella azteca, Amphipod Concentration, Units in1: Sediment Water 168.0 g/L Tissue (Sample Type) 855 g/g 884 g/g 971 g/g 988 g/g 1,265 g/g 1,375 g/g 746 g/g 896 g/g 1,208 g/g 1,302 g/g 1,382 g/g 1,445 g/g 1,581 g/g Day 1: 160 nmol/g Day 2: 140 nmol/g Day 3: 60 nmol/g Day 10: 90 nmol/g Day 17: 110 nmol/g Day 30: 120 nmol/g Day 1: 900 nmol/g Day 2: 1,050 nmol/g Day 3: 850 nmol/g Day 10: 700 nmol/g Day 17: 700 nmol/g Day 30:800 nmol/g Day 1: 1,000 nmol/g Day 2: 850 nmol/g Day 3: 950 nmol/g Day 10: 700 nmol/g Day 17: 800 nmol/g Day 30: 1,100 nmol/g Toxicity: Effects Ability to Accumulate2: Log BCF 0.61 0.59 0.60 0.58 0.59 0.60 0.57 0.58 0.57 0.59 0.59 0.58 0.57 Log BAF BSAF Source: Reference Comments3 184.7 g/L 158 nmol/g 634 nmol/g no mortality no mortality no mortality no mortality no mortality no mortality no mortality no mortality no mortality no mortality 40% mortality 40% mortality no mortality no mortality no mortality no mortality 35% mortality 65% mortality [11] L Hyalella azteca, Amphipod 1267 nmol/g 449 450 Species: Taxa Leptocheirus plumulosus, Amphipod Sediment Pontoporeia hoyi, Amphipod Rhepoxynius abronius, Amphipod Chironomus riparius, 4,040 g/kg Midge Chironomus tentans Midge 377 g/goc 1,853 ug/goc Summary of Biological Effects Tissue Concentrations for Fluoranthene Concentration, Units in1: Water 38 g/L or 187 nmol/L 36 nmol/L 77 nmol/L 143 nmol/L 285 nmol/L Toxicity: Tissue (Sample Type) Effects 0.68 mol/g 50% mortality Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [15] L; critical body residue 78 nmol/g 226 nmol/g 369 nmol/g 721 nmol/g 100% survival 100% survival 93% survival 46% survival [21] L 60 ng/g 5 ng/mL 270 ng/g 4 ng/mL 1000 ng/g 4 ng/mL 21.3 nmol/g 41.1 nmol/g 119.5 nmol/g 327.0 nmol/g 12.09 mg/kg 14.3 g/L 14.50 mg/kg 25.11 mg/kg 2,000 ng/g 2,000 ng/g 1,000 ng/g 7-12 nmol/g 28-57 nmol/g 68-149 nmol/g 71-614 nmol/g 23% mortality 52% mortality 92% mortality 1.04-1.36 [14] L [22] L 181,000 g/kg [23] L 4 g/L 1,220 g/goc 12 g/L 19 g/L 9,593 ng/g (larvae) 22 ng/g (adult) 33,455 ng/g (larvae) 257 ng/g (adult) 72,790 ng/g (larvae) 9,810 ng/g (adult) 0.36 0.36 0.41 0.41 0.56 0.56 [24] L Summary of Biological Effects Tissue Concentrations for Fluoranthene Species: Taxa Fishes Oncorhynchus mykiss, Rainbow trout Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 379 g/g, liver Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [25] F Cyprinus carpio, Common carp 183 mg/kg (liver) Physiological, NOED [29] L; no significant increase in erod enzyme and P450 1a protein content L Lepomis macrochirus, Bluegill 4,040 g/kg 600 g/kg [23] Pleuronectes vetulus, 320-25,000 English sole ng/g 1 2 3 4 <6.6 ng/g liver <2.6 ng/g muscle [26] F Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. 451 BIOACCUMULATION SUMMARY FLUORANTHENE References 1. IARC monographs, 1972-present, 1983, 32:356. (Cited in: USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Neff, J.M. 1995. Water quality criterion tissue level approach for establishing tissue residue criteria for chemicals. Report to U.S. Environmental Protection Agency. DeWitt, T.H., R.C. Swartz, and J.O. Lamberson. 1989. Measuring the acute toxicity of estuarine sediments. Environ. Toxicol. Chem. 8:1035-1048. Stegeman, J.J., and P.J. Kloepper-Sams. 1987. Cytochrome P-450 isozymes and monooxygenase activity in aquatic animals. Environ. Health Perspect. 71:87-95. McCarty, L.S., D. MacKay, A.D. Smith, G.W. Ozburn, and D.G. Dixon. 1992. Residue-based interpretation of toxicity and bioconcentration QSARs from aquatic bioassays: Neutral narcotic organics. Environ. Toxicol. Chem. 11:917-930. Kane-Driscoll, S., G.A. Harkey, and P.G. Landrum. 1997. Accumulation and toxicokinetics of flouranthene in sediment bioessays with freshwater amphipods. Environ. Toxicol. Chem. 16:742753. Brooke, L. 1994. Memorandum to Walter Berry. Summary of results of acute and chronic exposures of fluoranthene without and with ultraviolet (UV) light to various freshwater organisms. December 3. Harkey, G.A., S. Kane-Driscoll, and P. Landrum. 1997. Effect of feeding in 30-day bioaccumulation assays using Hyalella azteca in fluoranthene-dosed sediment. Environ. Toxicol. Chem. 16:762-769. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 452 BIOACCUMULATION SUMMARY 12. FLUORANTHENE Suedel, B.C., J.H. Rodgers, Jr., and P.A. Clifford. 1993. Bioavailability of fluoranthene in freshwater sediment toxicity tests. Environ. Toxicol. Chem. 12:155-165. McCarty, L.S., and D. MacKay. 1993. Enhancing ecotoxicological modeling and assessment. Environ. Sci. Technol. 27:1719-1728. Landrum, P.F., B.J. Eadie, and W.R. Faust. 1991. Toxicokinetics and toxicity of a mixture of sediment-associated polycyclic aromatic hydrocarbons to the amphipod Diporeia spp. Environ. Toxicol. Chem. 10:35-46. Driscoll S.K., L. Schaffnerm, and R. Dickhut. 1996. Bioaccumulation and critical body burden of fluoranthene in estuarine amphipods. Abstract, 17th Annual Meeting Society of Environmental Toxicology and Chemistry, Washington DC, November 17-21, 1996. Ankley, G.T., P.M. Cook, A.R. Carlson, D.J. Call, J.A. Swenson, H.F. Corcoran, and R.A. Hoke. 1990. Bioaccumulation of PCBs from sediments by oligochaetes and fishes. Can. J. Fish. Aquatic Sci. 49:2080-2085. Foster, G.D., and D.A. Wright. 1988. Unsubstituted polynuclear aromatic hydrocarbons in sediments, clams, and clam worms from Chesapeake Bay. Mar. Pollut. Bull. 19:459-465. Brannon, J.M., C.B. Price, F.J. Reilly, Jr., J.C. Pennington, and V.A. McFarland. 1993. Effects of sediment organic carbon on distribution of radiolabeled fluoranthene and PCBs among sediment, interstitial water and biota. Bull. Environ. Contam. Toxicol. 51:873-880. NOAA. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Technical Memorandum NOS OMA 52. National Oceanic and Atmospheric Administration, Office of Oceanography and Marine Assessment, Rockville, MD. Newsted, J.L., and J.P. Giesy. 1987. Predictive models for photoinduced acute toxicity of polycyclic aromatic hydrocarbons to Daphnia magna Strauss (Cladocera, Crustacea). Environ. Toxicol. Chem. 6:445-461. Eadie, B.J., P.F. Landrum, and W. Faust. 1982. Polycyclic aromatic hydrocarbons in sediments, pore water, and the amphipod Pontoporeia hoyi from Lake Michigan. Chemosphere 11:847-857. De Witt, T.H., R.J. Ozretich, R.C. Swartz, J.O. Lamberson, D.W. Schults, G.R. Ditsworth, J.K.P. Jones, L. Hoselton, and L.M. Smith. 1992. The influence of organic matter quality on the toxicity and partitioning of sediment-associated fluoranthene. Environ. Toxicol. Chem. 11:197-208. Clements, W.H., J.T. Oris, and T.E. Wissing. 1994. Accumulation and food chain transfer of fluoranthene and benzo[a]pyrene in Chironomus riparius and Lepomis macrochirus. Arch. Environ. Cont. Toxicol. 26:261-266. Bell, H.E. 1995. Bioaccumulation and photoinduced toxicity of fluoranthene at different lifestages of Chironomus tentans. Master's thesis, University of Wisconsin-Madison. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 453 BIOACCUMULATION SUMMARY 25. FLUORANTHENE Gerhart, E.H., and R.M. Carlson. 1978. Hepatic mixed-function oxidase activity in rainbow trout exposed to several polycyclic aromatic compounds. Environ. Res. 17:284-295. Malins, D.C., M.M. Krahn, M.S. Myers, L.D. Rhodes, D.W. Brown, C.A. Krone, B.N. McCain, and S.L. Chan. 1985. Toxic chemicals in sediments and biota from a creosote-polluted harbor: Relationships with hepatic neoplasms and other hepatic lesions in English sole (Parophrys vetulus). Carcinogenesis 6:1463-1469. Donkin, P., J. Widdows, S.V. Evans, C.M. Worrall, and M. Carr. 1989. Quantitative structure-activity relationships for the effect of hydrophobic organic chemicals on rate of feeding by mussels (Mytilus edulis). Aquat. Toxicol. 14:277-294. Eertman, R.H.M., C.L. Groenink, B. Sandee, and H. Hummel. 1995. Response of the blue mussel Mytilus edulis L. Following exposure to PAHs or contaminated sediment. Mar. Environ. Res. 39:169-173. Van Der Weidern, M.E.J., F.H.M Hanegraaf, M.L., Eggens, M., Celander, W. Seinen and M. Ven Den Berg. 1994. Temporal induction of cytochrome P450 1a in the mirror carp (Cyprinus carpio) after administration of several polycyclic aromatic hydrocarbons. Environ. Toxicol. Chem. 13:797-802 Weinstein, J.E. 1997. Fluoranthene-induced histological alterations in oysters, Crassostrea virginica: Seasonal field and laboratory studies. Mar. Environ. Res. 43(3):201-218. 26. 27. 28. 29. 30. 454 BIOACCUMULATION SUMMARY HEPTACHLOR Chemical Category: PESTICIDE (ORGANOCHLORINE) Chemical Name (Common Synonyms): HEPTACHLOR CASRN: 76-44-8 Chemical Characteristics Solubility in Water: 0.03 mg/L [1] Log Kow: 6.26 [3] Half-Life: No data [2] Log Koc: 6.15 L/kg organic carbon Human Health Oral RfD: 5 x 10-4 mg/kg/day [4] Confidence: Low, uncertainty factor = 300 [4] Critical Effect: Liver weight increases in rats; benign and malignant liver tumors in mice Oral Slope Factor: 4.5 x 10+0 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4] Wildlife Partitioning Factors: Partitioning factors for heptachlor in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for heptachlor in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Log BCFs ranged from 5.30 to 11.70 for invertebrates and log BCFs for fishes ranged from 3.87 to 19.34. Food Chain Multipliers: Food chain multipliers (FCMs) for trophic level 3 aquatic organisms were 20.8 (all benthic food web), 1.6 (all pelagic food web), and 12.7 (benthic and pelagic food web). FCMs for trophic level 4 aquatic organisms were 45.8 (all benthic food web), 3.4 (all pelagic food web), and 21.7 (benthic and pelagic food web) [18]. 455 BIOACCUMULATION SUMMARY Toxicity/Bioaccumulation Assessment Profile HEPTACHLOR Hepatchlor is the most widely used insecticide in the organochlorine class [5]. Heptachlor is resistent to degradation and, therefore, persistent in the environment. Heptachlor acute toxic effects in animals are principally due to hyperexcitation in the nervous system and death is frequently ascribed to respiratory failure [5]. Heptachlor is relatively toxic to aquatic invertebrates. The acute toxicity of heptachlor ranged from 0.11 g/L (96-h LC50) for Penaeus duorarum to 1.5 g/L (96-h LC50) for Crassostrea virginica [6]. Fish are also relatively sensitive to heptachlor. The 96-h LC50 values based on the exposure of sheepshead minnows, pinfish, and spot were 3.68, 3.77, and 0.85g/L, respectively [6]. Laboratory bioaccumulation exposures with spot showed that heptachlor was metabolized to heptachlor epoxide at all concentrations tested [7]. After 3 days of exposure, heptachlor concentrations averaged 52 percent of total residues. At the end of depuration the relative amount of heptachlor decreased to 10 percent, while heptachlor epoxide increased to 44 percent. Cooking (baking, charbroiling, canning, pan frying and deep frying) reduced the heptachlor contents by an average 40 percent in chinook salmon fillets [8]. Heptachlor was among chemicals responsible for the widespread decline of peregrine falcon populations [9]. Heptachlor concentrations above 4 mg/kg in brain is critical and could be associated with falcon mortality, while a concentration above 1.5 mg/kg in eggs was associated with lower reproductive success of falcons [9]. Birds whose life cycle depends on the aquatic environment contained higher residues of heptachlor in their tissue than the seed eaters [10]. The tissues of red-winged blackbirds and tree swallows demonstrated geographically distinct levels of chlorinated hydrocarbons including heptachlor [11]. The spatial variation of heptachlor concentration in eggs correlated significantly with those found in sediments. Higher concentrations of heptachlor in chick tissue rather than in eggs pointed to a local source of uptake through their diet [11]. 456 Summary of Biological Effects Tissue Concentrations for Heptachlor Species: Taxa Invertebrates Concentration, Units in1: Sediment Water Toxicity: Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Tissue (Sample Type) Effects Crassostrea virginica, Eastern oyster 0.08 g/L 0.4 g/L 0.91 g/L 4 g/L 14 g/L 0.43 g/g 3.1 g/g 7.7 g/g 18 g/g 55 g/g 30% shell reduction 28% shell reduction 33% shell reduction 78% shell reduction 98% shell reduction 7.59 [6] [6] [6] [6] [6] L L L L L Crassostrea virginica, Eastern oyster 0.021 mg/kg (whole body)4 0.016 mg/kg (whole body)4 0.11 mg/kg (whole body)4 Growth, ED18 Growth, NOED [6] [6] L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; no effect on feeding activity Mercenaria mercenaria, Quahog clam Mya arenaria, Soft shell clam Penaeus duorarum, Pink shrimp 0.04 g/L 0.2 g/L Behavior, NOED [15] 1.3 mg/kg (whole body)4 0.01 g/g 0.033 g/g Behavior, NOED [15] L; no effect on feeding activity 5% mortality 82% mortality 5.30 [6] [6] L L 457 458 Species: Taxa Palaemonetes vulgaris, Grass shrimp Sediment Fishes Oncorhynchus tshawytscha, Chinook salmon Cyprinodon variegatus, Sheepshead minnow Cyprinodon variegatus, Sheepshead minnow Cyprinodon variegatus, Sheepshead minnow Summary of Biological Effects Tissue Concentrations for Heptachlor Concentration, Units in1: Water 0.13 g/L 0.44 g/L 2 g/L 5 g/L Toxicity: Ability to Accumulate2: Log BCF 11.70 Log BAF BSAF Source: Reference Comments3 [6] [6] [6] [6] L L L L Tissue (Sample Type) Effects 0.062 ug/g 0.2 g/g 0.97 g/g 3.6 g/g 6% mortality 13% mortality 70% mortality 95% mortality 27.9 g/kg in eggs Rearing mortality [12] F 2.7 g/L 3.3 g/L 3.6 g/L 4.0 g/L 20 g/g 33 g/g 34 g/g 85 g/g 15% mortality 50% mortality 50% mortality 60% mortality 3.87 [6] [6] [6] [6] L L L L 8.8 g/L 133 g/g 85% mortality 4.33 [6] L 4.5 mg/kg (whole body)4 4.8 mg/kg (whole body)4 10.4 mg/kg (whole body)4 Behavior, LOED Behavior, LOED Behavior, NA [16] [16] [16] L; decreased swimming activity L; hyperkinetic behavior L; hyperkinetic behavior Summary of Biological Effects Tissue Concentrations for Heptachlor Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [16] [16] L; 39% decline in survivorship L; no effect on liver, kidney, pancreas, digestive tract histopathology L; no effect on liver, kidney, pancreas, digestive tract histopathology L; no effect on liver, kidney, pancreas, digestive tract histopathology L; no significant effect on mortality L; no significant effect on mortality L; increase in fry mortality L; decreased egg production of adults L; decreased fertility of eggs produced by adults L; exposure media 65% heptachlor (technical grade) L L L L L L Tissue (Sample Type) Effects 10.4 mg/kg (whole body)4 4.5 mg/kg (whole body)4 4.8 mg/kg (whole body)4 10.4 mg/kg (whole body)4 4.5 mg/kg (whole body)4 4.8 mg/kg (whole body)4 16 mg/kg (whole body)4 26 mg/kg (whole body)4 211 mg/kg (whole body)4 0.022 mg/kg (whole body)4 Mortality, NA Cellular, NOED Cellular, NOED [16] Cellular, NOED [16] Mortality, NOED Mortality, NOED Mortality, LOED Reproduction, LOED Reproduction, LOED Mortality, ED5 [16] [16] [17] [17] [17] [6] Leiostomus xanthurus, Spot 0.14 g/L 0.26 g/L 0.58 g/L 1.03 g/L 0.5 g/L 0.65 g/L 0.34 g/g 0.64 g/g 1.73 g/g 3.70 g/g 1.5 g/g 2.3 g/g 19.34 25% mortality 35% mortality [7] [7] [7] [7] [7] [7] 459 460 Species: Taxa Leiostomus xanthurus, Spot Sediment Lagodon rhomboides, Pinfish Wildlife Falco peregrinus anatum, American peregrine Falco peregrinus pealei, Peale's peregrine Falco peregrinus tundrius, Arctic peregrine Summary of Biological Effects Tissue Concentrations for Heptachlor Concentration, Units in1: Water Toxicity: Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [6] [6] [6] L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) L; exposure media 65% heptachlor (technical grade) Tissue (Sample Type) Effects 2.6 mg/kg (whole body)4 0.01 mg/kg (whole body)4 0.01 mg/kg (whole body)4 5.7 mg/kg (whole body)4 Mortality, ED40 Mortality, NOED Mortality, NOED Mortality, NOED [6] 0.018-2.070 mg/kg in eggs (1965-1986) [9] F 0.015-0.049 mg/kg in eggs (1965-1986) [9] F 0.087-2.710 mg/kg in eggs (1965-1987) [9] F Summary of Biological Effects Tissue Concentrations for Heptachlor Species: Taxa Martes americana, Marten Concentration, Units in1: Sediment Water Toxicity: Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [14] F Tissue (Sample Type) Effects 0.3 - 4.5 g/kg in muscle; 9.1 - 12.7 g/kg in liver Martes pennanti, Fishers 1 - 5.7 g/kg in muscle 5.8 -17g/kg in liver [14] F Quail 0.86 - 1.15 mg/kg [13] F Woodcock 0.86 - 1.29 mg/kg [13] F Agelaius phoeniceus, Red-winged blackbird 0.2 ng/g 0.2 ng/g 0.2 ng/g 4.1 ng/g in eggs 3.7 ng/g in eggs 4.3 ng/g in eggs 1.05 2.34 1.71 [11] [11] [11] F F F 1 2 3 4 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. 461 BIOACCUMULATION SUMMARY References 1. HEPTACHLOR Kenag, E.E.; Ecotoxicol and Environ. Safety 4:26-38. 1980. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated, and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January. Coats, J.R. 1990. Mechanisms of toxic action and structure-activity relationships for organochlorine and synthetic pyrethroid insecticides. Environ. Health Perspect. 87:255-262. Schimmel, S.C., J.M. Patrick, Jr., and J. Forester. 1976. Heptachlor toxicity and uptake by several estuarine organisms. J. Toxicol. Environ. Health 1:955-965. Schimmel, S.C., J.M. Patrick, Jr., and J. Forester. 1976. Heptachlor: Uptake, depuration, retention and metabolism by spot, Leiostomus xanthurus. J. Toxicol. Environ. Health 2:169-178. Zabik, M.E., M.J. Zabik, A.M. Booren, M. Nettles, J.H. Song, R. Welch, and H. Humphrey. 1995. Pesticides and total polychlorinated biphenyls in chinook salmon and carp harvested from the Great Lakes: Effects of skin-on and skin-off processing and selected cooking methods. J. Agric. Food Chem. 43:993-1001. Peakall, D.B., D.G. Noble, and J.E. Elliott. 1990. Environmental contaminants in Canadian peregrine falcons, Falco peregrinus: A toxicological assessment. Can. Field-Naturalist 104:244254. Frank, R., and H.E. Braun. 1990. Organochlorine residues in bird species collected dead in Ontario 1972-1988. Bull. Environ. Contam. Toxicol. 44:932-939. Bishop, C.A., M.D. Koster, A.A. Chek, D.J.T. Hussell, and K. Jock. 1995. Chlorinated hydrocarbons and mercury in sediments, red-winged blackbirds (Agelaius phoeniceus) and tree swallows (Tachycineta bicolor) from wetlands in the Great Lakes-St. Lawrence River basin. Environ. Toxicol. Chem. 14:491-501. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 462 BIOACCUMULATION SUMMARY 12. HEPTACHLOR Giesy, J.P., J. Newsted, and D.L. Garling. 1986. Relationships between chlorinated hydrocarbon concentrations and rearing mortality of chinook salmon (Oncorhynchus tshawytscha) eggs from Lake Michigan. J. Great Lakes Res. 12:82-98. Blevins, R.D. 1979. Organochlorine pesticides in gamebirds of eastern Tennessee. Water Air Soil Pollut. 11:633-657. Steeves, T., M. Strickland, R. Frank, J. Rasper, and C.W. Douglas. 1991. Organochlorine insecticide and polychlorinated biphenyl residues in martens and fishers from the Algonquin region of South-Central Ontario. Bull. Environ. Contam. Toxicol. 46:368-373. Butler, P.A. 1971. Influence of pesticides on marine ecosystems. Proc. Royal Soc. London, Series B 177:321-329. Goodman, L.R., D.J. Hansen, J.A. Couch, and J. Forester. 1977. Effects of heptachlor and toxaphene on laboratory-reared embryos and fry of the sheepshead minnow. Proceedings, 30th Annual Conference, Southeastern Association of Fish and Wildlife Agencies, pp. 192-202. Hansen, D.J., and P.R. Parrish. 1977. Suitability of sheepshead minnows (Cyprinodon variegatus) for life-cycle toxicity tests. In Aquatic toxicology and hazard evaluation, ed. F.L. Mayer et al., pp. 117-126. American Society of Testing and Materials, Philadelphia, PA. USEPA. 1998. Ambient water quality criteria derivation methodology human health: Technical support document. Final draft. EPA-822-B-98-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 13. 14. 15. 16. 17. 18. 463 464 BIOACCUMULATION SUMMARY Chemical Category: METAL Chemical Name (Common Synonyms): LEAD LEAD CASRN: 7439-92-1 Chemical Characteristics Solubility in Water: Insoluble [1] Log Kow: Half-Life: Not applicable, stable [1] Log Koc: Human Health Oral RfD: Not available [2] Confidence: Critical Effect: Changes in levels of certain blood enzymes, altered neurobehavioral development of children. (These changes may occur at blood lead levels so low as to be essentially without a threshold; therefore, the RfD workgroup determined that it was inappropriate to develop an RfD for inorganic lead.) Oral Slope Factor: Not available [2] Carcinogenic Classification: B2 [2] Wildlife Partitioning Factors: Partitioning factors for lead in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for lead in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Lead is most soluble in water and is bioavailable at low pH, low organic content, and low concentrations of calcium, iron, manganese, zinc, and cadmium. Lead is capable of forming insoluble metal sulfides and can easily complex with humic acid. The common forms of dissolved lead are lead sulfate, lead chloride, lead hydroxide, and lead carbonate, but the distribution of salts is highly dependent on the pH of the water. Most lead entering surface waters is precipitated in the sediment as carbonates or hydroxides [8]. Log BCFs of 5.15 (cladoceran) [12] and 3.56 (midge) [9] were reported in the literature. Food Chain Multipliers: Although methylated lead is rapidly taken out from the water, e.g., by rainbow trout, there is no evidence of biomagnification in the aquatic environment [6 and 7]. 465 BIOACCUMULATION SUMMARY Toxicity/Bioaccumulation Assessment Profile LEAD The amount of bioavailable lead in sediment is controlled, in large part, by the concentration of acid volatile sulfides (AVS) and organic mater [3,4,5]. Lead is accumulated by aquatic organisms equally from water and through dietary exposure [6]. In the sediments, a portion of lead can be transformed to trimethyllead and tetraalkyllead compounds through chemical and microbial processes. The organolead compounds are much more toxic to aquatic organisms than are the inorganic lead compounds [7]. Bioaccumulation of organolead compounds is rapid and high; these compounds concentrate in the fatty tissues of aquatic organisms. Babukutty and Chacko [8] and others reported a strong correlation between soft tissue concentration of lead in worms and that in the exchangeable fraction of the sediment. In vertebrates, lead is known to modify the structure and function of the kidney, bone, central nervous system, and the hematopoietic system. It produces adverse biochemical, histopathological, neuropsychological, ferotoxic, teratogenic, and reproductive effects. Inhibition of blood delta aminolevulnic acid dehydratase (ALAD), an enzyme critical in heme formation, has been observed as a result of exposure to lead in a variety of fish, invertebrates, and birds. At sufficiently high concentrations, lead effects are manifested in aquatic organisms as reduced growth, fecundity, and survivorship [9]. 466 Summary of Biological Effects Tissue Concentrations for Lead Species: Taxa Eichhornia crassipes, Water hyacinth Concentration, Units in1: Sediment Water Tissue (Sample Type) 4.4 mg/kg (leaf) 4.6 mg/kg (leaf) 135 mg/kg (root) 259 mg/kg (root) 598 mg/kg (root) 1030 mg/kg (root) 6 mg/kg (stem) 16.6 mg/kg (stem) 48.8 mg/kg (stem) 70.6 mg/kg (stem) 4.4 mg/kg (leaf) 4.6 mg/kg (leaf) 135 mg/kg (root) 259 mg/kg (root) 598 mg/kg (root) 1,030 mg/kg (root) 6 mg/kg (stem) 16.6 mg/kg (stem) 48.8 mg/kg (stem) 70.6 mg/kg (stem) 467 Toxicity: Effects Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Morphology, NOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference [20] [20] [20] [20] [20] [20] [20] [20] [20] [20] [20] [20] [20] [20] [20] [20] [20] [20] [20] [20] Comments3 L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on plant appearance L; no effect on plant appearance L; no effect on plant appearance L; no effect on plant appearance L; no effect on plant appearance L; no effect on plant appearance L; no effect on plant appearance L; no effect on plant appearance L; no effect on plant appearance L; no effect on plant appearance 468 Species: Taxa Invertebrates Invertebrates, field-collected Sediment Water Total SEM g/g g/g 679 569 113 62 99 55 86 50 38 19 14 4 365 g/g 138 g/g 375 g/g 297 g/g 283 g/g Tubificidae, Oligochaete worms Nereis diversicolor, 44 g/g Polychaete worm 154 g/g 35 g/g 21 g/g 299 g/g 287 g/g 359 g/g Dreissena polymorpha, Zebra mussel Summary of Biological Effects Tissue Concentrations for Lead Concentration, Units in1: Toxicity: Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 Tissue (Sample Type) Effects Filt Nonfilt g/L g/L <0.2 276 1.2 120 0.2 38 0.3 35 <0.2 9 0.4 24 Body 67 g/g 11 g/g 10 g/g 32 g/g 4 g/g 0.5 g/g 16.5 mg/g 3.7 mg/g 23.5 mg/g 35.8 mg/g 22.6 mg/g 5.9 g/g 4.4 g/g 3.4 g/g 0.7 g/g 5.8 g/g 4.9 g/g 3.5 g/g 200 mg/kg (whole body)6 200 mg/kg (whole body)6 30 mg/kg (whole body)6 2 mg/kg (whole body)6 Physiological, ED100 Mortality, LOED Physiological, LOED Mortality, NOED [15] F [14] F [10] F [21] [21] [21] [21] L; mussels stopped filtering L; increased mortality L; reduced filtration rate L; no effect on mortality Summary of Biological Effects Tissue Concentrations for Lead Species: Taxa Concentration, Units in1: Sediment Water Tissue (Sample Type) 4 mg/kg (whole body)6 6 mg/kg (whole body)6 30 mg/kg (whole body)6 2 mg/kg (whole body)6 4 mg/kg (whole body)6 6 mg/kg (whole body)6 ND4 (foot) ND (muscle) 5.8 g/g (visceral) 13.0 g/g (hepatopancreas) 18.8 g/g (gills) 13.9 g/g (mantle) 5.5 g/g (foot) 3.8 g/g (muscle) 6.9 g/g (visceral) 14.3 g/g (hepatopancreas) 36.0 g/g (gills) 33.3 g/g (mantle) Toxicity: Effects Mortality, NOED Mortality, NOED Mortality, NOED Physiological, NOED Physiological, NOED Physiological, NOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [21] L; no effect on mortality [21] [21] [21] [21] [21] L; no effect on mortality L; no effect on mortality L; no effect on filtration rate L; no effect on filtration rate L; no effect on filtration rate F Elliptio complanata, Freshwater mussel <0.9-28.8 g/g [16] <0.9-97.5 g/g 469 470 Species: Taxa Sediment <0.9-100.0 g/g Water Balanus crenatus, Barnacle Daphnia magna, Cladoceran Hyallela azteca, Amphipod Summary of Biological Effects Tissue Concentrations for Lead Concentration, Units in1: Toxicity: Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 Tissue (Sample Type) Effects ND (foot) ND (muscle) 6.0 g/g (visceral) 15.3 g/g (hepatopancreas) 35.4 g/g (gills) 35.6 g/g (mantle) 90 mg/kg (whole body)6 Behavior, NOED [23] L; regulation of metals endpoint - summer experiment L; 10% reduction in number of offspring L; lethal body burden after 21-day exposure L 1,880 mg/kg (whole body)6 5,040 mg/kg (whole body)6 3.3 g/L 2.6 g/L 11.6 g/L 8.8 g/L 12.6 g/L 24.0 g/L Total SEM Filt Nonfilt g/g g/g g/L g/L 679 569 <0.2 276 113 62 1.2 120 99 55 0.2 38 86 50 0.3 35 38 19 <0.2 9 14 4 0.4 24 5.8 g/g 7.1 g/g 15.8 g/g 19.2 g/g 30.0 g/g 20.9 g/g Body 7 g/g 7 g/g 6 g/g 2 g/g 6 g/g 0.4 g/g Reproduction, ED10 Mortality, ED50 [12] [12] 60% survival 65% survival 48% survival 31% survival 11% survival 4% survival [11] [15] F Summary of Biological Effects Tissue Concentrations for Lead Species: Taxa Hyalella azteca, Freshwater amphipod Concentration, Units in1: Sediment Water Tissue (Sample Type) 70 mg/kg (whole body)6 160 mg/kg (whole body)6 90 mg/kg (whole body)6 115 mg/kg (whole body)6 Toxicity: Effects Mortality, ED50 Mortality, ED50 Mortality, ED50 Mortality, ED50 Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [22] L; lethal body burden [22] [22] [22] L; lethal body burden L; lethal body burden L; lethal body burden Pontoporeia affiniss, Amphipod Total SEM g/g g/g 679 569 113 62 99 55 86 50 38 19 14 4 Chironomus riparius, Midge Chironomus gr. thummi, Midge 13.99 mg/kg 4 mg/kg (whole body)6 4 mg/kg (whole body)6 Filt Nonfilt Body g/L g/L <0.2 276 7 g/g 1.2 120 7 g/g 0.2 38 6 g/g 0.3 35 2 g/g <0.2 9 6 g/g 0.4 24 0.4 g/g 0.728 mg/L 2650 g/g Mortality, NOED Mortality, NOED [24] [24] [15] L; body burden estimated from graph L; body burden estimated from graph F 3.56 [9] L 12.80 mg/kg 16.22 mg/kg normal larvae deformed larvae [13] F 471 472 Species: Taxa Chironomus gr. thummi, Midge Fishes Salvelinus fontinalis, Brook trout Sediment Water Summary of Biological Effects Tissue Concentrations for Lead Concentration, Units in1: Toxicity: Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [13] L, 4th instar larvae Tissue (Sample Type) Effects 2.56 mg/kg Morphology, (whole body)6 NOED 24 mg/kg (gill) Behavior, LOED [19] 30 mg/kg (kidney) Behavior, LOED [19] 20 mg/kg (liver) Behavior, LOED [19] 3.2 mg/kg (red blood cells) 70 mg/kg (gill) 30 mg/kg (kidney) 25 mg/kg (liver) 4.02 mg/kg (whole body)6 4.02 mg/kg (whole body)6 70 mg/kg (gill) 30 mg/kg (kidney) Behavior, LOED [19] Development, LOED Development, LOED Development, LOED Development, LOED Growth, LOED Morphology, LOED Morphology, LOED [19] [19] [19] [19] [19] [19] [19] L; hyperactivity, erratic swimming, loss of equilibrium L; hyperactivity, erratic swimming, loss of equilibrium L; hyperactivity, erratic swimming, loss of equilibrium L; hyperactivity, erratic swimming, loss of equilibrium L; spinal deformities L; spinal deformities L; spinal deformities L; reduced embryo hatchability L; reduced weight gain L; darkening of caudal peduncle L; darkening of caudal peduncle Summary of Biological Effects Tissue Concentrations for Lead Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 25 mg/kg (liver) Morphology, LOED 4.02 mg/kg Morphology, (whole body)6 LOED 2.55 mg/kg Development, (whole body)6 NOED 1.6 mg/kg Development, (whole body)6 NOED 38 mg/kg (gill) Growth, NOED 70 mg/kg (gill) 60 mg/kg (gill) Growth, NOED Growth, NOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [19] L; darkening of caudal peduncle [19] L; deformed vertebral column [19] L; no effect on embryo hatchability [19] L; no effect on embryo hatchability [19] L; no effect on length or weight [19] L; no effect on growth [19] L; no effect on length or weight of first generation fish [19] L; no effect on length or weight of first generation fish [19] L; no effect on length or weight of first generation fish [19] L; no effect on length or weight [19] L; no effect on length or weight [19] L; no effect on growth [19] L; no effect on length or weight of first generation fish [19] L; no effect on length or weight of first generation fish 20 mg/kg (gill) Growth, NOED 6 mg/kg (gill) Growth, NOED 3.2 mg/kg (gonad) 43 mg/kg (kidney) 30 mg/kg (kidney) 100 mg/kg (kidney) Growth, NOED Growth, NOED Growth, NOED Growth, NOED 40 mg/kg (kidney) Growth, NOED 473 474 Species: Taxa Sediment Water Summary of Biological Effects Tissue Concentrations for Lead Concentration, Units in1: Toxicity: Tissue (Sample Type) Effects 8 mg/kg (kidney) Growth, NOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [19] L; no effect on length or weight of first generation fish [19] L; no effect on length or weight [19] L; no effect on growth [19] L; no effect on length or weight of first generation fish [19] L; no effect on length or weight of first generation fish [19] L; no effect on length or weight of first generation fish [19] L; no effect on length or weight [19] L; no effect on length or weight [19] L; no effect on length or weight of first generation fish [19] L; no effect on length or weight of first generation fish [19] L; no effect on length or weight of first generation fish [19] L; no effect on length or weight [19] L; no effect on weight gain 13.6 mg/kg (liver) 25 mg/kg (liver) 18 mg/kg (liver) Growth, NOED Growth, NOED Growth, NOED 16 mg/kg (liver) Growth, NOED 4 mg/kg (liver) Growth, NOED 0.6 mg/kg (muscle) 1.5 mg/kg (red blood cells) 4 mg/kg (red blood cells) 0.5 mg/kg (red blood cells) 0.2 mg/kg (red blood cells) 6 mg/kg (spleen) 2.55 mg/kg (whole body)6 Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Summary of Biological Effects Tissue Concentrations for Lead Species: Taxa Concentration, Units in1: Sediment Water Tissue (Sample Type) 1.6 mg/kg (whole body)6 2.55 mg/kg (whole body)6 1.6 mg/kg (whole body)6 38 mg/kg (gill) 70 mg/kg (gill) 60 mg/kg (gill) 20 mg/kg (gill) 6 mg/kg (gill) 3.2 mg/kg (gonad) 43 mg/kg (kidney) 30 mg/kg (kidney) 100 mg/kg (kidney) 40 mg/kg (kidney) 8 mg/kg (kidney) 13.6 mg/kg (liver) 25 mg/kg (liver) 18 mg/kg (liver) 16 mg/kg (liver) 4 mg/kg (liver) 475 Toxicity: Effects Growth, NOED Morphology, NOED Morphology, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [19] L; no effect on weight gain [19] [19] [19] [19] [19] [19] [19] [19] [19] [19] [19] [19] [19] [19] [19] [19] [19] [19] L; no effect on skeletal deformities L; no effect on skeletal deformities L; no effect on mortality L; no effect on mortality L; no effect on survival of first generation fish L; no effect on survival of first generation fish L; no effect on survival of first generation fish L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on survival of first generation fish L; no effect on survival of first generation fish L; no effect on survival of first generation fish L; no effect on mortality L; no effect on mortality L; no effect on survival of first generation fish L; no effect on survival of first generation fish L; no effect on survival of first generation fish 476 Species: Taxa Sediment Water Summary of Biological Effects Tissue Concentrations for Lead Concentration, Units in1: Tissue (Sample Type) 0.6 mg/kg (muscle) 1.5 mg/kg (red blood cells) 4 mg/kg (red blood cells) 0.5 mg/kg (red blood cells) 0.2 mg/kg (red blood cells) 6 mg/kg (spleen) 4.02 mg/kg (whole body)6 2.55 mg/kg (whole body)6 1.6 mg/kg (whole body)6 38 mg/kg (gill) 70 mg/kg (gill) Toxicity: Effects Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [19] L; no effect on mortality [19] L; no effect on mortality [19] [19] [19] [19] [19] [19] [19] [19] [19] L; no effect on survival of first generation fish L; no effect on survival of first generation fish L; no effect on survival of first generation fish L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on number of viable eggs produced L; no effect on number of viable eggs produced by second generation fish L; no effect on number of viable eggs produced L; no effect on number of viable eggs produced L; no effect on number of viable eggs produced L; no effect on number of viable eggs produced L; no effect on number of viable eggs produced 60 mg/kg (gill) 20 mg/kg (gill) 6 mg/kg (gill) 3.2 mg/kg (gonad) 43 mg/kg (kidney) [19] [19] [19] [19] [19] Summary of Biological Effects Tissue Concentrations for Lead Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 30 mg/kg (kidney) Reproduction, NOED 100 mg/kg (kidney) 40 mg/kg (kidney) 8 mg/kg (kidney) 13.6 mg/kg (liver) 25 mg/kg (liver) Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [19] L; no effect on number of viable eggs produced by second generation fish [19] L; no effect on number of viable eggs produced [19] L; no effect on number of viable eggs produced [19] L; no effect on number of viable eggs produced [19] L; no effect on number of viable eggs produced [19] L; no effect on number of viable eggs produced by second generation fish [19] L; no effect on number of viable eggs produced [19] L; no effect on number of viable eggs produced [19] L; no effect on number of viable eggs produced [19] L; no effect on number of viable eggs produced [19] L; no effect on number of viable eggs produced [19] L; no effect on number of viable eggs produced [19] L; no effect on number of viable eggs produced [19] L; no effect on number of viable eggs produced [19] L; no effect on number of viable eggs produced 18 mg/kg (liver) 16 mg/kg (liver) 4 mg/kg (liver) 0.6 mg/kg (muscle) 1.5 mg/kg (red blood cells) 4 mg/kg (red blood cells) 0.5 mg/kg (red blood cells) 0.2 mg/kg (red blood cells) 6 mg/kg (spleen) 477 478 Species: Taxa Pimephales promelas, Fathead minnow Sediment 107 g/g 365 g/g 138 g/g 241 g/g 375 g/g 508 g/g 297 g/g 377 g/g 283 g/g 286 g/g Water Pimephales promelas, Fathead minnow Pimephales promelas, Fathead minnow Summary of Biological Effects Tissue Concentrations for Lead Concentration, Units in1: Toxicity: Tissue (Sample Type) Effects 10.5 mg/g 5.7 mg/g 0.8 mg/g 0.9 mg/g 20.0 mg/g 13.6 mg/g 11.9 mg/g 19.5 mg/g 15.1 mg/g 9.3 mg/g 0.816 mg/kg (brain) Behavior, LOED Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [17] F [17] F [25] 0.451 mg/kg (brain) Behavior, LOED [25] 0.451 mg/kg (brain) Behavior, LOED [25] 44.2 mg/kg (whole body)6 Behavior, LOED [25] L; significant reduction in feeding rate and number of ineffective feeding behaviors with 1-day-old Daphnia L; significant reduction in number of ineffective feeding behaviors in lowest test concentration with 2day-old Daphnia L; significant reduction in feeding rate and number of ineffective feeding behaviors in lowest test concentration with 7-dayold Daphnia L; significant reduction in feeding rate and number of ineffective feeding behaviors with 1-day-old Daphnia Summary of Biological Effects Tissue Concentrations for Lead Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 26.2 mg/kg Behavior, LOED (whole body)6 Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [25] L; significant reduction in number of ineffective feeding behaviors in lowest test concentration with 2day-old Daphnia [25] L; significant reduction in feeding rate and number of ineffective feeding behaviors in lowest test concentration with 7-dayold Daphnia [25] L; significant reduction norepinephrine and serotonin levels in brain [25] L; significant reduction norepinephrine and serotonin levels in brain [25] L; no significant reduction in feeding rate and number of ineffective feeding behaviors with 1-day-old Daphnia [25] L; no significant reduction in number of ineffective feeding behaviors with 2day-old Daphnia [25] L; no significant reduction in feeding rate and number of ineffective feeding behaviors with 1-day-old Daphnia 26.2 mg/kg (whole body)6 Behavior, LOED 0.816 mg/kg (brain) Physiological, LOED Physiological, LOED Behavior, NOED 44.2 mg/kg (whole body)6 0.451 mg/kg (brain) 0.816 mg/kg (brain) Behavior, NOED 26.2 mg/kg (whole body)6 Behavior, NOED 479 480 Species: Taxa Sediment Water Wildlife Sterna hirundo, Common tern Sterna forsteri, Forster tern Sterna dougallii, Roseate tern Rynchops niger, Black skimmer Larus argentatus, Herring gull Summary of Biological Effects Tissue Concentrations for Lead Concentration, Units in1: Toxicity: Tissue (Sample Type) Effects 44.2 mg/kg Behavior, NOED (whole body)6 Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [25] L; no significant reduction in number of ineffective feeding behaviors with 2day-old Daphnia [25] L; no significant reduction norepinephrine and serotonin levels in brain [25] L; No significant reduction norepinephrine and serotonin levels in brain 0.451 mg/kg (brain) Physiological, NOED Physiological, NOED 26.2 mg/kg (whole body)6 247-389 ng/g (eggs) 912-1559 ng/g (feathers) 174 ng/g (eggs) 1527 ng/g (feathers) 318 ng/g (eggs) 2213 ng/g (feathers) 402-664 ng/g (eggs) 832-4091 ng/g (feathers) 1720-6743 ng/g (eggs) 1818-2101 ng/g (feathers) [18] F [18] F [18] F [18] F [18] F Summary of Biological Effects Tissue Concentrations for Lead Species: Concentration, Units in1: Water Tissue (Sample Type) 58.35-214.7 mg/kg dry wt (liver alive) 267.3 mg/kg dry wt (liver dead) 346-1,297.6 mg/kg dry wt (kidney alive) 1,901 mg/kg dry wt (kidney dead) Toxicity: Effects Cellular abnormalities increased with increasing tissue concentrations Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [26] L; dosage was ingested lead shot pellets Taxa Sediment Zenaida macroura, Mourning dove 1 2 3 4 5 6 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor.. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. ND = not detected. CBR = critical body residue. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. 481 BIOACCUMULATION SUMMARY References 1. LEAD Weast handbook of chemistry and physics, 68th edition, 1987-1988, B-99. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Di Toro, D.M., J.D. Mahony, D.J. Hansen, K.J. Scott, M.B. Hicks, S.M. Mayr, and M.S. Redmond. 1990. Toxicity of cadmium in sediments: The role of acid volatile sulfide. Environ. Toxicol. Chem. 9:1487-1502. Casas, A.M., and E.A. Crecelius. 1994. Relationship between acid volatile sulfide and the toxicity of zinc, lead and copper in marine sediments. Environ. Toxicol. Chem. 13:529-536. Kerndorff, H., and M. Schnitzer. 1980. Sorption of metals on humic acid. Geochim. Cosmochim. Acta 44:1701-1708. Woodward, D.F., W.G. Brumbaugh, A.J. DeLonay, E.E. Little, and C.E. Smith. 1994. Effects on rainbow trout fry of a metals-contaminated diet of benthic invertebrates from the Clark Fork River, Montana. Trans. Amer. Fish. Soc. 123:51-62. Hodson, P.V., D.M. Whittle, P.T.S. Wong, U. Borgmann, R.L. Thomas, Y.K. Chau, J.O. Nriagu, and D.J. Hallett. 1984. Lead contamination of the Great Lakes and its potential effects on aquatic biota. In Toxic contaminants in the Great Lakes, ed. J.O. Nriagu and M.S. Simmons, chapter 16: Advances in Environmental Sciences and Technology, Wiley and Sons, Toronto, Ontario. Babukutty, Y., and J. Chacko. 1995. Chemical partitioning and bioavailability of lead and nickel in an estuarine system. Environ. Toxicol. Chem. 14:427-434. Timmermans, K.R., W. Peeters, and M. Tonkes. 1992. Cadmium, zinc, lead, and copper in Chironomus riparius (Meigen) larvae (Diptera, Chironomidae): Uptake and effects. Hydrobiologia 241:119-134. 2. 3. 4. 5. 6. 7. 8. 9. 10. Bryan, G.W., and L.G. Hummerstone. 1971. Adaptation of the polychaete Nereis diversicolor to estuarine sediments containing high concentrations of heavy metals. Mar. Biol. Ass. 51:845-863. 11. Borgmann, U., W.O. Norwood, and C. Clarke. 1993. Accumulation, regulation and toxicity of copper, zinc, lead and mercury in Hyalella azteca. Hydrobiologia 259:79-89. 12. Enserink, E.L., J.L. Mass-Diepeveen, and C.J. Van Leeuwen. 1991. Combined effects of metals: An ecotoxicological evaluation. Water Res. 25:679-687. 482 BIOACCUMULATION SUMMARY LEAD 13. Janssens De Bisthoven, L.G., K.R. Timmermans, and F. Ollevier. 1992. The concentration of cadmium, lead, copper, and zinc in Chironomus gr. thummi larvae (Diptera, Chironomidae) with deformed versus normal antennae. Hydrobiologia 239:141-149. 14. Krantzberg, G. 1994. Spatial and temporal variability in metal bioavailability and toxicity of sediment from Hamilton Harbour, Lake Ontario. Environ. Toxicol. Chem. 13:1685-1698. 15. Ingersoll, C.G., W.G. Brumbaugh, F.J. Dwyer, and N. E. Kemble. 1994. Bioaccumulation of metals by Hyalella azteca exposed to contaminated sediments from the Upper Clark Fork River, Montana. Environ. Toxicol. Chem. 13:2013-2020. 16. Tessier, A., P.G.C. Campbell, J.C. Auclair, and M. Bisson. 1984. Relationships between the partitioning of trace metals in sediments and their accumulation in the tissues of the freshwater mollusk Elliptio complanata in a mining area. Can. J. Fish. Aquat. Sci. 41:1463-1472. 17. Krantzberg, G. 1994. Spatial and temporal variability in metal bioavailability and toxicity of sediment from Hamilton Harbour, Lake Ontario. Environ. Toxicol. Chem. 13:1685-1698. 18. Burger, P.M., and C.J. Gochfield. 1993. Lead and cadmium accumulation in eggs and fledgling seabirds in the New York Bight. Environ. Toxicol. Chem. 12:261-267. 19. Holcombe, G.W., D.A. Benoit, E.N. Leonard, and J.M. Mckim. 1976. Long-term effects of lead exposure on three generations of brook trout (Salvelinus fontinalis). J. Fish. Res. Bd. Can. 33:1731-1741. 20. Kay, S.H., W.T. Haller, and L.A. Garrard. 1984. Effects of heavy metals on water hyacinths (Eichhornia crassipes (mart.) Solms). Aquat. Toxicol. 5:117-128. 21. Kraak, M.H.S., Y.A. Wink, S.C. Stuijfzand, M.C. Buckert-de Jong, C.J. De Groot, and W. Admiraal. 1994. Chronic ecotoxicity of Zn and Pb to the zebra mussel Dreissena polymorpha. Aquat. Toxicol. 30:77-89. 22. Maclean, R.S., U. Borgmann, and D.G. Dixon. 1993. Lead accumulation and toxicity in Hyalella azteca. 14th Annual Meeting Society of Environmental Toxicology and Chemistry, Houston, TX, November 14-18, 1993. 23. Powell, M.I., and K.N. White. 1990. Heavy metal accumulation by barnacles and its implications for their use as biological monitors. Mar. Environ.Res. 30:91-118. 24. Sundelin, B. 1984. Single and combined effects of lead and cadmium on Pontoporeia affinis (Crustacea, Amphipoda) in laboratory soft-bottom microcosms. In Ecotoxicological testing for the marine environment, Vol. 2, ed. G. Persoone, E. Jaspers, and C. Claus. State University of Ghent and Institute of Marine Scientific Research, Bredene, Belgium. 25. Weber, D.N., A. Russo, D.B. Seale, and R.E. Spieler. 1991. Waterborne lead affects feeding abilities and neurotransmitter levels of juvenile fathead minnows (Pimephales promelas). Aquatic Toxicol. 21:71-80. 483 BIOACCUMULATION SUMMARY LEAD 26. Kendall, R.J., and P.F. Scanlon. 1983. Histologic and ultrastructural lesions of mourning doves (Zenaida macroura) poisoned by lead shot. Poult. Sci. 62:952-956. 484 BIOACCUMULATION SUMMARY Chemical Category: METAL Chemical Name: METHYLMERCURY METHYLMERCURY CASRN: 22967-92-6 Chemical Characteristics Solubility in Water: No data [1] Log Kow: Half-Life: No data [2] Log Koc: Human Health Oral RfD: 1 x 10-4 mg/kg-day [3] Confidence: Medium, uncertainty factor = 10 Critical Effect: Developmental neurologic abnormalities in infants On May 1, 1995, IRIS was updated to include an oral RfD of 1 x 10-4 mg/kg/d based on developmental neurological effects in human infants. An oral RfD of 3 x 10-4 mg/kg/d for chronic systemic effects of methylmercury among the general adult population was available in IRIS until May 1, 1995; however, it was not listed in the IRIS update on that date. For the purposes of calculating an SV for methylmercury that is protective of developing fetuses and nursing infants, EPA's Office of Water has chosen to continue to use the general adult population RfD of 3 x 10-4 mg/kg/d for chronic systemic effects of methylmercury until a value is relisted in IRIS, and to reduce this value by a factor of 5 to derive an RfD of 6 x 10-5 mg/kg/d for developmental effects among fetuses and nursing infants. The protective factor of 5 is based on experimental results that suggest a possible 5-fold increase in fetal sensitivity to methylmercury exposure. This more protective approach recommended by the Office of Water was deemed to be most prudent at this time. This approach should be considered interim until such time as the Agency has reviewed new studies on the chronic and developmental effects of methylmercury. Oral Slope Factor: Carcinogenic Classification: C [3] Wildlife Partitioning Factors: Over 90 percent of methylmercury is absorbed from the gastrointestinal tract in animals, and following such absorption most accumulates in erythrocytes, giving red cell to plasma ratios of up to 300 to 1 [4]. This allows for efficient transport through the body and results in a generally uniform pattern of distribution in tissues and organs--blood, kidney, and brain concentrations are within a range of one to three by ratio [5]. There is an exceptional ability of methylmercury to pass the bloodbrain barrier, and injury to the central nervous system then arises by strong binding of methylmercury to sulfhydryl residues and subsequent release of mercuric ions to binding sites in the central nervous system. The slow elimination of methylmercury from the body is a result of the high erythrocyte-plasma ratio [4]. Mercury will accumulate in both cerebellum and also cerebral cortex, where it will be tightly bound by sulfhydryl groups. Inside the cell, methylmercury will inhibit protein synthesis and RNA synthesis [6,7]. The effects are particularly important in the developing fetal and young brain of most animals. The ability 485 BIOACCUMULATION SUMMARY METHYLMERCURY of methylmercury to penetrate the placental barrier leads to accumulation in the fetus. The rate of transport across the placental barrier is 10-fold higher than for inorganic mercury. It appears that fetal tissue has a greater binding ability for methylmercury than does the pregnant mother. Exposure via milk is also important for feeding babies. It does appear that pregnant animals may detoxify themselves by transferences to their fetuses [8]. Food Chain Multipliers: In birds, there is a tendency for mercury concentrations to be highest in species feeding on fish (or on other seabirds) [9]. However, when one compares mercury levels among predominantly fish-eating species, levels apparently do not show clear patterns or any evident association with diet composition [10]. Particularly high concentrations have been found in some species of procellariiforms [11]. There is an inverse relationship between total mercury and percent methylmercury in tissues of various avian species [12,13]. Overall, the form of mercury in seabirds is predominantly inorganic, suggesting that biotransformation of ingested methylmercury is an important mechanism by which long-lived and slow-moulting seabirds avoid the toxic effects of accumulating large quantities of methylmercury [14,15]. Among furbearers, mecury burdens are higher in fish-eating species than in herbivorous ones [16]. Mink and river otter accumulate about 10 times more mercury than predatory fishes from the same areas [17]. Nonmarine mammals with mercury concentrations in the liver and kidney in excess of approximately 30 mg/kg of wet weight were likely to suffer mercury intoxification. The results of laboratory studies support this value and indicate that a dietary methylmercury concentration of aproximately 2 to 6 mg/kg of wet weight produced mercury poisoning in feeding experiments using a range of mammalian species [18]. Aquatic Organisms Partitioning Factors: Concentrations of total mercury in water are usually low, typically on the order of a few nanograms per liter. Elemental mercury adsorbs to sediments, where methylmercury can be produced and destroyed by microbial processes. This complex process is affected by environmental factors [1]. A significant fraction of the total mercury in water is found in the form of methylmercury, the species predominantly accumulated by aquatic organisms [19]. In the Onondaga Lake food web, the percent of total mercury occurring as methylmercury was determined as follows [20]: Lake water 5% Interstitial water 37% Phytoplankton 24% Zooplankton 40% Benthic macroinvertebrates 26% Fishes 96% Bioconcentration factors (BCFs) for methylmercury are highly variable. Log BCFs for methylmercury in brook trout range from 4.84 to 5.80, depending on the tissue analyzed. Methylmercury concentrations and bioaccumulation factors (BAFs) increased with higher trophic levels in both the pelagic and benthic components of aquatic food webs [20]. Food Chain Multipliers: Fish bioconcentrate methylmercury directly from water by uptake across the gills [21,22,23] and piscivores, such as walleye, readily accumulate mercury from dietary sources [24,25]. Methylmercury accumulation from either source may be substantial, but the relative contribution of each 486 BIOACCUMULATION SUMMARY METHYLMERCURY pathway may vary with fish species [26,27,28,29]. In addition, invertebrates generally have a lower percentage of methylmercury in their tissues than fish or marine mammals [30]. The percentage of methylmercury increases with age in both fish and invertebrates [30]. Mercury is accumulated by all trophic levels with biomagnification occurring up the food web. While sediment is usually the primary source of methylmercury in most aquatic systems, the food web is the main pathway for accumulation [24,25]. High concentrations of organic substances and reduced sulfur can complex free mercury ions in the sediment and reduce the availability to organisms [31,32]. Methylmercury can be accumulated directly from the water by uptake across the gills [21,22,23]. Hightrophic-level species tend to accumulate the most methylmercury, with concentrations highest in fisheating predators. Methylmercury concentrations in higher trophic species often do not correlate with concentrations in environmental media. Correlations have been made between sediment and lower trophic species that typically have a high percentage of inorganic mercury, and between mercury concentrations in higher trophic species and their prey items. The best measure of bioavailability of mercury in any system can be obtained through analysis of mercury concentrations in the biota at the specific site. The transfer efficiency of mercury through the food web is affected by the form of mercury. Although inorganic mercury is the dominant form in the environment and easily accumulated, it is also depurated quickly. Methylmercury accumulates quickly, depurates very slowly, and therefore has a greater potential to biomagnify in higher-trophic-level species. Pharmacologic half-lives of total mercury in tissues of aquatic organisms have been estimated at approximately 2 months to 1 year in saltwater mussels, 1 to more than 3 years in fishes, and 1.4 to 2.7 years in pinnipeds and dolphins [33]. As the concentration of methylmercury increases in prey items, the transfer efficiency also increases [34]. Methylmercury accumulation from either the water column or food sources might be substantial, but the relative contribution of each pathway varies from species to species [26,27,28,29]. Invertebrates generally have a lower percentage of methylmercury in their tissues than fish or marine mammals, but the percentage can vary greatly, from 1 percent in deposit-feeding polychaetes to almost 100 percent in crabs. The amount of methylmercury in animal tissues increases proportionately with the age of the organism, with the exception of marine mammals. Because marine mammals feed primarily on fish, they have the greatest potential for the highest tissue concentrations of methylmercury compared to other marine organisms. Contrary to other species or groups of animals, the tissue concentrations of methylmercury are higher in juvenile marine mammals than in adults because the adults can mineralize methylmercury into inorganic mercury [33]. Toxicity/Bioaccumulation Assessment Profile Methylmercury is the most hazardous mercury species due to its high stability, its lipid solubility, and its ionic properties that lead to a high ability to penetrate the membranes of living organisms [35]. Because methylmercury is lipid-soluble, it can rapidly penetrate the blood-brain barrier [36,37,38,39,40]. Injury to the central nervous system arises by accumulation in the cerebellum and cerebral cortex, where methylmercury binds tightly to sulfhydryl groups, resulting in pathological changes [41]. Inside the cell, methylmercury inhibits protein synthesis and RNA synthesis [6,7]. 487 BIOACCUMULATION SUMMARY METHYLMERCURY The early developmental stages of organisms are the most sensitive to the toxic effects of mercury, with methylmercury being more toxic than inorganic mercury. Mercury adversely affects reproduction, growth, behavior, osmoregulation, and oxygen exchange in aquatic organisms. In birds and mammals, comparatively low concentrations of mercury have adverse effects on growth and development, behavior, motor coordination, vision, hearing, histology, and metabolism [33]. Toxicity of methylmercury is dependent on temperature [42], oxygen conditions [43], salinity [44], and the presence of other metals such as zinc and lead [45]. The complex behavior of methylmercury in sediments makes it difficult to predict toxicity from bulk sediment chemistry. Toxicity of mercury has been linked with bioaccumulation, but the situation is complicated by the fact that some animals exposed to low concentrations of mercury can build up a tolerance to this contaminant, as well as detoxify the free metal within their cells via the production of metallothioneins and other metal-binding proteins. Brown et al. [46] propose that toxic effects occur as the binding capacity of these metal-binding proteins becomes saturated. 488 Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Invertebrates Phytoplankton Interstitial water: 0.003 g/L Lake water: 0.0003 g/L 32 g/kg 5.00 [20] F; estimated from chart; chart reported log BAF values Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Crepidula fornicata, Slipper limpet 9.00045013427734 mg/kg (whole body)5 Growth, ED25 [62] L; approximate 25% reduction in growth at lowest test concentration; algal food contained mercury at approximatley 2.9 g/L in addition to water concentration L; significant effect on fecundity (number of gametes); exposure includes mercury in food at approximately 9.5 g/L 15.0007495880126 mg/kg (whole body)5 Reproduction, LOED [62] 489 490 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 30.0014991760253 mg/kg (whole body)5 Development, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [62] L; no significant effect on number of live spat at peak settlement; exposure includes mercury in food at approximately 31 g/L L; no significant effect on ability to produce gametes; exposure includes mercury in food at approximately 31 g/L L; no significant effect on fecundity (number of gametes); exposure includes mercury in food at approximately 2.9 g/L 30.0014991760253 mg/kg (whole body)5 Reproduction, NOED [62] 9.00045013427734 mg/kg (whole body)5 Reproduction, NOED [62] Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Elliptio complanata, Freshwater mussel Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 43 g/kg Relative to least contaminated station (17.9 mg/kg, dry total Hg in sediment vs. 0.07 mg/kg, dry), whole animal ww was reduced by 97 percent Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [48] F; 42 and 84 days exposure; probable effects at tissue concentrations >34 g/kg, ww Rangia cuneata, Marsh clam 12 mg/kg (whole body)5 28 mg/kg (whole body)5 73.1399993896484 mg/kg (whole body)5 6 mg/kg (whole body)5 Mortality, ED50 Mortality, ED50 Mortality, LOED Mortality, NOED [54] [54] [54] [54] L; lethal to 50% of clams in 7 days L; lethal to 50% of clams in 7 days L; lethal body burden L; no effect on mortality Zooplankton, Cladocerans Interstitial water: 0.003 g/L Lake water: 0.0003 g/L 260 g/kg 5.94 [20] F; estimated from chart; chart reported log BAF values 491 492 Species: Taxa Diaptomus oregonensis Sediment Diaptomus minutus, Zooplankton Holopedium gibberum, Zooplankton Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF 7.10 Log BAF BSAF Source: Reference Comments3 [47] F; results were summarized for zooplankton and water samples taken from 12 lakes ranges are given Unfiltered 22-66 g/kg (dw) water: total Hg = 0.43-4.79 ng/L MeHg = 0.042.20 ng/L Filtered water: total Hg = 0.27-4.50 ng/L MeHg = 0.03-1.95 ng/L 4.04 [47] F; results were summarized for zooplankton and water samples taken from 12 lakes ranges are given Unfiltered 40-419 g/kg (dw) water: total Hg = 0.43-4.79 ng/L MeHg = 0.042.20 ng/L Filtered water: total Hg = 0.27-4.50 ng/L MeHg = 0.03-1.95 ng/L [47] F; results were summarized for biota and water samples taken from 12 lakes - ranges are given Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Bosmina longirostris, Cladoceran Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [47] F; results were summarized for biota and water samples taken from 12 lakes - ranges are given Unfiltered 479 g/kg (dw) water: total Hg = 0.43-4.79 ng/L MeHg = 0.042.20 ng/L Filtered water: total Hg = 0.27-4.50 ng/L MeHg = 0.03-1.95 ng/L Daphnia pulex Daphnia galeatra mendotae Daphnia ambigua, Cladocerans Unfiltered 1-211 g/kg (dw) water: total Hg = 0.43-4.79 ng/L MeHg4 = 0.042.20 ng/L Filtered water: total Hg = 0.27-4.50 ng/L MeHg = 0.03-1.95 ng/L [47] F; results were summarized for biota and water samples taken from 12 lakes - ranges are given Daphnia magna, Cladoceran 493 18.3999996185302 mg/kg (whole body)5 Mortality, ED25 [51] L; 25% reduction in survival compared to controls in 21 days 494 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 2.32800006866455 mg/kg (whole body)5 1.63999998569488 mg/kg (whole body)5 4.67000007629394 mg/kg (whole body)5 7.57000017166137 mg/kg (whole body)5 18.3999996185302 mg/kg (whole body)5 0.859000027179718 mg/kg (whole body)5 1.52600002288818 mg/kg (whole body)5 2.32800006866455 mg/kg (whole body)5 1.63999998569488 mg/kg (whole body)5 4.67000007629394 mg/kg (whole body)5 Reproduction, NA Reproduction, NA Reproduction, NA Reproduction, NA Reproduction, NA Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [51] L; 32% reduction in number of neonates produced in 21 days L; 35% reduction in number of neonates produced in 21 days L; 62% reduction in number of neonates produced in 21 days L; 63% reduction in number of neonates produced in 21 days L; 99% reduction in number of neonates produced in 21 days L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality [51] [51] [51] [51] [51] [51] [51] [51] [51] Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 7.57000017166137 mg/kg (whole body)5 0.859000027179718 mg/kg (whole body)5 1.52600002288818 mg/kg (whole body)5 Daphnia magna, Cladoceran 0.790000021457672 mg/kg (whole body)5 91.3000030517578 mg/kg (whole body)5 Mortality, NOED Reproduction, NOED Reproduction, NOED Reproduction, ED10 Mortality, ED50 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [51] [51] L; no effect on mortality L; no significant reproductive impairment L; no significant reproductive impairment L; 10% reduction in number of offspring L; lethal body burden after 21 day exposure [51] [55] [55] Benthic invertebrates Scientific names not given (amphipods and chironomids) Interstitial water: 0.003 g/L Lake water: 0.0003 g/L 25 g/kg 8.3x104 [20] F Palaemonetes pugio, Grass shrimp 1.09399998188018 mg/kg (whole body)5 Behavior, LOED [50] L; decreased sensitivity to physical disturbance 495 496 Species: Taxa Sediment Uca pugnax, Fiddler crab Fishes Squalus acanthias, Spiny dogfish Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 2.12299990653991 mg/kg (whole body)5 Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [50] L; no statistically significant increase in mortality 12.329999923706 mg/kg (whole body)5 Development, LOED [53] L; inhibition of limb regeneration and molting in male crabs L; inhibition of limb regeneration and molting in female crabs 19.4200000762939 mg/kg (whole body)5 Development, LOED [53] 0.0930000022053719 mg/kg (whole body)5 Mortality, NOED [57] L; no effect on mortality in 24 hours Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Oncorhynchus mykiss, Rainbow trout Concentration, Units in1: Sediment Water Exposure concentrations (CH3HgCl): 4 g/L Toxicity: Tissue (Sample Type) Effects kidney = 7430 (16-116 mg/kg) liver = 7619 (32-114 mg/kg) spleen = 8938 (32-118 mg/kg) brain = 198 (7-32 mg/kg) muscle = 3112 (9-52 mg/kg) gill = 6615 (42-93 mg/kg) 58.2 d21.4 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [49] L; d = mean days to death SD; n = 20 fish per treatment. Exposure whole fish =11.26.1 concentrations (4.0-27.3 mg/kg) (CH3HgCl): 9 g/L Exposure concentrations (CH3HgCl): 10 g/L kidney = 6420 (40-116 mg/kg) liver = 4710 (27-65 mg/kg) spleen = 7222 (37-112 mg/kg) brain = 133 (7-19 mg/kg) muscle = 185 (9-27 mg/kg) gill = 5112 (34-85 mg/kg) 24.2 d5.6 [49] 21.7 d6.0 [49] L; n = 20 per treatment; d = days to death; n = 20 per treatment. 497 498 Species: Taxa Sediment Oncorhynchus mykiss, Rainbow trout Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Exposure concentrations (CH3HgCl): 13 g/L Toxicity: Tissue (Sample Type) Effects kidney = 3921 (19-91 mg/kg) liver = 4227 (16-129 mg/kg) spleen = 5138 (19-194 mg/kg) brain = 7.75.6 (2.3-22 mg/kg) muscle = 6.27.7 (1.2-26 mg/kg) gill = 6415 (36-98 mg/kg) kidney = 6.22.7 (2.3-10 mg/kg) liver = 7.22.8 (3.0-12 mg/kg) spleen = 6.43.2 (2.7-14 mg/kg) brain = 1.10.3 (0.6-1.5 mg/kg) muscle = 0.70.3 (2.7-14 mg/kg) gill = 5612 (29-73 mg/kg) 7.6 d5.1 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [49] L; n = 20 per treatment; d = days to death; n = 20 per treatment. Exposure concentrations (CH3HgCl): 34 g/L 1.0 d [49] L; d = mean days to death (no SD reported) 1.60000002384185 mg/kg (blood)5 0.100000001490116 mg/kg (blood)5 Growth, NOED [52] L; no effect on growth L; no effect on growth Growth, NOED [52] Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.5 mg/kg (brain)5 0.100000001490116 mg/kg (brain)5 0.400000005960464 mg/kg (gill)5 0.100000001490116 mg/kg (gill)5 1.60000002384185 mg/kg (kidney)5 0.200000002980232 mg/kg (kidney)5 1 mg/kg (liver)5 0.100000001490116 mg/kg (liver)5 0.5 mg/kg (muscle)5 0.100000001490116 mg/kg (muscle)5 1.60000002384185 mg/kg (posterior intestine)5 499 Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [52] [52] [52] [52] [52] [52] [52] [52] [52] [52] [52] L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth 500 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 6 mg/kg (posterior intestine)5 1.29999995231628 mg/kg (spleen)5 0.300000011920929 mg/kg (spleen)5 0.140000000596046 mg/kg (whole body)5 0.469999998807907 mg/kg (whole body)5 1.60000002384185 mg/kg (blood)5 0.100000001490116 mg/kg (blood)5 0.5 mg/kg (brain)5 0.100000001490116 mg/kg (brain)5 0.400000005960464 mg/kg (gill)5 0.100000001490116 mg/kg (gill)5 1.60000002384185 mg/kg (kidney)5 Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [52] [52] [52] [52] [52] [52] [52] [52] [52] [52] [52] [52] L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on growth L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.200000002980232 mg/kg (kidney)5 1 mg/kg (liver)5 0.100000001490116 mg/kg (liver)5 0.5 mg/kg (muscle)5 0.100000001490116 mg/kg (muscle)5 1.60000002384185 mg/kg (posterior intestine)5 6 mg/kg (posterior intestine)5 1.29999995231628 mg/kg (spleen)5 0.300000011920929 mg/kg (spleen)5 0.140000000596046 mg/kg (whole body)5 0.469999998807907 mg/kg (whole body)5 501 Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [52] [52] [52] [52] [52] [52] L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on mortality L; no effect on survival L; no effect on survival [52] [52] [52] [52] [52] 502 Species: Taxa Oncorhynchus mykiss, Rainbow trout Sediment Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 15 mg/kg (whole body)5 20 mg/kg (whole body)5 6 mg/kg (whole body)5 4.76000022888183 mg/kg (whole body)5 5.69999980926513 mg/kg (whole body)5 Mortality, ED100 Mortality, ED100 Mortality, ED50 Mortality, ED50 Mortality, ED50 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [58] L; 100% mortality in 15 days L; 100% mortality in 15 days L; 50% mortality in 15 days L; 30 day ED50 for brain L; 15 day ED50 for single intraperitoneal injection L; 30 day ED50 for muscle L; 30 day ED50 for eye L; 83% mortality in 15 days L; 33% mortality in 15 days L; 83% mortality in 15 days L; 67% mortality in 15 days [58] [58] [58] [58] 3.91000008583068 mg/kg (whole body)5 2.02999997138977 mg/kg (whole body)5 10 mg/kg (whole body)5 2 mg/kg (whole body)5 5 mg/kg (whole body)5 8 mg/kg (whole body)5 Mortality, ED50 Mortality, ED50 Mortality, LOED Mortality, LOED Mortality, LOED Mortality, LOED [58] [58] [58] [58] [58] [58] Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 4 mg/kg (whole body)5 2 mg/kg (whole body)5 Salvelinus fontinalis, Brook trout 46.2000007629394 mg/kg (blood cells)5 16.8999996185302 mg/kg (brain)5 4.40000009536743 mg/kg (carcass)5 22.2000007629394 mg/kg (gill)5 Salvelinus fontinalis, Brook trout 12.3000001907348 mg/kg (gonad)5 26.8999996185302 mg/kg (kidney)5 24.3999996185302 mg/kg (liver)5 10.1999998092651 mg/kg (muscle)5 38.7000007629394 mg/kg (spleen)5 46.2000007629394 mg/kg (blood cells)5 Mortality, LOED Mortality, NOED Development, LOED Development, LOED Development, LOED Development, LOED Development, LOED Development, LOED Development, LOED Development, LOED Development, LOED Growth, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [58] [58] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] L; 13% mortality in 15 days L; no mortality in 15 days L; affected embryo development L; affected embryo development L; affected embryo development L; affected embryo development L; affected embryo development L; affected embryo development L; affected embryo development L; affected embryo development L; affected embryo development L; decreased weight 503 504 Species: Taxa Sediment Salvelinus fontinalis, Brook trout Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 16.8999996185302 mg/kg (brain)5 4.40000009536743 mg/kg (carcass)5 22.2000007629394 mg/kg (gill)5 12.3000001907348 mg/kg (gonad)5 26.8999996185302 mg/kg (kidney)5 24.3999996185302 mg/kg (liver)5 10.1999998092651 mg/kg (muscle)5 38.7000007629394 mg/kg (spleen)5 9.39999961853027 mg/kg (whole body)5 46.2000007629394 mg/kg (blood cells)5 16.8999996185302 mg/kg (brain)5 4.40000009536743 mg/kg (carcass)5 Growth, LOED Growth, LOED Growth, LOED Growth, LOED Growth, LOED Growth, LOED Growth, LOED Growth, LOED Mortality, LOED Reproduction, LOED Reproduction, LOED Reproduction, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; mortality of offspring L; reduced reproduction L; reduced reproduction L; reduced reproduction Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 22.2000007629394 mg/kg (gill)5 12.3000001907348 mg/kg (gonad)5 26.8999996185302 mg/kg (kidney)5 24.3999996185302 mg/kg (liver)5 10.1999998092651 mg/kg (muscle)5 38.7000007629394 mg/kg (spleen)5 3.40000009536743 mg/kg (whole body)5 2.70000004768371 mg/kg (whole body)5 Salvelinus fontinalis, Brook trout 21.3999996185302 mg/kg (blood cells)5 5.19999980926513 mg/kg (blood cells)5 2.29999995231628 mg/kg (blood cells)5 5.30000019073486 mg/kg (brain)5 Reproduction, LOED Reproduction, LOED Reproduction, LOED Reproduction, LOED Reproduction, LOED Reproduction, LOED Reproduction, LOED Development, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduction in reproduction L; no physical abnormalities L; decreased weight L; decreased weight L; decreased weight L; decreased weight 505 506 Species: Taxa Sediment Salvelinus fontinalis, Brook trout Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 1.70000004768371 mg/kg (brain)5 0.800000011920928 mg/kg (brain)5 1.60000002384185 mg/kg (carcass)5 0.589999973773956 mg/kg (carcass)5 0.400000005960464 mg/kg (carcass)5 6.19999980926513 mg/kg (gill)5 1.60000002384185 mg/kg (gill)5 0.699999988079071 mg/kg (gill)5 2.90000009536743 mg/kg (gonad)5 0.899999976158142 mg/kg (gonad)5 0.200000002980232 mg/kg (gonad)5 8.89999961853027 mg/kg (kidney)5 Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 2.5 mg/kg (kidney)5 1.20000004768371 mg/kg (kidney)5 8.30000019073486 mg/kg (liver)5 2.20000004768371 mg/kg (liver)5 0.699999988079071 mg/kg (liver)5 4.90000009536743 mg/kg (muscle)5 1.89999997615814 mg/kg (muscle)5 1 mg/kg (muscle)5 11.8000001907348 mg/kg (spleen)5 3.20000004768371 mg/kg (spleen)5 1.20000004768371 mg/kg (spleen)5 2.70000004768371 mg/kg (whole body)5 Salvelinus fontinalis, Brook trout 21.3999996185302 mg/kg (blood cells)5 507 Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Growth, NOED Mortality, NOED Reproduction, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; decreased weight L; no effect on mortality L; reduced reproduction 508 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 5.19999980926513 mg/kg (blood cells)5 2.29999995231628 mg/kg (blood cells)5 5.30000019073486 mg/kg (brain)5 1.70000004768371 mg/kg (brain)5 0.800000011920928 mg/kg (brain)5 1.60000002384185 mg/kg (carcass)5 0.589999973773956 mg/kg (carcass)5 0.400000005960464 mg/kg (carcass)5 6.19999980926513 mg/kg (gill)5 1.60000002384185 mg/kg (gill)5 0.699999988079071 mg/kg (gill)5 2.90000009536743 mg/kg (gonad)5 Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.899999976158142 mg/kg (gonad)5 Salvelinus fontinalis, Brook trout 0.200000002980232 mg/kg (gonad)5 8.89999961853027 mg/kg (kidney)5 2.5 mg/kg (kidney)5 1.20000004768371 mg/kg (kidney)5 8.30000019073486 mg/kg (liver)5 2.20000004768371 mg/kg (liver)5 0.699999988079071 mg/kg (liver)5 4.90000009536743 mg/kg (muscle)5 1.89999997615814 mg/kg (muscle)5 1 mg/kg (muscle)5 11.8000001907348 mg/kg (spleen)5 Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] [38] L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction L; reduced reproduction 509 510 Species: Taxa Sediment Esox lucius, Northern pike Planktivores: Dorosoma cepedianum, Gizzard shad Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 3.20000004768371 mg/kg (spleen)5 1.20000004768371 mg/kg (spleen)5 Reproduction, NOED Reproduction, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [38] [38] L; reduced reproduction L; reduced reproduction 7 mg/kg (whole body)5 Physiological, LOED [60] F; lowered blood alkaline phosphatase, serum cortisol, emaciation Interstitial water: 0.003 g/L Lake water: 0.0003g/L 680 g/kg 6.40 [20] F; mean methylmercury concentrations in whole bodies of fish were slightly lower than concentrations in fillets for 4 species evaluated (white perch, smallmouth bass, bluegill, and gizzard shad); differences were significant (P0.05, t-test) for bluegill only; BAF value estimated from chart as log BAF Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Benthivores: Cyprinus carpio; Carp; Ictalurus punctatus, Channel catfish; and Lepomis macrochirus, Bluegill Concentration, Units in1: Sediment Water Interstitial water: 0.003 g/L Lake water: 0.0003 g/L Toxicity: Tissue (Sample Type) Effects 480 g/kg Ability to Accumulate2: Log BCF Log BAF 6.20 BSAF Source: Reference Comments3 [20] F; mean methylmercury concentrations in whole bodies of fish were slightly lower than concentrations in fillets for 4 species evaluated (white perch, smallmouth bass, bluegill, and gizzard shad); differences were significant (P0.05, t-test) for bluegill only; BAF value estimated from chart as log BAF Oryzias latipes, Japanese medaka 54 mg/kg (whole body)5 56 mg/kg (whole body)5 54 mg/kg (whole body)5 56 mg/kg (whole body)5 Development, ED100 Development, ED100 Morphology, ED100 Morphology, ED100 [59] [59] [59] [59] L; complete failure of eggs to hatch L; complete failure of eggs to hatch L; subcutaneous hemorrhage, deformed vertebrae 511 512 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 29 mg/kg (whole body)5 Behavior, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [59] L; hatchlings unable to control fin movement, loss of equilibrium L; over 50% reduction in number of eggs which hatched L; subcutaneous hemorrhage, deformed vertebrae L; no effect on hatchability of eggs compared to controls L; no observations of subcutaneous hemorrhage or deformed vertebrae 29 mg/kg (whole body)5 Development, LOED [59] 29 mg/kg (whole body)5 16 mg/kg (whole body)5 Morphology, LOED Development, NOED [59] [59] 16 mg/kg (whole body)5 Morphology, NOED [59] Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Morone americana, White perch Concentration, Units in1: Sediment Water Interstitial water: 0.003 g/L Lake water: 0.0003 g/L Toxicity: Tissue (Sample Type) Effects 680 g/kg Ability to Accumulate2: Log BCF Log BAF 6.40 BSAF Source: Reference Comments3 [20] F; mean methylmercury concentrations in whole bodies of fish were slightly lower than concentrations in fillets for 4 species evaluated (white perch, smallmouth bass, bluegill, and gizzard shad); differences were significant (P0.05, t-test) for bluegill only; BAF value estimated from chart as log BAF F, controlled field study; two years but only 1-year-old fish analyzed; basin treated by reducing pH from about 6 to 5.6 Perca flavescens, Yellow perch 0.135000005364418 mg/kg (whole body)5 Growth, NOED [63] 513 514 Species: Taxa Piscivores: Microplerus dolomieui, Smallmouth bass; and Stizostedion vitreum, Walleye Sediment Stizostedion vitreum, Walleye Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Interstitial water: 0.003 g/L Lake water: 0.0003 g/L Toxicity: Tissue (Sample Type) Effects 1,100 g/kg Ability to Accumulate2: Log BCF Log BAF 3.7x106 BSAF Source: Reference Comments3 [20] F; mean methylmercury concentrations in whole bodies of fish were slightly lower than concentrations in fillets for 4 species evaluated (white perch, smallmouth bass, bluegill, and gizzard shad); differences were significant (P0.05, t-test) for bluegill only; BAF value estimated from chart as log BAF L; multifocal cell atrophy, testicular atrophy 0.25 mg/kg (whole body)5 2.36999988555908 mg/kg (whole body)5 0.25 mg/kg (whole body)5 2.36999988555908 mg/kg (whole body)5 Cellular, LOED Cellular, LOED Development, LOED Development, LOED [56] [56] [56] [56] L; decreased testicular development, lowered gonadosomatic index Summary of Biological Effects Tissue Concentrations for Methylmercury Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 2.36999988555908 mg/kg (whole body)5 Growth, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [56] L; significant reduction in length and weight of males, but not females L; reduced cortisol levels L; no effect on length or weight L; no statistically significant increase in mortality 0.25 mg/kg (whole body)5 0.25 mg/kg (whole body)5 0.25 mg/kg (whole body)5 2.36999988555908 mg/kg (whole body)5 2.36999988555908 mg/kg (whole body)5 Physiological, LOED Growth, NOED Mortality, NOED Mortality, NOED Physiological, NOED [56] [56] [56] [56] [56] L; no effect on cortisol levels Pseudopleuronectes americanus, Winter flounder 5 mg/kg (whole body)5 2 mg/kg (whole body)5 Mortality, LOED Physiological, LOED [61] L; increased mortality L; increased ornithine decarboxylase activity [61] 515 516 Species: Taxa Wildlife Larus californicus, California gull Sediment Pelecanus occidentalis, Brown pelican Phalacrocorax penicillatus, Brandts cormorant Summary of Biological Effects Tissue Concentrations for Methylmercury Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 0.404000014066696 mg/kg (brain)5 0.828999996185302 mg/kg (breast)5 1.08000004291534 mg/kg (liver)5 0.202999994158745 mg/kg (brain)5 0.347499996423721 mg/kg (breast)5 0.806500017642974 mg/kg (liver)5 Mortality, NA Mortality, NA Mortality, NA Mortality, NA [64] [64] [64] [64] L L L L Mortality, NA Mortality, NA [64] [64] L L 0.648999989032745 mg/kg (brain)5 0.986000001430511 mg/kg (breast)5 2.94000005722045 mg/kg (liver)5 3.06999993324279 mg/kg (liver)5 Mortality, NA [64] L Mortality, NA Mortality, NA Mortality, NA [64] [64] [64] L L L 1 2 3 4 5 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. MeHg = methylmercury. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. 517 BIOACCUMULATION SUMMARY References 1. METHYLMERCURY USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. March. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Norseth, T., and T.W. Clarkson. 1970. Studies on the biotransformation of mercury-203-labeled methyl mercury chloride in rats. Arch. Environ. Health. 21:717-27. Swensson, A., and U. Ulfvarson. 1968. Distribution and excretion of various mercury compounds after single injections in poultry. Acta Pharmacol. Toxicol. 26:259-72. Yoshino, Y., T. Mozai, and K. Nakao. 1966. Biochemical changes in the brain in rats poisoned with an alkymercury compound, with special reference to the inhibition of protein synthesis in brain cortex slices. J. Neurochem. 13:397-406. Chang, L.W., A.H. Martin, and H.A. Hartmann. 1972. Quantitative autoradiographic study on the RNA synthesis in the neurons after mercury and toxication. Exp. Neurol. 37:62-67. Syverson. 1974. Distribution of mercury in enzymatically characterized subcellular fractions from the developing rat brain after injections of methyl mercuric chloride and diethyl mercury. Biochem. Pharmacol. 23:2999-3007. Braune, B.M. 1987. Mercury accumulation in relation to size and age of Atlantic herring Clupea harengus harengus from the southwestern Bay of Fundy, Canada. Arch. Environ. Contam. Toxicol. 16:217-224. Elliott, J.E., A.M. Scheuhammer, F.A. Leighton, and P.A. Pearce. 1992 Heavy metal and metallothionein concentrations in Atlantic Canadian seabirds. Arch. Environ. Contam. Toxicol. 22:63-73. Muirhead, S.J., and R.W. Furness. 1988. Heavy metal concentrations in the tissues of seabirds from Gough Island South Atlantic Ocean. Mar. Pollut. Bull. 19:278-283. Norheim, G., L. Somme, and G. Holt. 1982. Mercury and persistent chlorinated hydrocarbons in Antarctic birds from Bouvetoya and Dronning Maud Land. Environ. Pollut. 28A:233-240. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 518 BIOACCUMULATION SUMMARY 13. METHYLMERCURY Karlog, O., and B. Clausen. 1983. Mercury and methylmercury in liver tissue from ringed herring gulls collected in three Danish localities. Nord. Vet. Med. 35:245-250. Thompson, D.R., and R.W. Furness. 1989. The chemical form of mercury stored in south Atlantic seabirds. Environ. Pollut. 60:305-317. Honda, K., J.E. Marcovecchio, S. Kan, R. Tatsukawa, and H. Ogi. 1990. Metal concentrations in pelagic seabirds from the north Pacific Ocean. Arch. Environ. Contam. Toxicol. 19:704-711. Sheffy, T.B., and J.R. St. Amant. 1982. Mercury burdens in furbearers in Wisconsin. J. Wildl. Manage. 46:1117-1120. Kucera, E. 1983. Mink and otter as indicators of mercury in Manitoba waters. Canad. J. Zool. 61:2250-2256. Thompson, D.R. 1996. Chapter 14: Mercury in birds and terrestrial mammals. In Environmental contaminants in wildlife: Interpreting tissue concentrations, ed. W.N. Beyer, G.H. Heinz, and A.W. Redmon-Norwood, pp. 341-356. Lewis Publishers, Boca Raton, FL. St. Louis, V., J.W.M. Rudd, C.A. Kelly, K.G. Beaty, N.S. Bloom, and R.J. Flett. 1994. Importance of wetlands as sources of methyl mercury to boreal forest ecosystems. Can. J. Fish. Aquat. Sci. 51(5):1065-1076. Becker, D.S., and G.N. Bigham. 1995. Distribution of mercury in the aquatic food web of Onondaga Lake, New York. (Water Air Soil Pollut. 80:563-571.) In Mercury as a global pollutant, ed. D.B. Porcella, J.W. Huckabee, and B. Wheatley, pp. 563-571. Kluwer Academic Publishers, New York, NY. Rodgers, D.W., and F.W.H. Beamish. 1981. Uptake of waterborne methylmercury by rainbow trout (Salmo gairdneri) in relation to oxygen consumption and methylmercury concentration. Can. J. Fish. Aquat. Sci. 38:1309-1315. Wren, C.D., H.R. MacCrimmon, and B.R. Loescher. 1983. Examination of bioaccumulation and biomagnification of metals in a Precambrian shield lake. Water Air Soil Pollut. 19:277-291. Xun, L., N.E.R. Campbell, and J.W.M. Rudd. 1987. Measurements of specific rates of net methylmercury production in the water column and surface sediment of acidified circumneutral lakes. Can. J. Fish. Aquat. Sci. 44:750-757. Mathers, R., and P. Johansen. 1985. The effects of feeding ecology on mercury accumulation in walleye (Stizostedion vitreum) and pike (Esox lucius) in Lake Simcoe. Can. J. Zool. 63:20062012. Wiener, J.G., and D.J. Spry. 1996. Toxicological significance of mercury in freshwater fish. In Interpreting concentrations of environmental contaminants in wildlife tissues, ed. G. Heinz and N. Beyer, pp. 297-339. Lewis Publishers, Chelsea, MI. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 519 BIOACCUMULATION SUMMARY 26. METHYLMERCURY Huckabee, J.W., S.A. Janzen, B.G. Blaylock, Y. Talmi, and J.J. Beauchamp. 1978. Methylated mercury in brook trout (Salvelinus fontinalis): Absence of in vivo methylating process. Trans. Amer. Fish. Soc. 107:848-852. Norstrom, R.J., A.F. McKinnon, and A.S.W. DeFreitas. 1976. A bioenergetics based model for pollutant bioaccumulation by fish: Simulation of PCB and methylmercury residues in Ottawa River perch (Perca flavescens). J. Fish. Res. Board Can. 33:248-267. Phillips, G.R., T.E. Lenhart, and R.W. Gregory. 1980. Relation between trophic position and mercury accumulation among fishes from the Tongue River, Montana. Environ. Res. 22:73-80. Rodgers, D.W., and S.U. Qadri. 1982. Growth and mercury accumulation in yearling yellow perch, Perca flavescens, in Ottawa River, Ontario. Environ. Biol. Fish. 7:377-383. Beckvar, N., J. Field, S. Salazar, and R. Hoff. 1996. Contaminants in aquatic habitats at hazardous waste sites: Mercury. National Oeanic and Atmospheric Administration and EVS Consultants, Seattle, WA. Luoma, S.N. 1977. The dynamics of biologically available mercury in a small estuary. Estuar. Coast. Mar. Sci. 5:643-652. Rubinstein, N.I., E. Lores, and N.R. Gregory. 1983. Accumulation of PCBs, mercury and cadmium by Nereis virens, Mercenaria mercenaria and Palaemonetes pugio from contaminated harbor sediments. Aquat. Toxicol. 3:249-260. Eisler, R. 1987. Mercury hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.10). 90 pp. Windom, H.L., and D. R. Kendall. 1979. Accumulation and biotransformation of mercury in coastal and marine biota. In The biogeochemistry of mercury in the environment, ed. J.O. Nriagu, pp. 277-302. Elsevier/North-Holland Biomedical Press, New York, NY. USEPA. 1985. Ambient water quality criteria for mercury - 1984. EPA 440/5-84-026. U.S. Environmental Protection Agency, Office of Water, Washington, DC. Feltier, J.S., E. Kahn, B. Salick, F.C. Van Natta, and M.W. Whitehouse. 1972. Heavy metal poisoning: Mercury and lead. Ann. Intern. Med. 76:779-792. Giblin, F.J., and E.J. Massaro. 1973. Pharmacodynamics of methyl mercury in rainbow trout (Salmo gairdneri): Tissue uptake, distribution and excretion. Toxicol. Appl. Pharmacol. 24:81-91. McKim, J.M., G.F. Olson, G.W. Holcombe, and E.P. Hunt. 1976. Long-term effects of methylmercuric chloride on three generations of brook trout (Salvelinus fontinalis): Toxicity, accumulation, distribution, and elimination. J. Fish. Res. B. Can. 33:2726-2739. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 520 BIOACCUMULATION SUMMARY 39. METHYLMERCURY Olson, K R., K.S. Squibb, and R.J. Cousins. 1978. Tissue uptake, subcellular distribution, and metabolism of 14CH3HgCl and CH3203 HgCl by rainbow trout, Salmo gairdneri. J. Fish. Res. Board Can. 35:381-90. Beijer, K., and A. Jernelov. 1979. Methylation of mercury in aquatic environments. In The biogeochemistry of mercury in the environment, ed. J.O. Nriagu, pp. 203-210. Elsevier/NorthHolland Biomedical Press, New York, NY. Sastry, K.V., and K. Sharma. 1980. Effects of mercuric chloride on the activities of brain enzymes in a freshwater teleost, Ophiocephalus (Channa) punctatus. Arch. Environ. Contam. Toxicol. 9:425-430. Armstrong, F.A.J. 1979. Effects of mercury compounds on fish. In The biogeochemistry of mercury in the environment, ed. J.O. Nriagu, pp. 657-670. Elsevier/North-Holland Biomedical Press, New York, NY. Slooff, W., P.F.H. Bont, M. van Ewijk, and J.A. Janus. 1991. Exploratory report mercury. Report no. 710401006. National Institute of Public Health and Environmental Protection, Bilthoven, The Netherlands. McKenney, C.L., Jr., and J.D. Costlow, Jr. 1981. The effects of salinity and mercury on developing megalopae and early crab stages of the blue crab Callinectes sapidus Rathbun. In Biological monitoring of marine pollutants, ed. F.J. Vernberg, A. Calabrese, F.P. Thurberg, and W.B. Vernberg, pp. 241-262. Academic Press, New York, NY. Parker, J.G. 1979. Toxic effects of heavy metals upon cultures of Uronema marinum (Ciliophora:Uronematidae). Mar. Biol. 54:17-24. Brown, D.A., R.W. Gosset, P. Hershelman, H.A. Schaefer, K.D. Jenkins, and E.M. Perkins. 1983. Bioaccumulation and detoxification of contaminants in marine organisms from Southern California coastal waters. In Waste disposal in the oceans, ed. D.F. Soule and D. Walsh, p. 171. Westview Press, Boulder, CO. Back, R.C., and C.J. Watras. 1995. Mercury in zooplankton of Northern Wisconsin lakes: Taxonomic and site-specific trends. (Water Air Soil Pollut. 80:931-9381.) In Mercury as a global pollutant, ed. D.B. Porcella, J.W. Huckabee, and B. Wheatley, pp. 931-938. Kluwer Academic Publishers, Hingham, MA. Salazar, S.M., N. Beckvar, M.H. Salazar, and K. Finkelstein. 1995. An in situ assessment of mercury contamination in the Sudbury River, Massachusetts, using bioaccumulation and growth in transplanted freshwater mussels. NOAA Technical Report. Submitted to U.S. Environmental Protection Agency, Massachusettes Superfund Program Region 1, Boston, MA. Niimi, A.J., and G.P. Kissoon. 1994. Evaluation of the critical body burden concept based on inorganic and organic mercury toxicity to rainbow trout (Oncorhynchus mykiss). Arch. Environ. Contam. Toxicol. 26:169-178. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 521 BIOACCUMULATION SUMMARY 50. METHYLMERCURY Barthalmus, G.T. 1977. Behavioral effects of mercury on grass shrimp. Mar. Pollut. Bull. 8:8790. Biesinger, K.E., L.E. Anderson, and J.G. Eaton. 1982. Chronic effects of inorganic and organic mercury on Daphnia magna: Toxicity, accumulation, and loss. Arch. Environ. Contam. Toxicol. 11:769-774. Boudou, A., and F. Ribeyre. 1985. Experimental study of trophic contamination of Salmo gairdneri by two mercury compounds - HgCl2 and CH3HgCl - Analysis at the organism and organ levels. Water Air Soil Pollut. 26:137-148. Callahan, P., and J.S. Weis. 1983. Methylmercury effects on regeneration and ecdysis in fiddler crabs (Uca pugilator, U. pugnax) after short-term and chronic pre-exposure. Arch. Environ. Contam. Toxicol. 12:707-714. Dillon, T.M. 1977. Mercury and the estuarine marsh clam, Rangia cuneata Gray. I. Toxicity. Arch. Environ. Contam. Toxicol. 6:249-255. Enserink, E.L., J.L. Maas-Diepeveen, and C.J. Van Leeuwen. 1991. Combined effects of metals; an ecotoxicological evaluation. Water Res. 25:679-687. Friedmann, A.S., M.C. Watzin, T. Brinck-Johnsen, and J.C. Leiter. 1996. Low levels of dietary methylmercury inhibit growth and gonadal development in juvenile walleye (Stizostedion vitreum). Aquat. Toxicol. 35:265-278. Guarino, A.M., and S.T. Arnold. 1979. Xenobiotic transport mechanisms and pharmacokinetics in the dogfish shark. In Pesticide and xenobiotic metabolism in aquatic organisms, ed. M.A.Q. Khan, J.J. Lech, and J.J. Menn, pp. 233-258. American Chemical Society, Washington, DC. Hawryshyn, C.W., and W.C. Mackay. 1979. Toxicity and tissue uptake of methylmercury administered interperitoneally to rainbow trout (Salmo gairdneri Richardson). Bull. Environ. Contam. Toxicol. 23:79-86. Heisinger, J.F., and W. Green. 1975. Mercuric chloride uptake by eggs of the ricefish and resulting teratogenic effects. Bull. Environ. Contam. Toxicol. 14:665-673. Lockhart, W.L., J.F. Uthe, A.R. Kenney, and P.M. Mehrle. 1972. Methylmercury in northern pike (Esox lucius): Distribution, elimination, and some biochemical characteristics of contaminated fish. J. Fish. Res. Bd. Can. 29:1519-1523. Manen, C.A., B. Schmidt-Nielsen, and D.N. Russell. 1976. Polyamine synthesis in liver and kidney of flounder in response to methylmercury. Amer. J. Physiol. 231:560-564. Thain, J.E. 1984. Effects of mercury on the prosobranch mollusc Crepidula fornicata: Acute lethal toxicity and effects on growth and reproduction of chronic exposure. Mar. Environ. Res. 12: 285-309. 51. 52. 53. 54. 55. 56. 57. 58. 59. 60. 61. 62. 522 BIOACCUMULATION SUMMARY 63. METHYLMERCURY Weiner, J.G., W.F. Fitzgerald, C.J. Watras, and R.G. Rada. 1990. Partitioning and bioavailability of mercury in an experimentally acidified Wisconsin lake. Environ. Toxicol. Chem. 9: 909-918. Young, D.R., and T.C. Heeson. 1977. Marine bird deaths at the Los Angeles Zoo. Coastal Water Research Program annual report. Southern California Coastal Water Research Project, El Segundo, CA. 64. 523 524 BIOACCUMULATION SUMMARY Chemical Category: METAL Chemical Name (Common Synonyms): NICKEL Chemical Characteristics Solubility in Water: Insoluble [1] Log Kow: NICKEL ASRN: 7440-02-0 Half-Life: Not applicable, stable [1] Log Koc: Human Health Oral RfD: 2 x 10-2 mg/kg/day [2] Critical Effect: Decreased body and organ weights Oral Slope Factor: Not available [2] Carcinogenic Classification: A [2] Confidence: Medium uncertainty factor = 300 Wildlife Partitioning Factors: Partitioning factors for nickel in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for nickel in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Nickel in the aquatic environment can partition to dissolved and particulate organic carbon. Also, the bioavailability of nickel can be influenced to some extent by the concentrations of calcium and magnesium in water. The bioavailability of nickel in sediments is controlled by the concentration of acid-volatile sulfides (AVS) [8]. Food Chain Multipliers: Little evidence exists to support the general occurrence of biomagnification of nickel in the aquatic environment [9 and 10]. Toxicity/Bioaccumulation Assessment Profile Bioaccumulation of nickel is most pronounced in sediments when the ratio of simultaneously extracted metals to acid-volatile sulfide (SEM/AVS) is greater than 1. Although nickel concentrations in animals from sediments with SEM/AVS ratios >1 were approximately 2- to 10-fold greater than nickel concentrations in benthic organisms from sediments with SEM/AVS ratio <1, nickel uptake (tissue concentration) was proportional to the concentration in sediment. Ankley et al. [3] have shown that bioaccumulation of nickel from the sediment by Lumbriculus variegatus was not predictable based on total sediment metal concentration, but was related to the sediment SEM/AVS ratio. 525 526 Species: Taxa Invertebrates Lumbriculus variegatus, Oligochaete worm Sediment Tubificidae 51 g/g 50 g/g 93 g/g 76 g/g 75 g/g Summary of Biological Effects Tissue Concentrations for Nickel Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 0.58 mol/L 16.44 mol/L 38.24 mol/L 31.40 mol/L 4.53 mol/L 32.77 mol/L 8.58 mol/L 14.43 mol/L 3.72 mol/L 17.96 mol/L 0.52 mol/L 2.75 mol/L 0.50 mol/L 3.51 mol/L 16.67 mol/L 17.20 mol/L 0.10 mol/g 5.00 mol/g 3.32 mol/g 0.87 mol/g 0.07 mol/g 0.33 mol/g 1.88 mol/g 0.97 mol/g 3.59 mol/g 2.77 mol/g 0.10 mol/g 0.29 mol/g 1.41 mol/g 1.91 mol/g 7.79 mol/g 0.95 mol/g [3] F 7.20 mg/g 3.19 mg/g 6.96 mg/g 12.04 mg/g 9.45 mg/g [6] L Summary of Biological Effects Tissue Concentrations for Nickel Species: Taxa Neanthes arenaceodentata, Polychaete worm Concentration, Units in1: Sediment Water <0.28 mol/L 0.42 mol/L 2.62 mol/L 0.16 mol/L <0.74 mol/L 3.72 mol/L 0.37 mol/L 0.80 mol/L 54.30 mol/L 1.28 mol/L 64.8 mol/L 67.4 mol/L 36.4 mol/L 0.86 mol/L 73.1 mol/L 52.4 mol/L 449 mol/L Toxicity: Tissue (Sample Type) Effects <0.002 mol/g 0.01 mol/g 0.01 mol/g <0.002 mol/g <0.001 mol/g 0.01 mol/g 0.02 mol/g <0.006 mol/g 0.12 mol/g <0.002 mol/g 0.05 mol/g 0.06 mol/g 0.12 mol/g 0.02 mol/g 0.10 mol/g 0.21 mol/g 1.69 mol/g 3% mortality 13% mortality 0% mortality 3% mortality 7% mortality 13% mortality 0% mortality 0% mortality 20% mortality 7% mortality 10% mortality 0% mortality 3% mortality 0% mortality 0% mortality 0% mortality 3% mortality Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [4] F [5] F Cerastoderma edule, Clam 56.6 mg/kg (whole body)4 Mortality, ED50 [12] L; estimated body residue by regression from other data values, number of replicates is 2 to 5 527 528 Species: Taxa Sediment Mytilus galloprovincialis, Mussel Lamellidans marginalis, 110 mg/L Freshwater mussel Summary of Biological Effects Tissue Concentrations for Nickel Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 128 mg/kg (adductor muscle)4 140 mg/kg (foot)4 209 mg/kg (gill)4 274 mg/kg (mantle)4 138 mg/kg (visceral tissue)4 167 mg/kg (whole body)4 Physiological, NOED Physiological, NOED Physiological, NOED Physiological, NOED Physiological, NOED Physiological,N OED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [12] [12] [12] [12] [12] [12] L; no significant effect on respiration rate at 100 g/L (highest test concentration at which body residues were measured), number of replicates is 2 to 5 1.1-1.4 mg/kg 0.22 [11] F Day 4: 1456.1 g/g (ctenidium) 432.7 g/g (mantle) 468.3 g/g (hepatopancreas) 328.4 g/g (foot) 373.9 g/g (adductor muscle) [5] L Summary of Biological Effects Tissue Concentrations for Nickel Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Day 15: 569.8 g/g (ctenidium) 277.1 g/g ( mantle) 327.1 g/g (hepatopancreas) 218.6 g/g (foot) 186.7 g/g (adductor muscle) Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [5] L Lamellidans marginalis, 22 mg/L Freshwater mussel Daphnia magna, Cladoceran 223 mg/kg (whole body)4 Mortality, ED50 [6] L; lethal body burden after 21-day exposure Fishes Cyprinus carpio, Carp 40 mg/L Day 4: 202.8 mg/L (gill) 226.3 mg/L (kidney) 82.2 mg/L (liver) 97.1 mg/L (brain) 118.1 mg/L (white muscle) Day 15: 103.0 mg/L (gill) 80.3 mg/L (kidney) 97.1 mg/L (liver) 40.6 mg/L (brain) 58.0 mg/L (white) muscle) [5] L 8 mg/L 529 530 Species: Taxa Sediment Pimephales promelas, Fathead minnow 31 g/g 51 g/g 50 g/g 57 g/g 93 g/g 73 g/g 76 g/g 60 g/g 75 g/g 53 g/g 1 2 Summary of Biological Effects Tissue Concentrations for Nickel Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 8.69 mg/g 8.19 mg/g 5.66 mg/g 4.02 mg/g 10.72 mg/g 10.10 mg/g 11.51 mg/g 13.32 mg/g 11.75 mg/g 10.90 mg/g [7] F Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. BIOACCUMULATION SUMMARY References 1. NICKEL Weast handbook of chemistry and physics, 68th edition, 1987-1988, B-110. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September). USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Ankley, .T., G.L. Phipps, E.N. Leonard, D.A. Benoit, V.R. Mattson, P.A. Kosian, A.M. Cotter, J.R. Dierkes, D.J. Hansen, and J.D.Mahony. 1991. Acid-volatile sulfide as a factor mediating cadmium and nickel bioavailability in contaminated sediments. Environ. Sci. Tech. 10:1299-1307. Pesch, C.E., D.J. Hansen, W.S. Boothman, W.J. Berry, and J.D. Mahony. 1995. The role of acidvolatile sulfide and interstitial water metal concentrations in determining bioavailability of cadmium and nickel from contaminated sediments to the marine polychaete Neanthes arenaceodentata. Environ. Toxicol. Chem. 14:129-141. Sreedevi, P., A. Suresh, B. Sivaramakrishna, B. Prabhavathi, and K. Radhakrishnaiah. 1992. Biaccumulation of nickel in the organs of the freshwater fish, Cyprinus carpio, and the freshwater mussel Lamellidens margina, under lethal/sublethal nickel stress. Chemosphere 24:29-36. Enserink, E.L., J.L. Mass-Diepeveen, and C.J. Van Leeuwen. 1991. Combined effects of metals: An ecotoxicological evaluation. Water Res. 25:679-687. Krantzberg, G. 1994. Spatial and temporal variability in metal bioavailability and toxicity of sediment from Hamilton Harbour, Lake Ontario. Environ. Toxicol. Chem. 13:1685-1698. Di Toro, D.M., J.D. Mahony, D.J. Hansen, K.J. Scott, M.B. Hicks, S.M. Mayr, and M.S. Redmond. 1990. Toxicity of cadmium in sediments: The role of acid volatile sulfide. Environ. Toxicol. Chem. 9:1487-1502. Krantzberg, G., and D. Boyd. 1992. The biological significance of contaminants in sediment from Hamilton Harbor, Lake Ontario. 2. 3. 4. 5. 6. 7. 8. 9. 10. Nriagu, J.O. 1980. Global cycle and properties of nickel. In Nickel in the environment, pp. 1-26, Wiley, New York, NY. 11. Houkal, D., B. Rummel, and B. Shephard. 1996. Results of an in situ mussel bioassay in the Puget Sound. Abstract, 17th Annual Meeting, Society of Environmental Toxicology and Chemistry, Washington, DC. November 17-21, 1996 531 BIOACCUMULATION SUMMARY NICKEL 12. Wilson, J.G. 1983. The uptake and accumulation of Ni by Cerastoderma edule and its effect on mortality, body condition and respiration rate. Mar. Environ. Res 8:129-148. 532 BIOACCUMULATION SUMMARY Chemical Category: PESTICIDE (CHLOROPHENOXY) Chemical Name (Common Synonyms): OXYFLUORFEN OXYFLUORFEN CASRN: 42874-03-3 Chemical Characteristics Solubility in Water: No data [1] Log Kow: No data [3] Half-Life: No data [2] Log Koc: -- Human Health Oral RfD: 3 x 10-3 mg/kg/day [4] Confidence: High, uncertainty factor = 100 Critical Effect: Increased absolute liver weight and nonneoplastic lesions in mice Oral Slope Factor: 1.3 x 10-1 per (mg/kg)/day [5] Carcinogenic Classification: C [5] Wildlife Partitioning Factors: Partitioning factors for in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for oxyfluorfen in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Partitioning factors for oxyfluorfen in aquatic organisms were not found in the literature. Food Chain Multipliers: Food chain multipliers for oxyfluorfen in aquatic organisms were not found in the literature. Toxicity/Bioaccumulation Assessment Profile A light activated herbicide, oxyfluorfen at 10-2 mM increased cell membrane permeability in Lemna minor [6]. The screening tissue value for fish for oxyfluorfen presented by the Chesapeake Bay Program is 800 ng/g [7]. 533 534 Species: Taxa Invertebrates Sediment Fishes Wildlife 1 2 Summary of Biological Effects Tissue Concentrations for Oxyfluorfen Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects [NO DATA] Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [NO DATA] [NO DATA] Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. BIOACCUMULATION SUMMARY References 1. OXYFLUORFEN USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long, 1995. Internal report on summary of measured, calculated, and recommended log values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1997. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. January. USEPA. 1992. Classification list of chemicals evaluated for carcinogenicity potential. U.S. Environmental Protection Agency, Office of Pesticide Programs, Washington, DC. O'Brien, M.C., and G.N. Prendeville. 1979. Effect of herbicides on cell membrane permeability in Lemna minor. Weed Res. 19:331-334. Chesapeake Bay Program. 1996. Finfish/shellfish tissue human health consumption thresholds compendium. CBP/TRS 96/XX. Chesapeake Bay Program Office, Annapolis, MD. 2. 3. 4. 5. 6. 7. 535 BIOACCUMULATION SUMMARY PCB 28 Chemical Category: BIPHENYLS Chemical Name (Common Synonyms): 2,4,4-TRICHLOROBIPHENYL Chemical Characteristics Solubility in Water: No data [1], 160 g/L [2] Log Kow: 5.60 [2] Half-Life: No data [3,4] Log Koc: 5.51 L/kg organic carbon CASRN: 7012-37-5 Human Health Oral RfD: No data [5] Critical Effect: -- Oral Slope Factor: No data [5] Carcinogenic Classification: No data [5] Confidence: -- Wildlife Partitioning Factors: No partitioning factors were identified for wildlife. Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and USACE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly waterinsoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. Log biomagnification factors of 1.07 and 1.97 were determined for total PCBs from alewife to herring gull eggs and from alewife to whole body herring gull, respectively [11]. No specific food chain multipliers were identified for PCB 28. Aquatic Organisms Partitioning Factors: Biota-sediment accumulation factors (BSAFs) range from 1.5 to 18.2 for aquatic invertebrate species. The highest BSAF was provided for marine crustaceans. Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify through the food web. Oliver and Niimi [12], studying accumulation of PCBs in various organisms in the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [13] reported that each trophic level 536 BIOACCUMULATION SUMMARY PCB 28 contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific food chain multipliers were identified for PCB 28 or other trichlorobiphenyls. Toxicity/Bioaccumulation Assessment Profile PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in various processes and products because of the extreme stability of many isomers, particularly those with five or more chlorines [14]. A common use of PCBs was as dielectric fluids in capacitors and transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture As a result of their stability and their general hydrophobic nature, PCBs released to the environment have dispersed widely throughout the ecosystem [14]. PCBs are among the most stable organic compounds known, and chemical degradation rates in the environment are thought to be slow. As a result of their highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water and at relatively high concentrations in sediment [15]. Individual PCB congeners have different physical and chemical properties based on the degree of chlorination and position of chlorine substitution, although differences with degree of chlorination are more significant [15]. Solubilities and octanol-water partition coefficients for PCB congeners range over several orders of magnitude [16]. Octanol-water partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest for the most chlorinated PCB congeners. Dispersion of PCBs in the aquatic environment is a function of their solubility [15], whereas PCB mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination [17]. The concentration of PCBs in sediments is a function of the physical characteristics of the sediment, such as grain size [18,19] and total organic carbon content [18,19,20,21]. Fine sediments typically contain higher concentrations of PCBs than coarser sediments because of more surface area [15]. Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [17]. Therefore, it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source [15]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment from reaching the overlying water via diffusion [17]. The persistence of PCBs in the environment is a result of their general resistance to degradation [16]. The rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [22]; other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation to a lesser extent [16]. Photochemical degradation, via reductive dechlorination, is also known to occur in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [21]. Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly than higher chlorinated congeners [23]. PCB congeners with no chlorine substituted in the ortho (2 and 2) positions but with four or more chlorine atoms at the meta (3 and 3) and para (4 and 4) positions can assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) [24]. Examples of these more toxic, coplanar congeners are 537 BIOACCUMULATION SUMMARY PCB 28 3,3,4,4-trachlorobiphenyl (PCB 77), 3,3,4,4,5-pentachlorobiphenyl (PCB 126), and 3,3,4,4,5,5hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of mixtures is to use toxic equivalency factors (TEFs) [25]. With this method, relative potencies for individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The following TEFs have been recommended [25,26]: Congener Class 3,3,4,4,5-PentaCB 3,3,4,4,5,5-HexaCB 3,34,4-TetraCB Monoortho coplanar PCBs Diortho coplanar PCBs Recommended TEF 0.1 0.05 0.01 0.001 0.00002 Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic organisms have a strong tendency to accumulate PCBs from water and food sources. The log bioconcentration factor for fish is approximately 4.70 [27]. This factor represents the ratio of concentration in tissue to the ambient water concentration. Aquatic organisms living in association with PCB-contaminated sediments generally have tissue concentrations equal to or greater than the concentration of PCB in the sediment [27]. Once taken up by an organism, partition primarily into lipid compartments [15]. Thus, differences in PCB concentration between species and between different tissues within the same species may reflect differences in lipid content [15]. PCB concentrations in polychaetes and fish have been strongly correlated to their lipid content [28]. Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higherchlorinated congeners [29, 30]. In some species, tissue concentrations of in females can be reduced during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred are eliminated from the female during spawning [31,32]. Fish and other aquatic organisms biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners [31]. Consequently, fish and other aquatic organisms may accumulate more of the higher chlorinated PCB congeners than is found in the environment [16]. The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate that PCB toxicity is directly related to the duration of exposure [33]. Toxic responses have been noted to occur at concentrations of 0.03 and 0.014 g/L in marine and freshwater environments, respectively [33]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 g/L [33]. Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [34], although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370 [35]. A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic organisms at low tissue concentrations [16]. Field and Dexter [16] suggest that a number of marine and 538 BIOACCUMULATION SUMMARY PCB 28 freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0 mg/kg and as low as 0.1 mg/kg. Spies et al. [36] reported an inverse relationship between PCB concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [37] also reported a significant correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with MFO induction by PCBs at tissue concentrations within the range of environmental exposures [16]. 539 540 Species: Taxa Invertebrates Microcystis 1.35 0.9 ng/g aeruginosa, dw (n = 11) Daphnia longispina, (0-20 cm) Plankton Sediment Plankton, 1.9494 (mean) Species not reported SD = 0.7309 (n = 9) g/kg dw Dreissena polymorpha, Zebra mussel 1.9494 (mean) SD = 0.7309 (n = 9) g/kg dw Dreissena polymorpha, Zebra mussel 1.35 0.9 ng/g dw (n = 11) (0-20 cm) Corbicula fluminea, Station B6: Bivalve 0.44 ng/g dw Station C10: 0.034 ng/g dw Summary of Biological Effects Tissue Concentrations for PCB 28 Concentration, Units in1: Water Toxicity: Ability to Accumulate2: Source: Tissue (Sample Type) Effects Log BCF Log BAF BSAF Reference Comments3 0.23 0.22 ng/g (n=14) 3.3 [38] F; Amsterdam; value is mean SD; mean sediment TOC = 9.7%; mean lipid = 0.65% 0.0084 (mean) 0.3504 (mean) SD = 0.0031 SD = 0.2353 (n = 3) ng/L (n = 5) g/kg [39] F; collected in western Lake Erie (offshore Middle Sister Island); sediment TOC = 7.4% (SD = 1.78), lipid = 1.2% (mean) SD = 0.24 0.0084 (mean) 0.4314 (mean) SD = 0.0031 SD = 0.4642 (n = 3) (n = 20) g/kg ng/L lipid = 1.3% (mean) SD = 0.34 0.52 0.36 ng/g (n = 5) 2.8 [38] F; Amsterdam; value is mean SD; mean sediment TOC = 9.7%; mean lipid = 1.74% [40] 1.14 ng/L 0.334 g/g5 of lipid (whole animal) 0.3 g/g5 of lipid <DL4 F; samples collected from the Rio de la Plata. Sediment depth samples was 0-5 cm. Water sample was filtered. Summary of Biological Effects Tissue Concentrations for PCB 28 Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Ability to Accumulate2: Source: Tissue (Sample Type) Effects 2.93 1.41 ng/g (n = 7) Log BCF Log BAF BSAF 18.2 Reference [38] Comments3 F; Amsterdam; value is mean SD; mean sediment TOC = 9.7%; mean lipid = 0.86% Crustaceans 1.35 0.9 ng/g Gammarus tigrinus, dw (n = 11) Assellus aquaticus, (0-20 cm) Orchestra carimana Gammarus fasciatus, Amphipod 1.9494 (mean) SD = 0.7309 (n = 9) g/kg dw 0.0084 (mean) 0.6664 (mean) SD = 0.0031 SD = 0.2768 (n = 3) ng/L (n = 4) g/kg lipid = 2.1% (mean) SD = 1.04 Orconectes propinquus, Crayfish 1.9494 (mean) SD = 0.7309 (n = 9) g/kg dw 0.0084 (mean) SD = 0.0031 (n = 3) ng/L 0.3924 (mean) SD = 0.2407 (n = 5) g/kg lipid = 1.7% (mean) SD = 0.11 Hydropsyche alterans, Caddisfly larva 1.9494 (mean) SD = 0.7309 (n = 9) g/kg dw 0.0084 (mean) 0.3694 SD = 0.0031 (n = 1) g/kg (n = 3) ng/L lipid = 1.7% (mean) Fishes Prochilodus platensis, Fish Station F17: 0.084 ng/g dw [40] <DL4 0.94g/g5 of lipid F; samples collected from the Rio de la Plata. Oligosarcus jenynsi, Station A1: Fish 64 ng/g dw 541 [40] 0.74 ng/L 0.34 g/g5 of lipid F; samples collected from the Rio Santiago. 542 Species: Taxa Anguilla anguilla, Eel Sediment 1.35 0.9 ng/g dw (n = 11) (0-20 cm) 1 2 Summary of Biological Effects Tissue Concentrations for PCB 28 Concentration, Units in1: Water Toxicity: Ability to Accumulate2: Source: Tissue (Sample Type) Effects 3.98 3.42 ng/g (n = 6) Log BCF Log BAF BSAF 1.5 Reference [38] Comments3 F; Amsterdam; value is mean SD; mean sediment TOC = 9.7%; mean lipid = 14.9% Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 Reported concentrations reflect both congeners 28 and 31. 5 Not clear from reference if concentration is based on wet or dry weight. BIOACCUMULATION SUMMARY References 1. PCB 28 USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February. Shiw, W.Y., and D. MacKay. 1986. A critical review of aqueous solubilities, vapor pressures, Henrys' Law Constants, and octanol-water partition coefficients of the polychlorinated biphenyls. J. Phys. Chem. Data 15: 911-929. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons, chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Jones, P.D., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145. Kay, 1984. Potential for biomagnification of contaminants within marine and freshwater food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. USACE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food chains. Environ. Sci. Technol. 23:699. Braune, B.M., and R. J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol. Chem. 8:957-968. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 543 BIOACCUMULATION SUMMARY 12. PCB 28 Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Rasmussen, J.B., D.J. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J. Fish. Aquat. Sci. 47:2030-2038. Rand, G. M., P. G. Wells, and L. S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology. In: Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M. Rand, pp. 3-67. Taylor and Francis. Washington, DC. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments. In PCBs and the environment, ed. J.S. Waid, pp. 127-182. CRC Press, Inc., Boca Raton, FL. Field, L. J., and R. N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments. Unpublished document. January 11, 1988. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ. Pollut. 5B:121-132. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ. Sci. Technol. 13:65-71. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop, pp. 273-287. American Society of Testing and Materials, Philadelphia, PA. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls. In: PCBs and the Environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton, FL. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In PCBs and the environment, ed. J.S. Waid,. pp. 47-65. CRC Press, Inc., Boca Raton, FL. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and the environment, ed. J.S. Waid,. Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop, "PCBs in Fish Tissue," May 10-11, 1993, pp. 3-9. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington, DC. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10- 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 544 BIOACCUMULATION SUMMARY PCB 28 11, 1993, pp. 3-9. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington, DC. 25. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(1):51-88. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group, Inc., Arlington, MA.) Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136. Shaw, G. R., and D. W. Connell. 1982. Factors influencing concentrations of polychlorinated biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution: A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments. Mar. Biol. 91:497-508. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'Itri and M.A. Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the Environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL. Eisler, R. 1986. Polychlorinated biphenyl hazards to fish, wildlife, and invertebrates: A synoptic review. U.S. Fish Wildl. Serv. Biol. Rep. 85(1.7). Mearns, A.J., M. Matta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G. Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric Administration. Seattle, WA. Long, E.R., and L.G. Morgan. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Tech. Memo. NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success, xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121. 545 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. BIOACCUMULATION SUMMARY 37. PCB 28 Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536. Van der Oost, R., H. Heida, and A. Opperhuizen. 1988. Polychlorinated biphenyl congeners in sediments, plankton, molluscs, crustaceans, and eel in a freshwater lake: Implications of using reference chemicals and indicator organisms in bioaccumulation studies. Arch. Environ. Contam. Toxicol. 17: 721-729. Morrison, H.A., F.A.P.C. Gobas, R. Lazar, and G.D. Haffner. 1996. Development and verification of a bioaccumulation model for organic contaminants in benthic invertebrates. Environ. Sci. Technol. 30:3377-3384. Columbo, J.C., M.F. Khalil, M. Arnac, and A.C. Horth. 1990. Distribution of chlorinated pesticides and individually polychlorinated biphenyls in biotic and abiotic compartments of the Rio de la Plata, Argentina. Environ. Sci. Technol. 24:498-505. 38. 39. 40. 546 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED BIPHENYLS PCB 77 Chemical Name (Common Synonyms): 3,3,4,4-TETRACHLOROBIPHENYL CASRN: 32598-13-3 Chemical Characteristics Solubility in Water: 0.18 mg/L [1] Log Kow: No data [4], 6.1 [5] Half-Life: No data [2,3] Log Koc: -- Human Health Oral RfD: No data [6] Critical Effect: -- Oral Slope Factor: No data [6] Carcinogenic Classification: No data [6] Confidence: -- Wildlife Partitioning Factors: Bioaccumulation factors (BAFs) were determined for mink. The mink had less PCB-77 in their tissues than was measured in their diet. BAF values ranged from 0.1 to 0.2. Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be selectively accumulated from organisms at one trophic level to the next [7]. At least three studies have concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and predators that feed primarily on aquatic organisms [8,9,10]. The results from Biddinger and Gloss [8] and USACE [10] generally agreed that highly water-insoluble compounds (including PCBs) have the potential to biomagnify in these types of food webs. Thomann's [11] model also indicated that highly water-insoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. Log biomagnification factors (BMFs) for tetrachlorobiphenyls from alewife to herring gulls ranged from 1.52 to 1.83, but were not measured specifically for PCB 77 [12]. A study of arctic marine food chains measured log biomagnification factors for tetrachlorobiphenyls that ranged from 0.08 to 0.40 for fish to seal, <0.40 for seal to bear, and <0.30 for fish to bear [13]. Log BMFs calculated for mink fed PCB 77-contaminated feed ranged from 1.00 to 0.70 [40]. Aquatic Organisms Partitioning Factors: Log bioconcentration factors (BCFs) for blue mussels deployed in New Bedford Harbor, MA, were approximately 6.40 and 6.60 during two years of the study, as reported in the attached summary table [42]. 547 BIOACCUMULATION SUMMARY PCB 77 Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify through the food web. Oliver and Niimi [14], studying accumulation of PCBs in various organisms in the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [15] reported that each trophic level contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific food chain multipliers were identified for PCB 77 or other tetrachlorobiphenyls. Toxicity/Bioaccumulation Assessment Profile PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in various processes and products because of the extreme stability of many isomers, particularly those with five or more chlorines [16]. A common use of PCBs was as dielectric fluids in capacitors and transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture. As a result of their stability and their general hydrophobic nature, PCBs released to the environment have dispersed widely throughout the ecosystem [16]. PCBs are among the most stable organic compounds known, and chemical degradation rates in the environment are thought to be slow. As a result of their highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water and at relatively high concentrations in sediment [17]. Individual PCB congeners have different physical and chemical properties based on the degree of chlorination and position of chlorine substitution, although differences with degree of chlorination are more significant [17]. Solubilities and octanol-water partition coefficients for PCB congeners range over several orders of magnitude [18]. Octanol-water partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest for the most chlorinated PCB congeners. Dispersion of PCBs in the aquatic environment is a function of their solubility [17] , whereas PCB mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination [19]. The concentration of PCBs in sediments is a function of the physical characteristics of the sediment, such as grain size [20,21] and total organic carbon content [20,21,22,23]. Fine sediments typically contain higher concentrations of PCBs than coarser sediments because of more surface area [17]. Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [19]. Therefore, it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source [17]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment from reaching the overlying water via diffusion [19]. The persistence of PCBs in the environment is a result of their general resistance to degradation [18]. The rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [24]; other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation to a lesser extent [18]. Photochemical degradation, via reductive dechlorination, is also known to occur in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [23]. 548 BIOACCUMULATION SUMMARY PCB 77 Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly than higher chlorinated congeners [25]. PCB congeners with no chlorine substituted in the ortho (2 and 2) positions but with four or more chlorine atoms at the meta (3 and 3) and para (4 and 4) positions can assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) [26]. Examples of these more toxic, coplanar congeners are 3,3,4,4-tetrachlorobiphenyl (PCB 77), 3,3,4,4,5-pentachlorobiphenyl (PCB 126), and 3,3,4,4,5,5hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of mixtures is to use toxic equivalency factors (TEFs) [27]. With this method, relative potencies for individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The following TEFs have been recommended [27,28]: Congener Class 3,3,4,4,5-PentaCB 3,3,4,4,5,5-HexaCB 3,34,4-TetraCB Monoortho coplanar PCBs Diortho coplanar PCBs Recommended TEF 0.1 0.05 0.01 0.001 0.00002 Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic organisms have a strong tendency to accumulate PCBs from water and food sources. The log bioconcentration factor for fish is approximately 4.70 [29]. This factor represents the ratio of concentration in tissue to the ambient water concentration. Aquatic organisms living in association with PCB-contaminated sediments generally have tissue concentrations equal to or greater than the concentration of PCB in the sediment [29]. Once taken up by an organism, PCBs partition primarily into lipid compartments [17]. Thus, differences in PCB concentration between species and between different tissues within the same species may reflect differences in lipid content [17]. PCB concentrations in polychaetes and fish have been strongly correlated to their lipid content [30]. Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higher-chlorinated congeners [31,32]. In some species, tissue concentrations of PCBs in females can be reduced during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred PCBs are eliminated from the female during spawning [33,34]. Fish and other aquatic organisms biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners [33]. Consequently, fish and other aquatic organisms may accumulate more of the higher chlorinated PCB congeners than is found in the environment [18]. The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate that PCB toxicity is directly related to the duration of exposure [35]. Toxic responses have been noted to occur at concentrations of 0.03 and 0.014 g/L in marine and freshwater environments, respectively [35]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 g/L [35]. Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [36], although the acute toxicity of PCBs is relatively low compared to that 549 BIOACCUMULATION SUMMARY PCB 77 of other chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370 g/kg [37]. A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic organisms at low tissue concentrations [18]. Field and Dexter [18] suggest that a number of marine and freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0 mg/kg and as low as 0.1 mg/kg. Spies et al [38] reported an inverse relationship between PCB concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [39] also reported a significant correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with MFO induction by PCBs at tissue concentrations within the range of environmental exposures [18]. 550 Summary of Biological Effects Tissue Concentrations for PCB 77 Species: Taxa Invertebrates Mytilus edulis, Blue mussel Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 1993: Particulate 1.7 g/L 0.5 n=9 Dissolved 1.0 g/L 0.1 n=9 ~6.60 [42] F; New Bedford Harbor, MA; deployment study; tissue concentrations were only presented for 1994 samples; BCF and tissue concentrations are approximations (~) as data were taken from figure Presented for 1994 samples; BCF and tissue concentrations are approximations (~) as data were taken from figure Mytilus edulis, Blue mussel 1994: Particulate 2.3 g/L 0.9 n=3 Dissolved 0.9 g/L 0.1 n=3 -360 ng/g dw (whole body) ~6.40 [42] 551 552 Summary of Biological Effects Tissue Concentrations for PCB 77 Species: Taxa Daphnia magna, Freshwater cladoceran Concentration, Units in1: Sediment Water exposure water 0.1 g/L Toxicity: Tissue (Sample Type) Effects ~6.5 ng/mg dw No significant effect on (n = 3) survival or reproduction; increased biomass ~55 ng/mg dw (n = 3) No significant effect on survival or reproduction; decreased biomass [41] L; mysids exposed to field contaminated sediments from Lake Champlain, NY; 24-day exposure; screened mysids were screened from direct contact with sediments (% lipid = 5.94 0.27) whole body; unscreened mysids were allowed to burrow into sediment.(% lipid = 5.80 0.18) whole body Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [40] L; 21-day static renewal tests; tissue concentrations are approximations (~), as data were taken from figures 1.0 g/L Mysis relicta, Epibenthic freshwater shrimp 118.47 g/kg dw (TOC = 22.8%) Screened mysids: 0.72 g/kg Unscreened mysids: 8.74 g/kg Summary of Biological Effects Tissue Concentrations for PCB 77 Species: Taxa Strongylocentrotus droebachiensis, Sea urchin Concentration, Units in1: Sediment 0.050 ng/g Water Toxicity: Tissue (Sample Type) Effects 0.087 ng/g Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [43] F; sediment and biota collected near or in Hamlet in Cambridge Bay, NW Territories, Canada. Fishes Myoxocephalus quadricornis, Fourhorn sculpin 0.050 ng/g dw 0.056 ng/g (liver) 0.11ng/g (whole body) [43] F; sediment and biota collected near or in Hamlet in Cambridge Bay, NW Territories, Canada. F Salmonids Wildlife Falco peregrinus, Peregrine falcon 1.5 ng/g (eggs) (n = 6) 11.4% eggshell thinning 0.29 [47] [46] F; Kola Peninsula, Russia White leghorn chicken (embryo) 2.6 g/kg (egg) 8.6 g/kg (egg) LD50 LD50 [44] L; PCBs were injected into the air cell of eggs 553 554 Summary of Biological Effects Tissue Concentrations for PCB 77 Species: Taxa Mustela vison, Mink Concentration, Units in1: Sediment Diet: 11 pg/g4 Water Toxicity: Tissue (Sample Type) Effects 50 pg/g4 (liver) NOAEL Ability to Accumulate2: Log BCF Log BAF No BMF reported Log BMF = 0.70 BSAF Source: Reference Comments3 L; BMF = lipid[45] normalized concentration in the liver divided by the lipid-normalized dietary concentration 300 pg/g4 45 pg/g4 (liver) LOAEL; reduced kit body weights followed by reduced survival Reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female 600 pg/g4 50 pg/g4 (liver) Log BMF = 1.00 1,100 pg/g4 90 pg/g4 (liver) Log BMF = 1.00 1 2 Concentration units expressed in wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 Not clear whether units are in dry or wet weight. BIOACCUMULATION SUMMARY References 1. PCB 77 National Academy of Science. 1979. Polychlorinated biphenyls (report), p.154. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH. February.) MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals, Vol. I, Monoaromatic hydrocarbons, chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. Shiw, W.Y., and D. MacKay. 1986. A critical review of aqueous solubilities, vapor pressures, Henrys' Law Constants, and octanol-water partition coefficients of the polychlorinated biphenyls. J. Phys. Chem. Data 15:911-929. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Jones, P.D., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater food webs. Technical Report D-84-7, U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. USACE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. 2. 3. 4. 5. 6. 7. 8. 9. 10. 555 BIOACCUMULATION SUMMARY 11. PCB 77 Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food chains. Environ. Sci. Technol. 23:699. Braune, B.M., and R. J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol. Chem. 8:957-968. Muir, D.C.G., R.J. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related compounds. Environ. Sci. Technol. 22:1071-1079. Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Rasmussen, J.B., D.J. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J. Fish. Aquat. Sci. 47:2030-2038. Rand, G. M., P. G. Wells, and L. S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M. Rand, pp. 3-67. Taylor and Francis, Washington, DC. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments. In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL. Field, L. J. and R. N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments. Unpublished document. January 11, 1988. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ. Pollut. 5B:121-132. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ. Sci. Technol. 13:65-71. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop, pp. 273-287. American Society of Testing and Materials, Philadelphia, PA. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls. In PBS and the Environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton, FL. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 556 BIOACCUMULATION SUMMARY 23. PCB 77 Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and the environment, ed. J.S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, pp. 37-53. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington, DC. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, pp. 3-9. EPA/823-R-93-003. U.S. Environmental Protection Agency, Washington, DC. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(1):51-88. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group, Inc., Arlington, MA.) Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136. Shaw, G. R. and D. W. Connell. 1982. Factors influencing concentrations of polychlorinated biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution: A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62. Pruell, R.J., J.L. Lake, W.R. Davis, and J.G. Quinn. 1986. Uptake and depuration of organic contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments. Mar. Biol. 91:497-508. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'Itri and M.A. Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 557 BIOACCUMULATION SUMMARY 35. PCB 77 USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH. February.) Mearns, A.J., M. Matta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G. Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric Administration. Seattle, WA. Long, E.R., and L.G. Morgan. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Technical Memorandum NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success, xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536. Van der Oost, R., H. Heida, and A. Opperhuizen. 1988. Polychlorinated biphenyl congeners in sediments, plankton, molluscs, crustaceans, and eel in a freshwater lake: Implications of using reference chemicals and indicator organisms in bioaccumulation studies. Arch. Environ. Contam. Toxicol. 17:721-729. Lester, D.C., and A. McIntosh. 1994. Accumulation of polychlorinated biphenyl congeners from Lake Champlain sediments by Mysis relicta. Environ. Toxicol. Chem. 13:1825-1841. Bergen, B.J., W.G. Nelson, and R.J.Pruell. 1996. Comparison of nonplanar and coplanar PCB congener partitioning in seawater and bioaccumulation in blue mussels (Mytilus edulis). Environ. Toxicol. Chem. 15:1517-1523. Bright, D.A., S.L. Grundy, and K.J. Reimer. 1995. Differential bioaccumulation of non-ortho substituted and other PCB congeners in coastal arctic invertebrates and fish. Environ. Sci. Technol. 29:2504-2512. Brunstrom, B., and L. Andersson. 1988. Toxicity and 7-ethoxyresorufin O-deethylase-inducing potency of coplanar polychlorinated biphenyls (PCBs) in chick embryos. Arch. Toxicol. 62:263266. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 558 BIOACCUMULATION SUMMARY 46. PCB 77 Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 47. 559 560 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED BIPHENYLS PCB 81 Chemical Name (Common Synonyms): 3,4,4,5-TETRACHLOROBIPHENYL CASRN: 70362-50-4 Chemical Characteristics Solubility in Water: No data [1,2] Log Kow: No data [2,4] Half-Life: No data [2,3] Log Koc: -- Human Health Oral RfD: No data [5] Critical Effect: -- Oral Slope Factor: No data [5] Carcinogenic Classification: No data [5] Confidence: -- Wildlife Partitioning Factors: Bioaccumulation factors were determined for mink. At PCB 81 concentration > 66 pg/g, the mink had less PCB 81 in their tissues (liver) than was measured in their diet. At low PCB 81 concentrations (e.g., 27 pg/g), there was an increase in the tissue burden. Log BAF values ranged from 0.10 to 0.23. Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and USACE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly waterinsoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. Log biomagnification factors for tetrachlorobiphenyls from alewife to herring gulls ranged from 1.52 to 1.83, but were not measured specifically for PCB 81 [11]. A study of arctic marine food chains measured log biomagnification factors for tetrachlorobiphenyls that ranged from 0.08 to 0.40 for fish to seal, <0.4 for seal to bear, and <0.3 for fish to bear [12]. No specific food chain multipliers were identified for PCB 81. Aquatic Organisms Partitioning Factors: No partitioning factors were identified for aquatic organisms. Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify through the food web. Oliver and Niimi [13], studying accumulation of PCBs in various organisms in 561 BIOACCUMULATION SUMMARY PCB 81 the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [14] reported that each trophic level contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific food chain multipliers were identified for PCB 81. Toxicity/Bioaccumulation Assessment Profile PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in various processes and products because of the extreme stability of many isomers, particularly those with five or more chlorines [15]. A common use of PCBs was as dielectric fluids in capacitors and transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture. As a result of their stability and their general hydrophobic nature, PCBs released to the environment have dispersed widely throughout the ecosystem [15]. PCBs are among the most stable organic compounds known, and chemical degradation rates in the environment are thought to be slow. As a result of their highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water and at relatively high concentrations in sediment [16]. Individual PCB congeners have different physical and chemical properties based on the degree of chlorination and position of chlorine substitution, although differences with degree of chlorination are more significant [16]. Solubilities and octanol-water partition coefficients for PCB congeners range over several orders of magnitude [17]. Octanol-water partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest for the most chlorinated PCB congeners. Dispersion of PCBs in the aquatic environment is a function of their solubility [16], whereas PCB mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination [18]. The concentration of PCBs in sediments is a function of the physical characteristics of the sediment, such as grain size [19,20] and total organic carbon content [19,20,21,22]. Fine sediments typically contain higher concentrations of PCBs than coarser sediments because of more surface area [16]. Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [18]. Therefore, it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source [16]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment from reaching the overlying water via diffusion [18]. The persistence of PCBs in the environment is a result of their general resistance to degradation [17]. The rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [23]; other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation to a lesser extent [17]. Photochemical degradation, via reductive dechlorination, is also known to occur in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [22]. Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly than higher chlorinated congeners [24]. PCB congeners with no chlorine substituted in the ortho (2 and 562 BIOACCUMULATION SUMMARY PCB 81 2) positions but with four or more chlorine atoms at the meta (3 and 3) and para (4 and 4) positions can assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) [25]. Examples of these more toxic, coplanar congeners are 3,3,4,4-tetrachlorobiphenyl (PCB 77), 3,3,4,4,5-pentachlorobiphenyl (PCB 126), and 3,3,4,45,5hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of mixtures is to use toxic equivalency factors (TEFs) [26]. With this method, relative potencies for individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The following TEFs have been recommended [26,27]: Congener Class 3,3,4,4,5-PentaCB 3,3,4,4,5,5-HexaCB 3,34,4-TetraCB Monoortho coplanar PCBs Diortho coplanar PCBs Recommended TEF 0.1 0.05 0.01 0.001 0.00002 Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic organisms have a strong tendency to accumulate PCBs from water and food sources. The log bioconcentration factor for fish is approximately 4.70 [28]. This factor represents the ratio of concentration in tissue to the ambient water concentration. Aquatic organisms living in association with PCB-contaminated sediments generally have tissue concentrations equal to or greater than the concentration of PCB in the sediment [28]. Once taken up by an organism, PCBs partition primarily into lipid compartments [16]. Thus, differences in PCB concentration between species and between different tissues within the same species may reflect differences in lipid content [16]. PCB concentrations in polychaetes and fish have been strongly correlated to their lipid content [29]. Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higherchlorinated congeners [30, 31]. In some species, tissue concentrations of PCBs in females can be reduced during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred PCBs are eliminated from the female during spawning [32,33]. Fish and other aquatic organisms biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners [32]. Consequently, fish and other aquatic organisms may accumulate more of the higher chlorinated PCB congeners than is found in the environment [17]. The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate that PCB toxicity is directly related to the duration of exposure [34]. Toxic responses have been noted to occur at concentrations of 0.03 and 0.014 g/L in marine and freshwater environments, respectively [34]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 g/L [34]. Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [35], although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370 g/kg [36]. 563 BIOACCUMULATION SUMMARY PCB 81 A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic organisms at low tissue concentrations [17]. Field and Dexter [17] suggest that a number of marine and freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0 mg/kg and as low as 0.1 mg/kg. Spies et al. [37] reported an inverse relationship between PCB concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [38] also reported a significant correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with MFO induction by PCBs at tissue concentrations within the range of environmental exposures [17]. 564 Summary of Biological Effects Tissue Concentrations for PCB 81 Species: Taxa Invertebrates Tubifex sp, Oligochaetes . Fishes Cyprinus carpio, Carp 0.0006 mg/kg (n = 1) 0.0210.012 mg/kg (n = 9) [39] F; lower Detroit River 0.0006 mg/kg (n = 1) 0.0003 mg/kg (one composite) [39] F; lower Detroit River Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Salmonids Wildlife Bucephala clangula, 0.0006 mg/kg Goldeneye (n = 1) 0.0170.0002 mg/kg (n = 3) 0.67 [42] F [39] F; lower Detroit River Aythya affinis, Lesser scaup 0.0006 mg/kg (n = 1) 0.310.017 mg/kg (n = 7) [39] F; lower Detroit River Aythya marila, Greater scaup 0.0006 mg/kg (n = 1) 0.0460.016 mg/kg (n = 3) [39] F; lower Detroit River Falco peregrinus, Peregrine falcon 565 0.14 ng/g (eggs) (n = 6) 11.4% eggshell thinning [40] F; Kola Peninsula, Russia 566 Summary of Biological Effects Tissue Concentrations for PCB 81 Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 50 pg/g4 (liver) NOAEL Ability to Accumulate2: Log BCF Log BAF No BMF reported Log BMF = 0.23 BSAF Source: Reference [41] Comments3 L; BMF = lipidnormalized concentration in the liver divided by the lipidnormalized dietary concentration Mustela vison, Mink Diet: 2 pg/g4 27 pg/g4 45 pg/g4 (liver) 66 pg/g4 150 pg/g4 50 pg/g4 (liver) LOAEL; reduced kit body weights followed by reduced survival 100 pg/g4 (liver) Reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female Log BMF = 0.10 Log BMF = 0.00 1 2 Concentration units in wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 Not clear whether units are in dry or wet weight. BIOACCUMULATION SUMMARY References 1. PCB 81 USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons, chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Jones, P.D., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. USACE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food chains. Environ. Sci. Technol. 23:699. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957-968. 2. 3. 4 5. 6. 7. 8. 9. 10. 11. 567 BIOACCUMULATION SUMMARY 12. PCB 81 Muir, D.C.G., R.J. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related compounds. Environ. Sci. Technol. 22:1071-1079. Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Rasmussen, J.B., D.J. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J. Fish. Aquat. Sci. 47:2030-2038. Rand, G.M., P.G. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M. Rand, pp. 3-67. Taylor and Francis, Washington, DC. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments. In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments. Unpublished document. January 11, 1988. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ. Pollut. 5B:121-132. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ. Sci. Technol. 13:65-71. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop, pp. 273-287. American Society of Testing and Materials, Philadelphia, PA. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls. In PCBs and the environment, ed. J.S. Waid, Vol.1, pp. 101-120. CRC Press, Inc. Boca Raton, FL. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and the environment, ed. J.S. Waid, Vol. 2., pp. 89-100. CRC Press, Inc., Boca Raton, FL. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 568 BIOACCUMULATION SUMMARY PCB 81 pp. 37-53. EPA/823-R-93003, U.S. Environmental Protection Agency, Office of Water, Washington, DC. 25. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, pp. 3-9. EPA/823-R-93003, U.S. Environmental Protection Agency, Office of Water, Washington, DC. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(1):51-88. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group, Inc., Arlington, MA.) Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution: A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62. Pruell, R. J., J.L. Lake, W.R. Davis, and J.G. Quinn. 1986. Uptake and depuration of organic contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments. Mar. Biol. 91:497-508. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'Itri and M.A. Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.) Mearns, A.J., M. Matta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G. Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 569 BIOACCUMULATION SUMMARY PCB 81 assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric Administration. Seattle, WA. 36. Long, E.R., and L.G. Morgan. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Technical Memorandum NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA. Spies, R. B., D.W. Rice, Jr., P.A. Montagna, and R.R. Ireland. 1985. Reproductive success, xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Patichthys stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536. Smith, E.V., J.M. Spurr, J.C. Filkins, and J.J. Jones. 1985. Organochlorine contaminants of wintering ducks foraging on Detroit River sediments. J. Great Lakes Res. 11(3):231-246. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 37. 38. 39. 40. 41. 42. 570 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED BIPHENYLS Chemical Name (Common Synonyms): 2,3,3,4,4-PENTACHLOROBIPHENYL PCB 105 CASRN: 32598-14-4 Chemical Characteristics Solubility in Water: No data [1], 0.0008 - 0.17 mg/L [2] Log Kow: 5.6 - 6.5 [2], No data [4] Half-Life: No data [2,3] Log Koc: 5.51 - 6.39 L/kg organic carbon Human Health Oral RfD: No data [5] Critical Effect: -- Oral Slope Factor: No data [5] Carcinogenic Classification: No data [5] Confidence: -- Wildlife Partitioning Factors: One study reported biomagnification factors (BMFs) for mink exposed to PCBcontaminated food. The lipid-normalized BMFs ranged from 3.8 to 6.8 indicating an accumulation of this PCB congener in the liver. Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and USACE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly waterinsoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. The log biomagnification factor for PCB 105 from alewife to herring gulls in Lake Ontario was 2.01 [11]. A study of arctic marine food chains measured log biomagnification factors for pentachlorobiphenyls that ranged from 0.71 to 1.05 for fish to seal, 0.28 to 0.49 for seal to bear, and 1.14 for fish to bear [12]. Aquatic Organisms Partitioning Factors: Two studies were found that reported laboratory-measured data to calculate nonnormalized log bioaccumulation factors (BAFs) and biota-sediment accumulation factors (BSAFs). In the first study the log BAFs determined for marine clams ranged from 0.86 to 1.35 [41]. The BSAFs ranged from 1.63 to 3.85, with the highest BSAF value associated with the lowest BAF. In the second 571 BIOACCUMULATION SUMMARY PCB 105 study, only BSAF for marine clams were reported. These values ranged from 0.22 to 0.68 [42]. A BSAF of 4.49 was determined for salmonids [46]. Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify through the food web. Oliver and Niimi [13], studying accumulation of PCBs in various organisms in the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [14] reported that each trophic level contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific food chain multipliers were identified for PCB 105 or other pentachlorobiphenyls. Toxicity/Bioaccumulation Assessment Profile PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in various processes and products because of the extreme stability of many isomers, particularly those with five or more chlorines [15]. A common use of PCBs was as dielectric fluids in capacitors and transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture. As a result of their stability and their general hydrophobic nature, PCBs released to the environment have dispersed widely throughout the ecosystem [15]. PCBs are among the most stable organic compounds known, and chemical degradation rates in the environment are thought to be slow. As a result of their highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water and at relatively high concentrations in sediment [16]. Individual PCB congeners have different physical and chemical properties based on the degree of chlorination and position of chlorine substitution, although differences with degree of chlorination are more significant [16]. Solubilities and octanol-water partition coefficients for PCB congeners range over several orders of magnitude [17]. Octanol-water partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest for the most chlorinated PCB congeners. Dispersion of PCBs in the aquatic environment is a function of their solubility [16], whereas PCB mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination [18]. The concentration of PCBs in sediments is a function of the physical characteristics of the sediment, such as grain size [19,20] and total organic carbon content [19,20,21,22]. Fine sediments typically contain higher concentrations of PCBs than coarser sediments because of more surface area [16]. Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [18]. Therefore, it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source [16]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment from reaching the overlying water via diffusion [18]. The persistence of PCBs in the environment is a result of their general resistance to degradation [17]. The rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [23]; other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation 572 BIOACCUMULATION SUMMARY PCB 105 to a lesser extent [17]. Photochemical degradation, via reductive dechlorination, is also known to occur in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [22]. Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly than higher chlorinated congeners [24]. PCB congeners with no chlorine substituted in the ortho (2 and 2) positions but with four or more chlorine atoms at the meta (3 and 3) and para (4 and 4) positions can assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) [25]. Examples of these more toxic, coplanar congeners are 3,3,4,4-tetrachlorobiphenyl (PCB 77), 3,3,4,4,5-pentachlorobiphenyl (PCB 126), and 3,3,4,4,5,5hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of mixtures is to use toxic equivalency factors (TEFs) [26]. With this method, relative potencies for individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The following TEFs have been recommended [26,27]: Congener Class 3,3,4,4,5-PentaCB 3,3,4,4,5,5-HexaCB 3,34,4-TetraCB Monoortho coplanar PCBs Diortho coplanar PCBs Recommended TEF 0.1 0.05 0.01 0.001 0.00002 Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic organisms have a strong tendency to accumulate PCBs from water and food sources. The log bioconcentration factor for fish is approximately 4.70 [28]. This factor represents the ratio of concentration in tissue to the ambient water concentration. Aquatic organisms living in association with PCB-contaminated sediments generally have tissue concentrations equal to or greater than the concentration of PCB in the sediment [28]. Once taken up by an organism, PCBs partition primarily into lipid compartments [16]. Thus, differences in PCB concentration between species and between different tissues within the same species may reflect differences in lipid content [16]. PCB concentrations in polychaetes and fish have been strongly correlated to their lipid content [29]. Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higherchlorinated congeners [30,31]. In some species, tissue concentrations of PCBs in females can be reduced during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred PCBs are eliminated from the female during spawning [32,33]. Fish and other aquatic organisms biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners [32]. Consequently, fish and other aquatic organisms may accumulate more of the higher chlorinated PCB congeners than is found in the environment [17]. The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate that PCB toxicity is directly related to the duration of exposure [34]. Toxic responses have been noted to occur at concentrations of 0.03 and 0.014 g/L in marine and freshwater environments, respectively [34]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 g/L [34]. 573 BIOACCUMULATION SUMMARY PCB 105 Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [35], although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370 g/kg [36]. A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic organisms at low tissue concentrations [17]. Field and Dexter [17] suggest that a number of marine and freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0 mg/kg and as low as 0.1 mg/kg. Spies et al. [37] reported an inverse relationship between PCB concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [38] also reported a significant correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with MFO induction by PCBs at tissue concentrations within the range of environmental exposures [17]. 574 Summary of Biological Effects Tissue Concentrations for PCB 105 Species: Taxa Invertebrates Plankton, Species not given Surface water: 0.003 0.666 (mean) (mean) SD = 0.1881 SD = 0.0020 (n = 5) fg/kg (n = 3) ng/L [39] F; collected in western Lake Erie (offshore Middle Sister Island). Sediment TOC = 7.4% (SD-1.78); lipid = 1.2% (mean) SD-0.24 F; Lake Ontario; value is mean SD; lipid content = 0.5% Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 2.703 (mean) SD = 1.0659 (n = 9) fg/kg dw Plankton (a mixture of primarily phytoplankton and some zooplankton) Mainly Tubifex tubifex and Limnodrilus hoffmeisteri, Oligochaete 14 5.1 ng/g 10 8.4 0.8 0.2 ng/g dw (0-3 cm) pg/L (surface (n = 3) (n = 38) water) (n = 7) [13] 14 5.1 ng/g 10 8.4 2.6 1.4 ng/g dw (0-3 cm) pg/L (surface (n = 6) (n = 38) water) (n = 7) [13] F; Lake Ontario; value is mean SD; lipid content = 1% Dreissena polymorpha, Zebra mussel 2.703 (mean) SD = 1.0659 (n = 9) fg/kg dw 0.003 (mean) 1.627 (mean) SD = 0.0020 SD = 1.6470 (n = 3) (n = 20) fg/kg ng/L lipid = 1.3% (mean) SD = 0.34 575 576 Summary of Biological Effects Tissue Concentrations for PCB 105 Species: Taxa Macoma nasuta, Bent-nose clam Concentration, Units in1: Sediment 52.6 ng/g dw (grain size < 1 mm) 43.2 ng/g dw (grain size < 0.25 mm) 48.8 ng/g dw (grain size < 0.125 mm) ng/g dw: 1.51 0.032 1.26 8.60.37 203.7 707.6 89.97 g/kg dw (TOC = 22.8%) Water Toxicity: Tissue (Sample Type) Effects 1,046 ng/g dw (n = 30) 575 ng/g dw (n = 30) 297 ng/g dw (n = 30) Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [41] L; steady state BAFs were calculated with average tissue residues and sediment concentrations from exposure days 42-119 22.2 (dw) 1.63 14.5 (dw) 2.87 7.3 (dw) 3.85 Macoma nasuta, Bent-nose clam ng/g dw: 6.60.83 1.80.67 8.20.75 11.90.84 20.32.83 Screened mysids: 1.46 g/kg (whole body) Unscreened mysids: 9.85 g/kg (whole body) [42] 0.68 0.22 0.64 0.56 0.39 [40] L; value given is mean SE; sediment TOC ranged from 0.84% to 7.4% Mysis relicta, Mysid L; mysids exposed to field contaminated sediments from Lake Champlain, NY; 24 day exposure; screened mysids were screened from direct contact with sediments (% lipid = 5.940.27); unscreened mysids were allowed to burrow into sediment.(% lipid = 5.800.18) Summary of Biological Effects Tissue Concentrations for PCB 105 Species: Taxa Mysis relicta, Mysid Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [13] F; Lake Ontario; value is mean SD; lipid content = 3% lipid = 2.1% (mean) SD = 1.04 14 5.1 ng/g 10 8.4 pg/L 8.5 3.5 ng/g dw (0-3 cm) surface water (n = 2) (n = 38) ( n = 7) 0.003 (mean) 1.611 (mean) SD = 0.0020 SD = 0.7505 (n = 3) (n = 4) fg/kg ng/L Gammarus fasciatus, 2.703 (mean) Amphipod SD = 1.0659 (n = 9) fg/kg dw Pontoporeia affinis, 14 5.1 ng/g 10 8.4 12 8 ng/g Amphipod dw (0-3 cm) pg/L (surface (n = 6) (n = 38) water) (n = 7) Orconectes propinquus, Crayfish 2.703 (mean) SD = 1.0659 (n = 9) fg/kg dw 2.703 (mean) SD = 1.0659 (n = 9) fg/kg dw 0.003 (mean) 0.606 (mean) SD = 0.0020 0.1101 (n = 3) (n = 5) fg/kg ng/L 0.003 (mean) 1.109 SD = 0.0020 (n = 1) fg/kg (n = 3) ng/L [13] F; Lake Ontario; value is mean SD; lipid content = 3% lipid = 1.7% (mean) SD = 0.11 Hydropsyche alterans, Caddisfly larva lipid = 1.7% (mean) Fishes Alosa pseudoharengus, Alewife 14 5.1 ng/g 10 8.4 pg/L 27 ng/g dw (0-3 cm) surface water (one composite) (n = 38) (n = 7) [13] F; Lake Ontario; value is mean SD; lipid content = 7% 577 578 Summary of Biological Effects Tissue Concentrations for PCB 105 Species: Taxa Cottus cognatus, Sculpin Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [13] F; Lake Ontario; value is mean SD; lipid content = 8% F; Lake Ontario; value is mean SD; lipid content = 4% F; Lake Ontario; value is mean SD; lipid content = 4% 14 5.1 ng/g 10 8.4 pg/L 39 ng/g dw (0-3 cm) surface water (one composite) (n = 38) (n = 7) Osmerus mordax, 14 5.1 ng/g 10 8.4 pg/L 15 2.0 ng/g Small rainbow smelt dw (0-3 cm) surface water (n = 4) (n = 38) (n = 7) Osmerus mordax, 14 5.1 ng/g 10 8.4 38 ng/g Large rainbow smelt dw (0-3 cm) pg/L (surface (one composite) (n = 38) water) (n = 7) Salmonids: Oncorhynchus kisutch, Coho salmon; Oncorhynchus mykiss (Salmo gairdner), Rainbow trout; Salvelinus namaycush, Lake trout; Salmo trutta, Brown trout 10 8.4 ng/g 14 5.1 pg/L 110 82 ng/g dw (0-3 cm) surface water (n = 60) (n = 38) (n = 7) [13] [13] [13] F; Lake Ontario; value is mean SD; lipid content = 11%; wild fish. 4.49 [46] Wildlife Falco peregrinus, Peregrine falcon White leghorn chicken embryo 72 ng/g (eggs) (n = 6) 11.4% eggshell thinning 2,200 g/kg (egg) LD50 [44] F; Kola Peninsula, Russia L; PCBs were injected into the air cell of eggs [43] Summary of Biological Effects Tissue Concentrations for PCB 105 Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 2,900 pg/g4 (liver) NOAEL Ability to Accumulate2: Log BCF Log BAF Log BMF = 0.58 Log BMF = 0.68 BSAF Source: Reference Comments3 [45] L; BMF = lipidnormalized concentration in the liver divided by the lipid-normalized dietary concentration Mustela vison, Mink Diet: 510 pg/g4 12,000 pg/g4 54,000 pg/g4 (liver) LOAEL; reduced kit body weights followed by reduced survival Reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female 23,000 pg/g4 105,000 pg/g4 (liver) Log BMF = 0.66 41,000 pg/g4 181,000 pg/g4 (liver) Log BMF = 0.83 1 2 Concentration units given in wet weight unless otherwise indicated. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 Not clear whether units are in dry or wet weight. 579 BIOACCUMULATION SUMMARY References 1. PCB 105 USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons, chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Jones, P.D., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. USACE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food chains. Environ. Sci. Technol. 23:699. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol. Chem. 8:957-968. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 580 BIOACCUMULATION SUMMARY 12. PCB 105 Muir, D.C.G., R.J. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related compounds. Environ. Sci. Technol. 22:1071-1079. Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Rasmussen, J.B., D.J. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J. Fish. Aquat. Sci. 47:2030-2038. Rand, G.M., P.G. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M. Rand, pp. 3-67. Taylor and Francis, Washington, DC. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments. In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments. Unpublished document. January 11, 1988. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ. Pollut. 5B:121-132. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ. Sci. Technol. 13:65-71. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop (eds.), pp. 273-287. American Society of Testing and Materials, Philadelphia, PA. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls. In PCBs and the environment, ed. J.S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton, FL. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and the environment, ed. J.S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc., Boca Raton, FL. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, pp. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 581 BIOACCUMULATION SUMMARY PCB 105 37-53. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington, DC. 25. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, pp. 3-9. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington, DC. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Crit. Rev.Toxicol. 21(1):51-88. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group, Inc., Arlington, MA.) Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution: A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62. Pruell, R.J., J.L. Lake, W.R. Davis, and J.G. Quinn. 1986. Uptake and depuration of organic contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments. Mar. Biol. 91:497-508. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'Itri and M.A. Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the Environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/580-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.) Mearns, A.J., M. Matta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G. Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric Administration. Seattle, WA. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 582 BIOACCUMULATION SUMMARY 36. PCB 105 Long, E.R., and L.G. Morgan. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Tech. Memo. NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA. Spies, R.B., D.W. Rice, Jr., P.A. Montagna, and R.R. Ireland. 1985. Reproductive success, xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536. Morrison, H.A., F.A.P.C. Gobas, R. Lazar, and G.D. Haffner. 1996. Development and verification of a bioaccumulation model for organic contaminants in benthic invertebrates. Environ. Sci. Technol. 30:3377-3384. Lester, D.C., and A. McIntosh. 1994. Accumulation of polychlorinated biphenyl congeners from Lake Champlain sediments by Mysis relicta. Environ. Toxicol. Chem. 13:1825-1841. Boese, B.L., M. Winsor, H. Lee II, S. Echols, J. Pelletier, and R. Randal. 1995. PCB congeners and hexachlorobenzene biota sediment accumulation factors for Macoma nasuta exposed to sediments with different total organic carbon contents. Environ. Toxicol. Chem. 14(2): 303-310. Ferraro, S.P., H. Lee II, L.M. Smith, R.J. Ozretich, and D.T. Sprecht. 1991. Accumulation factors for eleven polychlorinated biphenyl congeners. Bull. Environ. Contam. Toxicol. 46:276-283. Brunstrom, B. 1990. Mono-ortho-chlorinated chlorobiphenyls: Toxicity and induction of 7-ethoxyresorufin O-deethylase (EROD) activity in chick embryos. Arch. Toxicol. 64:188-192. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 583 584 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED BIPHENYLS Chemical Name (Common Synonyms): 2,3,4,4,5-PENTACHLOROBIPHENYL PCB 118 CASRN: 31508-00-6 Chemical Characteristics Solubility in Water: No data [1] Log Kow: -- Half-Life: No data [2,3] Log Koc: 5.51 - 6.39 L/kg organic carbon Human Health Oral RfD: No data [5] Critical Effect: -- Oral Slope Factor: No data [5] Carcinogenic Classification: No data [5] Confidence: -- Wildlife Partitioning Factors: In a laboratory study with mink, the lipid-normalized ratios of PCB 118 in liver to food ranged from 3.4 to 5.9 (log BMF = 0.53 to 0.77) [49]. The ratio of PCB 118 in three species of duck to sediment in the lower Detroit River ranged from 21 to 35 [40]. Food Chain Multipliers: For PCBs as a class, the most toxic congeners have been shown to be selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and USACE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly waterinsoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. The biomagnification factor for PCB 118 from alewife to herring gulls in Lake Ontario was 80 [11]. A study of arctic marine food chains measured log biomagnification factors for pentachlorobiphenyls that ranged from 0.71 to 1.05 for fish to seal, 0.28 to 0.49 for seal to bear, and 1.14 for fish to bear [12]. Aquatic Organisms Partitioning Factors: Steady-state BSAFs for the bent-nose clam ranged from 0.59 to 4.7 in two laboratory studies. The ratio of PCB 118 in carp tissue to sediment from the lower Detroit River was 25. Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify through the food web. Oliver and Niimi [13], studying accumulation of PCBs in various organisms in the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving 585 BIOACCUMULATION SUMMARY PCB 118 from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [14] reported that each trophic level contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific food chain multipliers were identified for PCB 118 or other pentachlorobiphenyls. Toxicity/Bioaccumulation Assessment Profile PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in various processes and products because of the extreme stability of many isomers, particularly those with five or more chlorines [15]. A common use of PCBs was as dielectric fluids in capacitors and transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture. As a result of their stability and their general hydrophobic nature, PCBs released to the environment have dispersed widely throughout the ecosystem [15]. PCBs are among the most stable organic compounds known, and chemical degradation rates in the environment are thought to be slow. As a result of their highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water and at relatively high concentrations in sediment [16]. Individual PCB congeners have different physical and chemical properties based on the degree of chlorination and position of chlorine substitution, although differences with degree of chlorination are more significant [16]. Solubilities and octanol-water partition coefficients for PCB congeners range over several orders of magnitude [17]. Octanol-water partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest for the most chlorinated PCB congeners. Dispersion of PCBs in the aquatic environment is a function of their solubility [16], whereas PCB mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination [18]. The concentration of PCBs in sediments is a function of the physical characteristics of the sediment, such as grain size [19,20] and total organic carbon content [19,20,21,22]. Fine sediments typically contain higher concentrations of PCBs than coarser sediments because of more surface area [16]. Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [18]. Therefore, it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source [16]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment from reaching the overlying water via diffusion [18]. The persistence of PCBs in the environment is a result of their general resistance to degradation [17]. The rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [23]; other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation to a lesser extent [17]. Photochemical degradation, via reductive dechlorination, is also known to occur in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [22]. Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly than higher chlorinated congeners [24]. PCB congeners with no chlorine substituted in the ortho (2 and 2) positions but with four or more chlorine atoms at the meta (3 and 3) and para (4 and 4) positions can assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8586 BIOACCUMULATION SUMMARY PCB 118 tetrachlorodibenzo-p-dioxin (TCDD) [25]. Examples of these more toxic, coplanar congeners are 3,3,4,4-tetrachlorobiphenyl (PCB 77), 3,3,4,4,5-pentachlorobiphenyl (PCB 126), and 3,3,4,4',5,5'hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of mixtures is to use toxic equivalency factors (TEFs) [26]. With this method, relative potencies for individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The following TEFs have been recommended [26,27]: Congener Class 3,3,4,4,5-PentaCB 3,3,4,4,5,5-HexaCB 3,34,4TetraCB Monoortho coplanar PCBs Diortho coplanar PCBs Recommended TEF 0.1 0.05 0.01 0.001 0.00002 Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic organisms have a strong tendency to accumulate PCBs from water and food sources. The log bioconcentration factor for fish is approximately 4.70 [28]. This factor represents the ratio of concentration in tissue to the ambient water concentration. Aquatic organisms living in association with PCB-contaminated sediments generally have tissue concentrations equal to or greater than the concentration of PCB in the sediment [28]. Once taken up by an organism, PCBs partition primarily into lipid compartments [16]. Thus, differences in PCB concentration between species and between different tissues within the same species may reflect differences in lipid content [16]. PCB concentrations in polychaetes and fish have been strongly correlated to their lipid content [29]. Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higherchlorinated congeners [30,31]. In some species, tissue concentrations of PCBs in females can be reduced during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred PCBs are eliminated from the female during spawning [32,33]. Fish and other aquatic organisms biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners [32]. Consequently, fish and other aquatic organisms may accumulate more of the higher chlorinated PCB congeners than is found in the environment [17]. The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate that PCB toxicity is directly related to the duration of exposure [34]. Toxic responses have been noted to occur at concentrations of 0.03 and 0.014 g/L in marine and freshwater environments, respectively [34]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 g/L [34]. Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [35], although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370 g/kg [36]. A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic organisms at low tissue concentrations [17]. Field and Dexter [17] suggest that a number of marine and 587 BIOACCUMULATION SUMMARY PCB 118 freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0 mg/kg and as low as 0.1 mg/kg. Spies et al. [37] reported an inverse relationship between PCB concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [38] also reported a significant correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with MFO induction by PCBs at tissue concentrations within the range of environmental exposures [17]. 588 Summary of Biological Effects Tissue Concentrations for PCB 118 :Species Taxa Invertebrates Plankton 4.514 (mean) SD = 1.8449 (n = 9) g/kg dw 0.007 (mean) 0.750 (mean) SD = 0.0044 SD = 0.4919 (n = 3) (n = 5) fg/kg ng/L [42] F; collected in western Lake Erie (offshore Middle Sister Island); sediment TOC = 7.4%; SD = 1.78 lipid = 1.2% (mean) SD = 0.24 F; lower Detroit River L; value given is mean SE; sediment TOC ranged from 0.84% to 7.4% Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 Tubifex sp., Oligochaetes Macoma nasuta, Bent-nose clam 0.017 mg/kg 0.0069 mg/kg [40] ng/g dw: 2.93 0.067 2.5 16.5 1.42 45 9.2 162 16.5 44.2 ng/g dw (grain size < 1 mm) 36.2 ng/g (grain size < 0.25 mm) 41.6 ng/g dw (grain size < 0.125 mm) ng/g dw: 20 3.0 12.0 1.89 28.9 2.60 40.3 2.64 66 8.9 1,049 ng/g dw (n = 30) 550 ng/g dw (n = 30) 296 ng/g dw (n = 30) [43] 1.08 0.73 1.17 0.82 0.54 30.3 (dw) 2.02 [41] Macoma nasuta, Bent-nose clam 18.5 (dw) 3.28 8.4 (dw) 4.74 L; steady state BAFs were calculated with average tissue residues and sediment concentrations from exposure days 42-119. 589 590 :Species Taxa Dreissena polymorpha, Zebra mussel Sediment 4.514 (mean) SD = 1.8449 (n = 9) g/kg dw Mytilus edulis, Blue mussel Daphnia magna, Freshwater cladoceran Gammarus fasciatus, 4.514 (mean) Amphipod SD = 1.8449 (n = 9) g/kg dw Summary of Biological Effects Tissue Concentrations for PCB 118 Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 Lipid = 1.3% (mean) SD = 0.34 0.007 (mean) 2.156 (mean) SD = 0.0044 SD = 0.8847 (n = 3) (n = 20) g/kg ng/L Water column: Whole body: ~16.0 ng/L ~4.0 ng/L ~0.8 ng/L ~1,780 ng/g dw ~1,000 ng/g dw ~130 ng/g dw ~3.5 ng/mg dw (n = 3) No significant effect on survival, reproduction, or biomass No significant effect on survival, reproduction, or biomass [45] F; New Bedford Harbor, MA; deployment study; ~ -read all values off figures 0.1 fg/L [39] L; 21-day static renewal tests; tissue concentrations are approximations (~), as data were taken from figures 1.0 fg/L ~130 ng/mg dw (n = 3) 0.007 (mean) 3.113 (mean) SD = 0.0044 SD = 1.7881 (n = 3) (n = 4) g/kg ng/L Lipid = 2.1% (mean) SD = 1.04 Summary of Biological Effects Tissue Concentrations for PCB 118 :Species Taxa Orconectes propinquus, Crayfish Concentration, Units in1: Sediment 4.514 (mean) SD = 1.8449 (n = 9) g/kg dw 4.514 (mean) SD = 1.8449 (n = 9) g/kg dw 135.73 g/kg dw (TOC = 22.8%) Water 0.007 (mean) SD = 0.0044 (n = 3) ng/L Toxicity: Tissue (Sample Type) Effects 2.242 (mean) SD = 0.3628 (n = 5) g/kg Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 Lipid = 1.7% (mean) SD = 0.11 Hydropsyche alterans, Caddisfly larva 0.007 (mean) 4.780 SD = 0.0044 (n = 1) (n = 3) g/kg ng/L Screened mysids: 2.39 g/kg (whole body) [44] Lipid = 1.7% (mean) Mysis relicta, Mysid Unscreened mysids: 15.67 g/kg (whole body) L; mysids exposed to field contaminated sediments from Lake Champlain, NY; 24-day exposure screened mysids were screened from direct contact with sedi-ments (% lipid = 5.94 0.27); unscreened mysids were allowed to burrow into sediment.(% lipid = 5.80 0.18) 591 592 :Species Taxa Fishes Salvelinus namaycush namaycush, Lake trout 0.87 ng/g 0.11 n=4 Sediment Coregonus culpeaformis neohantoniensus, Whitefish Salmonids 0.87 ng/g 0.11 n=4 Cyprinus carpio, Carp 0.017 mg/kg (n = 1) Wildlife Bucephala clangula, 0.017 mg/kg Goldeneye (n = 1) Summary of Biological Effects Tissue Concentrations for PCB 118 Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 0.20 ng/L 0.29 n = 11 290 ng/g lipid [46, 47] F; Siskiwit Lake, Isle Royale, Lake Superior; tissue concentrations are means of concentrations measured in several size classes; organic carbon content of sediment was not presented. 0.20 ng/L 0.29 n = 11 280 ng/g lipid 8.15 4.09 [13] F; %lipid = 11; %sed OC = 2.7 F F; lower Detroit River 1.72 0.42 0.26 mg/kg (n = 9) [50] [40] 0.36 0.041 mg/kg (n = 3) [40] F; lower Detroit River Summary of Biological Effects Tissue Concentrations for PCB 118 :Species Taxa Aythya affinis, Lesser scaup Concentration, Units in1: Sediment 0.017 mg/kg (n = 1) Water Toxicity: Tissue (Sample Type) Effects 0.52 0.26 mg/kg (n = 7) Ability to Accumulate2: Log Log BCF BAF BSAF Source: Reference Comments3 [40] F; lower Detroit River Aythya marila, Greater scaup Falco peregrinus, Peregrine falcon 0.017 mg/kg (n = 1) 0.59 0.10 mg/kg (n = 3) 450 ng/g (eggs) (n = 6) 11.4% eggshell thinning [40] F; lower Detroit River F; Kola Peninsula, Russia [48] Mustela vison, Mink Diet: 1,660 pg/g4 35,000 pg/g 4 8,500 pg/g4 (liver) 20,000 pg/g4 (liver) NOAEL LOAEL; reduced kit body weights followed by reduced survival Reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female log BMF = 0.53 log BMF = 0.56 [49] L; BMF = lipidnormalized concentration in the liver divided by the lipid-normalized dietary concentration 284,000 pg/g4 (liver) 68,000 pg/g 4 log BMF = 0.63 478,000 pg/g4 (liver) 125,000 pg/g4 log BMF = 0.77 1 2 Concentration units expressed in wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, SAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 Not clear whether units are in dry or wet weight. 593 BIOACCUMULATION SUMMARY References 1. PCB 118 USEPA. 1996. Hazardous Substances Data Bank (SDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals, Vol. I, Monoaromatic hydrocarbons, chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Jones, P.D., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. USACE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food chains. Environ. Sci. Technol. 23:699. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol. Chem. 8:957-968. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 594 BIOACCUMULATION SUMMARY 12. PCB 118 Muir, D.C.G., R.J. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related compounds. Environ. Sci. Technol. 22:1071-1079. Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Rasmussen, J.B., D.J. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J. Fish. Aquat. Sci. 47:2030-2038. Rand, G.M., P.G. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M. Rand, pp. 3-67. Taylor and Francis, Washington, DC. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments. In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments. Unpublished document. January 11. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ. Pollut. 5B:121-132. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ. Sci. Technol. 13:65-71. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop, pp. 273-287. American Society of Testing and Materials, Philadelphia, PA. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls. In PCBs and the environment, ed. J.S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton, FL. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc. Boca Raton, FL. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, pp. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 595 BIOACCUMULATION SUMMARY PCB 118 37-53. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington, DC. 25. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop"PCBs in Fish Tissue," May 10-11, 1993, pp. 3-9. EPA/823-R-93-003. U.S. Environmental Protection Agency, Office of Water, Washington, DC. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(1):51-88. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group, Inc., Arlington, MA.) Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution: A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments. Mar. Biol. 91:497-508. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'Itri and M.A. Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/5-80-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.) Mearns, A.J., M. Matta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G. Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric Administration. Seattle, WA. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 596 BIOACCUMULATION SUMMARY 36. PCB 118 Long, E.R., and L.G. Morgan. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Technical Memorandum NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success, xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536. Dillon, T.M., W.H. Benson, R.A. Stackhouse, and A.M. Crider. 1990. Effects of selected PCB congeners on survival, growth, and reproduction in Daphnia magna. Environ. Toxicol. Chem. 9:1317-1326. Smith., E.V., J.M. Spurr, J.C. Filkins, and J.J. Jones. 1985. Organochlorine contaminants of wintering ducks foraging on Detroit River sediments. J. Great Lakes Res. 11(3):231-246. Boese, B.L., M. Winsor, H. Lee II, S. Echols, J. Pelletier, and R. Randal. 1995. PCB congeners and hexachlorobenzene biota sediment accumulation factors for Macoma nasuta exposed to sediments with different total organic carbon contents. Environ. Toxicol. Chem. 14(2): 303-310. Morrison, H.A., F.A.P.C. Gobas, R. Lazar, and G.D. Haffner. 1996. Development and verification of a bioaccumulation model for organic contaminants in benthic invertebrates. Environ. Sci. Technol. 30:3377-3384. Ferraro, S.P., H. Lee II, L.M. Smith, R.J. Ozretich, and D.T. Sprecht. 1991. Accumulation factors for eleven polychlorinated biphenyl congeners. Bull. Environ. Contam. Toxicol. 46:276283. Lester, D.C., and A. McIntosh. 1994. Accumulation of polychlorinated biphenyl congeners from Lake Champlain sediments by Mysis relicta. Environ. Toxicol. Chem. 13:1825-1841. Bergen, B.J., W.G. Nelson, and R.J. Pruell. 1996. Bioaccumulation of PCB congeners by blue mussels (Mytilus edulis) deployed in New Bedford Harbor, Massachusetts. Environ. Toxicol. Chem. 12:1671-1681. Swackhamer, D.L., B.D. McVeety, and R.A. Hites. 1988. Deposition and evaporation of polychlorobiphenyl congeners to and from Siskiwit Lake, Isle Royale, Lake Superior. Environ. Sci. Tech. 22:664-672. Swackhamer, D.L., and R.A. Hites. 1988. Occurrence and bioaccumulation of organochlorine compounds in fishes from Siskiwit Lake, Isle Royale, Lake Superior. Environ. Sci. Tech. 22:543548. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 597 BIOACCUMULATION SUMMARY PCB 118 Kola Peninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. 49. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 50. 598 BIOACCUMULATION SUMMARY PCB 126 Chemical Category: POLYCHLORINATED BIPHENYLS Chemical Name (Common Synonyms): 3,3,4,4,5-PENTACHLOROBIPHENYL Chemical Characteristics Solubility in Water: No data [1] 0.004 - 0.099 mg/L [2] Log Kow: 6.2 - 6.85 [2], No data [4] Half-Life: No data [2,3] CASRN: 57465-28-8 Log Koc: 6.09 - 6.73 L/kg organic carbon Human Health Oral RfD: No data [5] Critical Effect: -- Oral Slope Factor: No data [5] Carcinogenic Classification: No data [5] Confidence: No data [5] Wildlife Partitioning Factors: Partitioning factors for PCB 126 in wildlife were not found. Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and USACE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly waterinsoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. The log biomagnification factor for pentachlorobiphenyls from alewife to herring gulls in Lake Ontario ranged from 1.18 to 2.00 [11]. A study of arctic marine food chains measured biomagnification factors for pentachlorobiphenyls that ranged from 0.71 to 1.05 for fish to seal, 0.28 to 0.49 for seal to bear, and 1.14 for fish to bear [12]. No specific food chain multipliers were identified for PCB 126. Aquatic Organisms Partitioning Factors: In an 83-day laboratory study with three-spined stickleback, the lipid-normalized ratio of PCB 126 in food to fish tissue ranged from 3.8 to 6.1. A log bioconcentration factor (BCF) for deployed mussels in New Bedford Harbor, MA, was approximately 6.90, as reported in the attached table. 599 BIOACCUMULATION SUMMARY PCB 126 Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify through the food web. Oliver and Niimi [13], studying accumulation of PCBs in various organisms in the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [14] reported that each trophic level contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific food chain multipliers were identified for PCB 126 or other pentachlorobiphenyls. Toxicity/Bioaccumulation Assessment Profile PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in various processes and products because of the extreme stability of many isomers, particularly those with five or more chlorines [15]. A common use of PCBs was as dielectric fluids in capacitors and transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture. As a result of their stability and their general hydrophobic nature, PCBs released to the environment have dispersed widely throughout the ecosystem [15]. PCBs are among the most stable organic compounds known, and chemical degradation rates in the environment are thought to be slow. As a result of their highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water and at relatively high concentrations in sediment [16]. Individual PCB congeners have different physical and chemical properties based on the degree of chlorination and position of chlorine substitution, although differences with degree of chlorination are more significant [16]. Solubilities and octanol-water partition coefficients for PCB congeners range over several orders of magnitude [17]. Octanol-water partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest for the most chlorinated PCB congeners. Dispersion of PCBs in the aquatic environment is a function of their solubility [16], whereas PCB mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination [18]. The concentration of PCBs in sediments is a function of the physical characteristics of the sediment, such as grain size [19,20] and total organic carbon content [19,20,21,22]. Fine sediments typically contain higher concentrations of PCBs than coarser sediments because of more surface area [16]. Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [18]. Therefore, it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source [16]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment from reaching the overlying water via diffusion [18]. The persistence of PCBs in the environment is a result of their general resistance to degradation [17]. The rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [23]; other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation to a lesser extent [17]. Photochemical degradation, via reductive dechlorination, is also known to occur in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [22]. 600 BIOACCUMULATION SUMMARY PCB 126 Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly than higher chlorinated congeners [24]. PCB congeners with no chlorine substituted in the ortho (2 and 2) positions but with four or more chlorine atoms at the meta (3 and 3) and para (4 and 4) positions can assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) [25]. Examples of these more toxic, coplanar congeners are 3,3,4,4-tetrachlorobiphenyl (PCB 77), 3,3,4,4,5-pentachlorobiphenyl (PCB 126), and 3,3,4,4,5,5hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of mixtures is to use toxic equivalency factors (TEFs) [26]. With this method, relative potencies for individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The following TEFs have been recommended [26,27]: Congener Class 3,3,4,4,5-PentaCB 3,3,4,4,5,5-HexaCB 3,34,4-TetraCB Monoortho coplanar PCBs Diortho coplanar PCBs Recommended TEF 0.1 0.05 0.01 0.001 0.00002 Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic organisms have a strong tendency to accumulate PCBs from water and food sources. The log bioconcentration factor for fish is approximately 4.70 [28]. This factor represents the ratio of concentration in tissue to the ambient water concentration. Aquatic organisms living in association with PCB-contaminated sediments generally have tissue concentrations equal to or greater than the concentration of PCB in the sediment [28]. Once taken up by an organism, PCBs partition primarily into lipid compartments [16]. Thus, differences in PCB concentration between species and between different tissues within the same species may reflect differences in lipid content [16]. PCB concentrations in polychaetes and fish have been strongly correlated to their lipid content [29]. Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higherchlorinated congeners [30,31]. In some species, tissue concentrations of PCBs in females can be reduced during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred PCBs are eliminated from the female during spawning [32,33]. Fish and other aquatic organisms biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners [32]. Consequently, fish and other aquatic organisms may accumulate more of the higher chlorinated PCB congeners than is found in the environment [17]. The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate that PCB toxicity is directly related to the duration of exposure [34]. Toxic responses have been noted to occur at concentrations of 0.03 and 0.014 g/L in marine and freshwater environments, respectively [34]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 g/L [34]. Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [35], although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses 601 BIOACCUMULATION SUMMARY PCB 126 at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370 g/kg [36]. A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic organisms at low tissue concentrations [17]. Field and Dexter [17] suggest that a number of marine and freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0 mg/kg and as low as 0.1 mg/kg. Spies et al. [37] reported an inverse relationship between PCB concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [38] also reported a significant correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with MFO induction by PCBs at tissue concentrations within the range of environmental exposures [17]. 602 Summary of Biological Effects Tissue Concentrations for PCB 126 Species: Taxa Invertebrates Mytilus edulis, Blue mussel Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Source: Log Log BAF BAF BSAF Reference Comments3 1993: particulate 0.2 g/L 0.1 n=9 dissolved 0.02 g/L 0.01 n=9 1994: particulate 0.2 g/L 0.1 n=3 dissolved 0.03 g/L 0.01 n=3 ~20 ng/g dw (whole body) 6.90 [39] F; New Bedford Harbor, MA; deployment study; tissue concentrations were only presented for 1994 samples; BCF and tissue concentrations read from figures (~) Fishes Gasterosteus aculeatus, Three-spined stickleback 0.78 (male) 0.58 (female) [41] L; 83-day dosing study; BAF = lipidnormalized concentration in fish divided by the lipidnormalized concentration in food F; collected in or near Hamlet in Cambridge Bay, NW Territories, Canada F Myoxocephalus 0.013 ng/g quadricornis, dw Four-horn sculpin 0.035 ng/g (liver) 0.068 ng/g (whole body) [40] Salmonids 603 3.21 [45] Summary of Biological Effects Tissue Concentrations for PCB 126 Species: Taxa Wildlife Sterna hirundo, Common tern (embryo) Falco peregrinus, Peregrine falcon Falco sparverius, American kestrel (embryo) Falco sparverius, American kestrel (nestling) Colinus virginianus, Bobwhite (embryo) White leghorn chicken (embryo) Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 45 g/kg4 (egg) 35% embryo mortality (through hatching) 11.4% eggshell thinning LD50 (through hatching) Ability to Accumulate2: Source: Log Log BAF BAF BSAF Reference Comments3 [42] L; PCBs were injected into the air cell of eggs F; Kola Peninsula, Russia L; PCBs were injected into the air cell of eggs L 604 White leghorn chicken (embryo) 1 2 1.3 ng/g (eggs) (n = 6) 65 g/kg4 (egg) [44] [42] 156 g/kg4 (liver) Histopathology of liver, thyroid, and spleen LD50 (through hatching) [42] 24 g/kg4 (egg) [42] L; PCBs were injected into the air cell of eggs 0.4 g/kg (egg) LD50 [42] L; PCBs were injected into the air cell of eggs from day 4 of incubation through hatching L; PCBs were injected into the air cell of eggs from day 7 through day 10 of incubation 3.1 g/kg (egg) LD50 [43] Concentration units expressed in wet weight unless otherwise indicated. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 2 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 Not clear from reference if concentration is based on wet or dry weight. BIOACCUMULATION SUMMARY References 1. PCB 126 USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons, chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Jones, P.D., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. USACE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food chains. Environ. Sci. Technol. 23:699. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario gulls. Environ. Toxicol. Chem. 8:957-968. 605 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. BIOACCUMULATION SUMMARY 12. PCB 126 Muir, D.C.G., R.J. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related compounds. Environ. Sci. Technol. 22:1071-1079. Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Rasmussen, J.B., D.J. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J. Fish. Aquat. Sci. 47:2030-2038. Rand, G.M., P.G. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M. Rand, pp. 3-67. Taylor and Francis, Washington, DC. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments. In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments. Unpublished document. January 11, 1988. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ. Pollut. 5B:121-132. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ. Sci. Technol. 13:65-71. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop, pp. 273-287. American Society of Testing and Materials, Philadelphia, PA. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls. In PCBs and the environment, ed. J. S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton, FL. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In PCBs and the environment, ed. J. S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and the environment, ed. J. S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc. Boca Raton, FL. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue", May 10-11, 1993, pp. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 606 BIOACCUMULATION SUMMARY PCB 126 37-53. EPA/823-R-93-003, U.S. Environmnetal Protection Agency, Office of Water, Washington, DC. 25. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue", May 10-11, 1993, pp. 3-9. EPA/823-R-93-003, U.S. Environmnetal Protection Agency, Office of Water, Washington, DC. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(1):51-88. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group, Inc., Arlington, MA.) Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution: A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments. Mar. Biol. 91:497-508. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'Itri and M.A. Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the Environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/580-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.) Mearns, A.J., M. Matta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G. Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 607 BIOACCUMULATION SUMMARY PCB 126 assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric Administration. Seattle, WA. 36. Long, E.R., and L.G. Morgan. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Technical Memorandum NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success, xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536. Bergen, B.J., W.G. Nelson, and R.J.Pruell. 1996. Comparison of nonplanar and coplanar PCB congener partitioning in seawater and bioaccumulation in blue mussels (Mytilus edulis). Environ. Toxicol.Chem. 15:1517-1523. Bright, D.A., S.L. Grundy, and K.J. Reimer. 1995. Differential bioaccumulation of non-ortho substituted and other PCB congeners in coastal arctic invertebrates and fish. Environ. Sci. Technol. 29:2504-2512. Van Bavel, B., P. Andersson, H. Wingfors, J. Ahgren, P. Bergqvist, L. Norrgren, C. Rappe, and M. Tysklind. 1996. Multivariate modeling of PCB bioaccumulation in three-spined stickleback (Gasterosteus aculeatus). Environ. Toxicol. Chem. 6:947-954. Hoffman, D.J., M.J. Melancon, J.D. Eisemann, and P.N. Klein. 1995. Comparative toxicity of planar PCB congeners by egg injection. Abstract, 16th Annual Meeting, Society of Environmental Toxicology and Chemistry, Washington, DC, November 17-21, 1995. Brunstrom, B., and L. Andersson. 1988. Toxicity and 7-ethoxyresorufin O-deethylase-inducing potency of coplanar polychlorinated biphenyls (PCBs) in chick embryos. Arch. Toxicol. 62:263266. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today, ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. USEPA. 1995. Great Lakes Water Quality Initiative technical support document for the procedure to determine bioaccumulation factors. EPA-820-B-95-005. U.S. Environmental Protection Agency, Office of Water, Washington, DC. 37. 38. 39. 40. 41. 42. 43. 44. 45. 608 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED BIPHENYLS Chemical Name (Common Synonyms): 2,3,3,4,4,5-HEXACHLOROBIPHENYL PCB 156 CASRN: 38380-08-4 Chemical Characteristics Solubility in Water: No data [1], 0.004 - 0.038 mg/L [2] Log Kow: 6.7 - 7.3 [2] Half-Life: No data [2,3] Log Koc: 6.59 - 7.18 L/kg organic carbon Human Health Oral RfD: No data [5] Critical Effect: -- Oral Slope Factor: No data [5] Carcinogenic Classification: No data [5] Confidence: -- Wildlife Partitioning Factors: In a laboratory study with mink, the lipid-normalized ratios of PCB 156 in liver to food ranged from 5.5 to 11.6. The ratio of PCB 156 in tissues of three species of duck to sediment in the lower Detroit River ranged from 27 to 41. Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and USACE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly waterinsoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. The log biomagnification factors for hexachlorobiphenyls from alewife to herring gulls in Lake Ontario ranged from 1.30 to 2.14 [11]. A study of arctic marine food chains measured log biomagnification factors for hexachlorobiphenyls that ranged from 0.99 to 1.36 for fish to seal, 0.97 to 1.26 for seal to bear, and 2.23 for fish to bear [12]. No specific food chain multipliers were identified for PCB 156. Aquatic Organisms Partitioning Factors: In Lake Ontario, ratios of PCB-156 in tissue (wet weight) to sediment (dry weight) for plankton, oligochaetes, mysids, and amphipods were 0.10, 0.14, 0.57, and 1.9 respectively; ratios in sculpin, alewife, rainbow smelt, and salmonids were 6.7, 3.0, 2.9, and 16, respectively. In carp from the lower Detroit River the tissue to sediment ratio (wet weight) was 25. BSAFs for clam in a laboratory study ranged from 0.16 to 0.67. 609 BIOACCUMULATION SUMMARY PCB 156 Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify through the food web. Oliver and Niimi [13], studying accumulation of PCBs in various organisms in the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [14] reported that each trophic level contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific food chain multipliers were identified for PCB 156 or other hexachlorobiphenyls. Toxicity/Bioaccumulation Assessment Profile PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in various processes and products because of the extreme stability of many isomers, particularly those with five or more chlorines [15]. A common use of PCBs was as dielectric fluids in capacitors and transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture. As a result of their stability and their general hydrophobic nature, PCBs released to the environment have dispersed widely throughout the ecosystem [15]. PCBs are among the most stable organic compounds known, and chemical degradation rates in the environment are thought to be slow. As a result of their highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water and at relatively high concentrations in sediment [16]. Individual PCB congeners have different physical and chemical properties based on the degree of chlorination and position of chlorine substitution, although differences with degree of chlorination are more significant [16]. Solubilities and octanol-water partition coefficients for PCB congeners range over several orders of magnitude [17]. Octanol-water partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest for the most chlorinated PCB congeners. Dispersion of PCBs in the aquatic environment is a function of their solubility [16], whereas PCB mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination [18]. The concentration of PCBs in sediments is a function of the physical characteristics of the sediment, such as grain size [19,20] and total organic carbon content [19,21,22]. Fine sediments typically contain higher concentrations of PCBs than coarser sediments because of more surface area [16]. Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [18]. Therefore, it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source [16]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment from reaching the overlying water via diffusion [18]. The persistence of PCBs in the environment is a result of their general resistance to degradation [17]. The rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [23]; other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation to a lesser extent [17]. Photochemical degradation, via reductive dechlorination, is also known to occur in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [22]. 610 BIOACCUMULATION SUMMARY PCB 156 Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly than higher chlorinated congeners [24]. PCB congeners with no chlorine substituted in the ortho (2 and 2) positions but with four or more chlorine atoms at the meta (3 and 3) and para (4 and 4) positions can assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) [25]. Examples of these more toxic, coplanar congeners are 3,3,4,4-tetrachlorobiphenyl (PCB 77), 3,3,4,4,5-pentachlorobiphenyl (PCB 126), and 3,3,4,4,5,5hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of mixtures is to use toxic equivalency factors (TEFs) [26]. With this method, relative potencies for individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The following TEFs have been recommended [26,27]: Congener Class 3,3,4,4,5-PentaCB 3,3,4,4,5,5-HexaCB 3,34,4-TetraCB Monoortho coplanar PCBs Diortho coplanar PCBs Recommended TEF 0.1 0.05 0.01 0.001 0.00002 Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic organisms have a strong tendency to accumulate PCBs from water and food sources. The log bioconcentration factor for fish is approximately 4.70 [28]. This factor represents the ratio of concentration in tissue to the ambient water concentration. Aquatic organisms living in association with PCB-contaminated sediments generally have tissue concentrations equal to or greater than the concentration of PCB in the sediment [28]. Once taken up by an organism, PCBs partition primarily into lipid compartments [16]. Thus, differences in PCB concentration between species and between different tissues within the same species may reflect differences in lipid content [16]. PCB concentrations in polychaetes and fish have been strongly correlated to their lipid content [29]. Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higherchlorinated congeners [30,31]. In some species, tissue concentrations of PCBs in females can be reduced during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred PCBs are eliminated from the female during spawning [32,33]. Fish and other aquatic organisms biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners [32]. Consequently, fish and other aquatic organisms may accumulate more of the higher chlorinated PCB congeners than is found in the environment [17]. The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate that PCB toxicity is directly related to the duration of exposure [34]. Toxic responses have been noted to occur at concentrations of 0.03 and 0.014 g/L in marine and freshwater environments, respectively [34]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 g/L [34]. Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [35], although the acute toxicity of PCBs is relatively low compared to that of other chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses 611 BIOACCUMULATION SUMMARY PCB 156 at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370 g/kg [36]. A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic organisms at low tissue concentrations [17]. Field and Dexter [17] suggest that a number of marine and freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0 mg/kg and as low as 0.1 mg/kg. Spies et al. [37] reported an inverse relationship between PCB concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [38] also reported a significant correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with MFO induction by PCBs at tissue concentrations within the range of environmental exposures [17]. 612 Summary of Biological Effects Tissue Concentrations for PCB 156 Species: Taxa Invertebrates Plankton (a mixture 2.1 1.4 ng/g Not detected in 0.2 0.1 ng/g of primarily dw (0-3 cm) surface water (n = 3) phytoplankton and (n = 38) (n = 7) some zooplankton) Mainly Tubifex tubifex and Limnodrilus hoffmeisteri, Oligochaete Tubifex sp, Oligochaetes 2.1 1.4 ng/g Not detected in 0.3 0.4 ng/g dw (0-3 cm) surface water (n = 6) (n = 38) (n = 7) [13] F; Lake Ontario; value is mean SD; lipid content = 0.5% Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Source: Log Log BCF BAF BSAF Reference Comments3 [13] F; Lake Ontario; value is mean SD; lipid content = 1% 0.0024 mg/kg (n = 1) 0.0016 mg/kg (n = 1) [39] F; lower Detroit River Macoma nasuta, Bent-nose clam ng/g dw: 0.60 0.019 0.48 NA 11.6 2.29 34 5.3 ng/g dw: 2.6 0.59 1.93 0.284 2.61 0.192 2.89 0.215 4.1 0.77 0.67 0.61 0.51 0.23 0.16 [40] L; values given are mean SE; sediment TOC ranged from 0.84% to 7.4%. Macoma were exposed to 5 sediments containing different PCB concentrations; NA means number was not legible. F; Lake Ontario; value is mean SD; lipid content = 3% Pontoporeia affinis, 2.1 1.4 ng/g Not detected in 3.9 2.3 ng/g Amphipods dw (0-3 cm) surface water (n = 6) (n = 38) (n = 7) [13] 613 Summary of Biological Effects Tissue Concentrations for PCB 156 Species: Taxa Mysis relicta, Mysids Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Source: Log Log BCF BAF BSAF Reference Comments3 [13] F; Lake Ontario; value is mean SD; lipid content = 3% 614 2.1 1.4 ng/g Not detected in 1.2 0.1 ng/g dw (0-3 cm) surface water (n = 2) (n = 38) (n = 7) Fishes Salmonids: 2.1 1.4 ng/g Not detected in 34 27 ng/g dw (0-3 cm) surface water (n = 60) Oncorhynchus (n = 7) velinus namaycush, (n = 38) Coho salmon; Oncorhynchus mykiss (Salmo gairdneri), Rainbow trout; Salvelinus namaycush, Lake trout; Salmo trutta, Brown trout Cyprinus carpio, Carp Cottus cognatus, Sculpin 0.0024 mg/kg (n = 1) 0.0610.024 mg/kg (n = 9) 3.97 [13] F; Lake Ontario; value is mean SD; lipid content = 11% [39] F; lower Detroit River F; Lake Ontario; value is mean SD; lipid content = 8% F; Lake Ontario; value is mean SD; lipid content = 7% F; Lake Ontario; value is mean SD; lipid content = 4% 2.1 1.4 ng/g Not detected in 14 ng/g dw (0-3 cm) surface water (one composite) (n = 38) (n = 7) 2.1 1.4 ng/g Not detected in 6.3 ng/g dw (0-3 cm) surface water (one composite) (n = 38) (n = 7) 2.1 1.4 ng/g Not detected in 2.7 1.9 ng/g dw (0-3 cm) surface water (n = 4) (n = 38) (n = 7) [13] Alewife [13] Osmerus mordax, Small rainbow smelt [13] Summary of Biological Effects Tissue Concentrations for PCB 156 Species: Taxa Osmerus mordax, Large rainbow smelt Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Source: Log Log BCF BAF BSAF Reference Comments3 [13] F; Lake Ontario; value is mean SD; lipid content = 4% 2.1 1.4 ng/g Not detected in 6.1 ng/g dw (0-3 cm) surface water (one composite) (n = 38) (n = 7) Wildlife Bucephala clangula, Goldeneye Aythya affinis, Lesser scaup Aythya marila, Greater scaup Falco peregrinus, Peregrine falcon 0.0024 mg/kg (n = 1) 0.0640.018 mg/kg (n = 3) [39] F; lower Detroit River 0.0024 mg/kg (n = 1) 0.0024 mg/kg (n = 1) 0.0900.044 mg/kg (n = 7) 0.0980.0091 mg/kg (n = 3) 82 ng/g (eggs) (n = 6) 11.4% eggshell thinning [39] F; lower Detroit River F; lower Detroit River F; Kola Peninsula, Russia [39] [41] 615 Summary of Biological Effects Tissue Concentrations for PCB 156 Species: Taxa Mustela vison, Mink Concentration, Units in1: Sediment Diet: 110 pg/g4 Water Toxicity: Tissue (Sample Type) Effects 920 pg/g4 (liver) NOAEL Ability to Accumulate2: Source: Log Log BCF BAF BSAF Reference Comments3 [42] Log BMF = 0.74 Log BMF = 0.96 L; BMF = lipidnormalized concentration in the liver divided by the lipid-normalized dietary concentration 616 1,300 pg/g4 12,000 pg/g4 (liver) LOAEL; reduced kit body weights followed by reduced survival reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female 2,800 pg/g4 23,000 pg/g4 (liver) Log BMF = 0.91 Log BMF = 1.06 5,000 pg/g4 37,100 pg/g4 (liver) 1 Concentration units expressed in wet weight unless otherwise noted. 2 BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 Not clear whether units are in dry or wet weight. BIOACCUMULATION SUMMARY References 1. PCB 156 USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons, chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1996. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Jones, P.D., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. USACE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food chains. Environ. Sci. Technol. 23:699. 2. 3. 4. 5. 6. 7. 8. 9. 10. 617 BIOACCUMULATION SUMMARY 11 PCB 156 Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol. Chem. 8:957-968. Muir, D.C.G., R.J. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related compounds. Environ. Sci. Technol. 22:1071-1079. Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Rasmussen, J.B., D.J. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J. Fish. Aquat. Sci. 47:2030-2038. Rand, G.M., P.G. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M. Rand, pp. 3-67. Taylor and Francis,Washington, DC. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments. In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL. Field, L.J., and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments. Unpublished document. January 11, 1988. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ. Pollut. 5B:121-132. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ. Sci. Technol. 13:65-71. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop, pp. 273-287. American Society of Testing and Materials, Philadelphia, PA. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls. In PCBs and the environment, ed. J.S. Waid, Vol. 1, pp. 101-120. CRC Press, Inc. Boca Raton, FL. Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 618 BIOACCUMULATION SUMMARY 23. PCB 156 Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and the environment, ed. J.S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc. Boca Raton, FL. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, pp. 37-53. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington, DC. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, pp. 3-9. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington, DC. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(1):51-88. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group, Inc., Arlington, MA.) Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution: A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments. Mar. Biol. 91:497-508. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'Itri and M.A. Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI. Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/580-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and 619 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. BIOACCUMULATION SUMMARY PCB 156 Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February.) 35. Mearns, A.J., M. Matta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G. Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric Administration. Seattle, WA. Long, E.R., and L.G. Morgan. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Technical Memorandum NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success, xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536. Smith, E.V., J.M. Spurr, J.C. Filkins, and J.J. Jones. 1985. Organochlorine contaminants of wintering ducks foraging on Detroit River sediments. J. Great Lakes Res. 11(3):231-246. Ferraro, S.P., H. Lee II, L.M. Smith, R.J. Ozretich, and D.T. Sprecht. 1991. Accumulation factors for eleven polychlorinated biphenyl congeners. Bull. Environ. Contam. Toxicol. 46:276-283. Henny, C.J., S.A. Ganusevich, F.P. Ward, and T.R. Schwartz. 1994. Organochlorine pesticides, chlorinated dioxins and furans, and PCBs in peregrine falcon Falco peregrinus eggs from the Kola Penninsula, Russia. In Raptor conservation today., ed. B.U. Meyburg and R.D. Chancellor, pp. 739-749. WWGPB/The Pica Press. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. 36. 37. 38. 39. 40. 41. 42. 620 BIOACCUMULATION SUMMARY Chemical Category: POLYCHLORINATED BIPHENYLS Chemical Name (Common Synonyms): 3,3,4,4,5,5-HEXACHLOROBIPHENYL PCB 169 CASRN: 32774-16-6 Chemical Characteristics Solubility in Water: No data [1], 0.5 mg/L [2] Log Kow: 7.4 [5] Half-Life: No data [2,3] Log Koc: 7.27 L/kg organic carbon Human Health Oral RfD: No data [5] Critical Effect: -- Oral Slope Factor: No data [5] Carcinogenic Classification: No data [5] Confidence: -- Wildlife Partitioning Factors: In a laboratory study with mink, the lipid-normalized ratios of PCB 169 in liver to food ranged from 12.4 to 21.4. Food Chain Multipliers: For PCBs as a class the most toxic congeners have been shown to be selectively accumulated from organisms at one trophic level to the next [6]. At least three studies have concluded that PCBs have the potential to biomagnify in food webs based on aquatic organisms and predators that feed primarily on aquatic organisms [7,8,9]. The results from Biddinger and Gloss [7] and USACE [9] generally agreed that highly water-insoluble compounds (including PCBs) have the potential to biomagnify in these types of food webs. Thomann's [10] model also indicated that highly waterinsoluble compounds (log Kow values 5 to 7) showed the greatest potential to biomagnify. The log biomagnification factors for hexachlorobiphenyls from alewife to herring gulls in Lake Ontario ranged from 1.30 to 2.14 [11]. A study of arctic marine food chains measured log biomagnification factors for hexachlorobiphenyls that ranged from 0.99 to 1.36 for fish to seal, 0.99 to 1.26 for seal to bear, and 2.23 for fish to bear [12]. Log BMFs ranged from 1.09 to 1.33 for mink fed PCB 169 in the diet [40]. Aquatic Organisms Partitioning Factors: In an 83-day laboratory study with three-spined stickleback, the lipid-normalized ratio of PCB 169 in food to fish tissue (log BAF) ranged from 0.50 to 0.79. 621 BIOACCUMULATION SUMMARY PCB 169 Food Chain Multipliers: Polychlorinated biphenyls as a class have been demonstrated to biomagnify through the food web. Oliver and Niimi [13], studying accumulation of PCBs in various organisms in the Lake Ontario food web, reported concentrations of total PCBs in phytoplankton, zooplankton, and several species of fish. Their data indicated a progressive increase in tissue PCB concentrations moving from organisms lower in the food web to top aquatic predators. In a study of PCB accumulation in lake trout (Salvelinus namaycush) of Lake Ontario, Rasmussen et al. [14] reported that each trophic level contributed about a 3.5-fold biomagnification factor to the PCB concentrations in the trout. No specific food chain multipliers were identified for PCB 169 or other hexachlorobiphenyls. Toxicity/Bioaccumulation Assessment Profile PCBs are a group (209 congeners/isomers) of organic chemicals, based on various substitutions of chlorine atoms on a basic biphenyl molecule. These manufactured chemicals have been widely used in various processes and products because of the extreme stability of many isomers, particularly those with five or more chlorines [15]. A common use of PCBs was as dielectric fluids in capacitors and transformers. In the United States, Aroclor is the most familiar registered trademark of commercial PCB formulations. Generally, the first two digits in the Aroclor designation indicate that the mixture contains biphenyls, and the last two digits give the weight percent of chlorine in the mixture. As a result of their stability and their general hydrophobic nature, PCBs released to the environment have dispersed widely throughout the ecosystem [15]. PCBs are among the most stable organic compounds known, and chemical degradation rates in the environment are thought to be slow. As a result of their highly lipophilic nature and low water solubility, PCBs are generally found at low concentrations in water and at relatively high concentrations in sediment [16]. Individual PCB congeners have different physical and chemical properties based on the degree of chlorination and position of chlorine substitution, although differences with degree of chlorination are more significant [16]. Solubilities and octanol-water partition coefficients for PCB congeners range over several orders of magnitude [17]. Octanol-water partition coefficients, which are often used as estimators of the potential for bioconcentration, are highest for the most chlorinated PCB congeners. Dispersion of PCBs in the aquatic environment is a function of their solubility [18], whereas PCB mobility within and sorption to sediment are a function of chlorine substitution pattern and degree of chlorination [18]. The concentration of PCBs in sediments is a function of the physical characteristics of the sediment, such as grain size [19,20] and total organic carbon content [19,20,21,22]. Fine sediments typically contain higher concentrations of PCBs than coarser sediments because of more surface area [16]. Mobility of PCBs in sediment is generally quite low for the higher chlorinated biphenyls [18]. Therefore, it is common for the lower chlorinated PCBs to have a greater dispersion from the original point source [16]. Limited mobility and high rates of sedimentation could prevent some PCB congeners in the sediment from reaching the overlying water via diffusion [18]. The persistence of PCBs in the environment is a result of their general resistance to degradation [19]. The rate of degradation of PCB congeners by bacteria decreases with increasing degree of chlorination [23]; other structural characteristics of the individual PCBs can affect susceptibility to microbial degradation to a lesser extent [17]. Photochemical degradation, via reductive dechlorination, is also known to occur in aquatic environments; the higher chlorinated PCBs appear to be most susceptible to this process [22]. 622 BIOACCUMULATION SUMMARY PCB 169 Toxicity of PCB congeners is dependent on the degree of chlorination as well as the position of chlorine substitution. Lesser chlorinated congeners are more readily absorbed, but are metabolized more rapidly than higher chlorinated congeners [24]. PCB congeners with no chlorine substituted in the ortho (2 and 2) positions but with four or more chlorine atoms at the meta (3 and 3) and para (4 and 4) positions can assume a planar conformation that can interact with the same receptor as the highly toxic 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) [25]. Examples of these more toxic, coplanar congeners are 3,3,4,4-tetrachlorobiphenyl (PCB 77), 3,3,4,4,5-pentachlorobiphenyl (PCB 126), and 3,3,4,4,5,5hexachlorobiphenyl (PCB 169). A method that has been proposed to estimate the relative toxicity of mixtures is to use toxic equivalency factors (TEFs) [26]. With this method, relative potencies for individual congeners are calculated by expressing their potency in relation to 2,3,7,8-TCDD. The following TEFs have been recommended [26,27]: Congener Class 3,3,4,4,5-PentaCB 3,3,4,4,5,5-HexaCB 3,34,4-TetraCB Monoortho coplanar PCBs Diortho coplanar PCBs Recommended TEF 0.1 0.05 0.01 0.001 0.00002 Due to the toxicity, high Kow values, and highly persistent nature of many PCBs, they possess a high potential to bioaccumulate and exert reproductive effects in higher-trophic-level organisms. Aquatic organisms have a strong tendency to accumulate PCBs from water and food sources. The log bioconcentration factor for fish is approximately 4.70 [28]. This factor represents the ratio of concentration in tissue to the ambient water concentration. Aquatic organisms living in association with PCB-contaminated sediments generally have tissue concentrations equal to or greater than the concentration of PCB in the sediment [28]. Once taken up by an organism, PCBs partition primarily into lipid compartments [16]. Thus, differences in PCB concentration between species and between different tissues within the same species may reflect differences in lipid content [16]. PCB concentrations in polychaetes and fish have been strongly correlated to their lipid content [29]. Elimination of PCBs from organisms is related to the characteristics of the specific PCB congeners present. It has been shown that uptake and depuration rates in mussels are high for lower-chlorinated PCBs and much lower for higherchlorinated congeners [30,31]. In some species, tissue concentrations of PCBs in females can be reduced during gametogenesis because of PCB transfer to the more lipophilic eggs. Therefore, the transferred PCBs are eliminated from the female during spawning [32,33]. Fish and other aquatic organisms biotransform PCBs more slowly than other species, and they appear less able to metabolize, or excrete, the higher chlorinated PCB congeners [32]. Consequently, fish and other aquatic organisms may accumulate more of the higher chlorinated PCB congeners than is found in the environment [17]. The acute toxicity of PCBs appears to be relatively low, but results from chronic toxicity tests indicate that PCB toxicity is directly related to the duration of exposure [34]. Toxic responses have been noted to occur at concentrations of 0.03 and 0.014 g/L in marine and freshwater environments, respectively [34]. The LC50 for grass shrimp exposed to PCBs in marine waters for 4 days was 6.1 to 7.8 g/L [34]. Chronic toxicity of PCBs presents a serious environmental concern because of their resistance to degradation [35], although the acute toxicity of PCBs is relatively low compared to that of other 623 BIOACCUMULATION SUMMARY PCB 169 chlorinated hydrocarbons. Sediment contaminated with PCBs has been shown to elicit toxic responses at relatively low concentrations. Sediment bioassays and benthic community studies suggest that chronic effects generally occur in sediment at total PCB concentrations exceeding 370 g/kg [36]. A number of field and laboratory studies provide evidence of chronic sublethal effects on aquatic organisms at low tissue concentrations [17]. Field and Dexter [17] suggest that a number of marine and freshwater fish species have experienced chronic toxicity at PCB tissue concentrations of less than 1.0 mg/kg and as low as 0.1 mg/kg. Spies et al. [37] reported an inverse relationship between PCB concentrations in starry flounder eggs in San Francisco Bay and reproductive success, with an effective PCB concentration in the ovaries of less than 0.2 mg/kg. Monod [38] also reported a significant correlation between PCB concentrations in eggs and total egg mortality in Lake Geneva char. PCBs have also been shown to cause induction of the mixed function oxidase (MFO) system in aquatic animals, with MFO induction by PCBs at tissue concentrations within the range of environmental exposures [17]. 624 Summary of Biological Effects Tissue Concentrations for PCB 169 Species: Taxa Fishes Gasterosteus aculeatus, Threespined stickleback Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log Log BCF BAF BSAF 0.79 (male) 0.50 (female) Source: Reference Comments3 [39] L; 83-day dosing study; BAF = lipid-normalized concentration in fish divided by the lipid-normalized concentration in food Wildlife Mustela vison, Mink Diet: 2 pg/g4 65 pg/g4 (liver) NOAEL Log BMF = 1.33 Log BMF = 1.10 [40] 5 pg/g4 65 pg/g4 (liver) LOAEL; reduced kit body weights followed by reduced survival Reduced kit body weights followed by reduced survival Significant decrease in number of live kits whelped per female L; BMF = lipidnormalized concentration in the liver divided by the lipidnormalized dietary concentration 10 pg/g4 120 pg/g4 (liver) Log BMF = 1.09 20 pg/g4 205 pg/g4 (liver) Log BMF = 1.20 625 626 1 2 Concentration units expressed as wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. 3 L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. 4 Not clear from reference if concentration is based on wet or dry weight. BIOACCUMULATION SUMMARY References 1. PCB 169 USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. February. MacKay, D.M., W.Y. Shiw, and K.C. Ma. 1992. Illustrated handbook of physical-chemical properties and environmental fate for organic chemicals. Vol. I, Monoaromatic hydrocarbons, chlorobenzenes and PCBs. Lewis Publishers, Boca Raton, FL. USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. Debruyn, J.F. Busser, W. Seinen, and J. Hermens. 1989. Determinination of octanol/water partition coefficients for hydrophobic organic chemicals with the Aslow stirring method. Environ. Toxicol. Chem. 8: 499-512. Jones, P.D., J.P. Giesy, T.J. Kubiak, D.A. Verbrugge, J.C. Newstead, J.P. Ludwig, D.E. Tillit, R. Crawford, N. De Galan, and G.T. Ankley. 1993. Biomagnification of bioassay-derived 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin equivalents. Chemosphere 26:1203-1212. Biddinger, G.R., and S.P. Gloss. 1984. The importance of trophic transfer in the bioaccumulation of chemical contaminants in aquatic ecosystems. Residue Rev. 91:103-145. Kay, S.H. 1984. Potential for biomagnification of contaminants within marine and freshwater food webs. Technical Report D-84-7. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. USACE. 1995. Trophic transfer and biomagnification potential of contaminants in aquatic ecosystems. Environmental Effects of Dredging, Technical Notes EEDP-01-33. U.S. Army Corps of Engineers, Waterways Experiment Station, Vicksburg, MS. Thomann, R.V. 1989. Bioaccumulation model of organic chemical distribution in aquatic food chains. Environ. Sci. Technol. 23:699. 627 2. 3. 4. 5. 6. 7. 8. 9. 10. BIOACCUMULATION SUMMARY PCB 169 11. Braune, B.M., and R.J. Norstrom. 1989. Dynamics of organochlorine compounds in herring gulls: III. Tissue distribution and bioaccumulation in Lake Ontario Gulls. Environ. Toxicol. Chem. 8:957-968. Muir, D.C.G., R.J. Norstrom, and M. Simon. 1988. Organochlorine contaminants in arctic marine food chains: Accumulation of specific polychlorinated biphenyls and chlordane-related compounds. Environ. Sci. Technol. 22:1071-1079. Oliver, B.G., and A.J. Niimi. 1988. Trophodynamic analysis of polychlorinated biphenyl congeners and other chlorinated hydrocarbons in the Lake Ontario ecosystem. Environ. Sci. Technol. 22:388-397. Rasmussen, J.B., D.J. Rowan, D.R.S. Lean, and J.H. Carey. 1990. Food chain structure in Ontario lakes determines PCB levels in lake trout (Salvelinus namaycush) and other pelagic fish. Can. J. Fish. Aquat. Sci. 47:2030-2038. Rand, G.M., P.G. Wells, and L.S. McCarty. 1995. Chapter 1. Introduction to aquatic toxicology. In Fundamentals of aquatic toxicology: Effects, environmental fate, and risk assessment, ed. G.M. Rand, pp. 3-67. Taylor and Francis, Washington, DC. Phillips, D.J.H. 1986. Use of organisms to quantify PCBs in marine and estuarine environments. In PCBs and the environment, ed. J.S. Waid, pp.127-182. CRC Press, Inc., Boca Raton, FL. Field, L.J. and R.N. Dexter. 1998. A discussion of PCB target levels in aquatic sediments. Unpublished document. January 11, 1988. Fisher, J.B., R.L. Petty, and W. Lick. 1983. Release of polychlorinated biphenyls from contaminated lake sediments: Flux and apparent diffusivities of four individual PCBs. Environ. Pollut. 5B:121-132. Pavlou, S.P., and R.N. Dexter. 1979. Distribution of polychlorinated biphenyls (PCB) in estuarine ecosystems: Testing the concept of equilibrium partitioning in the marine environment. Environ. Sci. Technol. 13:65-71. Lynch, T.R., and H.E. Johnson. 1982. Availability of hexachlorobiphenyl isomer to benthic amphipods from experimentally contaminated sediments. In Aquatic Toxicology and Hazard Assessment: Fifth Conference, ASTM STP 766, ed. J.G. Pearson, R.B. Foster, and W.E. Bishop, pp. 273-287. American Society of Testing and Materials, Philadelphia, PA. Chou, S.F.J., and R.A. Griffin. 1986. Solubility and soil mobility of polychlorinated biphenyls. In PCBs and the environment, Vol. 1, pp. 101-120. CRC Press, Inc., Boca Raton, FL. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 628 BIOACCUMULATION SUMMARY 22. PCB 169 Sawhney, B.L. 1986. Chemistry and properties of PCBs in relation to environmental effects. In PCBs and the environment, ed. J.S. Waid, pp. 47-65. CRC Press, Inc., Boca Raton, FL. Furukawa, K. 1986. Modification of PCBs by bacteria and other microorganisms. In PCBs and the environment, ed. J.S. Waid, Vol. 2, pp. 89-100. CRC Press, Inc. Boca Raton, FL. Bolger, M. 1993. Overview of PCB toxicology. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, pp. 37-53. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington, DC. Erickson, M.D. 1993. Introduction to PCBs and analytical methods. In Proceedings of the U.S. Environmental Protection Agency's National Technical Workshop "PCBs in Fish Tissue," May 10-11, 1993, pp. 3-9. EPA/823-R-93-003, U.S. Environmental Protection Agency, Office of Water, Washington, DC. Safe, S. 1990. Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related compounds: Environmental and mechanistic considerations which support the development of toxic equivalency factors (TEFs). Crit. Rev. Toxicol. 21(1):51-88. USEPA. 1991. Workshop report on toxicity equivalency factors for polychlorinated biphenyl congeners. EPA/625/3-91/020. U.S. Environmental Protection Agency. (Eastern Research Group, Inc., Arlington, MA.) Neff, J.M. 1984. Bioaccumulation of organic micropollutants from sediments and suspended particulates by aquatic animals. Fres. Z. Anal. Chem. 319:132-136. Shaw, G.R., and D.W. Connell. 1982. Factors influencing concentrations of polychlorinated biphenyls in organisms from an estuarine ecosystem. Aust. J. Mar. Freshw. Res. 33:1057-1070. Tanabe, S., R. Tatsukawa, and D.J.H. Phillips. 1987. Mussels as bioindicators of PCB pollution: A case study on uptake and release of PCB isomers and congeners in green-lipped mussels (Perna viridis) in Hong Kong waters. Environ. Pollut. 47:41-62. Pruell, R. J., J. L. Lake, W. R. Davis, and J. G. Quinn. 1986. Uptake and depuration of organic contaminants by blue mussels (Mytilus edulis) exposed to environmentally contaminated sediments. Mar. Biol. 91:497-508. Lech, J.J., and R.E. Peterson. 1983. Biotransformation and persistence of polychlorinated biphenyls (PCBs) in fish. In PCBs: Human and environmental hazards, ed. F.M. D'Itri and M.A. Kamrin, pp. 187-201. Ann Arbor Science Publishers, Inc., Ann Arbor, MI. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 629 BIOACCUMULATION SUMMARY 33. PCB 169 Stout, V.F. 1986. What is happening to PCBs? Elements of effective environmental monitoring as illustrated by an analysis of PCB trends in terrestrial and aquatic organisms. In PCBs and the Environment, ed. J.S. Waid. CRC Press, Inc., Boca Raton, FL. USEPA. 1980. Ambient water quality criteria document: Polychlorinated biphenyls. EPA 440/580-068. (Cited in USEPA. 1996. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cinncinati, OH. February.) Mearns, A.J., M. Matta, G. Shigenaka, D. MacDonald, M. Buchman, H. Harris, J. Golas, and G. Lauenstein. 1991. Contaminant trends in the Southern California Bight: Inventory and assessment. Technical Memorandum NOAA ORCA 62. National Oceanic and Atmospheric Administration. Seattle, WA. Long, E.R., and L.G. Morgan. 1991. The potential for biological effects of sediment-sorbed contaminants tested in the National Status and Trends Program. NOAA Technical Memorandum NOS OMA 52. National Oceanic and Atmospheric Administration, Seattle, WA. Spies, R. B., D. W. Rice, Jr., P. A. Montagna, and R. R. Ireland. 1985. Reproductive success, xenobiotic contaminants and hepatic mixed-function oxidase (MFO) activity in Platichthys stellatus populations from San Francisco Bay. Mar. Environ. Res. 17:117-121. Monod, G. 1985. Egg mortality of Lake Geneva char (Salvelinus alpinus) contaminated by PCB and DDT derivatives. Bull. Environ. Contam. Toxicol. 35:531-536. Van Bavel, B., P. Andersson, H. Wingfors, J. Ahgren, P. Bergqvist, L. Norrgren, C. Rappe, and M. Tysklind. 1996. Multivariate modeling of PCB bioaccumulation in three-spined stickleback (Gasterosteus aculeatus). Environ. Toxicol. Chem. 6:947-954. Tillitt, D.E., R.W. Gale, J.C. Meadows, J.L. Zajicek, P.H. Peterman, S.N. Heaton, P.D. Jones, S.J. Bursian, T.J. Kubiak, J.P. Giesy, and R.J. Aulerich. 1996. Dietary exposure of mink to carp from Saginaw Bay. 3. Characterization of dietary exposure to planar halogenated hydrocarbons, dioxin equivalents, and biomagnification. Environ. Sci. Technol. 30:283-291. 34. 35. 36. 37. 38. 39. 40. 630 BIOACCUMULATION SUMMARY Chemical Category: SUBSTITUTED PHENOLS PENTACHLOROPHENOL Chemical Name (Common Synonyms): PENTACHLOROPHENOL (PCP) CASRN: 87-86-5 Chemical Characteristics Solubility in Water: 14 mg/L at 20C [1] Half-Life: 23 - 178 days, sediment grab sample, estimated unacclimated aqueous aerobic biodegradation [2] Log Koc: 5.00 L/kg organic carbon Log Kow: 5.09 [3] Human Health Oral RfD: 3 x 10-2 mg/kg/day [4] Critical Effect: Liver and kidney pathology Oral Slope Factor: 1.2 x 10-1 per (mg/kg)/day [4] Carcinogenic Classification: B2 [4] Confidence: Medium, uncertainty factor = 100 Wildlife Partitioning Factors: Partitioning factors for pentachlorophenol in wildlife were not found in the literature. Food Chain Multipliers: Food chain multipliers for pentachlorophenol in wildlife were not found in the literature. Aquatic Organisms Partitioning Factors: Partitioning factors for pentachlorophenol in aquatic organisms were not found in the literature. Food Chain Multipliers: Food chain multipliers for pentachlorophenol in aquatic organims were not found in the literature. 631 BIOACCUMULATION SUMMARY PENTACHLOROPHENOL Toxicity/Bioaccumulation Assessment Profile Technical PCP has been reported to contain chlorodiphenylethers, chlorodibenzo-p-dioxins, chlorodibezofurans, and hydroxychlorodiphenylethers, whereas commercial PCP contains significant quantities of tetrachlorophenol [5]. These impurities contribute to PCP toxicity, especially sublethal effects at low concentrations of PCP. PCP undergoes rapid degradation (by chemical, microbiological, or photochemical processes) in the environment. PCP affects energy metabolism by increasing oxygen consumption and altering the activities of several glycolytic and citric acid cycle enzymes and by increasing the consumption rate of stored lipid [6]. PCP toxicity ranged from 3 to 100 g/L for invertebrates and 1 to 68 g/L for fish. In oral doses PCP was fatal to birds at 380 to 580 mg/kg. Adverse sublethal effects in birds were observed in a diet containing 1 mg/kg of PCP [5]. Residues above 11 mg/kg in bird tissues were associated with acute toxicity. Studies with birds showed that PCP killed various species at single oral doses of 380 to 504 mg/kg at dietary concentration of 3,850 mg/kg, fed over a 5-day period. Residues of PCP in dead birds were 11 mg/kg in brain, 20 mg/kg in kidney, and 46 mg/kg in liver [7]. Chickens fed 1 mg/kg PCP over an 8-week period accumulated substantial amounts of PCP: 2 mg/kg in muscle, 80 mg/kg in kidney, 25 mg/kg in liver [8]. Residues of PCP in dead organisms after treatment in rice fields were 8.1 mg/kg in frogs and 36.8 mg/kg in snails, and the residues ranged from 31.2 to 59.5 mg/kg in three fish species [7]. Accumulation of PCP is pH-dependent; at pH 4, PCP is completely protonated and therefore highly lipophilic. At this pH, PCP has the greatest accumulation potential. Conversely, PCP is completely ionized at pH 9. Early studies estimated the lethal body burden or critical body residue for goldfish was 0.36 mmol PCP/kg [12] and 0.75 mmol PCP/kg for brown trout [13] (these were prior to 1985 and are not included in the following table). Experiments with rainbow trout [9] showed that neither the twofold difference in body weight nor the 3-percent difference in body lipid content gave fish resistance to the toxicity of PCP. Mean lethal body residues (= critical body residue) ranged from 0.08 to 0.15 mmol/kg. The PCP accumulation by medaka (Oryzias latipes) acclimated in freshwater and saltwater decreased with increased salinity [10]. However, the amount of PCP accumulated by killifish acclimated to freshwater was greater than that accumulated by killifish acclimated to saltwater. The growth rate of bluegill was reduced by 75 percent during the 22-day subchronic exposure to 173 g/L of PCP [11]. The critical body residue for chlorophenols for fathead minnows ranged from 1.1 to 1.7 mmol/kg [14]. PCP is rapidly accumulated and rapidly excreted, and it has no tendency to persist in living organisms. However, PCP tends to accumulate in mammalian tissues unless it is efficiently conjugated into a readily excretable form [15]. Humans eliminate 75 percent of all PCP in the urine. Rats (Rattus sp.) and mice can eliminate PCP in the urine very efficiently; however, rhesus monkeys (Macaca mulatta) are unable to excrete PCP efficiently. 632 Summary of Biological Effects Tissue Concentrations for Pentachlorophenol Species: Taxa Invertebrates Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 Glycera dibranchiata, Polychaete 6.64 mg/kg (whole body)4 Cellular, LOED [20] L; reduced ability of amebocytes to recognize foreign material L; reduced antibacterial activity L; significant reduction in coelomic fluid glucose level, number of replicates is 8 to 10 L; decrease in tissue glycogen L; lethal body burden 1.55 mg/kg (whole body)4 Neanthes virens, Polychaete sandworm 28 mg/kg (whole body)4 Physiological, LOED Physiological, LOED [20] [23] 112 mg/kg (whole body)4 13.8 mg/kg (whole body)4 469 mg/kg (extractable lipid)4 Physiological, LOED Mortality, ED100 Mortality, ED50 [23] [32] [9] L; median survival time with fish fed low fat diet for 11 weeks then PCP exposure L; median survival time with fish fed high fat diet for 11 weeks then PCP exposure 471 mg/kg (extractable lipid)4 Mortality, ED50 [9] 633 634 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Pentachlorophenol Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 29.8 mg/kg (whole body)4 Mortality, ED50 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [9] L; median survival time with fish fed low fat diet for 11 weeks then PCP exposure L; median survival time with fish fed high fat diet for 11 weeks then PCP exposure 39.4 mg/kg (whole body)4 Mortality, ED50 [9] Summary of Biological Effects Tissue Concentrations for Pentachlorophenol Species: Taxa Eisenia fetida, Earthworm, Concentration, Units in1: Sediment 6.75 mmol/kg 3.75 mmol/kg 2.10 mmol/kg 1.20 mmol/kg 0.68 mmol/kg 0.38 mmol/kg 0.21 mmol/kg 0.12 mmol/kg 0.068 mmol/kg 0.038 mmol/kg Water Toxicity: Tissue (Sample Type) Effects 1.39-2.65 mmol/kg 0.74-1.19 mmol/kg 0.62-1.35 mmol/kg 0.56-1.16 mmol/kg 0.59-1.58 mmol/kg 0.51-0.80 mmol/kg 0.33-0.84 mmol/kg 0.79-1.16 mmol/kg 0.44-1.29 mmol/kg 0.21 mmol/kg 0.33 mg/kg (whole body)4 Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [19] L Physa sp., Snail [28] L; no effect on survivorship in 24 hours 635 636 Species: Taxa Anodonta anatina, Duck mussel Sediment Mytilus edulis, Blue mussel 5 g/kg Mytilus edulis, Mussel Summary of Biological Effects Tissue Concentrations for Pentachlorophenol Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 3.1 mg/kg (whole body)4 1.5 mg/kg (whole body)4 3.1 mg/kg (whole body)4 Behavior, LOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [30] L; behavioral changes, distended foot could not be retracted L; no effect on behavior L; no effect on mortality Behavior, NOED Mortality, NOED [30] [30] 32-244 g/kg [16] F 2.34 mg/kg (whole body)4 Physiological, LOED [34] L; significant increase in anoxic heat dissipation (j/h/g)at test concentration L; 10% reduction in anoxia tolerance as percent of controls L; 36% reduction in anoxia tolerance as percent of controls L; 54% reduction in anoxia tolerance as percent of controls 2.34 mg/kg (whole body)4 9.9 mg/kg (whole body)4 29.4 mg/kg (whole body)4 Physiological, NA Physiological, NA Physiological, NA [34] [34] [34] Summary of Biological Effects Tissue Concentrations for Pentachlorophenol Species: Taxa Mercenaria mercenaria, Quahog clam Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 0.498 mg/kg (whole body)4 0.498 mg/kg (whole body)4 Physiological, LOED Mortality, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [21] L; impaired ability to clear flavobacterium L; no effect on mortality [21] Daphnia magna, Cladoceran 0.45 mg/kg (whole body)4 Mortality, NOED [28] L; no effect on survivorship in 24 hours Pontoporeia hoyi, Amphipod 48.6 mg/kg (whole body)4 200 mmol/L 3.8 mmol/kg 300 mmol/L 5.6 mmol/kg 430 mmol/L 7.6 mmol/kg CBR = 0.33 to1.1 mmol/kg Survival, ED50 lethal lethal lethal [27] [17] L L Chironomus riparius, Midge 1.1 mg/kg (whole body)4 0.87 mg/kg (whole body)4 0.38 mg/kg (whole body)4 Behavior, NOED Behavior, NOED Behavior, NOED [29] L; no effect on swimming behavior L; no effect on swimming behavior L; no effect on swimming behavior [29] [29] 637 638 Species: Taxa Sediment Strongylocentrotus purpuratus, Purple sea urchin Fishes Oncorhynchus kisutch, Coho salmon Oncorhynchus mykiss, Rainbow trout Summary of Biological Effects Tissue Concentrations for Pentachlorophenol Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 95 mg/kg (whole body)4 927 mg/kg (whole body)4 662 mg/kg (whole body)4 Development, LOED Development, LOED Reproduction, LOED [22] L; increase in number of abnormal embryos L; genotoxicity, anaphase aberrations L; reduced fertilization of embryos [22] [22] 1.3 g/L 21 g/kg [17] L 1.3 g/L 24 g/kg Summary of Biological Effects Tissue Concentrations for Pentachlorophenol Species: Taxa Concentration, Units in1: Sediment Water 1100 mmol/L 1150 mmol/L 1300 mmol/L 1400 mmol/L 1600 mmol/L 1700 mmol/L 2300 mmol/L Toxicity: Tissue (Sample Type) Effects 3.8 mmol/kg 4.0 mmol/kg 4.3 mmol/kg 4.4 mmol/kg 5.2 mmol/kg 6.0 mmol/kg 8.0 mmol/kg CBR = 0.08 to 0.15 mmol/kg lethal lethal lethal lethal lethal lethal lethal Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [17] L Salmo trutta, Brown trout 0.2 mg/l 200 mg/kg (whole body)4 Mortality, ED50 [13] L; lethal body burden Salvelinus namaycush, Lake trout 1.3 g/L 11 g/kg [17] L Carassius auratus, Goldfish 82 mg/kg (whole body)4 97 mg/kg (whole body)4 89 mg/kg (whole body)4 Mortality, ED100 Mortality, ED100 Mortality, ED100 [25] L; lethal body burden [25] L; lethal body burden [25] L; lethal body burden 639 640 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Pentachlorophenol Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 88 mg/kg (whole body)4 97 mg/kg (whole body)4 99 mg/kg (whole body)4 87 mg/kg (whole body)4 86 mg/kg (whole body)4 82 mg/kg (whole body)4 107 mg/kg (whole body)4 92 mg/kg (whole body)4 89 mg/kg (whole body)4 100 mg/kg (whole body)4 82 mg/kg (whole body)4 Mortality, ED100 Mortality, ED100 Mortality, ED100 Mortality, ED100 Mortality, ED100 Mortality, ED100 Mortality, ED100 Mortality, ED100 Mortality, ED100 Mortality, ED100 Mortality, ED100 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [25] L; lethal body burden [25] L; lethal body burden [25] L; lethal body burden [25] L; lethal body burden [25] L; lethal body burden [25] L; lethal body burden [25] L; lethal body burden [25] L; lethal body burden [25] L; lethal body burden [25] L; lethal body burden [25] L; lethal body burden Summary of Biological Effects Tissue Concentrations for Pentachlorophenol Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 99 mg/kg (whole body)4 86 mg/kg (whole body)4 95 mg/kg (whole body)4 Mortality, ED100 Mortality, ED100 Mortality, ED50 Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [25] L; lethal body burden [25] L; lethal body burden [26] L; mortality Pimephales promelas, Fathead minnow CBR = 1.1-1.7 mmol/kg 50% mortality [14] L Pimephales promelas, Fathead minnow 69 mg/kg (whole body)4 22.1 mg/kg (whole body)4 25.1 mg/kg (whole body)4 43.8 mg/kg (whole body)4 69 mg/kg (whole body)4 Growth, LOED [33] L; pH was 8.5 Growth, LOED [33] L; pH was 8.0 Growth, LOED [33] L; pH was 7.5 Morphology, LOED Morphology, LOED [33] L; pH was 8.0 [33] L; pH was 8.5 641 642 Species: Taxa Sediment Summary of Biological Effects Tissue Concentrations for Pentachlorophenol Concentration, Units in1: Water Toxicity: Tissue (Sample Type) Effects 35.1 mg/kg (whole body)4 45.9 mg/kg (whole body)4 45.9 mg/kg (whole body)4 43.8 mg/kg (whole body)4 12.6 mg/kg (whole body)4 12.3 mg/kg (whole body)4 45.9 mg/kg (whole body)4 35.1 mg/kg (whole body)4 35.1 mg/kg (whole body)4 22.1 mg/kg (whole body)4 21.5 mg/kg (whole body)4 Mortality, LOED Mortality, LOED Mortality, LOED Mortality, LOED Growth, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [33] L; pH was 8.5 [33] L; pH was 6.5 [33] L; pH was 6.5 [33] L; pH was 8.0 [33] L; pH was 8.0 Growth, NOED [33] L; pH was 7.5 Growth, NOED [33] L; pH was 6.5 Growth, NOED [33] L; pH was 8.5 Morphology, NOED Morphology, NOED Morphology, NOED [33] L; pH was 8.5 [33] L; pH was 8.0 [33] L; pH was 6.5 Summary of Biological Effects Tissue Concentrations for Pentachlorophenol Species: Taxa Concentration, Units in1: Sediment Water Toxicity: Tissue (Sample Type) Effects 25.1 mg/kg (whole body)4 17.8 mg/kg (whole body)4 22.1 mg/kg (whole body)4 25.1 mg/kg (whole body)4 21.5 mg/kg (whole body)4 25.1 mg/kg (whole body)4 45.9 mg/kg (whole body)4 69 mg/kg (whole body)4 43.8 mg/kg (whole body)4 Morphology, NOED Mortality, NOED Mortality, NOED Mortality, NOED Mortality, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Reproduction, NOED Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [33] L; pH was 7.5 [33] L; pH was 8.5 [33] L; pH was 8.0 [33] L; pH was 7.5 [33] L; pH was 6.5 [33] L; pH was 7.5 [33] L; pH was 6.5 [33] L; pH was 8.5 [33] L; pH was 8.0 Ictalurus nebulosus, Brown bullhead 643 5.7 g/L 260 g/kg [18] F 644 Species: Taxa Oryzias latipes, Medaka Sediment Gambusia affinis, Mosquito fish Osmerus mordax, Rainbow smelt Leuciscus idus, Golden ide Micropterus salmoides, Largemouth bass Summary of Biological Effects Tissue Concentrations for Pentachlorophenol Concentration, Units in1: Water 100 g/L Toxicity: Tissue (Sample Type) Effects 41.02 g/g 38.02 g/g 37.50 g/g Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [10] L 0.8 mg/kg (whole body)4 Mortality, NOED [28] L; no effect on survivorship in 24 hours 1.3 g/L 6 g/kg [17] L 13 mg/kg (whole body)4 Mortality, NOED [24] L; no effect on survivorship in 3 days 9.6 mg/kg (whole body)4 9.6 mg/kg (whole body)4 9.6 mg/kg (whole body)4 10.8 mg/kg (whole body)4 Behavior, LOED [31] L; reduced success rate of prey capture L; reduction in growth Growth, LOED [31] Physiological, LOED Mortality, NOED [31] L; reduced food conversion efficiency, condition factor L; no effect on mortality [31] Summary of Biological Effects Tissue Concentrations for Pentachlorophenol Species: Taxa Perca flavescens, Yellow perch Concentration, Units in1: Sediment Water 5.7 g/L Toxicity: Tissue (Sample Type) Effects 260 g/kg Ability to Accumulate2: Log BCF Log BAF BSAF Source: Reference Comments3 [18] F 1 2 3 4 Concentration units based on wet weight unless otherwise noted. BCF = bioconcentration factor, BAF = bioaccumulation factor, BSAF = biota-sediment accumulation factor. L = laboratory study, spiked sediment, single chemical; F = field study, multiple chemical exposure; other unusual study conditions or observations noted. This entry was excerpted directly from the Environmental Residue-Effects Database (ERED, www.wes.army.mil/el/ered, U.S. Army Corps of Engineers and U.S. Environmental Protection Agency). The original publication was not reviewed, and the reader is strongly urged to consult the publication to confirm the information presented here. 645 BIOACCUMULATION SUMMARY References 1. PENTACHLOROPHENOL Iverschueren handbook of environmental data for organic chemicals, 1983, p. 953. (Cited in: USEPA. 1995. Hazardous Substances Data Bank (HSDB). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September.) USEPA. 1989. Chemical fate rate constants for SARA section 313 chemicals and Superfund Health Evaluation Manual chemicals. Prepared by Chemical Hazard Assessment Division, Syracuse Research Corporation, for U.S. Environmental Protection Agency, Office of Toxic Substances, Exposure Evaluation Division, Washington, DC, and Environmental Criteria and Assessment Office, Cincinnati, OH. August 11. Karickhoff, S.W., and J.M. Long. 1995. Internal report on summary of measured, calculated and recommended log Kow values. Draft. Prepared by U.S. Environmental Protection Agency, Office of Research and Development, Environmental Research Laboratory-Athens, for E. Southerland, Office of Water, Office of Science and Technology, Standards and Applied Science Division, Washington, DC. April 10. USEPA. 1995. Integrated Risk Information System (IRIS). National Library of Medicine online (TOXNET). U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH. September. Eisler, R. 1989. Pentachlorophenol hazards to fish, wildlife, and invertebrates: A synoptic review. Fish and Wildlife Service, Biological Report 85(1.17). Brown, J.A., P.H. Johansen, P.W. Colgan, and R.A. Mathers. 1987. Impairment of early feeding behavior of largemouth bass by pentachlorophenol exposure: A preliminary assessment. Trans. Am. Fish. Soc. 116:71-78. Vermeer, K., R.W. Risebrough, A.L. Spaans, and L.M. Reynolds. 1974. Pesticide effects on fishes and birds in rice fields of Surinam, South America. Environ. Pollut. 7:217-236. Prescott, C.A., B.N. Wilke, B. Hunter, and R.J. Julian. 1982. Influence of a purified grade of pentachlorophenol on the immune response of chickens. Amer. J. Vet. Res. 43:481-487. Van den Heuvel, M.R., L.S. McCarty, R.P.Lanno, B.E. Hickie, and D.G. Dixon. 19