Tobacco_facts_sheets[1]

Tobacco_facts_sheets[1] - The Surgeon General’s Report on...

Info iconThis preview shows page 1. Sign up to view the full content.

View Full Document Right Arrow Icon
This is the end of the preview. Sign up to access the rest of the document.

Unformatted text preview: The Surgeon General’s Report on The Health Consequences of Smoking Four Major Conclusions of the 2004 Report ◗ Smoking harms nearly every organ of the body, causing many diseases and reducing the health of smokers in general. ◗ Quitting smoking has immediate as well as long-term benefits, reducing risks for diseases caused by smoking and improving health in general. ◗ Smoking cigarettes with lower machine-measured yields of tar and nicotine provides no clear benefit to health. ◗ The list of diseases caused by smoking has been expanded to include abdominal aortic aneurysm, acute myeloid leukemia, cataract, cervical cancer, kidney cancer, pancreatic cancer, pneumonia, periodontitis, and stomach cancer. These are in addition to diseases previously known to be caused by smoking, including bladder, esophageal, laryngeal, lung, oral, and throat cancers, chronic lung diseases, coronary heart and cardiovascular diseases, as well as reproductive effects and sudden infant death syndrome. Citation U.S. Department of Health and Human Services. The Health Consequences of Smoking: A Report of the Surgeon General. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Smoking remains the leading cause of preventable death and has negative health impacts on people at all stages of life. It harms unborn babies, infants, children, adolescents, adults, and seniors. Department of Health and Human Services The Surgeon General’s Report on The Health Consequences of Smoking How Smoking Harms People of All Ages ◗ Toxic ingredients in cigarette smoke travel throughout the body, causing damage in several different ways. (p. 616) ◗ Nicotine reaches the brain within 10 seconds after smoke is inhaled. It has been found in every part of the body and in breast milk. (p. 616) ◗ Carbon monoxide binds to hemoglobin in red blood cells, preventing affected cells from carrying a full load of oxygen. (p. 616) ◗ Cancer-causing agents (carcinogens) in tobacco smoke damage important genes that control the growth of cells, causing them to grow abnormally or to reproduce too rapidly. (p. 44–45) ◗ The carcinogen benzo[a]pyrene binds to cells in the airways and major organs of smokers. (p. 616) ◗ Smoking affects the function of the immune system and may increase the risk for respiratory and other infections. (p. 616) ◗ There are several likely ways that cigarette smoke does its damage. One is oxidative stress that mutates DNA, promotes atherosclerosis, and leads to chronic lung injury. Oxidative stress is thought to be the general mechanism behind the aging process, contributing to the development of cancer, cardiovascular disease, and COPD. (p. 619) ◗ The body produces antioxidants to help repair damaged cells. Smokers have lower levels of antioxidants in their blood than do nonsmokers. (p. 618–619) ◗ Smoking is associated with higher levels of chronic inflammation, another damaging process that may result from oxidative stress. (p. 619) Citation U.S. Department of Health and Human Services. The Health Consequences of Smoking: A Report of the Surgeon General. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Smoking remains the leading cause of preventable death and has negative health impacts on people at all stages of life. It harms unborn babies, infants, children, adolescents, adults, and seniors. Department of Health and Human Services The Surgeon General’s Report on The Health Consequences of Smoking Smoking Among Adults in the United States: Cancer ◗ Cancer is the second leading cause of death and was among the first diseases causally linked to smoking. (p. 39) ◗ Lung cancer is the leading cause of cancer death, and cigarette smoking causes most cases. (p. 61) ◗ Compared to nonsmokers, men who smoke are about 23 times more likely to develop lung cancer and women who smoke are about 13 times more likely. Smoking causes about 90% of lung cancer deaths in men and almost 80% in women. (p. 39) ◗ In 2003, an estimated 171,900 new cases of lung cancer occurred and approximately 157,200 people died from lung cancer. (p. 42) ◗ The 2004 Surgeon General’s report adds more evidence to previous conclusions that smoking causes cancers of the oral cavity, pharynx, larynx, esophagus, lung, and bladder. (pp. 42, 62, 63, 116, 166) ◗ Cancer-causing agents (carcinogens) in tobacco smoke damage important genes that control the growth of cells, causing them to grow abnormally or to reproduce too rapidly. (p. 44–45) ◗ Cigarette smoking is a major cause of esophageal cancer in the United States. Reductions in smoking and smokeless tobacco use could prevent many of the approximately 12,300 new cases and 12,100 deaths from esophageal cancer that occur annually. (p. 119) ◗ The combination of smoking and alcohol consumption causes most laryngeal cancer cases. In 2003, an estimated 3,800 deaths occurred from laryngeal cancer. (p. 62) ◗ In 2003, an estimated 57,400 new cases of bladder cancer were diagnosed and an estimated 12,500 died from the disease. (p. 166) ◗ For smoking-attributable cancers, the risk generally increases with the number of cigarettes smoked and the number of years of smoking, and generally decreases after quitting completely. (pp. 39, 42) ◗ Smoking cigarettes that have a lower yield of tar does not substantially reduce the risk for lung cancer. (p. 61) ◗ Cigarette smoking increases the risk of developing mouth cancers. This risk also increases among people who smoke pipes and cigars. (p. 67) ◗ Reductions in the number of people who smoke cigarettes, pipes, cigars, and other tobacco products or use smokeless tobacco could prevent most of the estimated 30,200 new cases and 7,800 deaths from oral cavity and pharynx cancers annually in the United States. (p. 67) Department of Health and Human Services factsheet no:12 What’s in a cigarette Action on Smoking and Health – August 2001 Cigarette composition Cigarettes look deceptively simple, consisting of paper tubes containing chopped up tobacco leaf, usually with a filter at the mouth end. In fact, they are highly engineered products, designed to deliver a steady dose of nicotine. Cigarette tobacco is blended from two main leaf varieties: yellowish ‘bright’, also known as Virginia where it was originally grown, contains 2.5-3% nicotine; and ‘burley’ tobacco which has a higher nicotine content (3.5-4%). US blends also contain up to 10% of imported ‘oriental’ tobacco which is aromatic but relatively low (less than 2%) in nicotine. 1 In addition to the leaf blend, cigarettes contain ‘fillers’ which are made from the stems and other bits of tobacco which would otherwise be waste products. These are mixed with water and various flavourings and additives. The ratio of filler varies among brands. For example, a high filler content makes a less dense cigarette with a slightly lower tar delivery. Additives are used to make tobacco products more acceptable to the consumer. They include humectants (moisturisers) to prolong shelf life; sugars to make the smoke seem milder and easier to inhale; and flavourings such as chocolate and vanilla. While some of these may appear to be quite harmless in their natural form they may be toxic in combination with other substances. Also when additives are burned, new products of combustion are formed and these may be toxic. The full list of 600 permitted additives can be viewed on the Department of Health’s website 2 For further information on tobacco additives, see also the ASH/ICRF report, Tobacco Additives. 3 The nicotine and tar delivery can also be modified by the type of paper used in the cigarette. Using more porous paper will let more air into the cigarette, diluting the smoke and (in theory) reducing the amount of tar and nicotine reaching the smoker’s lungs. Filters are made of cellulose acetate and trap some of the tar and smoke particles from the inhaled smoke. Filters also cool the smoke slightly, making it easier to inhale. They were added to cigarettes in the 1950s, in response to the first reports that smoking was hazardous to health. Tobacco companies claimed that their filtered brands had lower tar than others and encouraged consumers to believe that they were safer. Tobacco Smoke Tobacco smoke is made up of “sidestream smoke” from the burning tip of the cigarette and “mainstream smoke” from the filter or mouth end. Tobacco smoke contains thousands of different chemicals which are released into the air as particles and gases. Many toxins are present in higher concentrations in sidestream smoke than in mainstream smoke and, typically, nearly 85% of the smoke in a room results from sidestream smoke. 4 The particulate phase includes nicotine, "tar" (itself composed of many chemicals), benzene and benzo(a)pyrene. The gas phase includes carbon monoxide, ammonia, dimethylnitrosamine, formaldehyde, hydrogen cyanide and acrolein. Some of these have marked irritant properties and some 60, including benzo(a)pyrene and dimethylnitrosamine, have been shown to cause cancer. One study has established the link between smoking and lung cancer at the cellular level. It found that a substance in the tar of cigarettes, benzo(a)pyrene diol epoxide (BPDE), damages DNA in a key tumour suppresser gene. 5 What is tar? “Tar”, also known as total particulate matter, is inhaled when the smoker draws on a lighted cigarette. In its condensate form, tar is the sticky brown substance which can stain smokers’ fingers and teeth yellow-brown. All cigarettes produce tar but the brands differ in amounts. The average tar yield of British cigarettes (as measured by a standard machine method by the Government Chemist) has declined from about 30mg per cigarette in the period 1955-61 to 11mg today. There have also been reductions in nicotine (from an average of about 2mg in 1955-61 to about 0.9mg by 1996). 6 7 Until January 1992, information about tar yields of cigarettes was given in a general fashion on cigarette packets and advertisements as a result of a voluntary agreement between the tobacco industry and the Government. Under the terms of The Tobacco Products Labelling (Safety) Regulations 1991, which implement EU requirements for health warnings on tobacco, cigarette packets must include a statement of both the tar and the nicotine yield per cigarette on the packet itself. The same figures are printed on cigarette advertising, along with the health warning, as part of a voluntary agreement between the industry and the Department of Health. Under the current EU tar yield directive, cigarettes with a tar yield of 15mg or more were phased out by the end of 1992. From the 1st January 1998, an upper limit of 12mg per cigarette was applied to all cigarettes sold in the EU with the exception of Greece which was granted an extension until 2006. Both the labelling and tar yield directives will be replaced by a new directive, 8 effective from September 2000, which will place an upper limit of 10mg of tar, 10mg of carbon monoxide and 1mg of nicotine on all cigarettes sold in the EU. For further information on tobacco regulation, see Fact Sheet 20, Tobacco Policy in the European Union. Why low tar cigarettes are no safer than higher tar cigarettes Following the discovery in the 1950s that it was the tar in tobacco smoke which was associated with the increased risk of lung cancer, tobacco companies, with the approval of successive governments, embarked on a programme to gradually reduce the tar levels in cigarettes. Although there is a moderate reduction in lung cancer risk associated with lower tar cigarettes, research suggests that the assumed health advantages of switching to lower tar may be largely offset by the tendency of smokers to compensate for the reduction in nicotine (cigarettes lower in tar also tend to be lower in nicotine) by smoking more or inhaling more deeply. 9 Also, a study by the American Cancer Society found that the use of filtered, lower tar cigarettes may be the cause of adenocarcinoma, a particular kind of lung cancer. 10 There is no evidence that switching to lower tar cigarettes reduces coronary heart disease risk. Nicotine Nicotine, an alkaloid, is an extremely powerful drug. The Royal College of Physicians has affirmed that the way in which nicotine causes addiction is similar to drugs such as heroin and cocaine. 11 Only 60mg of pure nicotine placed on a person's tongue would kill within minutes. Nicotine is contained in the moisture of the tobacco leaf: when the cigarette is lit, it evaporates, attaching itself to minute droplets in the tobacco smoke inhaled by the smoker. It is absorbed by the body very quickly, reaching the brain within 10-19 seconds. It stimulates the central nervous system, increasing the heart beat rate and blood pressure, leading to the heart needing more oxygen. Carbon Monoxide Carbon monoxide, the main poisonous gas in car exhausts, is present in all cigarette smoke. It binds to haemoglobin much more readily than oxygen, thus allowing the blood to carry less oxygen. Heavy smokers may have the oxygen carrying power of their blood cut by as much as 15%. 12 For further information see ASH’s briefing on tobacco smoke composition. 13 References and links 1 2 3 4 5 6 7 8 9 10 11 12 13 Milne, A. Smoking – the inside story. Woodside Communications, 1998 Permitted Additives to Tobacco Products in the United Kingdom, March 2000. [View list] Tobacco Additives – cigarette engineering and nicotine addiction. ASH/ICRF, 1999 [View report] US Surgeon General. The Health Consequences of Smoking: Chronic obstructive lung disease. USGPO, 1984. Moon-shong Tang et al. Science 1996; 274: 430-32. Kiryluk, S. and Wald, N. Trends in cigarette smoking habits in the United Kingdom, 1905-1985. In Wald, N. and Froggatt, P. Nicotine, Smoking and the Low Tar Programme. OUP, 1989. Consumers and the changing cigarette. Health Education Authority, 1999 EU Directive concerning the manufacture, presentation and sale of tobacco products 1999/0244 (COD) C50086/2001 [View text] Jarvis, M and Bates, B. Why low tar cigarettes don’t work. ASH, 1999 [View report] Thun, M; et al. Cigarette smoking and changes in the histopathology of lung cancer. Journal of the National Cancer Institute, 1997; 89 (21): 1580-86. [View abstract] Royal College of Physicians. Nicotine Addiction in Britain. 2000 . [View report] Royal College of Physicians. Smoking or Health. London, Pitman, 1977. ASH briefing What goes in? What comes out? Cigarette and smoke composition - ASH sources of information, February 2001 [View document] 986 MMWR November 5, 1999 Achievements in Public Health, 1900–1999 Tobacco Use — United States, 1900–1999 Smoking—once a socially Tobacco Use — Continued accepted behavior—is the leading preventable cause of death and disability in the United States. During the first decades of the 20th century, lung cancer was rare; however, as cigarette smoking became increasingly popular, first among men and later among women, the incidence of lung cancer became epidemic (Figure 1). In 1930, the lung cancer death rate for men was 4.9 per 100,000; in 1990, the rate had increased to 75.6 per 100,000 (1 ). Other diseases and conditions now known to be caused by tobacco use include heart disease, atherosclerotic peripheral vascular disease, laryngeal cancer, oral cancer, esophageal cancer, chronic obstructive pulmonary disease, intrauterine growth retardation, and low birthweight. During the latter part of the 20th century, the adverse health effects from exposure to environmental tobacco smoke also were documented. These include lung cancer, asthma, respiratory infections, and decreased pulmonary function (2 ). Large epidemiologic studies conducted by Ernst Wynder (see box) and others in the 1940s and 1950s linked cigarette smoking and lung cancer. In 1964, on the basis of approximately 7000 articles relating to smoking and disease, the Advisory Committee to the U.S. Surgeon General concluded that cigarette smoking is a cause of lung and laryngeal cancer in men, a probable cause of lung cancer in women, and the most important cause of chronic bronchitis in both sexes (3 ). The committee stated that “Cigarette smoking is a health hazard of sufficient importance in the United States to warrant appropriate remedial action.” Substantial public health efforts to reduce the prevalence of tobacco use began shortly after the risk was described in 1964. With the subsequent decline in smoking, the incidence of smoking-related cancers (including cancers of the lung, oral cavity, and pharynx) have also declined (with the exception of FIGURE 1. Annual adult per capita cigarette consumption and major smoking and health events — United States, 1900–1998 1st World Conference on Smoking and Health 1st Surgeon General's Report 5000 End of WW II Broadcast Ad Ban 1st Great American Smokeout Number 4000 Nicotine Medications Available Over the Counter Fairness Doctrine Messages on TV and Radio 3000 1st SmokingCancer Concern 2000 1000 Master Settlement Agreement Nonsmokers' Rights Movement Begins Surgeon General's Report on Environmental Tobacco Smoke Federal Cigarette Tax Doubles Great Depression 0 1900 1910 1920 1930 1940 1950 1960 1970 1980 1990 1998 Year Sources: United States Department of Agriculture; 1986 Surgeon General’s Report. 988 MMWR November 5, 1999 Tobacco Use — Continued lung cancer among women) (4 ). In addition, age-adjusted death rates per 100,000 persons (standardized to the 1940 population) for heart disease (i.e., coronary heart disease) have decreased from 307.4 in 1950 to 134.6 in 1996 (4 ). During 1964–1992, approximately 1.6 million deaths caused by smoking were prevented (5 ). Smoking Trends During the Century Early in the 20th century, several events coincided that contributed to increases in annual per capita consumption, including the introduction of blends and curing processes that allowed the inhalation of tobacco, the invention of the safety match, improvements in mass production, transportation that permitted widespread distribution of cigarettes, and use of mass media advertising to promote cigarettes (6,7 ). Cigarette smoking among women began to increase in the 1920s when targeted industry marketing and social changes reflecting the liberalization of women’s roles and behavior led to the increasing acceptability of smoking among women (8,9 ). Annual per capita cigarette consumption increased from 54 cigarettes in 1900 to 4345 cigarettes in 1963 and then decreased to 2261 in 1998 (10,11 ). Some decreases correlate with events, such as the first research suggesting a link between smoking and cancer in the 1950s, the 1964 Surgeon General’s report, the 1968 Fairness Doctrine, and increased tobacco taxation and industry price increases during the 1980s (Figure 1). An important accomplishment of the second half of the 20th century has been the reduction of smoking prevalence among persons aged ≥18 years from 42.4% in 1965 to 24.7% in 1997, with the rate for men (27.6%) higher than for women (22.1%) (Figure 2). The percentage of adults who never smoked increased from 44% in the mid-1960s to 55% in 1997. In 1998, tobacco use varied within and among racial/ethnic groups. The prevalence of smoking was highest among American Indians/Alaska Natives, and second highest among black and Southeast Asian men. The prevalence FIGURE 2. Trends in cigarette smoking* among persons aged ≥18 years, by sex — United States, 1955–1997 60 Percentage Smokers Men 50 40 30 Women 20 10 0 1955 1960 1965 1970 1975 1980 1985 1990 1995 Year *Before 1992, current smokers were defined as persons who reported having smoked ≥100 cigarettes and who currently smoked. Since 1992, current smokers were defined as persons who reported having smoked ≥100 cigarettes during their lifetime and who reported now smoking every day or some days. Sources: 1955 Current Population Survey; 1965–1997 National Health Interview Survey. Vol. 48 / No. 43 MMWR 993 Tobacco Use — Continued 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. Pacific Islanders, and Hispanics: report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, CDC, 1998. Fielding JF, Husten CG, Eriksen MP. Tobacco: health effects and control. In: Wallace RB, Doebbeling BN, Last JM, eds. Public health and preventive medicine. 14th ed. Stamford, Connecticut: Appleton & Lange, 1998. CDC. State-specific prevalence of cigarette smoking among adults, and children’s and adolescents’ exposure to environmental tobacco smoke—United States, 1996. MMWR 1997; 46:1038–43. Chaloupka FJ, Warner KE. The economics of smoking. In: Newhouse J, Culyer A, eds. The handbook of health economics. Amsterdam, The Netherlands: Elsevier Science, 1999 (in press). CDC. Projected smoking-related deaths among youth—United States. MMWR 1996;45:971–4. CDC. Response to increases in cigarette prices by race/ethnicity, income, and age groups— United States, 1976–1993. MMWR 1998;47:605–9. Johnston LD, O’Malley PM, Bachman JG. National survey results on drug use from the Monitoring the Future study, 1975–1998. Vol I: secondary school students. Rockville, Maryland: National Institutes of Health, National Institute on Drug Abuse, 1999 (NIH publication no. 994660). CDC. Cigarette smoking among adults—United States, 1997. MMWR 1999;48:994–9. Pirkle JL, Flegal KM, Bennert JT, Brody DJ, Etzel RA, Maurer KR. Exposure of the U.S. population to environmental tobacco smoke. JAMA 1996;275:1233–40. Warner KE, Slade J, Sweanor DT. The emerging market for long-term nicotine maintenance. JAMA 1997;278:1087–92. CDC. Bidi use among urban youth—Massachusetts, March–April 1999. MMWR 1999;48:796–9. Byers R, Mouchawa J, Marks J, et al. The American Cancer Society challenge goals: how far can cancer rates decline in the U.S. by the year 2015? Cancer 1999;86:715–27. Tobacco Use — Continued Cigarette Smoking Among Adults — United States, 1997 Cigarette Smoking Among Adults — Continued In the United States, cigarette smoking is the leading cause of preventable morbidity and mortality and results in approximately 430,000 deaths each year (1 ). One of the national health objectives for 2000 is to reduce the prevalence of cigarette smoking among adults to no more than 15% (objective 3.4) (2 ). To assess progress toward meeting this objective, CDC analyzed self-reported data about cigarette smoking among U.S. adults from the 1997 National Health Interview Survey (NHIS) Sample Adult Core Questionnaire. This report summarizes the findings of this analysis, which indicate that, in 1997, 24.7% of adults were current smokers and that the overall prevalence of current smoking in 1997 was unchanged from the overall prevalence of current smoking from the 1995 NHIS. The 1997 NHIS Sample Adult questionnaire was administered to a nationally representative sample (n=36,116) of the U.S. noninstitutionalized civilian population aged ≥18 years; the overall response rate for the survey was 80.4%. Participants were asked, “Have you smoked at least 100 cigarettes in your entire life?” and “Do you now smoke cigarettes every day, some days, or not at all?” Current smokers were persons who reported having smoked ≥100 cigarettes during their lifetime and who smoked every day or some days at the time of the interview. Former smokers were those who had smoked ≥100 cigarettes during their lifetime but who did not smoke currently. Attempts to quit were determined by asking current daily smokers, “During the past 12 months, have you stopped smoking for one day or longer because you were trying to stop smoking?” Data were adjusted for nonresponse and weighted to provide national estimates. Confidence intervals (CIs) were calculated using SUDAAN. 994 MMWR November 5, 1999 Cigarette Smoking Among Adults — Continued In 1997, an estimated 48.0 million (24.7%) adults, including 25.7 million (27.6%) men and 22.3 million (22.1%) women, were current smokers (Table 1). Overall, 20.1% (95% CI=±0.5) of adults were every-day smokers, and 4.4% (95% CI=±0.2) were someday smokers (every-day smokers constituted 81.9% [95% CI=±0.9] of all smokers). Prevalence of smoking was highest among persons aged 18–24 years (28.7%) and aged 25–44 years (28.6%) and lowest among persons aged ≥65 years (12%). Prevalence of current smoking was significantly higher among American Indians/Alaska Natives (34.1%), non-Hispanic blacks (26.7%), and non-Hispanic whites (25.3%) than among Hispanics (20.4%) or Asians/Pacific Islanders (16.9%). Current smoking prevalence was highest among persons with nine to 11 years of education (35.4%) and lowest among persons with ≥16 years of education (11.6%), and was higher among persons living below the poverty level* (33.3%) than among those living at or above the poverty level (24.6%). *Published 1996 poverty thresholds from the Bureau of the Census are used in these calculations. TABLE 1. Percentage of persons aged ≥18 years who were current smokers,* by selected characteristics — United States, National Health Interview Survey, 1997 Men (n=15,361) Characteristic Total Total (n=35,816) % (95% CI†) % (95% CI) % (95% CI) 27.4 32.1 26.2 (± 1.0) (± 2.4) (± 2.1) 23.3 22.4 14.3 (±0.8) (±1.7) (±1.4) 25.3 26.7 20.4 (±0.7) (±1.4) (±1.4) 37.9 21.6 (±13.7) (± 4.4) 31.3 12.4 (±8.8) (±3.5) 34.1 16.9 (±7.7) (±2.7) 29.9 41.3 31.8 27.4 13.0 (± (± (± (± (± 3.0) 3.1) 1.7) 1.7) 1.2) 15.1 30.5 25.7 23.1 10.1 (±2.2) (±2.4) (±1.3) (±1.4) (±1.0) 22.5 35.4 28.4 25.1 11.6 (±1.9) (±2.0) (±1.0) (±1.1) (±0.8) 31.7 31.2 27.6 12.8 (± (± (± (± 2.8) 1.3) 1.5) 1.4) 25.7 26.1 21.5 11.5 (±2.4) (±1.1) (±1.3) (±1.1) 28.7 28.6 24.4 12.0 (±1.9) (±0.8) (±1.0) (±0.9) 27.3 38.7 23.4 (± 1.0) (± 2.8) (± 2.0) 21.8 29.8 18.2 (±0.8) (±1.9) (±1.5) 24.6 33.3 20.5 (±0.7) (±1.7) (±1.2) 27.6 (± 0.9) 22.1 (±0.7) 24.7 (±0.6) Race/Ethnicity§ White, non-Hispanic Black, non-Hispanic Hispanic American Indian/ Alaska Native¶ Asian/Pacific Islander Education (yrs)** ≤8 9–11 12 13–15 ≥16 Age group (yrs) 18–24 25–44 45–64 ≥65 Poverty status†† At or above Below Unknown Women (n=20,455) * Persons who reported having smoked ≥100 cigarettes during their lifetime and who reported now smoking every day or some days. Excludes 300 respondents for whom smoking status was unknown. † Confidence interval. § Excludes 74 respondents of unknown, multiple, and other racial/ethnic categories. ¶ Wide variances on estimates reflect the small sample sizes. **Persons aged ≥25 years. Excludes 305 persons with unknown years of education. †† Published 1996 poverty thresholds from the Bureau of the Census are used in these calculations. M e th o d s to d e te c t to b a c c o b y - p r o d u c ts a n d th e a b ility to c o r r e la te le v e ls to s m o k in g h a v e b e e n a v a ila b le fo r a c o u p le o f d e c a d e s . S o m e b y - p r o d u c ts a r e d e te c ta b le u p to 1 0 d a y s a fte r e x p o s u re . H e r e is a s u m m a r y f r o m o n e jo u r n a l: V o l. 7 2 , N o . 4 , 2 0 0 4 C lin ic a l C o r r e la tio n b e tw e e n th e C o n s u m p tio n o f N ic o tin e a n d C o tin in e C o n c e n tr a tio n s in U r in e a n d S e r u m b y C o m p e titiv e E n z y m e -L in k e d Im m u n o s o r b e n t A s s a y U l r i c h E . Z i e g l e r a, J e n s K a u c z o k a, U l r i c h A n d r e a s D i e t z a, H . B e r n d R e i t h b, K a r s t e n S c h m i d t a aP l a s t i c a n d H a n d S u r g e r y , D e p a r t m e n t o f S u r g e r y , U n i v e r s i t y o f W ü r z b u r g , W ü r z b u r g a n d bK l i n i k f ü r V i s c e r a l - , T h o r a x - u n d G e f ä s s c h i r u r g i e , K l i n i k u m K o n s t a n z , K o n s t a n z , G e r m a n y P h a r m a c o lo g y 2 0 0 4 ;7 2 :2 5 4 - 2 5 9 ( D O I: 1 0 .1 1 5 9 /0 0 0 0 8 0 3 8 1 ) K e y W o rd s C o tin in e E L IS A S m o k e r s , c o tin in e in s e r u m a n d u r in e N ic o tin e m e ta b o lite A b s tra c t Different negative effects of smoking are known (e.g. postoperative complications), which lead, especially in plastic surgery, to unsatisfactory results. The aim of this study was to examine the appropriateness of a cotinine enzyme-linked immunosorbent assay (ELISA) for routine usage in operative disciplines. By correlation of smoking habits and concentration of cotinine in serum and urine, we tried to ascertain reference values for smokers, passive smokers and non-smokers. The reliability and sensitivity of the cotinine ELISA concerning nicotine exposure need to be proven. 165 (108 men, 57 women) test persons were examined by detecting cotinine in serum and urine by ELISA. The study shows a very good sensitivity, precision and reproducibility of the cotinine ELISA according to the laboratory criteria. The test shows significance of a good differentiation between smokers, passive smokers and non-smokers in urine. In serum, cotinines are excellent to differentiate between smokers and nonsmokers/passive smokers. Urine and serum tests demonstrate valid and comparable results. C o p y r ig h t © 2 0 0 4 S . K a r g e r A G , B a s e l A r tic le In fo r m a tio n R e c e iv e d : M a r c h 1 0 , 2 0 0 4 A c c e p te d a fte r r e v is io n : M a y 1 0 , 2 0 0 4 N u m b e r o f P r in t P a g e s : 6 N u m b e r o f F ig u r e s : 4 , N u m b e r o f T a b le s : 0 , N u m b e r o f R e fe r e n c e s : 3 6 ...
View Full Document

Ask a homework question - tutors are online