Secondhand smoke (Environmental Tobacco Smoke)

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Summary

TBD.

Studies and Reports

  • Enstrom J, Defending legitimate epidemiologic research: combating Lysenko pseudoscience, Epidemiologic Perspectives & Innovations 2007, 4:11, October 10, 2007.
    • Abstract. This analysis presents a detailed defense of my epidemiologic research in the May 17, 2003 British Medical Journal that found no significant relationship between environmental tobacco smoke (ETS) and tobacco-related mortality. In order to defend the honesty and scientific integrity of my research, I have identified and addressed in a detailed manner several unethical and erroneous attacks on this research. Specifically, I have demonstrated that this research is not “fatally flawed,” that I have not made “inappropriate use” of the underlying database, and that my findings agree with other United States results on this relationship. My research suggests, contrary to popular claims, that there is not a causal relationship between ETS and mortality in the U.S. responsible for 50,000 excess annual deaths, but rather there is a weak and inconsistent relationship. The popular claims tend to damage the credibility of epidemiology. In addition, I address the omission of my research from the 2006 Surgeon General’s Report on Involuntary Smoking and the inclusion of it in a massive U.S. Department of Justice racketeering lawsuit. I refute erroneous statements made by powerful U.S. epidemiologists and activists about me and my research and I defend the funding used to conduct this research. Finally, I compare current ETS epidemiology in the U.S. with pseudoscience in the Soviet Union during the period of Trofim Devisovich Lysenko. Overall, this paper is intended to defend legitimate research against illegitimate criticism by those who have attempted to suppress and discredit it because it does not support their ideological and political agendas. Hopefully, this defense will help other scientists defend their legitimate research and combat “Lysenko pseudoscience.”
  • Sagiv S et al., Active and passive cigarette smoke and breast cancer survival, Ann Epidemiol. 2007 May;17(5):385-93. Epub 2007 Mar 28.
    • Conclusion. "These data do not provide strong evidence for an association between smoking and all-cause or breast cancer-specific mortality, although smokers who are postmenopausal or obese at diagnosis may be at higher risk."
  • Lee P & Hamling J, Environmental tobacco smoke exposure and risk of breast cancer in nonsmoking women: a review with meta-analyses, Inhal Toxicol. 18(14):1053-70, December 2006.
    • Abstract. "Recent authoritative reviews consider smoking has no effect on breast cancer risk, but some studies report an increase from environmental tobacco smoke (ETS). We reviewed the overall evidence on ETS and breast cancer in nonsmoking women. We extracted details of available studies, derived relative risk (RR) estimates with confidence intervals (CIs) for various ETS exposure indices and conducted meta-analyses. Using an index for each study most closely equivalent to "spouse ever smoked," a weak, but significant, association was seen (random-effects RR = 1.12, 95% CI = 1.02-1.24, n = 22). However, the estimates were heterogeneous: close to 1.0 for prospective, North American and larger studies, and those adjusting for many potential confounders, but significantly (p < .05) elevated in case-control, European, and smaller studies, and those accounting for fewer potential confounders. Risk was increased in premenopausal women (RR = 1.54, 95% CI = 1.16-2.05, n = 10), but not postmenopausal women. Dose-response findings were similarly heterogeneous. No significant increase was seen for ETS in childhood or the workplace or from the spouse specifically, but an increase was seen for total exposure (RR = 1.54, 95% CI = 1.17-2.04, n = 6). Increases mainly derive from case-control studies asking detailed ETS histories, where RRs depend heavily on who is classified in the totally unexposed reference group, and may be prone to recall bias. Results from prospective studies using similar histories are needed. Study weaknesses and possible publication bias also limit interpretation. Because of the inherent implausibility that ETS exposure might cause breast cancer, given the similar risks of smokers and nonsmokers, one cannot confidently conclude ETS exposure increases risk in nonsmokers."
  • Stranges S et al., Lifetime cumulative exposure to secondhand smoke and risk of myocardial infarction in never smokers: results from the Western New York health study, 1995-2001, Arch Intern Med. 2006 Oct 9;166(18):1961-7.
    • Results and Conclusion. "RESULTS: After adjustment for covariates, exposure to SHS was not significantly associated with an increased risk of MI. Compared with participants in the bottom tertile of SHS exposure, those in the top tertile had an odds ratio of 1.19 [95% confidence interval, 0.78-1.82] for MI. Virtually all subjects reported some exposure to SHS over their lifetime, but self-reported exposures declined over time, especially in the period closest to the interview. CONCLUSIONS: Exposure to SHS has declined sharply among nonsmokers in recent years. In the absence of high levels of recent exposure to SHS, cumulative lifetime exposure to SHS may not be as important a risk factor for MI as previously thought."
    • Lifetime cumulative exposure to secondhand smoke and risk of myocardial infarction in never smokers: results from the Western New York health study, 1995-2001
  • Study. Enstrom J and Kabat G, Environmental tobacco smoke and coronary heart disease mortality in the United States--a meta-analysis and critique, Inhal Toxicol. 2006 Mar;18(3):199-210.
    • Abstract. "Several major meta-analyses have concluded that exposure to environmental tobacco smoke (ETS) increases the risk of coronary heart disease (CHD) by about 25% among never smokers. However, these reviews have excluded a large portion of the epidemiologic evidence on questionable grounds and have been inconsistent in the selection of the results that are included. We conducted an updated meta-analysis and critique of the evidence on ETS exposure and its relationship to death from CHD among never smokers. Our focus is on the U.S. cohort studies, which provide the vast majority of the available evidence. ETS exposure is assessed in terms of spousal smoking, self-reported estimates, and personal monitoring. The epidemiologic results are summarized by means of overall relative risks and dose-response relationships. The methodological issues of publication bias, exposure misclassification, and confounding are discussed. Several large studies indicate that spousal smoking history is a valid measure of relative exposure to ETS, particularly for females. Personal monitoring of nonsmokers indicates that their average ETS exposure from a smoking spouse is equivalent in terms of nicotine exposure to smoking less than 0.1 cigarettes per day. When all relevant studies are included in the meta-analysis and results are appropriately combined, current or ever exposure to ETS, as approximated by spousal smoking, is associated with roughly a 5% increased risk of death from CHD in never smokers. Furthermore, there is no dose-response relationship and no elevated risk associated with the highest level of ETS exposure in males or females. An objective assessment of the available epidemiologic evidence indicates that the association of ETS with CHD death in U.S. never smokers is very weak. Previous assessments appear to have overestimated the strength of the association."
  • Gammon M et al., Environmental tobacco smoke and breast cancer incidence, Environ Res. 2004 Oct;96(2):176-85.
    • Abstract. "To evaluate whether environmental tobacco smoke (ETS) influences breast cancer incidence, data from a population-based case-control study were analyzed. Respondents with available ETS information assessed by in-person questionnaires included 1356 newly diagnosed cases and 1383 controls. Relative to nonsmokers who reported no residential ETS exposure throughout the life course, the odds ratios (OR) for breast cancer were not substantially elevated in relation to ETS exposure, active smoking, or a joint measure of active and passive smoking (OR, 1.15, 95% CI, 0.90, 1.48). An increased OR, however, was noted among nonsmokers who lived with a smoking spouse for over 27 years (2.10, 95% CI, 1.47, 3.02), although no dose-response was evident. Also, among women with hormone-receptor-positive tumors only, the OR for both active and passive smoking was increased (1.42 for ER+ PR+, 95% CI, 1.00, 2.00). Our data suggest that if there is an effect for ETS on breast cancer, that effect is restricted to selected subgroups of women, such as those with long-term exposure from a smoking spouse."
  • Enstrom J and Kabat G, Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98, BMJ. 2003 May 17;326(7398):1057.
    • Conclusions. "The results do not support a causal relation between environmental tobacco smoke and tobacco related mortality, although they do not rule out a small effect. The association between exposure to environmental tobacco smoke and coronary heart disease and lung cancer may be considerably weaker than generally believed."
    • Authors' reply to letters to the BMJ editor.
  • Lee P, Difficulties in assessing the relationship between passive smoking and lung cancer, Stat Methods Med Res. 7(2):137-63, June 1998.
    • Abstract. "Since 1981, numerous epidemiological studies have investigated the relationship between passive smoking and lung cancer in nonsmokers. The overall evidence, predominantly relating to women, indicates a weak association with the husband's smoking and many reviewers have concluded that this demonstrates a causal effect of exposure to environmental tobacco smoke (ETS). Interpreting weak associations is notoriously difficult, however, and this paper reviews problems specific to the ETS-lung cancer relationship. After describing how to select relevant studies and appropriate data, the methods for combining evidence together ('meta-analysis') are discussed, and the need to investigate sources of heterogeneity is emphasized. Separate consideration is given to various forms of bias that may affect overall relative risk estimates, including misclassification of active smoking status, confounding, systematic case-control differences, recall bias, diagnostic bias and publication bias. Sections on dose-response, multiple ETS exposure sources and other issues follow. The problems are illustrated from the available literature. It is shown there is no significant association of lung cancer with workplace, childhood or social ETS exposure or with smoking by the wife. Though statistically significant, the association with husband's smoking is weak and heterogeneous and varies widely according to various study characteristics. The association is markedly weakened by the adjustment for smoking misclassification bias and is likely to be affected by confounding and other sources of bias. While the precise extent of all the biases remains unclear, it seems impossible to conclude with any certainty that ETS causes lung cancer."
  • Cardenas V et al., Environmental tobacco smoke and lung cancer mortality in the American Cancer Society's Cancer Prevention Study. II, Cancer Causes Control. 1997 Jan;8(1):57-64.
    • Abstract. "Environmental tobacco smoke (ETS) has been classified as a human lung carcinogen by the United States Environmental Protection Agency (EPA), based both on the chemical similarity of sidestream and mainstream smoke and on slightly higher lung cancer risk in never-smokers whose spouses smoke compared with those married to nonsmokers. We evaluated the relation between ETS and lung cancer prospectively in the US, among 114,286 female and 19,549 male never-smokers, married to smokers, compared with about 77,000 female and 77,000 male never-smokers whose spouses did not smoke. Multivariate analyses, based on 247 lung cancer deaths, controlled for age, race, diet, and occupation. Dose-response analyses were restricted to 92,222 women whose husbands provided complete information on cigarette smoking and date of marriage. Lung cancer death rates, adjusted for other factors, were 20 percent higher among women whose husbands ever smoked during the current marriage than among those married to never-smokers (relative risk [RR] = 1.2, 95 percent confidence interval [CI] = 0.8-1.6). For never-smoking men whose wives smoked, the RR was 1.1 (CI = 0.6-1.8). Risk among women was similar or higher when the husband continued to smoke (RR = 1.2, CI = 0.8-1.8), or smoked 40 or more cigarettes per day (RR = 1.9, CI = 1.0-3.6), but did not increase with years of marriage to a smoker. Most CIs included the null. Although generally not statistically significant, these results agree with the EPA summary estimate that spousal smoking increases lung cancer risk by about 20 percent in never-smoking women. Even large prospective studies have limited statistical power to measure precisely the risk from ETS."
    • Study. Environmental tobacco smoke and lung cancer mortality in the American Cancer Society's Cancer Prevention Study. II
  • Koo L et al., Dietary and lifestyle correlates of passive smoking in Hong Kong, Japan, Sweden, and the U.S.A., Soc Sci Med. 1997 Jul;45(1):159-69.
    • Abstract. "From epidemiologic studies in several countries, passive smoking has been associated with increased risk for lung cancer, respiratory diseases, and coronary heart disease. Since the relative risks derived from those studies are weak, i.e. relative risk less than two, we investigated whether poorer diets and less healthy lifestyles might act as confounders and be correlated with having a smoking husband on a cross-cultural basis. Characteristics of never-smoked wives with or without smoking husbands were compared between 530 women from Hong Kong, 13,047 from Japan, 87 from Sweden, and 144 from the U.S. In all four sites, wives with smoking husbands generally ate less healthy diets. They had a tendency to eat more fried food but less fruit than wives with nonsmoking husbands. Other healthy traits, e.g. avoiding obesity, dietary cholesterol and alcohol, or taking vitamins and participating in preventive screening were also less prevalent among wives with smoking husbands. These patterns suggest that never-smoked wives with smoking husbands tend to share the same less healthy dietary traits characteristic of smokers, and to have dietary habits associated with increased risk for lung cancer and heart disease in their societies. These results emphasize the need to take into account the potential confounding effects of diet and lifestyle in studies evaluating the health effects of passive smoking, especially since it is known that the current prevalence rates of smoking among men is indirectly associated with social class and education in affluent urban societies."
  • Steenland K et al., Environmental tobacco smoke and coronary heart disease in the American Cancer Society CPS-II cohort, Circulation. 1996 Aug 15;94(4):622-8.
  • Muscat J and Wynder E, Exposure to environmental tobacco smoke and the risk of heart attack, Int J Epidemiol. 24(4):715-9, August 1995.
    • Conclusion. "Exposure to ETS comes from a variety of sources besides the spouse including parents, workplace employees and motorists. Exposure to ETS during childhood is not associated with an increased risk of heart disease. However, ETS exposure during adulthood increased the risk of myocardial infarction approximately 50% in this data although the findings were not statistically significant."
  • Kabat G et al., Relation between exposure to environmental tobacco smoke and lung cancer in lifetime nonsmokers, Am J Epidemiol. 142(2):141-8, July 1995.
    • Abstract. "To assess the relation between exposure to environmental tobacco smoke throughout life and lung cancer in lifetime nonsmokers, the authors conducted in-person interviews with 41 male and 69 female never-smoking lung cancer cases and 117 male and 187 female never-smoking controls between 1983 and 1990 as part of a hospital-based case-control study of tobacco-related cancers. Cases had newly diagnosed, histologically confirmed primary carcinoma of the lung. Controls were matched to cases on age (+/- 5 years), sex, race, hospital, and year of interview. Subjects were asked about environmental tobacco smoke exposure in childhood, in adulthood at home, in different jobs, and in transportation and social situations. In addition to amount smoked by family members in the subject's presence, subjects were asked to rate the intensity of each exposure, and married subjects were asked whether their spouse smoked in the bedroom. Several independent indicators of exposure to smoking by spouses were strongly correlated, thereby increasing confidence in the classification of exposure status. The reproducibility of environmental tobacco smoke variables was good for qualitative measures (yes/no), in agreement with previous studies. There were few associations of exposure in specific settings with lung cancer. Males whose wives smoked had odds ratio of 1.60 (95% confidence interval (CI) 0.67-3.82) and females whose husbands smoked had an odds ratio of 1.08 (95% CI 0.60-1.94). While this study had limited sample size, the pattern of odds ratios shows little indication of an association of environmental tobacco smoke with lung cancer in nonsmokers."
  • Gori G, Environmental tobacco smoke and coronary heart syndromes: absence of an association, Regul Toxicol Pharmacol. 21(2):281-95, April 1995.
    • Abstract. "Concerns about possible cardiovascular and especially coronary effects of environmental tobacco smoke (ETS) derive from the reported effects of active smoking. Despite similarities, however, ETS has composition and physical characteristics different from the mainstream smoke (MS) that active smokers inhale and appears relatively more chemically inert and less biologically active. ETS doses to nonsmokers are small and often below the sensitivity of detection technologies. They are several orders of magnitude less than MS doses in active smokers. Numerous epidemiologic studies report that the active smoking of less than 10 cigarettes/day is not associated with measurable risk of coronary heart disease (CHD). Thus, even assuming that ETS and MS have equivalent biologic activities, conceivable ETS doses to nonsmokers are far below apparent no-effect thresholds for active smoking. Hence, it is no surprise that epidemiologic reports are inconclusive about a possible association of ETS exposure and CHD, some suggesting a slight elevation, others a reduction of risk. Often, the elevations reported are higher than the CHD risk values associated with active smoking. Such equivocations likely result from the presence of contrasting protective or aggravating confounders, of which more than 200 have been reported in the literature--confounders that were not and could not be adequately controlled by any epidemiologic study. By scientific standards, the weight of evidence continues to falsify the hypothesis that ETS exposure might be a CHD risk factor."
  • Rodgman P, Environmental Tobacco Smoke, Regulatory Toxicology and Pharmacology (16:3;223-244), December 1992.
    • Abstract. "In 1992, the U.S. Environmental Protection Agency (EPA) issued a “draft” assessment of ETS and lung cancer in adults and respiratory disorders in children. Relying on weak and inconclusive epidemiological data, the supposed similarity between ETS and MS, the presence of 'known or suspected carcinogens' in MS and by extrapolation in ETS, and the “biological plausibility” of an adverse relationship between ETS and health, the EPA recommended that ETS be classified as a “Group A (known human) carcinogen.” Fundamental physical and quantitative chemical differences among ETS, MS, and SS and human exposure to each smoke were disregarded: The three are not equivalent nor is ETS exposure a quantitative variant of cigarette smoking. A substantial difference in retention percentage overlays the huge dosimetric difference between exposures. As a result, the “dosage” of ETS retained is miniscule relative to MS. Also, conclusions reached by the EPA and the use of tenuous relationships as bases for Group A classification are unwarranted because of failure to consider the data upon which the “tumorigenicity” of the ETS components was based, questions on the presence and/or levels of these components in MS, and data indicating that a 25- to 30-fold decrease of a high-level dose of MS or MS condensate diminished the effects observed in bioassays from pronounced to zero, i.e., a threshold was demonstrated. Finally, EPA overlooked the more than 100 tobacco smoke components known to inhibit the tumorigenic action of many of the listed 'tumorigens'."
  • Gori G, Mainstream and environmental tobacco smoke, Regul Toxicol Pharmacol. 14(1):88-105, August 1991.
    • Abstract. "Environmental tobacco smoke (ETS) is derived from cigarette smoldering and active smoker exhalation. Its composition displays broad quantitative differences and redistributions between gas and respirable suspended particulate (RSP) phases when compared with the mainstream smoke (MSS) that smokers puff. This is because of different generation conditions and because ETS is diluted and ages vastly more than MSS. Such differences prevent a direct comparison of MSS and ETS and their biologic activities. However, even assuming similarities on an equal mass basis, ETS-RSP inhaled doses are estimated to be between 10,000- and 100,000-fold less than estimated average MSS-RSP doses for active smokers. Differences in effective gas phase doses are expected to be of similar magnitude. Thus the average person exposed to ETS would retain an annual dose analogous to the active MSS smoking of considerably less than one cigarette dispersed over a 1-year period. By contrast, consistent epidemiologic data indicate that active smoking of some 4-5 cigarettes per day may not be associated with a significantly increased risk of lung cancer. Similar indications also obtain for cardiovascular and respiratory diseases. Since average doses of ETS to nonsmoking subjects in epidemiologic studies are several thousand times less than this reported intake level, the marginal relative risks of lung cancer and other diseases attributed to ETS in some epidemiologic studies are likely to be statistical artifacts, derived from unaccounted confounders and unavoidable bias."
  • Garfinkel L, Time trends in lung cancer mortality in nonsmokers and a note on passive smoking, JNCI 1981;66:1061-1066.
    • Abstract. "Lung cancer mortality rates were computed for nonsmokers in the American Cancer Society's prospective study for three 4-year periods from 1960 to 1972 and in the Dorn study of veterans for three 5-year periods from 1954 to 1969. There was no evidence of any trend in these rates by 5-year age groups or for the total groups. No time trend was observed in nonsmokers for cancers of other selected sites except for a decrease in cancer of the uterus. Compared to nonsmoking women married to nonsmoking husbands, nonsmokers married to smoking husbands showed very little, if any, increased risk of lung cancer."
    • Study. Time trends in lung cancer mortality in nonsmokers and a note on passive smoking

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