Studies Of Environmental Tobacco Smoke Research Articles

Exposure misclassification bias in studies of environmental tobacco smoke and lung cancer.

It is now recognized that exposure to environmental tobacco smoke (ETS) in the workplace and other settings outside the home may be equally as important as residential ETS exposure. This review examines the sources of misclassification in the assessment of workplace ETS exposure in questionnaire-based epidemiologic studies. Cogent to this discussion is the role of misclassification of ever smokers as never smokers, which is important in studies of both workplace and residential ETS exposure and lung cancer and is discussed first. The collective evidence from studies that have used direct or indirect approaches to estimate smoker misclassification shows that although some misclassification of ever smokers as never smokers exists in studies of ETS and lung cancer, the potential bias from the misclassification of smokers is unlikely to explain the observed increased risk of lung cancer associated with ETS exposure.

Exposure Misclassification Bias in Studies of Environmental Tobacco Smoke and Lung Cancer

Exposure Misclassification Bias in Studies of Environmental Tobacco Smoke and Lung Cancer

Studies of Environmental Tobacco Smoke Generated by Different Cigarettes

ABSTRACT A method was developed to reproducibly measure environmental tobacco smoke (ETS) components generated by different cigarettes. Measurements were carried out in an unventilated, controlled environment chamber. True ETS (the aged and diluted combination of exhaled mainstream plus sidestream smoke) was generated by human smokers. To reliably quantitate components normally present at trace levels, the comparisons were carried out at elevated ETS concentrations—greater than 40 times those typically encountered in “real-world” settings. The method was applied to four commercially available cigarettes and a cigarette prototype that primarily heats tobacco. Forty-three properties and components of the gas and particulate phases of ETS generated by the different cigarettes were measured. Good precision of measurement was obtained both within and between tests. Statistically significant differences in the concentration of ETS components were observed among the different commercial cigarettes and between the commercial and prototype cigarettes. Most ETS components from the prototype cigarette were reduced by >90% when compared to the commercial cigarettes. The method was used to determine the effect of cigarette design changes on the generation of ETS.

Differential Exposure Misclassification in Case-Control Studies of Environmental Tobacco Smoke and Lung Cancer

We review some of the literature on the effects of exposure misclassification on the statistical analysis of case-control studies. In particular, we focus on evidence for exposure misclassification which may be different for cases and controls in studies of environmental tobacco smoke (ETS). For example, such misclassification could induce relative risk estimates below unity for low exposure which appears to be the case in U.S. lung cancer and ETS studies. We describe procedures for systematically examining the sensitivity of dose-response statistics on exposure misclassification. These procedures demonstrate how p-values for the null hypothesis of no dose-response trend could be adjusted to account for exposure misclassification. The adjustment procedures were applied to an example based on a recently published large study of ETS and lung cancer in which a p-value for trend was reported as 0.03. In this example it is seen that modest differential exposure misclassification can induce substantial increases in the actual p-value, changing what appears to be statistically significant to decidedly nonsignificant.

Exposure of Puerto Rican Children to Environmental Tobacco Smoke

Background.Many studies of environmental tobacco smoke (ETS) have been conducted in northern, industrialized countries. As yet, however, no studies have been carried out on ETS exposure with nonsmokers living in tropical environments.Methods.Urine specimens were collected from 175 healthy Puerto Rican children (2–11 years) living in an industrial area and were analyzed for cotinine, a quantitative biomarker for exposure to ETS. Their parents completed a questionnaire covering smoking habits.Results.Seventy percent of children were exposed to ETS. Quantitatively, exposure to smoke in households consuming more than 1 pack per day (ppd) caused a doubling of cotinine excretion compared with households consuming less than 1 ppd. Smoke from mothers made the greatest contribution to cotinine, followed by smoke from fathers, with smoke from other persons having no effect. Degree of exposure was inversely related to age of the child.Conclusions.Young children (2–4 years) were detected to have significantly greater exposure to ETS than older children (5–11 years) and in the younger group the effect seemed to be from the mother's smoking much more than the father's, with other persons contributing negligible amounts. This suggests an obvious strategy for prevention of exposure to ETS in young children.

Industry-Funded Research and Conflict of Interest: An Analysis of Research Sponsored by the Tobacco Industry Through the Center for Indoor Air Research

The Center for Indoor Air Research (CIAR) was created by three United States tobacco companies in 1988. Its stated mission is to fund high-quality, objective research related to indoor air, including studies of environmental tobacco smoke (ETS). Because CIAR is financed by the tobacco industry and funds research related to tobacco, it fosters an inherent conflict of interest. We consider whether this conflict of interest has affected the content, quality, or use of research funded by CIAR. We hypothesize that the tobacco industry might be using CIAR to develop scientific data to support its position that ETS is not harmful to health. CIAR funds two types of projects: "Peer-reviewed" projects are awarded after peer review by a group of scientists, whereas "special-reviewed" projects are awarded directly by tobacco industry executives. CIAR's special-reviewed projects are more likely than its peer-reviewed projects to be related to ETS, to support the tobacco industry position, and to be used by the industry to argue that smoking should not be regulated in public places. Our findings suggest that the tobacco industry is funding special-reviewed projects through CIAR to develop scientific data that it can use in legislative and legal settings. The industry may be financing peer-reviewed projects through CIAR to enhance its credibility, to provide good publicity, and to divert attention from ETS as an indoor air pollutant. CIAR's stated mission of funding high-quality, objective research has been compromised by conflict of interest, and at least some of CIAR's projects are being used to promote the tobacco industry's agenda.

Inconsistency between workplace and spousal studies of environmental tobacco smoke and lung cancer: LeVois ME, Layard MW. Environmental Health Resources, Tiburon, CA 94920. Regul Toxicol Pharmacol 1994;1:309–316

Inconsistency between workplace and spousal studies of environmental tobacco smoke and lung cancer: LeVois ME, Layard MW. Environmental Health Resources, Tiburon, CA 94920. Regul Toxicol Pharmacol 1994;1:309–316

Lung cancer pathology in smokers, ex-smokers and never smokers.

The histologic distribution of lung cancer is markedly different in smokers and non-smokers. It is not known whether the histology among former smokers varies according to the number of years since quitting. Using data from a large case-control study of lung cancer, we found that for both men and women, the proportion of adenocarcinomas increased with the number of years since quitting smoking. Among long-term quitters (> 25 years), the proportion of adenocarcinomas was similar to that in never smokers. These findings have implications for studies of environmental tobacco smoke and lung cancer.

Inconsistency between Workplace and Spousal Studies of Environmental Tobacco Smoke and Lung Cancer

In a risk assessment released at the end of 1992, the U.S. Environmental Protection Agency (EPA) concluded that environmental tobacco smoke (ETS) is a known human lung carcinogen. The Agency reached that conclusion primarily on the basis of epidemiologic studies of self-reported never-smoking women, in which the exposure index was marriage to a smoker. However, the use of the spousal smoking exposure surrogate introduces many potential confounding factors. Such confounding and bias due to denial of active smoking are likely explanations for weak and inconsistent reported ETS-lung cancer associations. This contention is supported by the results of 14 worldwide studies of lung cancer and ETS exposure in the workplace, which in combination indicated no risk elevation. Workplace ETS-lung cancer studies are not subject to the bias and confounding introduced by the spousal smoking exposure surrogate. The EPA ignored the workplace studies in its risk assessment and extrapolated the results of spousal smoking studies to workplace and other sources of ETS exposure. In its estimate of ETS-attributable lung cancer deaths in the United States, the EPA ascribed over 70% of the deaths to nonspousal ETS exposure, primarily workplace exposure. Considered in their entirety, the ETS-lung cancer epidemiologic data do not support a causal inference or provide a scientific basis for government regulation of smoking in the workplace.

The background adjustment in risk assessment of environmental tobacco smoke and lung cancer

Most epidemiologic studies of environmental tobacco smoke (ETS) and lung cancer in non-smokers have used marriage to a smoker as the ETS exposure index. Several risk assessments of ETS and lung cancer have calculated a summary relative risk from a meta-analysis of epidemiologic studies, and have increased that relative risk by applying a “background” adjustment. The aim of the background adjustment is to compensate for the ETS exposure received by nominally unexposed subjects, namely persons married to nonsmokers. Estimates of the ratio of ETS exposure of subjects married to smokers to that of subjects married to nonsmokers have been based on measurements of cotinine, a metabolite of nicotine, in body fluids. The validity of those estimates of relative ETS exposure is questionable, because of analytical problems and the possibility of exposure to nicotine from sources other than ETS. Attempts to explain differences between relative risks reported in U.S. and foreign studies of ETS and lung cancer on the basis of lower U.S. background exposure ratios, or higher foreign ETS exposures, are not supported by the available evidence.

602 Dose response studies of environmental tobacco smoke (ETS) reactivity by serial inhalation challenges in a dynamic test chamber

602 Dose response studies of environmental tobacco smoke (ETS) reactivity by serial inhalation challenges in a dynamic test chamber

Exposure of nonsmoking women to environmental tobacco smoke: a 10-country collaborative study

The interpretation and interpretability of epidemiologic studies of environmental tobacco smoke (ETS) depend largely on the validity of self-reported exposure. To investigate to what extent questionnaires can indicate exposure levels to ETS, an international study was conducted in 13 centers located in 10 countries, and 1,369 nonsmoking women were interviewed. The present paper describes the results of the analysis of self-reported recent exposure to ETS from any source in relation to urinary concentrations of cotinine. Of the total, 19.7 percent of the subjects had nondetectable cotinine levels, the median value was 6 ng/mg, and the cut-point of the highest decile was 24 ng/mg. The proportion of subjects misreporting their active smoking habit was estimated at between 1.9 and 3.4 percent, depending on whether cut-points of 50 or 100 ng/mg creatinine were used. Large and statistically significant differences were observed between centers, with the lowest values in Honolulu, Shanghai, and Chandigarh, and the highest in Trieste, Los Angeles, and Athens. Mean cotinine/creatinine levels showed a clear linear increase from the group of women not exposed either at home or at work, to the group of those exposed both at home and at work. Values were significantly higher for women exposed to ETS from the husband but not at work, than for those exposed at work but not from the husband. The results of linear regression analysis indicated that duration of exposure and number of cigarettes to which the subject reported being exposed were strongly related to urinary cotinine. ETS exposure from the husband was best measured by the number of cigarettes, while exposure at work was more strongly related to duration of exposure. After adjustment of number of cigarettes for volume of indoor places, a similar increase in cotinine (5 ng/mg) was predicted by the exposure to 7.2 cigarettes/8 h/40 m3 from the husband and 17.9 cigarettes/8 h/40 m3 at work. The results indicate that, when appropriately questioned, nonsmoking women can provide a reasonably accurate description of ETS exposure. Assessment of individual exposure to ETS should focus on daily duration and volume of indoor places where exposure occurred.

Lung Cancer and Exposure to Tobacco Smoke in the Household

The relation between passive smoking and lung cancer is of great public health importance. Some previous studies have suggested that exposure to environmental tobacco smoke in the household can cause lung cancer, but others have found no effect. Smoking by the spouse has been the most commonly used measure of this exposure. In order to determine whether lung cancer is associated with exposure to tobacco smoke within the household, we conducted a population-based case--control study of 191 patients with histologically confirmed primary lung cancer who had never smoked and an equal number of persons without lung cancer who had never smoked. Lifetime residential histories including information on exposure to environmental tobacco smoke were compiled and analyzed. Exposure was measured in terms of "smoker-years," determined by multiplying the number of years in each residence by the number of smokers in the household. Household exposure to 25 or more smoker-years during childhood and adolescence doubled the risk of lung cancer (odds ratio, 2.07; 95 percent confidence interval, 1.16 to 3.68). Approximately 15 percent of the control subjects who had never smoked reported this level of exposure. Household exposure of less than 25 smoker-years during childhood and adolescence did not increase the risk of lung cancer. Exposure to a spouse's smoking, which constituted less than one third of total household exposure on average, was not associated with an increase in risk. The possibility of recall bias and other methodologic problems may influence the results of case-control studies of environmental tobacco smoke. Nonetheless, our findings regarding exposure during early life suggest that approximately 17 percent of lung cancers among nonsmokers can be attributed to high levels of exposure to cigarette smoke during childhood and adolescence.

A genotoxic assessment of environmental tobacco smoke using bacterial bioassays

Recently, the National Research Council in the U.S.A. stated that laboratory studies of environmental tobacco smoke (ETS) should be important in identifying ETS carcinogens, their concentrations in typical daily environments, and in understanding how these compounds contribute to ETS dose-response relationships. This paper demonstrates that integrated chemical and bacterial mutagenicity information can be used to identify ETS genotoxicants, monitor human exposure, and make comparative assessments. Approximately 1 3 of the ETS constituents for which there is quantitative analytical chemistry information also have associated genotoxicity information. For example, 11 of the quantitated compounds are animal carcinogens. Work presented in this paper demonstrates that both the nonparticle-bound semi-volatile and the particulate-bound organic material contain bacterial mutagens. These ETS organics give an equivalent of ∼86000 revertants per cigarette. In addition, this article summarized efforts to estimate ETS bacterial mutagenicity, to use bacterial tests for the monitoring of ETS-impacted indoor environments, and to use bacterial assays for the direct monitoring of human exposure.

INDOOR AIR POLLUTION IN DEVELOPING COUNTRIES AND ACUTE RESPIRATORY INFECTION IN CHILDREN

Indoor air pollution emerges as an important risk factor for acute respiratory infections (ARI) in developing countries. In many developing countries in addition to an increasing amount of tobacco smoke many homes contain high levels of smoke from the combustion of biofuels such as wood crop residues and animal dung for cooking or heating. In about half the worlds households such fuels are used for cooking daily usually without a flue or chimney and with poor ventilation. Results of investigations in 6 developing nations have shown the range of indoor pollution in such circumstances. The best single indicator for comparison of toxic noncarcinogenic effects is most likely respirable particulates similar to tar reported for cigarette emissions. Results of studies in animals suggest any difference in respiratory-system toxicity according to mass is not likely to be large. On the basis of the small amount of evidence available peak and daily exposures to indoor particulate levels in villages in developing countries seem to be about 20 times greater than in developed nations. The results of a semi-quantitative epidemiological study conducted in Nepal showed a direct relation between reported hours/day spent near the stove by infants and children aged under 2 years and episodes of life threatening acute respiratory infections. If one discounts the many possible confounding factors extrapolation shows that by moving all children into the lowest smoke exposure groups as much as 25% of moderate and severe infections would be eliminated. Extrapolation from studies of both ARI and environmental tobacco smoke also indicates indirectly the potential effect of indoor smoke from biofuels. Some environmental tobacco smoke studies have reported a dose-response relation between the number of cigarettes smoked in the home and respiratory symptoms in children. In sum biofuel smoke is likely to be a factor in ARI but its importance in relation to other risk factors is difficult to establish. It may be that prevention of acute respiratory infections could be best realized by initially addressing other risk factors or by addressing smoke solely in the context of broad based programs for several risk factors.

Misclassification of environmental tobacco smoke exposure: Its potential influence on studies of environmental tobacco smoke and lung cancer

The effects of selection, confounding, misclassification and bias must be eliminated from case-control studies of ‘passive smoking’ and lung cancer before a meaningful interpretation can be made. Misclassification includes the misclassification of the subject's non-smoking status, of the disease status or of the spouse's smoking habits. This paper shows that inflation of the amount smoked by the husbands of female lung cancer cases may have accounted for the apparent ‘dose-response’ relationships in 3 widely referenced case-control studies.