The effects of passive smoking on ischemic heart disease are reviewed. Short-term exposures of 20 min to 8 h result in increased platelet sensitivity and decreased ability of the heart to receive and process oxygen. Longer term exposure results in plaque buildup and adverse effects on blood cholesterol. The available epidemiology is reviewed, and it is concluded that passive smoking increases the coronary death rate among U.S. never smokers by 20% to 70%. The newest Environmental Protection Agency procedures for estimating deaths from passive smoking, when applied to the epidemiologic results on heart disease and passive smoking, indicate that in 1985 an estimated 62,000 ischemic heart disease deaths in the United States were associated with exposure to environmental tobacco smoke. Clinicians are advised to counsel their patients to avoid tobacco smoke at home, at work and in transportation settings.

In recent years, concerns have been raised that the association between passive smoking and lung cancer could in whole or in part be ascribed to an upward bias caused by misclassification of smokers as never smokers.' These concerns arise because a small proportion of subjects is known who report as never having smoked, through either tests of their body fluids or repeated questionnaires, to probably smoke currently or to have smoked in the past.Because most of the passive smoking studies involve spousal exposure of women who say they have never smoked, such misclassification could create the impression of a passive smoking effect because smokers tend to marry smokers. Therefore, if misclassification is appreciable, more of the smokers misclassified as never smokers will be found among those reporting as never smokers married to smokers than among those reporting as never smokers married to nonsmokers. In the case of lung cancer, the high relative risks of even a small percentage of misclassified smokers would increase the incidence of cancer among the self-reported never smokers married to the smokers relative to those married to the nonsmokers and would create a spurious passive smoking effect. The emphasis here is on the misclassification of self-reported never smokers rather than a category that would include former smokers, because the various passive smoking studies deal almost entirely with subjects who never smoked.Several methods'" have been proposed to determine the effect of smoker misclassification on the observed passive smoking relative risks. These methods require a knowledge of misclassification rates for current and former smokers, the degree of concordance of smoking status between spouses, the prevalence of smoking in the subject population, and the proportion of never smokers who are exposed to tobacco smoke. All of these factors are important, but among the most important, and least easily derived from the published literature, are the degree to which current smokers are misclassified as never smokers and the level at which they smoked.Misclassification rates for current smokers can be measured with biomarkers in body fluids. The best biomarker is thought to be cotinine,5 a metabolite of nicotine but with a longer half-life of about 20 hours, which is specific to tobacco smoke and can be measured in saliva, urine, or serum. Unfortunately, none of the passive smoking studies includes detailed information on cotinine levels in the body fluids of subjects. Therefore, estimates of misclassification rates for smokers must be derived from other studies.In most of the literature on cotinine levels, one or more of the essential factors needed for the passive smoking bias calculation is missing. Such studies lack either breakdown by sex or separation of selfreported never smokers from self-reported former smokers, or the misclassification rate is stated simply as the number or percent of reported nonsmokers (never smokers plus former smokers) who had cotinine levels

OBJECTIVES: This study was undertaken to determine whether exposure at work to environmental tobacco smoke is associated with an increased risk of lung cancer. METHODS: Data from 14 studies providing information on lung cancer and exposure to environmental tobacco smoke at work were examined. Six quality criteria were developed for determining usable data. A meta-analysis was performed to obtain a combined risk for those data that met the quality restrictions. RESULTS: Five studies met the quality standards. Their combined relative risk was 1.39 (95% confidence interval [CI] = 1.15, 1.68) based on 835 lung cancer cases. In various meta-analyses prepared by tobacco industry employees or consultants, no increase in risk was found. The main reason for this difference is that the earlier analysts failed to find errors in 2 underlying studies that resulted in overweighting of the odds ratios from those studies, both of which were less than unity. CONCLUSIONS: When appropriate cognizance is taken of the quality of data inputs, the increase in lung cancer risk from workplace exposure to environmental tobacco smoke is about the same as that from household exposure.

The RRs for heart disease from passive smoking at work are roughly equal to those from home-based exposure.