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dismisses it as unimportant on the ground:;.that_elevated risks-- were reported in studies conducted in countries where no social stigma against smoking exists. In view of the dat-a elicited by Lee (1988b) in his intensive examination of the smoker misclassification question, this argument appears to be facile and insubstantial. Finally, little attention was given :; in the Surgeon General's report to the important matter of uncontrolled confounding in the analysis of study results. Samet concludes his lung cancer discussion by mentioning three ETS-lung cancer risk assessments, which he says can provide insight into the magnitude of the problem in spite of the fact that they are subject to substantial uncertainty. He first refers to Repace and Lowrey's (1985) estimate of lung cancer deaths attributab:_e to ETS exposure, but offers no critical evaluation of its validity. Primarily because it was based on a comparison of mortality rates in two populations which could not be assumed to be comparable in respects other than ETS exposure, the Repace and Lowrey risk assessment has been strongly criticized and largely disregarded by the scientific community (i:he NRC report did not mention it, for example). The other -=wo risk assessments mentioned by Samet are those of Robins (in an appendix to the NRC-report) and Wells (1988). Both are biased on data from the epidemiologic•studies, and have no validi:y in view of the fact that it cannot be definitely concluded that the 11

associations repor-ted.in_those.-studies.reflect-a causal. - relationship. In the- last section of-his review, Samet discusses epidemiologic studies of ETS exposure and cancer other than of the lung. Surprisingly, he states that the Miller (1984) study linked ETS exposure to a generally increased risk of malignancy. That study showed an age-adjusted cancer mortality relative risk of 0.97 for all women, and a nonsignificant relative risk of 1.25 for women not employed outside the home. Samet does not mention the cohort study of Sandler et al. (1989), which reported all-site cancer - mortality relative risks of 1.01 and 1.00 for men and women respectively. Nor does he mention criticisms that have been made of other ETS cancer studies, for example that they failed to control for known risk factors for specific cancers, such as sexual activity in the case of cervical cancer. No review committee ha's concluded that ETS exposure is linked to an elevated risk of cancer at sites other ti-an the lung. Some ETS studies have reported increased risks for cancers not associated with smoking, and, as Samet notes, such findings are biologically implausible. Thus bias and confounding are likely contributors to these observed risks. There seems nb reason to suppose that these distorting factors have not also been present in the lung cancer studies themselves : -- 12

To summarize, _ this chapter prov'.des -a rather cursory_ and uncritical review of the epidemiologic-evidence-concerning ETS and cancer. It offers little in the way of systematic analysis or new insights, merely endorsiny the conclusions of some of the studies without considering the merits of opposing viewpoints. It falls short of being an adequate source of technical information on this important subject. V:O 13

ADDITIONAL REFERENCES (NOT LISTED IN 'PHE EPA DOCUMENT)-- Buffler, P.A., L.W. Pickle, T.J. Mason, and C. Constant (1984). The causes of cance•r in Texas. In: Lung Cancer: Causes and Prevention (Eds. Mizell and Correa). Verlag-Chemie International, New York. Layard, M.W. (1990). Environmental tobacco smoke and cancer: the epidemiologic evidence. In: Environmental Tobacco Smoke: Proceedings of the Interational Symposium at McGill University 1989 (Eds. Ecobichon and Wu). D.C. Heath & Co., Lexington, MA. Layard, M.W., and J.R. Viren (1989). Assessing the validity of a Japanese cohort study. In: Present and Future of Indoor Air Quality (Eds. Bieva et al.). Excerpta Medica, Amsterdam. Lee, P.N. (1988a). An alternative explanation for the increased risk of lung cancer in non-smokers married to smokers. In: Indoor Air and Ambient Air Quality (Eds. Perry and Kirk). Selper Ltd., London. Lee, P.N. (1988b). Misclassification of Smoking Habits and Passive Smoking. A Review of the Evidence. Springer-Verlag, Heidelberg. Lee, P.N. (1989). Passive smoking and lung cancer; fact or fiction? In: Present and Future of Indoor Air Quality (Eds. Bieva et al.). Excerpta Medica, Amsterdam. McAugtiey, J.J., J.N. Pritchard, and A. Black (1989). Relative lung cancer risk from exposure to mainstream and sidestream smoke particulates. In: Present and Future of Indoor Air Quality (Eds. Bieva et al.). Excerpta Medica, Amsterdam. Robins, J.M., D. Blevins, and M. Schneiderman (1989). The effective number of cigarettes inhaled daily by passive smokers: are epidemiologic and dosimet.ric estimates equivalent? J. Hazardous Materials 2].:215-238. Samet, J.M. (1985). Relationship between passive exposure to cigarette smoke and cancer. In: Indoor Air and Human Health (Eds. Gammage and Kaye). Lewis Publishers Inc., Chelsea, MI. Sandler, D.P., G.W. Comstock, K.J. Helsing, and D.L. Shore (1989). Deaths from all causes in non--smokers who lived with smokers. Am. J. Publ. Health 79::.63=167: 14

Wynder, E.L., and G.C. Kabat (1989). Health-care.and-society• environmental tobacco smoke and lung cancer. In: Present • and Future of Indoor Air Quality (Eds. Bieva-et-al.). Excerpta Medica, Amsterdam. Ziegler, R.G., T.J. Mason, A. Stemhagen, et al. (1984). Dietary carotene and vitamin A and risk of lung cancer among white men in New Jersey. J. Natl. Cancer Inst. 73:1429-1435. 15