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SUBJECT: Repace and Lowrey's Estimate of the Nonsmokers' Lung Cancer Risk From Passive Smoking FROM: Herman.J. Gibb Epidemfol ogi st Carcinogen Assessment Group (RD-689) TO: Elizabeth L. Anderson Di'rector Office of Health and Environmental Assessment (RD-689) THRU: Robert E. McGaughy Acting~ Technical Director Carcinogen Assessment Group (RD-689) As requested, I have reviewed the report by Repace and Lowrey entitled "Estimate of the Nonsmokers' Lung Cancer Risk from Passive Smoktng". The authors have derived two estimates of the annual lung cancer risk to passive smokers. One estimate is 0.87 x 10-5 per year and is based on a one-hit model (P = 1-e-Bd where B is the response in smokers and d is the dose from passive smoking). The second estimate of 8.0 x 10-5, an order of magnitude higher than the estimate from the one-hit model, is a so-called "phencmenological" estimate and is based on the excess lung cancer incidence rate for nonsmoking non-Seventh Day Adventists over that of nonsmoking Seventh Day Adventists (SDAs). Since SDAs do not smoke, Repace and Lowrey assumed that they would not be exposed to passive smoking from spouses. Moreover, a substantial portion of SDAs were reported to "work for an organization owned and operated by the SDA church" and thus would probably not be exosed to smoking at their place of employment. -Differences in susceptibility, dose-rate, and dose to the target tissue between smokers and nonsmokers would, the authors theorized, make the higher "phenomenoiogical" estimate more val'id than the one-hit mod'el'l which uti lii zed a dose-response i n smokers. The lung cancer risk estimate for nonsmokers deri'ved by the authors with a one-hit model is a rather crude approach that utilized a slope derived by dividing a lung cancer excess risk of all smokers as a group by the average amount of tar smoked by a smoker. In an independent anaylsis, however, Thorsiund (1982) of the Carcinogen Assessment Group (CAG), using a more sophisticated model, achieved a result similar to that of Repace and Lowrey's. Thorslund (1982) used Doll's (1978) model of the lung cancer risk to British physictans due to smoking cigarettes and a 1982 estimate by Repace and Lowrey of the tar intake for a passive smoker to calculate the l1ung cancer risk to a

passive smoker. The major problem with the uphenomenological" estimate is the authors' assumption that the difference in the lung cancer rate between non-SDA and SOA nonsmokers is due to passive smoking. SOAs are a very unique group and may differ from the general population with regard, to lung cancer risk by more than just their lack of exposure to passive smoking. In addition to not smoking, SOAs do not drink, and they maintain rather strict diets. As indicated above, they tend to work in SDA businesses. Repace and Lowrey, by their discussion, attemptedito mimimize the possibility that lifestyle differences other than smoking may be partially accountable for the difference in lung cancer risk, but the issue has not been resoived. A separate problem with the "phenomenological" estimate is Repace and Lowrey's calculation of the age-adjusted lung cancer rates for SDAs and'non- SDAs. They have multiplied an age-adjusted iung!cancer mortality ratio of SDA non-smokers to non-SDA non-smokers, provided by the author of the SDA study, by the crude lung cancer mortality rate for non-SDA nonsmokers to arrive at an age-adjusted lung cancer mortality rate for SDA non-smokers. This approach will not provide the age-adjusted rate. The calculation of the age-adjusted rate for both SDA non-smokers and non-SDA non-smokers would require information not provided by the authors of the SDA study in the original report. Lastly, the authors indicate that the age-adjusted lung cancer rate attributable to passive smoking from the SDA study is similar to that of the Hirayama study of non-smoking females married~to smokers. The Hirayama study has been severely criticized in letters to the British Medical Journal where the study was published. Two of the issues whicn~se considerab'Te concern to this reviewer are: 1) it is unclear from the Hirayama study and from his replies to the criticism whether the rates are age-adjusted for the females or not; 2) there does not appear to have been any analysis by length of exposure. The many issues raised by other reviewers of the Hirayama study are too lengthy to go into here, but further discussion can be provided if necessary. In summary, the estimate of the annual lung cancer risk to passive smokers derived by the authors using a one-hit model (0.87 x 10-5) i's more reasonable than their "phenomenological!" estimate (8.0 x 10-5). The assumptiion of the "phenomenological" estimate that the entire difference between the lung cancer rate in non-SDA.nonsmokers andISDA nonsmokers iis due to passive smoking is questionable. The use of data from the Hirayama study in an attempt to verify this absolute difference is also questionable because of the shortcomings iin the Hirayama study. As a final note, it would be interesting to attempt to validate the authors' theories with regard to susceptibility, dose rate, and dose-to-the-target tissue irn nonsmokers. Information derived from such studies m might then be used to improve the risk model for passive smokers. C cc: Charles Ris (RD-68?) Todd Thors l und ( RD-689 ). James Repace ( ANR-445 )~ 2

1 Ab REFERENCES Doll, Richard and Richard Peto. 1978. Cigarette smoking and'bronchial carcinoma: dose and time relationships among regular smokers and lifelong non-smokers. Journal of Epidemiology and Ccmnunity Health. 32:303-313. Thorslund, Todd. 1984. Estimation of the effects of exposure to a carcinogen that fl uctuate over time on the lifetime risk of cancer death. Presented at the Pacific Division of the American Association for the Advancement of Science Annual Meeting, Santa Barbara, California, August 1982. r.0 3