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They concluded that dietary B-earotene intake was a potential confounder of the relationship between El'S and lung eancer.. Other potential' confounders included: occupation, domestic radon exposure, a history of exposure to therapeutic x-rays, and keeping pet birds in the bome. This last is raised by a recent study from the Netherlands which found that the odds ratio for lung cancer among people who kept pet birds in their Lome was 63 (95% eonfidence interval 22•20.0) aRer adjustment for active smoking and vitamin C intake (16). This study did not assess ETS exposure among the subjects. THE AMERICAN HEA].TH FOUNDATION STUDY Since 1483, a study of ETS and lung cancer in never smokers has been in progress at the Americaa Health Foundation. All lung cancer cases interviewed in the eontext of a large, muhi- eenter study of tobaeco-rolated diseases.vho report never having smoked more than one cigarette per day for a year are pvea a detailed ETS questionnaire. For each ease, 2-3 hospitalized eontrols.vho have diagnoses not known to be associated with tobacco use and who are also lifetime non-amokers are interviewcd. Controls are matehed to cases on age (+/- S years), sex. race, hospital, and date of interview (within 3 months). The items in the questionnaire include exposure in utero; in childhood (specific family members.vho smoked, years of exposure and average number of hours of exposure per day, and a subjective rating of the intensity of exposure), in adulthood at home (specific family members who smoke(d)y number o( cpd smoked by each, years of exposure, number of hours per day, subjective rating of exposure, aad.vbere a spouse smoked,.vhetber be or she smoked in the bedroom); in the workplace (number of hours per week, years of exposure, number of smokers within ten feet of subject,, rating of exposure) for up to four different jobs; and in various forms of transpo'rtation and in social~ situations. In addition to ETS questions, information is obtained on demographic factors, occupation, alcohol consumption, medical history, diet, and other factors. To date, this study has accrued a total of 90 lung cancer cases and 247 matched controls. We plan to continue recruiting subjects for the study in order to reach a sample size of 1S0 cases. Table 4®ves a breakdown of the bistology of lung cancer by sez. Prelimiaary analyses of the data do not indicate any striking ETS exposure differences between eases and controls. Tables S and 6 give crude odds ratios and confidence intervals for overall exposure in childhood, adulthood at home, and in the workplace, in males and females, respectively. With the possible exception of exposure in childhood and among women, there is little suggestion of ata.ss risk due to E'TS. A fuller analysis of these data, inc]uding adjustment for otrvariates, is in progress. CONCLUSION Epidemiologic studies of ETS and lung cancer g+enerally suffer from small sample sizc. Givea the small magnitude of the observed RR assodated with pasaive smoking and the problems assoaated with multiple histologic types bias, mt • r:fisation, and eonfoundin,g, iaaeasing the sample size is ooe way to attempt to answer the E7S-lung cancer question with greater cenainry. A case-control study of i0;p001ung cancer cases (7,500 males and 2,500 females) could be eqeaed to 190 ! i

yield approxrimately 1S0 male and 250 femalc never amokers, based on estimates of the frequenc}~ of lung cancer among never smokers (2% for males and 10°Tc for females 171)., Table 7 sbows the aample sizes necessary in each group (usuming equal numbers of cases and controls) to detect RRs between 1.25 and 2.00, with a one-tailcd alpha of 5% and 80°Xo- power, Bven various proportions of czposcd controls. While it is highly unlikely that such a study would be funded solely to assess the effects of ETS exposure, the study could be duigaed to make an important contribution to the radon-lung cancer issue as well. Specifically, studies of domestic radon exposure have also :uffered from small sample sizes and have produced variable and unstable estimates of the risk of radon exposure in never smokers. In addition, tbere is a aced to better assess the interactive eQects of active smoking and radon exposure. Since ETS and radon exposure are both risk factors for hutQ cancer, and since one may confound, or interact with, the other, a large study designed to measure both fauors as reliably as possible would have considerable scientific merit. 191

table I Epidemiologic Studies Prospective Studies Relative Risk Hirayama (1981) 1.63 Garfinkel (1981) 1.18 Case-Contro/ Studies ._.~.~. Trichopoulos, et al. (1981) 2.1 1.18 - 3.78 Chan & Fung (1982) 0.75 0.44 - 1.30 ~ Correa, et al. (1983) 2.03 0.83 - 5.03 Koo, et ai. (1983) 1.54 0.90 - 2.64 Kabat & Wynder (1984) 0.79 0,26 - 2.43 Wu, et al. (1985) 1.2 0.6 - 2.5 Garfinkel, et al.. (1985) 1.12 0.74 - 1.69 Lee, et ai. (1985) 1.03 0.41 - 2.47 Akiba, et al. (1986) 1.48 0.88 - 2.50 Dalager, et al. (1986) 1.5 0.8 - 2.8 Pershagen, et al. (1987) 1.28 0.75 - 2.16 Lam, et al. (1987) 1.65 1.16 - 2.35 Koo, et al. (1987) 1.55 0.94 - 3.08 8~szs~~~oz

Cell Type Related to Spouse's Smoking 9 * Study Histo%gio Type N Odds I4atlo 95% C. /. Adenocarcinoma 16 1.02 0.33 - 3.16 Dalager et al. (1986) Squamous & Small 14 2.88 ~ 0.91 -- 9.10 Cell Ca. Other 18 1.31 * 0.48 - 3. 5 7 Squamous or 20 3.3 1.1 -1 1.4 Pershagen et al. Small Cell Ca. (1987) Other 47 0.8 0.4 - 1.5 Adenocarcinotna 131 2.12 1.32 - 3.39 Lam et al. (1987) Squamous Cell Ca. 27 0.85 0.35 - 2.06 Small Cell Ca. 8 3.00 O.. 53 -16.9 Adjusted for gender, age, and study area. fiTS28cezUZ'

Table 3 Reproducibility of ETS Exposure Data r Ouesf/on Ka a value Ever lived with regular smoker? 0.66 Ever exposed to smoke at work? 0.46 No. of resident smokers? 0.55 No. of job sites reported? 0.37 Duration of residential •xposure? 0.45 Source: Pron et al., 1988 194 ~

Histology of LunQCancer Arnong Never-Smokers ro U Ma/es N ( 10/. ~ Females N ( •r. ~ Squamous & 5 (13 . 5) 10 (18.9) Small Cell Ca. Adenoca. 25 (67.6) 26 (49.1) Large Ceil Ca. 5 (13.5) 6 (11.3) BAC 1 (2.7) 7 (13.2) Other 1 (2.7) 4 (7.5) 37 53 izszscuzoz

Table 5 American Health Foundation Study Males Cases Controls OR 95% C.I. Exposed in Childhood: No Yes 15 21 36 69 1.00 0.73 0.34 - 1.59 ~ Exposed in Adulthood- at home: No 23 68 1.00 ----- Yes 13 32 1.20 0.54 - 2.68 Exposed at Work (ever): No 16 45 1.00 - --- Yes 21 60 0.98 0.46 - 2.10 zzszSeEZOz

Table 6 American Health Foundation Study Females Cases Controls OR 9 5% C.I. Exposed in Childhood: No 17 6 1 1.00 ----- Yes 36 77 1.68 0.86 - 3.27 Exposed in Adulthood- at home: No 18 45 1.00 ----- Yes 35 97 0.90 0.46 - 1.76 Exposed at Work (ever): No Yes 17 27 4 3 68 1.00 1.00 0.49 - 2.06 E%sz&EczOz

Table 7 Power Caiculation Odds Ratio Percent Controls Exposed To Detect 20% 40% 60'/• 1.25 1616 1124 1172 1.50 419 303 329 1.75 214 161 179 2.00 134 104 119 c< = .05 (1-tailed) 1-t3-.80 R = I vzszsEEzOz

REFERENCES 1. National Research Council. Environmental Tobacco Smoke: Measuring exposures and' assessing health effects. National Academy Press, Washington, D.C., 1986. 2. Dalager NA, Pickle LW, Mason TJ, Corrca P, Fontham E, Stembagen A, Buffler PA, Ziegler RG, Fraumeni JF. The relation of passive smoking to lung cancer. Caacer Res 46: 4808-4811, 1986. 3. Pershagen G, Hrubec Z, Svenuoa C. Passive smoking in Swedisb women. Am J Epidemiol 125:17-24,1987. 4. Lam TH, Kung 1TM, Wong CM, Lam WK, Kleeveas JWL, Saw D, Hsu C, Seneviratne S, Lam SY, La KK, Chan WC. Smoking, passive smoking and histological types of lung cancer in Hong Kong Chinese women. Br J Cancer 56: 67'}678, 1987. 5. H'srayama T. Non-smoking wives of heavy smokers have a higher ruk of lung cancer: A study from Japan. Br Med J 282:183-185, 1981. 6. Tricbopoulos D, Kalandidi A, Sparros L Lung cancer and passive smoking: conclusion of Greek studv: Lancet 2: 677-678, 1983. 7. Kabat GC, Wynder EL Lung cancer in aon-smokers. Cancer 53; 1214-1221, 1984. 8. Garfinkel L, Auerbacb 0, Joubert L Involuntary smoking and lung canter: A case- control study. J Natl Cancer Inst 75: 463-469, 1985. 9. Lee PN. Passive smoking and lung cancer association: A result of bias! Human Toxicol 6: 517-524, 1987: 10. Lee PN. Misdassif cation of Smoking Habits and Passive Smoking: A review of the evidence. Springer V'erlsg, Berlin, 1988. 11. Fleiss J.Statistical Methods for Rates and Proportions. W"iley and Sons, New York, 1951. 12. Pron GE, Burch JD, Howe GR, Miller AB., The reliability of passive smoking histories reported in a case-control study of lung cancer. AM J Epidemiol 127: 267-273, 1988. 13. Friedman GD, Petiti DB, Bawol RD. Prevalence and correlates of passive smoking. Am J Publ Health 73; 401-405, 1983. 14. Koo LC, Ho J H-C, Rylander R. Life-history correlates of environmental tobacco smoke: A study on non-smoking Hong Kong C.hinese wives with smoking versus aon-smokiag busbands. Soc Sci Med 26- 751-760,1988. ].S. Sidney S, Caan BJ, Friedman GD. Dietary intake of carotene in aon-smokers.vitlt and without psssi.re smoking at home. Am J Epidemio1129: 1305-13U9, 1989: 16. Ho1tt PA, Kromhout D, Brand R. For debate: Pet birds as an independent risk factor for ln=g cancer. Br Med J 197: 1319-1321,1988. 199