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EFFECTS OF PASSiVE SMOKING 793 I ies show a higher prevalence of exposure to passive smoking amo:rg the cases compared with the controls. The estimated odds ra- tios have generally ranged from 1.5 to 2.5. The largest prospective studies have been reported from Japan (37, 38) and the United States (39). In both studies, the populations at risk were predominantly women, and the exposure sources were spouses who smoked. The study in Japan by Hirayama (37, 38) demonstrated a con- sistent increased risk of lung cancer and other cancers among the nonsmoking wives of men who smoked A smaller study amongg nonsmoking men as index subjects also demonstrated an increased risk of lung can- cer among men married to women who smoked cigarettes (40). Our findings on~totalian& coronary heart disease mortality and morbidity are similar to those of two other studies. A study by Garland et al. (41) specifically related en- vironmental tobacco smoke to coronary heart disease. This study followed for an average of 10 years 695 married women, initially examined in 1972-1974, in a re- tirement community in California The women were classified by the self-reported smoking status of their husbands at entry into the study. After 10 years, nonsmoking wives of'current or former cigarette smok- ers had a higher ischemie heart disease death rate than nonsmoking wives of' non- smokers. There were, however, only two ischemic heart disease deaths among the wives of the men who never smoked, 15 among the wives of former smokers, and two among the wives of current cigarette smokers. There were no differences in age- adjusted aTl-cause mortality rates among the wives of never, former, or current cig- arette smokers. In the longitudinaL study in Japan by Hirayama (40), the wives of men who smoked'cigarettes also had higher coronary heart disease mortality rates. Several reasons for the higher overall mortality among the passive smokers have been considered. First, it is possible that some passive nonsmokers were actively smoking cigarettes. The careful'chemical measuremente at baseline and follow-up would almost certalnly' rule out this hy- pothesis in the MRFIT study. Practically all cigarette smokers in the MRFIT study had thiocyanate levels over 100 µmol/liter. Among the passive smokers, 7.5 per cent had thiocyanate levels over 100 Kmol/liter,, compared with 7.3 per cent among the non- passive smokers. If some men were smok- ing, they were equally divided among the two groups. A second hypothesis is that key risk factors may be different among passive and nonpassive smokers. The risk factors in the MRFIT trial, socialLbehavioral, physiologic, and biochemical, were gener- ally similar between the passive and' non- passive smokers. These have been further reviewed in detail by Martin et al. (42). Adjustment for these other risk factors did not decrease the relative risks associated with passive smoking. Third, certain other behavioral and so- cial factors may be different among passive and nonpassive smokers. There is an in- verse relation between education and'other measures of social class and total coronary heart disease mortality (43). Similarly, there is an inverse relation between ciga- rette smoking and social class (44). Thus, it is more likely that passive smokers will be in the lower socioeconomic group. Ad- justment for education or other measures of social class in the MRFIT trial did not reduce the increased relative risk. It is pos- sible, although unlikely, that these adjust- ments did not completely deal with the potential, differences in social and behav- ioral characteristics between the passive smokers and nonexposed men. More de- tailed analyses have failed to demonstrate other significant differences between these two groups. Fourth, the passive smokers at baseline may have been less likely during the trial to change important risk factors that were related& to subsequent mortality and mor- bidity. Analyses of risk factor changes in table 2 do not support this hypothesis. Finally„ follow-up was complete for all MRFIT men, and endpoints were assessed

i 794 SVEI3IDSEAI ET Ai.L without knowledge of passive smoking sta- tus. It is very unlikely that differential as- certainment of morbidity or mortality could account for the differences in mortality be- tween passive and nonpassive smokers that were notedl It is aNways possible that other unknown factors can explain the increased relative risk of morbidity and mortality among the passive smokers. The men were obviously not randomized to wives who smoked and to those who did not smoke. A man who did not'smoke married to a woman who smoked may have had other llnmeasured health behaviors that increased morbidity and mortality. The consistency of the re- sults of the current studies with many of the other case-control and longitudinal studies plus the biologic plausibility of the hypothesis based'on biochemical measure- ments of exposure to environmental! to- bacco smoke and'knowledge of the patbolL ogy and physiologic changes suggest that passive smoking may result in an increased morbidity and mortality among non- smokers. Environmental tobacco smoke is a major indoor pollutant to which a substantial seg- ment of the population is exposed (45)'. O6viously„ the most successful method of reducing environmental tobacco smoke would be the further reduction of active cigarette smoking in the population. On the basis of these data, a continued red'uction in active cigarette smoking willl have a ben- eficial effect on both the cigarette smoker and on the nonsmoking population. RI.IERtr7QS L Hoffmann D;,Brunnemaan KD, Adams JD, et al. Indoor pollution by tobacoo smoke: model atudies on the uptake by nonsmokers. In: Indoor air, radon, passive smoking.,partieuletes and bousing epidemiology. Proceedings of the 3r& Interna- tional Conference on Indoor Air Quality and Cli- mate. Stockholm. 1984;2(Suppl D17)~313-18. 2 Stober W. Lung dynamies and uptake of smoke oonstitaents by nonsmoken-a survey. Prev Med 1984;11589-W1. 3. Brunnemann KD, Hoffman D. Analysis of volatile nitroaamines in tobacco smoke and polluted in- door environments. IARC Sei PubIi1978;19:343= 56: •: Fsiedman GD, Petitti'DB; Bawol RD. Prevalence and aorrelates of puaive smoking. Am J' Public Health 1983;73:401-5. 5. Repace JL Lavrey AH'. A quantitative estimate of nonsmokers' lung cancer risk from passive smoking. Environ !nt 1985;11:3-22. 6. Division of Lung D'rse.aea, National Heart„Lung, and Blood Institute. Report of Workahopan Rbs- piratory, Effects of Involuntary Smoke Exposure: epidemiologic studies, Bethesda, MD, May 1-3, 1983. 7: Sherwin R. Kaelber CT,,Kezdi P, et al. The Mu]- tiple Risk Factor Intervention Trial i(MRFIT); !1.. The development of the protoeol. Prev Med 1981;10:402-25. & MRFIT Research Group. Multiple Risk Factor Intervention Trial: quality control of technical procedures and data acqy3isition. Controlled Clin Trials 1986;7:179S-192S. 9. MRFIT Research Group: Coronary beart disease death, non-fatal acute myocardial infarction and other clinical outcomes in the Multiple Risk Fac- tor Intervention TriaL Am' J Cardiol 1986:$8:1- 13: 10. Cox DR Regression models and life tables. (with diacuaaion):J~R'Star Soc B 1972;34:187-220:, I1. Brealow NE. Covariance analysis of censored sur- vival data. Biometrics I974;30:89-99. 12:, Hoffmann D, Haley IQJ; Adams JD, et al. Tobacco aidestream smoke: upt.lie by nonsmokers. Prev Med 1984;13:608-18. 13: Jarvis M, Tunstall-Pedoe H„Feyerabend C, et al. Biochemical markers of smoke absorption and self-reported exposure to passive smoking.. J'Epi- demioi Community Health 1984;38:335-9. 14. Matsukura S, Tominato T, Kitono N, et al. Effects of environmental tobacco smoke on urinary cotin - iae excretion in nonsmokers. N Engll J Med 1984;311:828-32. 15. Wald NJ; Boreham J, Bailey A, et al. Urinaryy cotinine as marker of breathing other people's tobacco smoke. Lancet 1984;1:230-1. 16. Avudb DM. Carbon monoxide as an index of environmental tobacco smoke exposure. Eur J RespirDis 1984:65(Suppl 133):47-60. 17. Aronow WS, Iabell MW. Carbon monoxide effect on e:ercise-induud angina pectoris: Ann Intern Med 1973;79:392-5.. 1& Anderson E14', Andeltrun RJ; Strauch JM, et al. Effect of low-level carbon monoxide exposure on onset and duration of angina pectoris::a study in ten patients with iacbemic heart disease. Ann Intern Med 1973;79:46-50. 19. US Environmental! Protection Agency, Office of Health and Environmental Asses.ment Revised evaluation of health effects associated with carbon monoxide exposure: an addendum to the 1979 EPA air quality criteria. Document for Carbon Monoxide, Final Report. EPA-600/8-83-033F, August 1984. 20. Scbievelbein H. Richter F. The influence of pas- sive smoking on the cardiovascular system. Prev Med 1984;13:626-44. 21. Kuller LH, Perper JA, Cooper MC: Sudden and unexpected death due to arteriosclerotic beart dis- e.ae. In: Oliver MF, ad Modern trends in cardiol- ogy-3. London: Butterworth, 1975. f

EFFECTS OF PASSIVE SMOKING 795 ic e s r 1 x 22. Kuller LH, Radford E, Swift D, eL al. Carbon monoxide and heart attacks. Arch Environ Health 1975;30:477-52. 23. White JR; Ftoeb HF. Small-airways dysfunction in nonsmokers chronically exposed to tobacco smoke. N Engl J M'ed 1980;302:724-3. 24. Kauffmann F, Tessier J-F, Oriol P. Adult passive smoking in the home environment a risk factor for chronic airflow limitation: Am J Epidemiol 1983;117:269-80. 25. Brunekreef B, Fischer P, Remijn B, et al. Indoor air pollution and its effect on pulmonary function of adult nonamoking women., IIl. Passive smoking and pulmonary function. Int J Epidemiol 1985;14:227-0. 26. Comstock GW, Meyer MB, Kelsing KJ, et aL Respiratory effects of household exposures to to- bacco smoke and gas cooking. Am Rev Respir Dia 1981;124i 143--8: 27, Schilliag RSF, Letai AD, Hui SL, et al. Lung function, respiratory disease, and smoking in fam- iliea. Am J Epidemiol 1977;106:274-83:. 28. Kentner M, Triebig G, Weltle D; The influence of passive smoking on pulmonary function-a study of 1,351 office workers. Prev Med'1964;13:65Cr69. 29. Lebowitz MD; Influence of passive smoking on pulmonary function: a survey. Prev Med 1984;13:645-55. 30. Trichopoulos D, Katandidi A, Sparros L Lung cancer and passive smoking conclusion of Greek study. Lancet 1983;2:677-8. 31. Sandler DP, Everson RB, Wilcox AJ. Passive smoking in adulthood and cancer risk. Am J Epi- demiol 1985;121.37-48: 32. Garfinkel L,,Auerbacb 0, Joubert L Involuntary smoking and lung cancer. a caae<ontrol study. JNCI 1985;75:463-9. 33. Wu AH. Henderson BE;,Pike MC, et al. Smoking and other risk factors for lung cancer in women. JNCI 1985;74:747-51. 34. Cban WC, Fung SC. Lung cancer in nonsmokers in Hong Kong. Im Grundmaan E, ed Cancer campaign: cancer epidemiology. Vol!6. Stuttgart: Gustav Fischer Verlag, 1982:199-202. 35. Knoth A, Bohn H, Schmidt F. Passive smoking as a causal factor ofbronchial carcinoma in female nonsmokers. (English translation). Msd Kliaik 1963;78:66-9. 36. Koo LC, Ho JH-C, Fraumeni J,,et aL Me.sore- ments of passive smoking and estimates of risk for lung cancer among nonsmoking Chine~e fe- malss. (Abstract). Fourth World Conference on Lung Cancer, Toronto, Canada. August 25-.'i0, 1985. 37. Hisayama T. Nonsmoking wives oGheavy smokers have a higher risk of lung cancer. a study from Japan. Br Med J 1981;282:183-5. 38. Hirayama T. Cancer mortality in nonsmoking women with smoking huabands based on a large- scale cohort study in Japan. Prsv Med' 1984;13:680-90. 39. GarfinJcel'L. Time trends in lung cancer mortality among nonsmokers and a note on passive smok- ing. JNCI 1981;66:1061-6. 40. Hirayama T. Passive smoking and lung cancer, nasal sinus cancer, brain tumor and iacbemic heart disease. (Abstract). Proceedings of the Fifth World Conference on Smoking and Health, Win- nipeg. Canada„Jlily 1983: 41', Garland C, Barrett-Connor E; Suarez L, et al. Effects of passive smoking on uchemic heart dis- ease mortality of nonsmokere: a prospective study. Am J Epidemiol 1985;121:6i5-50. 42. Martin MJ, Svendsen KH, Kuller LH. Nonsmok- ing men married~ to smokers are similar to non- smoking men msrried'to nonsmokers. (Abstract). Society of Behavioral Medicine, 7th Annual Sci- entific Sessions, San Francism March 5-8, 1986. 43. Kraus JF, Borhani N0, Franti CE. Socioeconomic status, ethnicity, and risk of coronary heart dia- ease. Am J Epidemiol 198o-111:407-14. 44. Kuller L. Meilahn E, Ockene J. Smoking and coronary heart disease. In: Connor WE, Bristow JD, eds. Coronary heart disease-prevention, complications, and treatment. Philadelphia: JB Lippincott Company, 1985: 45. Spengler JD, Sexton K. Indoor air pollution: a public health perspective. Science 1983;221:9-17.