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192 N ~) T~ ~ t Letiern to the edttor ~s materr,al may 5e protected try c3a-FVt tj,d (fit1e 17 U.S. Code',• Possible reasons would be (1) a longer follow-up period and moie,cases in the 1984 report than in the 1981 report, or Z'2„l husbands' age and occupation were standardized"For data in 1981, while data reporte& in 1984 was andardized by age only. However, the latter is 'nitely not the reason responsible for the discrepan as age-occupat standardized data in 1'984 showe most sim' re- sulu„ corresponding relative risks (r. ' & 1.00; 1.11, and 1.36 (trend p: 0.009),, respecti (Table 1). The results were also similar rnpisks(r. tandar ' ed by wives' age, corresponding r.rs ng 1.00, 1.0~, nd 1.34 (trend p: 0.019). The ore, it should be cdn; cluded that the more cig ttes the husbands smoke, the higher the ische`nrlc heart disease risk in non- smoking wives. In 1980-198, r.rs of ischemic heart disease in nonsmoking~ivives were 1.00, 1.29, and 1.87 (trend p: 0.0. 'f) when husbands were nonsmokers, ezs ers/10-19 daily, and 20+ daily respectively. O may further consider as the possible reasons for this discrepan the influence of the changing qual- i'ty of side eam smoke coming out of the ignited end' of ' arettes in recent years due to the intensive che cal manipulation of the products (e,g., inclu- n of tobacco additives) in order to lower tar and nicotine, to improve the flavor, etc. Al'so, the recent i'ncrease in fat consumption in Japan may interact on the risk of ischemic heart disease when exposed to passive smoking. Tateshi' Hirayama Institute of Preventive Medicine Tokyo,Japan ERENCES ~ Hinyama, T. Noe-smonin{ wives of heavr ®okers have a digser riek of lon{ cancer, a etedy f'rom Japaa. Br. Mcd. 1. 2t2:113'- 1a9; 1911. "Hinyama, T. Lnnj t•eacer in Japaa. Effects of natriuon and pu- sive smoting. In: Miis11, M.; Ccrre.a.,P.. eds. New Yort: Verlas Cbeenie tnurseuooaJ'Ioc-1~49 i4:17S-1'99. T., L. u.,,S 1...-o w, e y, A, ik. S ~. vlr c ~. 3,,, t REBUTTAL TO LEE/KATZENSTEIN COMMENTARY ON PASSIVE SMOKING RISK Dear Editor. Let (1989) and Katzenstein (1989), in their com- mentary on Wells"(1988) paper, take issue not only with Wells'' estimates of the magnitude of the mortal- ity effect of passive smoking on nonsmokers, but question whether mortality occurs at all. Their argu- ments are based upon the alleged fragility of the epidemiological studies of passive smoking and dis- ease; the potential for misclassification of subjects, disease, or exposure; possible confounding factors; and the lower doses of smoke to which nonsmokers are exposed relative to smokers. Let us examine these issues one by one. Are non- smokers exposed to such low doses of environmental tobacco smoke (ETS) that Wells' estimates of 46 000 nonsmokers' deaths per year from passive smoking are about '46 000 too high', as Lee asserts? Perhaps the most salient point to be considered: active smok- ing is a cause of more than one out of every six deaths in the U.S.A. every year (USSO 1989). Intentional exposure to tobacco smoke has been judged to cause coronary hean disease, atherosclerotic peripheral vas- LL (.Z_) , (t, l19`l0 cular disease, lung and laryWal cancer. oral cancer, esophageal cancer, chronic obstructive pulmonary disease, chronic bronchitis, intrauterine growth re- tardation, and low birthweighr babies. In addition, probable causality has also been established for un- successful pregnancies, increased infant mortal'uty, and' peptic ulcer disease, as well as cancers of the bladder, pancreas, and kidney, and associations have been reported for cancer of the stomach (USSG 1989). Hardly an organ system of the human body remains undiseased' upon exposure to tobacco smoke. To argue, as do Lee and Kauenstein, that the diseases of smok- ing are not even plausible in nonsmokers does not give us confidence in their deductive abilities. To be sure, it is possible that thresholds for effect may exist for one or more of the diseases of smoking, but neither Lee nor Katzenstein present any evidence whatsoever that such low dose thresholds exist, let alone that all nonsmokers have exposures and sus- ceptibilities which place them within an adequate margin of safety below such thresholds. Are the epidemiological studies of passive smok- ing and lung cancer really all to be explained by misclassification of smokers as nonsmokers as Lee has proposed? Nonsmokers who report no passive smoking nevertheless possess levels of nicotine and cotinine in body fluids which are significant frac- tions of those who report a lot of exposure. For 202_03511S93

Lettera to the editor example, of 100 nonsmokers studied by Jarvis ('1987), the 46% who reported "no" exposure had measured urinary cotinine levels which were neari!y a third of the levels of those 27% of nonsmokers who reported "some" or "a lot" of passive smoking exposure. This suggests that there is major misclassification of non- smoking controls as "unexposed". The result of this kind of misclassification of nonsmokers is to cause epidemiological studies to lack statistical signifi- cance or to find no effect. Nevertheless, despite such misclassification of controls, fully two-thirds of the studies shown by Katzenstein in his Table 1 showed a positive result. Are confounding factors such as higher exposure to carcinogenic organic chemicals from non-ETS sources in the spouses of smokers, as Katzenstein assera, really responsible for the consistent reports linking lung cancer to passive smoking from 15 different researchers in six different countries? To the con- trary: Wallace (1989). in making measurements of personal exposure to benzene, a known human carcinogen and a prominent constituent of tobacco smoke, found that benzene exposures were 50% higher in the nonsmoking children and spouses of smokers than for nonsmokers in nonsmoking households. Finally, what of the magnitude of Wells' (1988) estimates which Lee asserts are 46 000 too high? Let us take lung cancer, which Wells has estimated at 3000 U.S. lung cancer deaths (LCDs) per year. Lee selectively contrasts the estimate of 12 LCDs/yr from passive smoking by Arundel ecal. (1987), buromits the mention of eight other risk assessments with which Wells' assessment agrees, all eight of which taken together average 5000 ± 2400 LCDs/yr. (Repace and Lowrey 1990). It is Arundel et al. who are out of step with the rest, not Wells. This lends credence to Wells' risk assessment methodology. As far as heart disease mortal'ity is concerned, this is primarily a disease of those aged 2 35 years. In 1985 there were roughly 105 million Americans in this age bracket, roughly 72 million nonsmokers, and 33 million smokers. Among the 33 million smok- ers, there were 120 000 active smoking-attribut- able bean disease deaths (HDDs) in 1985, or 3.6 x 10'3 HDD/smoker. By comparison, Wells' estimates 32 000 passive smoking-attributable nonsmokers' HDDs per year in a population of 72 miuion, or 4.4 x 10-4HDD/non- smoker.Thus, the ratio of ETS-induced heart disease deaths per nonsmoker to smoking-induced heart dis- ease deaths per smoker is only 1296, which does not seem excessive considering that tobacco smoke is known to be one of three major risk factors for HDD, and synergistic (USSG 1989) with the other two fac- 163 tors (hypertension and elevated serum cholesterol) which are also commom in nonsmokers. A final note on Katzenstein's attack on the risks of passive smoking-induced lung cancer death (LCD) estimated by Repace and Lowrey (11'985, 1986, 1987). The radical difference in lifestyle between never- smoking Seventh Day Adventist (SDA) controls and never-smoking non-SDAs is the avoidance of passive smoking in the SDA lifestyle, which we believe con- vincingly accounts for their lower lung cancer rate. As Katzenstein selectively notes, we were criticised by OTA (1985) and by tobacco industry consultants for attributing the entire LCD rate difference to pas- sive smoking, but what our critics have conveniently ignored' is that, since 60% of the SDA control group were potentially exposed to passive smok- ing, this was in fact a conservative estinlate. More- over, Katzenstein selectively omits mention of the analysis of our work by Weiss (198b), who found our figures to be "the best current estimates of lung can- cer deaths from passive smoking". In sum, contrary to the assertions of Lee and Katzenstein, we find Wells' predictions of 46 000 deaths per year from passive smoking to be credible,, and to indicate, as Wells concluded, that exposure to ETS can have adverse long-term health effects that are more serious than previously thought. James L. Repace Office of Air & Radiation U.S. Environmental Protection Agency• Washington, DC 20460 and Alfred H. Lowrey Laboratory for the Structure of Matter Naval Research Laboratory• Washington, DC 20375 •The comments of the authors represent their opin- ions, and do not necessarily represent the policies of their respective federal agencies. REFERENCES Armdal, A.; Steriiaa, T;, Wsinkam, J. Atsanmoker 1®a eancer riekefrom e:poenrs to putieulatts tobacco amoka. fia.ieoo. lat. 13:409-426; 19a7. Jar+vir, M. J. Upuka of snviroemeaul tobacco smoka. 1a:,0'Nei11. LK., Bratwcmaa4 K.D., Dodet,, B., and Hoffmatm. D., sds. Environmeotaz earciaojeot, metbodt of aaaiyru and ezposu» measurcment. IAAC Scientific Pubticatioae No. 91. Vol. 9. Pucive Smoking. Lyon: Iotarnational A{cocyior Reeeareb oa . Caacer, 1'9i7,

184 Lee, P. N: An estimate of adult mortality in the U.S. from pustve smoking„a response.,Envaroo. lnt. 16:179-181; 1990:, Katzenstetn, A. W. An esrimate of adult monaliiy,in the li.S: from passiNe smoking; a response. Environ. Int. 161173'-177;, 1990. Rcpace„Ji. L.; Lowrey„A. H. Rssk aasessmenrmetAodolopes in passiNe smokinj. J. Risk Anal. (in press] 1990. LSSG (U. S. Surgeon General)!Rcducinj the health eonsequences of smoking. 25 years of' proyress„ a report of the Surgeon AN ESTIMATE OF ADULT MORTALITY IN THE UNITMSTATES FROM PASSIVE SMOKING; A RESPONSE Dear Editor: An article in Inside EPA (January 13, 1989) is headlined: 'EPA weighs_Impact of Study Linking Passive Smoke Exposure to Heart Deaths..." lt leads with the statement: "EPA is giving serious attention to~a recently published study that pinpoints passive smoking ... as a significant cause,of heart disease and cancer-related deaths'. The articl; states: "Pas- sive smoking causes 46 000 deaths a year, according to~a study by A. Judson Wells published lot month in Environmenr lnternarional'. An EPA source is quoted: 'The 46 000 mortality was surprisi,ng,be- cause such a large eomponenvwas from heartdisease Lei:ert :o cmc :-ucr General. Washington. D.C.: U S. Dept. of Health & Human Servicer, 1989. W'allace, L. A Major sources of benzene eaposure. Environ Health Perspect. 82: 165 • 169; 1989. Wetca, S., T Passive smokin8 and lung eancer: .har ts the rssk? American Rev: of Resp. Dts. 133463-465, 1986 Wells, A. J. An estima:e ot adult monality in the Lot,tcd States. Environ. Int. 14':2+9-I65; 1988. with ETS exposure. These calculations do not in any way establish that ETS does, in fact, cause death in expose& individuals. Rather, such calculations rely on an independent conclusion, based on a review of the available data, that ETS causes lung cancer, other cancers, and cardiovascular diseases. If such a con. clusion cannot be supported, then the estimate of ETS-associated mortality rests on the aswmption that ETS causes these diseases, and it is incumbent upon the author to state this underlying assumption when reporting the results of his calculations. The issue ofeausation is neveraddressed by Wells. The studies cited in Wells' Tables 1-4 are discussed below with -particular attention to whether they es- tablish a,causal relationshi'p between ETS and dis- ease in yi~on- or never-smokers. The vast majority of the stud'ies were included in reviews publishedty the Natipnal Academy of' Sciences (NAS 1986) and' the Su1•geon Generall(USSG 1986). Therefore, these re- addressin the i iat f d g ng po or as a start ." Thi's statement is similar to one made by EPA's , pprts are use James Repact on national television when the report '~ '~uestion of causality. was first released. Lung Cancer: A1mosP all of the epidemiological' What is surprising is'that' anyone from the EPA can~ st9dies listed in Wells' Tables I and 2'were consid- consider this recent review surprising. Dr. Wells has ered in the NAS and Surgeon, General's reports, as not completed an epidemiological study, new or ~`'h- well',~s other reviews appearing at about the same erwise, and has in no way contributed to pinpoig #ing time (c'lot and Fraumeni 1986; Uberla 1987), The l passive smoking as a significant cause of hea dis- ease, lung cancer, or other cancer deaths. Wh he did udang Surgeon\General s Report was alone in conc that ETS c^~uses lung cancer in nonsmokers; the other was publish the results of a series of calfftlations reviews genErally concluded that although a statisti- based on the results of existing epidemiolo$ tcal stud- cal associat'taqn appeared to exist between marriage ies and a number of assumptions (Wells!1988). Dr. to a smokec aT.Q the risk of lung cancer, the lack of Wells presented a similar analysis at tp'e 1986 Air adequate expos Pollution Control Association meettng, which was fluence of differ e information, and'the potential in- tial misclassification of smoking onclusion of causality. The lung published in the meeting proceedings. (Wells 1986). status precluded a There should have been no sudden sitrprise at EPA; cancer studies publi an EPA official chaired the 1986 session in which this same limitations as i ed since these reviews have the e previous studies. Little has paper was presented. Dr. Wells eneourages the view been published since l that he had done something new by failing to even the issues of exposure a 86 that adequately addresses d misclassification. ting to link cancer to ETS acknowledge his previous presentation. All of the studies atterri Wells used the data of previously published (and have been epidemiologicaf, : An epidemiology study in some cases, unpublished) studies as a basis for attempts to relate the frequeqcy' of a certain health calculating annual mortality statistically associated effect or disease with the frequency of specific envi-