Tobacco Documents Online

N 0 T 1 ~ E l/ l Laun to the editor 1!h15 maiEr.a1 'nty ht OT,aected by cc;Y,nrn qw (f~t1e 17 U.S. ~cai! Helsin6, K. ].; Saadler D. P.; Comstoek„ C. W.; Chee, 5. Hean Lee, P. N. Ao elternative ezplaUS, ia6lor the incnatcd risk of 11m6 ditease mortality in nonemoken livin$ with emokerc. Am. J'. cancer in non-amokerr ed to cmoken.:ln: Perry, R.; Kirk, Epidemioll 127:915-922; 1982. P. W:,, edt. Ind and' ambient air quality. London: Selper. Hinyama, T. Non-emoking wives of heavy tmoken have a higher 19tttb:t a. risk oflun6 cancer. a study ftom Japan. Br. Med: J. 2E2:113- Lee p Passive smoking Fact or fiction7 Paper presented at 195: 1991. ~onfereaa on Prssent and Future of ladoor Air Quality. Brw- Hirayama, T. Lung cancerin Japan: aHecu of nutrition and pate •~ ec1a, February 14-16, 1939; 19/9a. rmokin6. In: Miseil.,M.,Correa, P., eds. Lung cane auses Lec, P. N. Problemt in interpreting epidemiolosical dan. Paper and prevention: Ner York: Verlri Chemie ernatioaaln presented at Conference on Aueeemcaaof Inbalacion Hasards. 1984:175-1'9!. Hanover, February 19-24. 1989; 1919b. Lec, P. N. Lifctime passive emokia nd cancer risk. Laneat Sandler, D. P. et al. Passive emokia= in adulthood and eancer risk. 1:1444: 1915. Am. J. Epidcmiol. 121:Y1-N; 1985. Lee„P. N. Passive emokin d lung cancer. Asaoaation a tsault USSO (U.S. Surgeon Geoeral) Reducing the health eonaequenca of bias? Hi:man T- oti. 6:517-524; 19a7. of smoking. 25 yean of prvgrcu.: A report of the Surgeon Lee„P. N. Mis tficatioa of amokin8 habiu and paeeive emok- General. Rockvillc, MD: U.S.,Public Hkaltb Service; 1949. ina. A ew of the evidence. In: International' Archives of Welle, A. J. An estimate of adult mortality in the United States Oc ational and' H'ealth Snpplemaat. Heidelberg: Springer- from passive smoking. Envirtm. lat. 1:4:249•263; 1991. V'erlaa; 19Eta. ,~.v-a~~we; ~tck "10 ISCHEMIC HEART DISEASE; RESPONSE TO LEE Dear Editor: The 1981 report was based on a 14 year follow-up (n-400) and the 1984 report was based on a 16 year follow-up (nm,494) of nonsmoking wives. The rela- tive risks of ischemic heart, disease when husbands were nonsmokers, exsmokers, or daily smokers of 1 00' i 0 garettes were . , or more c Dr. P. Lee questioned the reuons for a discrepancy 1'-19 cigarettes and 2 of my reports in 1981 and in 1984 on husbands' 1.06, and 1.18 (trend p: 0.061 not;ignificant)'in the smoking and ischemic heart disease risk in nonsmok- 14: year follow-up; and 1.00, 1.10, and, 1.31 (trend ing wives. p : 0.019 significant) in the 1984 report. Table 1. Ischemic heartdiuus mortality in women by age 6roup;,by occupauon, and by husbands' smoking habit (patient benelf a nonsmoker). Husband's sn+oking habit ------------------------------------- " ' Hus-0and s oceupation Husband s age group Nonsmoker Agricultural, 40-49 8 2,502 worker S0-59 15 3,497 60-69 36 4,084 70- S 323 Tota1' 64 10.406 Other 40-49 5 3.727 50-59 11 4,294 60-69 29 3.036 70- 9 432 Tota1 54 11.489 The .1iQnted'point eat4i.ate of rate ratio and test-based 90% confddenca Ttadts E,csa+oker 1~19/day 20•/day Total! 25 5,941 17 3.636 50 12.079 27 6.812 27 3,514 69 13,923 79 6.645 27 2,152 142 13,081 11 446 2 89 18 a58 142 20.044 73 9,391 279 39,841 1S 9.093 1S 7,1Z8 35 19„948 29 b,a3'0 23 6.306 63 19„430 46 5,596 20 2.499 95 11.133 a 619 5 137 22 1.188 98 24.140 63 16,070 215 51,699 1.33 /1.6a 1. 00 1'-11 ~ 1. 36,~ 0.92 1.09 0.882 2.331 rtintel-Kaens=el cni 0.19889 0.00988 One-tatl p value /lantel entensiCn chi 2.539 One tail p valut 0.00916

1/2 Possible reasons would be (1) a longer follow-up period;and more cases in the 1984 report than in the 1981 report, or (2) husbands' age and occupation were standardized for data in 1991, while data reported in 1984 was standardized by age only. However, the latter is definitely not the reason responsible for the discrepancy, as age-occupation standardized data in 1984 showed almost similar re- sults, corresponding relative risks (r.rs) being 1.00, 1.11, and 1.36 (trend p: 0.009), respectively (Table I). The resulu were also similar when stand'ardized by wives' age, corresponding r.ts being 1.00, 1.09, and 1.34 (irend' p : 0.019). Therefore, it should be con- cluded that the more cigarettes the husbands smoke, the higher the ischemic heart disease risk in non- smoking wives. In 1980-198L, r.rs of ischemic heart disease in nonsmoking wives were 1.00,, 1.29, and 1.87 (trend p : 0.041) when husbands were nonsmokers, exsmokers/10-19 daily, and 20+ daily respectively. One may further consider as the possible reasons for REBUTTAL TO LEE/KATZENSTEIN COMMENTARY ON PASSIVE SMOKING RISK Lee (1989) an anstein (1989), in their com- mentary on Wells"(198 per, take issue not only with Wells"estimates of the m itude of the mortal- ity effect of passive smoking on nsmokers, but question whether mortality occurs at a Their argu- ments are based upon the alleged fragiit of the epidemiological' studies of passive smoking an is- ease; the potential for misclassification of subjec disease, or exposure; possible eonfounding f ors; and the lower doses of smoke to which no moken are exposed relative to smokers. Let us examine these issues one one. A?e DOn- smokers exposed to such low do of environmental tobacco smoke (ETS) that W s' estimates of 46 000 nonsmokers' deaths per from passive smoking are about '46 000 too gh', as Lee assertsl Perhaps the most salient p' t to be considered: active smok- ing is a cause o ore than one out of every six deaths in the U.S.y4/~very year (USSO 1989). Intentional exposure'{o tobacco smoke has been judged to cause coron~ry heart disease, atherosclerotic peripheral vas- L` 1-enrn to dte editor this discrepancy the influence of the changing qual- ity of side-stream smoke coming out of the ignited end of cigarettes in recent years due to the intensive chemical manipulation of the products (e.g., inclu- sion of tobacco additives) in order to lower tar and nicotine, to improve the flavor, etc. Also, the recent increase in fat consumption in Japan may interact on the risk of ischemic heart disease when exposed to passive smoking. Takeshi Hirayama Institute of Preventive Medicine Tokyojapan REFERENCES Hiraynma, T. Btoe-smokinj wives of heavy ®oken heve a hi3ber riek of lnag eaoesr, a study from Japan. Br. M,ed. J. 2R2:1f3- 1aJ; 1981. Ftirayama, T. Lung cancer ie Jefpan. Effecu of autriuoo and paa- .ive.motin{. In: itiull„M.; Correa, P., ads. New Yort: Veriaa Chemie Iauraatioeal 1sc.; 19a4:17S-J91. cular disease, lung and larytsgsal cancer, oral cancer, esophageal cancer, chronic obstructive pulmonary disease, chronic bronchitis, intrauterine growth re- tardation, and low birthweight babies. In addition, probable causality has also be successful pregnancies, in and peptic ulcer diseas bladder, pancreas, been reported fo Hardly an o undi as d esublished for un- ased infant mortality. 'as well as cancers of the kidney, and associations have cer of the stomach (USSG 1989). n system of the human body remains upon exposure to tobacco smoke. To argue, e and Katzenstein, that the diseases of smok- 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 or one or more of the diseases of smoking, but ne wha er Lee nor Katzenstein present any evidence ver that such low dose thresholds exist, let alone th al1 nonsmokers have exposures and sus- ceptibilitiei hieh place them within an adequate margin of safef Are the epideai l'ow, such thresholds. ogical studies of passive smok- ing and lung cancer ly all to be explained by n.as nonsmokers as Lee misclassification of smok has proposed? Nonsmokers who report no passive smokirg nevertheless possess levels of nicotine and cotinine in body fluids which are significant frac- tions of those who report a lot of exposure. For 2V I:r 3ti11 V92