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LE7TERS TO THE EDITOR' 227 givenl. In this analysis, the 13 coronary heart disease deaths imthe never smokers are again included and the proportions to which they contribute are tested for statistical significance three more times. The ap- propriate analysis would have examined only the 2,222 ex-smokers in the same terms, as suggested for table 7. The reader who is interested in outcomes other than coronary heart disease death is forced to use guesswork to subtract this effect from the other data in the tables. For example, even though we are not told the numbers of men imtable 9, the much lower p vahie for "death from any cause" than in table 7 suggests that this difference is due to the contribution of the ex-smokers. Had'these been analyzed sepa- rately, the difference in risk of "death from any cause"' between the exposed and nonexposed ex-smokers would probably have beem even more marked. This would have suggested'that the men who stopped smok- ing were especially susceptible to second-hand tobacco smoke. A presentation of the data that did' not lump and overlap the subsets of interest would have made such speculation unnecessan. The study by Svendsen et al. is presented as an exploration without hyTothesis. This "blurred" anah- sis could have been avoided if,this,repon had set out to investigate an explicit hypothesis that specified the target groupand the expected endpoint. Paradoxicalh, focussing in on a specific research question and follow- ing the method'appropriate to address that question often allows the researchers to isolate and investigate secondary or unexpected results more accurately. RErERENCE 1. Svendnen K.H. Kuller LH, Manin Ma;.etal: Ettects of passive smoking intheMuluple.Risk,Factor Intenrnttmn Trial. Am J EpidemioV 19fiT.:126.'&3-95.. Peter Morgan 118:Mill'Street Lanork, Ontario Conada KOG 1X0 J ` / A ~ VRE: 'EFFECTS OF PASSIVE SMOKING IN THE MULTIRLE RISK FACTOR C1` l..- '- INTERVENTIQN' TRIAL" 7 c. . lkg'i ~.Z2 Svendsen et al. (l') analyze data from the Multiple Risk Factor Intervention Trial (MRFITI'study and report the relative risks of various endpoint events for men who never smoked in relation to spousal smoking. They assert that their data provide "further evidence of a potential'serious health risk for a large segmentt of the nonsmoking population" (1„p. 792). This con- clusion does not appear to be supported by the data presented. For morbidity and mortality, the relative risks are noostatistically significant; except for the "all deaths" category for the group combining 'never smoked" and "ex-smoker" males. Since the relative risk for "coro- nary heart disease deaths" was not significantly ele- vated for that group, the increased relative risk for `all deaths" requires some explenation before the sta- tistics can be assumed to indicate a meaningful in- crease in health risk related to spousal smoking. While the statistics alone raise serious doubt about the conclusion of increased health risk for nonsmokers exposed to environmental tobacco smoke based on spousal smoking, questions also need to be raised about the quality of the evidence on w-hich the assess- ments are based, notably the nonhomogeneity between the groups based on spousal smoking classification. The lack of homogeneity was implicit when adjust- ments were made for differences in some coronary hearo disease risk factors„e.g., age, weight, blood pres- sure, and alcohol consumption;,but there is no indi- cation that the adjustment inclUded'consideration of the additive effect of multiple risk factors, as has been demonstrated in numerous other studies, notably the Framingham Heart Study. There is no indication that other coronary heart disease risk factors, e.g., familyy history and exercise„were considered or adjusted for. Differences in forced'expiratory volume in one second (FEV,) among the groups were also cited. The numer, ous confounding coronary heart disease risk factors should not be disregarded& nor can statistical adjust• ments be made to eliminate their possible roles. Thus. while the MRFIT'study was well designed to assess the effect of various interventions according to se- lected risk factors, it does not appear to have been designed to assess the environmental tobacco smoke exposure as a coronary heart disease risk factor. Svendsen et al: observe that men whose wives smoked had "significant1Y lower levels of pulmonan function at baseline"' (1, p. 786). The authors fail; however, to note and to interpret the data in table 6. which shows FEV,,levels for men whose wives smoked 20+, cigarettes/day were markedly htFh'cr than those of men whose wives smoked 1-19 cigarettes/day, both at baseline and averaged over all visits. R'ithisuch a notable reversal of the dose•response relation; which must be demonstrated! if causal inferenees are to be supported, there seems to be little basis for suggesting the possibility of' any relhtiom bet..een pulmonary function and spousal smoking from this studi: The weakness ofithe evidence thus raise~ imponant questions about the conclitsion that `paai.e smokinF is associated with an increase in morbiditv and mor- tality, among nonsmokers" (1, p. 791)i There ic. cer- tainly no convincing demonstration that spousal smoking constitutes a"potential serious health riak" for anyy segment of the nonsmoking popularion. REFERF.r:CE' 1. CtYndsen KH. Kuller l:H,,\txnin Slll. ev sl EflrrtF of pe~ivexmokinR in thr 1\tuhiple Hi,A FarvIr, lmet+ent.un Triali Am J F.pidemiol 19++ i:1 L'h. S r:'i- p5: Alan 11'. }Catzenstein ltiSotZCrtsatctn r1s.-uCrOtPs. 57 Ruckuuod I)rinr Larchmctn/, .^''V 1033t;