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Philip Morris

the Authors Reply

Date: 19890100/P
Length: 1 page
2023511846
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Author
Kuller, L.H.
Svendsen, K.H.
Type
PSCI, PUBLICATION SCIENTIFIC
BIBL, BIBLIOGRAPHY
Area
SCIENTIFIC AFFAIRS/BLACK LATERAL OLD S&T
Document File
2023511660/2023512308/Ets: Heart Disease 930900
Litigation
Okag/Privilege Withdrawn
Okag/Produced
Characteristic
EXTR, EXTRA
Site
R529
Named Organization
Multiple Risk Factor Interven Trial Grou
Author (Organization)
Am J Epidem
Univ of Mn Minneapolis
Univ of Pittsburgh
Named Person
Katzenstein
Martin
Morgan
Master ID
2023511661/2307
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Date Loaded
24 May 1999
UCSF Legacy ID
phc02a00

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k- . 7 C i') -Jio:.. 1-,gl 228 IiE7TERS TO THE EDITOR / THE AUTHORS REPL}' Dr. Morgan (1)states that our investigation was not initiated' with an explicit hypothesis. Quite the contrary:,This research investigation (2) within the Multiple Risk Factor Intenrntion Trial!(MRFIT) was carefully planned and undertaken because of the grow- ing body, of' evidence that environmental tobacco smoke is a health hazard to nonsmokers. Reports that document exposure of nonsmokers to environmental tobacco smoke, such as elevated carboxyhemoglobin or cotinine in exposed persons, as well as reports of a possible relation between environmental tobecco~ smoke and diseases such as lung: cancer, pulmonary' disease, and' coronary heart disease prompted this investigation. An advantage of large acale clinicall trials is that data are often collected which can be used to investigate other research questions. Our re- search h}pothesis was formulated to utilizedata that we re collected in t'he !vI RF lIT for anot her purpose. The NfRFIT group had collected data on smoking habits of wives for all of'the 12.866 participants prior to this studv of the relation between environmental tobacco smoke and disease. These data were collected not because of an interest in em•ironmental' tobacco smoke; but rather because we believed'the wife's smok- ing behavior might impact the participant's ability to change risk factors, in particular, the ability to quin smoking for participants,who were smokers. , The endpoints presented in our paper-coronary heart disease (CHD) death. fatal or nonfatal CHD event, and death from any cause-were the endpoints used' for the primary MRFIT trial. Dr. Morgan is correct in observing that the CHD deaths are counted when considering the endpoints fatal or nonfatal ICHD event and death from any'cause. The intent was not to repeatedly test the difference betweem the same proportions: butto investigate ifthe smoking behavior of the participant's,wife was related to these major MRFIT endpoints defined at the beginning of the study: The focus of our paper (2) was on MRFIT men who ha&neversmoked tobacco products. We repeated the table of relative risk estimates for all nonsmokers (which included never smokers and ex-smokers who quit prior to entn• into the MRFIT) to provide data for comparisons with, other studies which may not have such detailed lifetime smoking histories. The lower p value for the endpoint "death from any cause"' in table 9 primarily reflects increased sample size and not strength of association. The hypothesis that the relative risk for this endpoint would be higher if the ex-smokers were considered alone is false. The relative risk is 1.60 (p - 0.08, 95 per cent confidence interval - 0.95-2.69). compared with 1.96 for never smokers (table 8) and 1.72 for allinonsmokers (table 9). Dr. Kat¢enstein (3) suggests lack of homogeneity between the men who had neveramoked tobaecoprodo ucts whose wives smoked versus those whose wives did not smoke. As noted in our paper (2) one of the strengths of the MRFIT data set was the large amount of information available regarding the biologic, social, and behavioral characteristics of the participanu at entry to the trial. Baseline characteristics of men whose wives smoked and men whose wives did not smoke were similar, as we noted in table 2 of ourpsper P, Z..I- i, I and as observed by Martin et' al. (4): The significant differences were men whose wives smoked weighed 4.2 lbs (1.9 kg) more, consumed 2.1' more drinks per week, and had 0.5 years less formal education, than men whose wives did not smoke. Weight was notassociated with coronary heart disease death or total mortality in the MRFIT study (5). Adjustment for baseline differences in weight, alcohol consumption, and ed'u- cation (used'as a measure of'socioeconomic statua)i as well as age, blood pressure, and cholesterol did nott change the relative risk estimates appreciably. Clearly, however, not every' variable that might possibly differ between the husbands of women who smoke and those who do not smoke were measured. There are almost certainly social and behavioral dif- ferences between a man who is a lifetime nonsmoker married to a woman who smokes, and a man married to a woman who also does not smoke. It is possible that a man who does not smoke married to a wife who smokes makes behavioral changes because of the habit of'his,wife which increases his risks of death, inde- pendent of'the known toxic chemicals in the environ- ment from his wife's cigarette smoke.'I1he ideal study, randomizing nonsmoking men to smoking or non- smoking wives, cannot be done. We agree with Dr. Katzenstein that the lack of a dose-response relation makes the pulmonary function data weaker. The difference in FEV,, between men whose wives smoke 1-19 cigarettes per day and those whose wives smoke 20 or more cigarettes per day' is not significant so the dose-response relation is lacking, not reversed; In view of our carbon monoxide and mortality findings, along,with otherstudies referenced in our paper, we see no reason to alter our cortclusions. REf ERENCES 1. MorQan P. Re,'Effectsof passive smoking in the Multiple R sk Factor I ntervrnt ion Trial '(Letter.) Am J:Epidemiol , 1989;129:226-- 2: Svendsen KH, Kuller LH. Martin MJ. et all F-f&cts of passivesmokinR in theMultiple.Risk.Factor Intervention Trial. Am J iEpidemtol l9(3 7,:126:783-95: 3:. Katzenstein AW. Re: `Effects.ofpassivesmoking in,the Multiple Risk Factor: Intervention Tnal.' (Letter.) Am J~ Epldbmol'.19ii9:'129i227:. 4. Martin MJ. Svendsen KH, Kuller LH. Nonsmoking men married to smokers.are similarito nonsmokingmen,mar- ried to nonsmokers. (Atistract.l Sooiet) y ofBehavtoral Medicine. Sth Annual Scientific Sessions. San Francisco, CA. March 5-H, 1986. 5. Multiple Risk Factor Intervention Trial Research Group.. Relationship.be.tween baselinr riskk factors and coronary heart dtsease and total morultty.in the Muhiple Risk. Factor InterventionTriall PrtvMed 19F,6:I5:354-73. Kenneth H. Svendsen Coordinating Centers for Biometric Research '~. School of Public Health Uniuersity of Minnesota Minneapoiu, MN 55414 lv' ~ Lewis H. Kuller Graduate School'oJ Public Health 1rl~l 1" Universiiy of Pittsburgh ~ Pittsburgh;,PA' 15261 TM"~ W V•

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