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Philip Morris

Re: 'effects of Passive Smoking in the Multiple Risk Factor Intervention Trial'

Date: 19880700/P
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Author
Gantt, R.C.
Lincoln, J.E.
Document File
2023511660/2023512308/Ets: Heart Disease 930900
Area
SCIENTIFIC AFFAIRS/BLACK LATERAL OLD S&T
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PSCI, PUBLICATION SCIENTIFIC
BIBL, BIBLIOGRAPHY
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2023511661/2307
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Characteristic
EXTR, EXTRA
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Svendsen
Litigation
Okag/Privilege Withdrawn
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Author (Organization)
Am J Epidemiol
PM, Philip Morris
Site
R529
Date Loaded
24 May 1999
UCSF Legacy ID
mhc02a00

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t ,4,>, 242 lLETi'ERS TO THE EDITOR RE: 'EFFECTS OF PASSIVE SMOKING IN THE MULTIPLE RISK' FACTOR N O T I C E INTERVENTION TRIAL' This material' may b2 Based on the Multiple Risk Factor Intervention Trial data. Svendsen et al. ( i)'have reported a relative risk of' 1.72 for death from any cause among male passive smokers Imalt nonsmokers married to a smok- ing wife vs. male nonsmoker marned to a nonsmoking wife): This riak compares with a relative risk for male active smoking (mak smokers vs. male nonsmokers) of 1.66, which we caleulated: from the Multiple Risk Factor Intervention Trial data (2). To the other explanations that may be offered for this surprising comparison, we wish to add an alter- native possibility that may not occur to those who are not predisposed to give cigarettes the benefit of the doubt. The effect measured by Svendsen er al. may be caused by stress rather tban by passive exposure to cigarette smoke.. There is considerable evidence that psychologic stress is capable of increasing the risk of developing diseases that are major causes of death. Both Type A behavior and'hi`h levels of hostility have been shown in prospective studies of human populations to predict increased risk of coronary heart disease (3) and death due to all causes (4„5). There is additional evidence from animal studies that behavioral stress and its physiologic concomitants promote the developmentof both cancer 16, 7) and coronary atherosclerosis (8). As we have previously argued (9)i there are sub- stantial grounds for believing that nonsmoking spouses of smokers are subjected to stresses arising therefrom. While the health authorities., given their convictions, have no honorable alternative, it is never- theless stressful to the nonsmoking apouse to be told constantly that the smoking spouse is "killing herself (or himself)" by smoking cigarettes. Repeated at- tempu to persuade the spouse to give up smoking would be a source of contention and their failure an additional soueee of stress. Also, there is reason to believe that smokers are len supportive as spouses than nonamokera, thus ere- ating a stress-relatsd risk for their mates. Current female smokers are nearly three times as likely to be divorced as women who have never smoked cigarettes / rate calculated from data in reference 10). In addition, it has been demonstrated from the Frnmingham Heart Study data ('11) that occupations, ambition, and:symp- toms of anger among wives were more strongly related' to their husbands' coronary health outcomes than the husbands' conventional "risk factors":, More generally, the inferences dra.rrt by Svendlen et al. may be an example of the error potential in attributing a mortality difference between two groups of people to what is presumed by the inveatig.ton to be the only relevant average difference between them. If there is menr in the foregoing. it may also be ttue that the scientific community has been incorrect in, attributing to smoking the mortality rate differ- ences so often reported for active cigarette smokers compared' with nonsmokers. A hitherto undiscussed difference is that the constant ad'atonitions that their smoking u`self:-destructive" must also be stressful to the smoker, while cessation of smoking may have a placebo effect.. RE/EaEMCEs1., Svendsen KH. Kuller LH. Martin M.1;,et al. Effects of pusiveamokina in the Multiple Risk Factor Inurvenuon Trial. Am J Eptderniol 1987:126:783-95.. 2. Multiple Risk Factor Interrention Trial. JAMA 1962.248:1485-77. 3. Rosenman RH. Brand RJ, Jenkins CD. er all Coronary iieart disease in the Western Collaborative Group Study: final follo-up ecperience of. 8 1/2yean. JAMA 1975:233S72-7L 4. Barefoot JC, Daitlstmm WG, Williams RB. Hostility. CHDtncidence and tottl morultty: a 25-year follow-up studyof255physietana. Psyehosom Med 1963:45:59-63 5. Shekelle RB. Gale M. Ostfeld AM, et sl. Hostility, riak of coronary disease. and mortality. Psychosam Med 1983:45:109-14. 6., Rtley % ' Psychoneuroendocnne tn0uencer on immuno- competence snd;nedpla.u. Science 1981-212:1100-9. 7. VwntatneT MA. Volptcelli JR. Seligman ME Tumor, re- pcnon in nu after inestap.bleor escapable shock. Sci- ence 1982116:437-9. 8.. Manuck SB. Kaplan JR. Matthews KA. Behavionl an- tecedenu of coronary heart diseoe and,atherouclerosis. Atherosclerosis 1986;6:2-14. 9. Gann RC. Lincoln JE. Marriage to a attwk'er and cancer nsk. (Letter.i AmJ Public Health. 1988:7B99. 10. Adultuse of iobaceo-1975. Atlanta, GA:. Center for Dis- ease Conttol. 1975: 11. Haynn SC. Eaker ED, Feinkib M. Spouse behavior and coronary hesrt disease in men: prtrpective results from the Framtnaham Hean Study., 1.. Concordance of risk factors and the relacionship,ofpsycholopcalsutus to caronary.tnrndence. AmJ Epidrmioll1983;118:1-22:. Rebecca C. Gantt Jetson E. Lincoln Philip Morris Managerrtent Corp. 120 Pdrk Atxnu[ New York NY 10017 Editor't Notr. In ortordancnu-ithJournal.pol.ey. Dr. Strnd.en et o1: urre Ruvn the opportututvto respond too th'urletrer. 6ut chost not:todo.o.: RE: 'ENVIRONMENTAL AND BEHAVIORAL DETERMINANTS OF FASTING PLASMA GLUCOSE IN WOMEN: A MATCHED CO-TWIN ANALYSIS' Over, 45 years ago, Gesell' (1) described the metliod' of co-twin control, an experimental method that was applied to the study of child'development. Since mon- orygotic co-twins share environment as children and are genetically identical, differences between treated and untreated co-twins were interpreted to result from treatment'Chis method wu recently extended to con- tinuous outcomes in observational studies (2, 3). The method compares associations in an unmatched sam- ple to associations within twin pairs (matched) to identify associations that are independent of familial variables shared by co-twins. The matched analysis consists of a multivariate linear, reegreaaion forced through a ttro ~ intercept with dependent and inde- protected by ccp.;;:~ -t law (Title 17 U-S: Code).

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