Philip Morris
the Authors Reply
Fields
- 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- Okag/Privilege Withdrawn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
- 2023511661-2307 Environmental Tobacco Smoke and Heart Disease
- 2023511710 the Relationship of Passive Smoking to Various Health Outcomes Among Seventh-Day Adventists in California.
- 2023511714-1718 Passive Smoking and the Risk of Heart Attack or Coronary Death
- 2023511722-1727 Effects of Passive Smoking on Ischemic Heart Disease Mortality of Nonsmokers A Prospective Study
- 2023511728 Erratum
- 2023511729 'effects of Passive Smoking on Ischemic Heart Disease Mortality of Nonsmokers: A Prospective Study'
- 2023511730 the First Author Replies
- 2023511734-1737
- 2023511738-1744 Passive Smoking in Females and Coronary Heart Disease
- 2023511749-1756 Original Contributions Heart Disease Mortality in Nonsmokers Living with Smokers
- 2023511760-1781 Lung Cancer in Japan: Effects of Nutrition and Passive Smoking
- 2023511785-1789 Passive Smoking and Cardiorespiratory Health in A General Population in the West of Scotland
- 2023511790 Passive Smoking and Cardiorespiratory Health in Scotland
- 2023511791-1792 Passive Smoking and Cardiorespiratory Health in Scotland
- 2023511793-1795 Passive Smoking and Cardiorespiratory Health in Scotland
- 2023511800-1802 Public Health Briefs Passive Smoking and 20-Year Cardiovascular Disease Mortality Among Nonsmoking Wives, Evans County, Georgia
- 2023511806-1816 Relationship of Passive Smoking to Risk of Lung Cancer and Other Smoking-Associated Diseases
- 2023511818 Increased Incidence of Heart Attacks in Nonsmoking Women Married to Smokers
- 2023511822-1824 Cvd Epidemiology Newsletter
- 2023511829-1841 Original Contributions Effects of Passive Smoking in the Multiple Risk Factor Intervention Trial
- 2023511842 Re: 'effects of Passive Smoking in the Multiple Risk Factor Intervention Trial'
- 2023511843-1844 Re: 'effects of Passive Smoking in the Multiple Risk Factor Intervention Trial'
- 2023511845 Re: 'effects of Passive Smoking in the Multiple Risk Factor Intervention Trial'
- 2023511849-1853 Smoking As A Risk Factor for Cerebral Ischemia
- 2023511857-1862 Urinary Cotinine Measurement in Patients with Buerger's Disease - Effects of Active and Passive Smoking on the Disease Process
- 2023511865-1881 An Estimate of Adult Mortality in the United States From Passive Smoking
- 2023511882 Editorial Cardiovascular Risks of Environmental Tobacco Smoke
- 2023511883-1887 An Estimate of Adult Mortality in the United States From Passive Smoking: A Response
- 2023511888-1890 An Estimate of Adult Mortality in the United States From Passive Smoking: A Response
- 2023511891-1892 Ischemic Heart Disease: Response to Lee
- 2023511893-1895 Rebuttal to Lee / Katzenstein Commentary on Passive Smoking Risk
- 2023511896-1899 An Estimate of Adult Mortality in the United States From Passive Smoking: A Response
- 2023511900-1906 An Estimate of Adult Mortality in the United States From Passive Smoking: A Response to Criticism
- 2023511908-1911 Deaths From Lung Cancer and Ischemic Heart Disease Due to Passive Smoking in New Zealand
- 2023511912 Deaths From Lung Cancer and Ischemic Heart Disease Due to Passive Smoking in New Zealand
- 2023511913 Passive Smoking in New Zealand
- 2023511914 Passive Smoking in New Zealand
- 2023511915 Passive Smoking in New Zealand
- 2023511916 Passive Smoking and Passive Thinking
- 2023511918-1937 Cardiovascular Diseases and the Work Environment A Critical Review of the Epidemiological Literature on Chemical Factors
- 2023511939-1950 Clinical Progress Series Passive Smoking and Heart Disease Epidemiology, Physiology, and Biochemistry
- 2023511952-1957 Review Passive Smoking and the Risk of Heart Disease
- 2023511958-1961 Aha Medical / Scientific Statement Position Statement Environmental Tobacco Smoke and Cardiovascular Disease A Position Paper From the Council on Cardiopulmonary and Critical Care, American Heart Association
- 2023511965-1983 the Health Consequences of Involuntary Smoking A Report of the Surgeon General
- 2023511985-1998 Environmental Tobacco Smoke Measuring Exposures and Assessing Health Effects
- 2023512000-2015 Environmental Tobacco Smoke Proceedings of the International Symposium at Mcgill University 890000 Environmental Tobacco Smoke and Cardiovascular Disease: A Critique of the Epidemiological Literature and Recommendations for Future Research
- 2023512016-2028 Panel Discussion on Cardiovascular Disease
- 2023512030-2037 Indoor Air Quality and Ventilation Environmental Tobacco Smoke (Ets) and Cardiovascular Disease
- 2023512039-2054 A Critique of the Methods Used to Assess the Toxic Effects on Man of Combustion Products.
- 2023512056-2066 Coronary Heart Disease and Involuntary Smoking
- 2023512068-2077 7. Environmental Tobacco Smoke and Coronary Heart Disease
- 2023512079-2088 Environmental Tobacco Smoke and Coronary Heart Disease
- 2023512090-2091 Editorial Give A Dog-End A Bad Name
- 2023512093-2108 Weaknesses in Recent Risk Assessments of Environmental Tobacco Smoke
- 2023512110-2129 Environmental Tobacco Smoke and Mortality A Detailed Review of Epidemiological Evidence Relating Environmental Tobacco Smoke to the Risk of Cancer, Heart Disease and Other Causes of Death in Adults Who Have Never Smoked - 5 Heart Disease
- 2023512131-2155 Environmental Tobacco Smoke Exposure and Occupational Heart Disease
- 2023512157-2171 Passive Smoking and Coronary Artery Disease. Biological Plausibility and Severity of Effect
- 2023512173-2180 Carbon Monoxide and Cardiovascular Disease: An Analysis of the Weight of Evidence
- 2023512185-2189 the Effects of Passive Inhalation of Cigarette Smoke on Excercise Performance
- 2023512192-2195 Effect of Passive Smoking on Angina Pectoris
- 2023512199-2202
- 2023512203-2213 Effect of 'passive' Smoking on the Physical Load Tolerance of Coronary Heart Disease Patients
- 2023512216-2220 Indoor Passive Smoking: Its Effect on Cardiac Performance
- 2023512223-2224 Passive Smoking Severely Decreases Platelet Sensitivity to Antiaggregatory Prostaglandins
- 2023512227-2230 Platelet Sensitivity to Prostacyclin in Smokers and Non-Smokers
- 2023512233-2237 Besitzen Passivraucher Ein Erhohtes Thromboserisiko?
- 2023512241-2244 Passive Smoking Affects Endothelium and Platelets
- 2023512247-2253 Lipoprotein and Oxygen Transport Alterations in Passive Smoking Preadolescent Children the Mcv Twin Study
- 2023512256-2257 Abstracts of the 30th Annual Conference on Cardiovascular Disease Epidemiology Children's Hdl-Chol: the Effects of Tobacco: Smoking, Smokeless and Parental Smoking
- 2023512261-2266 Passive Smoking Alters Lipid Profiles in Adolescents
- 2023512269-2274 Serum Lipids & Lipoprotein Profiles of Cigarette Smokers & Passive Smokers
- 2023512278-2279 8th Worldconference on Tobacco or Health Building A Tobacco-Free World 920330 - 920403 Buenos Aires - Argentina Abstracts, Posters and Videos. Serum Lipoproteins in Nonsmokers Chronically Exposed to Tobacco Smoke in the Workplace
- 2023512282 the Association Between Carotid Arterial Wall Thickness and Active and Passive Cigarette Smoking
- 2023512285 Passive Smoking and Carotid Artery Wall Thickness: the Aric Study
- 2023512290-2297 Passive Smoking Increases Experimental Atherosclerosis in Cholesterol-Fed Rabbits
- 2023512300-2301 Supplement to Circulation Abstracts From the 65th Scientific Sessions New Orleans Convention Center New Orleans, Louisiana 921116 - 921119
- 2023512304-2307 Association of Passive Smoking with Increased Coronary Heart Disease Risk Is Not Explained by Elevation of Leucocyte Count
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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 emironmental' 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"~
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