Philip Morris
Environmental Tobacco Smoke and Heart Disease
Fields
- Author
- S, W.L.
- Named Person
- Adena, M.A.
- Alderson, M.R.
- Alexander, H.M.
- Armitage, A.
- Arnold, J.
- Aronow
- Aronow, W.S.
- Aviado, D.
- Bansal, A.K.
- Barrettconnor, E.
- Bernheim, J.
- Bertanelli, F.
- Bodurtha, J.N.
- Bossano, R.
- Buerger
- Burghuber, O.C.
- Butler
- Butler, T.
- Caldwell, Ads
- Casper, M.
- Chamberlain, J.
- Chee, E.
- Chopra, C.
- Clarke, W.
- Comstock, G.W.
- Correa, P.
- Crepat, J.
- Criqui, M.
- Criqui, M.H.
- Croft, J.
- Davis
- Davis, J.W.
- Dobson, A.J.
- Donnan, G.A.
- Doyle, A.E.
- Eckfeldt, J.
- Etzel, R.A.
- Evans, G.
- Fabiano, P.
- Feldman, J.
- Filippelli, M.
- Fortmann, S.P.
- Froeb, H.F.
- Garland, C.
- Gerber, A.
- Gillis, C.R.
- Glantz, S.A.
- Green
- Green, J.
- Green, M.S.
- Haber, P.
- Hames, C.G.
- Harari, G.
- Hawthorne, V.M.
- He, Y.
- Heiss, G.
- Heller, R.F.
- Helsing, K.J.
- Hewitt, J.K.
- Hicks, L.L.
- Hirayama, T.
- Hole, D.J.
- Hollarbush, J.
- Howard, G.
- Humble
- Humble, C.
- Hunt, S.C.
- Isenberg, W.M.
- Jacobson, M.S.
- Kawachi
- Kefalides, A.
- Khalfen, E.S.
- Klochkov, V.A.
- Kristensen
- Kulik, J.A.
- Kuller, L.H.
- Lauer, R.
- Lee, P.N.
- Leone
- Leone, A.
- Lilienfield, D.E.
- Lloyd, D.M.
- Martin
- Martin, M.J.
- Matsumoto, T.
- Matsushita
- Matsushita, M.
- Mcmurray
- Mcmurray, R.G.
- Mcneil, J.J.
- Mennear, J.
- Mizell, M.
- Mori, L.
- Moskowitz, W.B.
- Mosteller, M.
- Munby, J.
- Neill, G.C.
- Nussbaum, M.
- Ockene, J.K.
- Omalley, H.M.
- Palmer
- Palmer, J.R.
- Parmley, W.W.
- Pomrehn, P.
- Punzengruber, C.
- Rosenberg, L.
- Sandler, D.P.
- Schieken, R.M.
- Segrest, J.P.
- Shaham, J.
- Shapiro, S.
- Shelton, L.
- Shenkder, I.R.
- Shionoya, S.
- Sievers, R.E.
- Silberbauer, K.
- Singh, C.B.
- Sinsheimer, P.J.
- Sinzinger, H.
- Soni, G.L.
- Spierto, F.W.
- Steenland, K.
- Suarez, L.
- Sun, Y.P.
- Surgeon General
- Svendsen
- Svendsen, K.H.
- Szklo, M.
- Taylor
- Tell, G.
- Thompson, D.L.
- Tribble, D.L.
- Tyroler, H.A.
- Virgolini, I.
- Watanabe, I.S.
- Weetman, D.F.
- Wells, A.J.
- Wexler, L.
- Whig, J.
- White, J.R.
- Williams, R.R.
- Wingard, D.L.
- Zhu
- Zhu, B.Q.
- Alderson, M.R.
- Type
- REPT, REPORT, OTHER
- BIBL, BIBLIOGRAPHY
- Site
- R529
- Document File
- 2023511660/2023512308/Ets: Heart Disease 930900
- Characteristic
- PARE, PARENT
- Master ID
- 2023511661/2307
Related Documents:- 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'
- 2023511846 the Authors Reply
- 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
- Area
- SCIENTIFIC AFFAIRS/BLACK LATERAL OLD S&T
- Named Organization
- 30th Annual Conf Cardiovasc Disease Epid
- 7th World Conference on Tobacco + Health
- 8th World Conference Tobacco or Health
- American Cancer Society
- American Heart Assn
- American Journal of Epidemiology
- American Journal of Public Health
- American Lung Assn
- American Public Health Assn
- Arch Intern Med
- Arteriosclerosis + Thrombosis
- Atmospheric Health Sciences
- Austrian Research Group
- Bowman Gray School of Med Winston Salem
- British Journal of Cancer
- British Medical Journal
- Ca 7th Day Adventists
- Campbell Univ
- Cardiovascular Disease Epidemiology Conf
- Chest
- Chung Hua Yu Fang I Hsuch Tsa Chih
- Circulation
- Conference on Ets
- Cvd Epidemiology Newsletter
- European Journal of Applied Physiology
- European Journal of Public Health
- High Ets Group
- Indian J Med Res
- Intl Conference on Indoor Air Quality
- Intl Journal of Cardiology
- J Vasc Surg
- Jacc
- Journal of Smoking Related Diseases
- Lancet
- Low Ets Group
- Mcgill Univ
- Medical Journal of Australia
- Nas, Natl Academy of Sciences
- Natl Research Council
- New England Journal of Medicine
- Niosh, Natl Inst for Occupational Safety & Health
- Non Ets Exposed Group
- Ny Medical College
- Pediatrics
- Sunderland Polytechnic
- Ter Arkh
- Tobacco Research Council Lab
- Univ of Ca San Diego
- Univ of Ca San Francisco
- Univ of Dijon
- Univ of Munich
- Verlag Chemie Intl
- Who, World Health Org
- Wiener Klinische Wochenschrift
- 7th World Conference on Tobacco + Health
- Litigation
- Okag/Privilege Withdrawn
- Okag/Produced
- Date Loaded
- 24 May 1999
- UCSF Legacy ID
- sgc02a00
Document Images
}
5. Failure to control adequately for biases stemming
from potential confounding!variables.
6. Failure to confirm causes of death via autopsy or
other histological methods.
Reviews claiming ETS-associated risk ("unfavorable" reviews)
Despite the scientific weaknesses in the epidemiologic
literature on ETS and heart disease, several recent reviews have
concluded that ETS is associated with an increased risk of heart
disease and that, in~fact, such exposure causes a large number of
deaths each year. Each of these reviews attempted to estimate an
overall risk based on the combined data from the epidemiologic
studies. These estimated risk ratios are provided in the following
table.
8
Epidemiological data have also been reported for ETS
exposure in~relation to Buerger's disease. Buerger's disease is an
inflammatory condition leading to arterial occl~usion in the
peripheral vascular system. It has been, reported to be
statistically associated with cigarette smoking. Matsushita, et
al.14 studied 40 Buerger's disease patients, in relation to smoking
history and history of ETS exposure. Based on an examination of
the progression or "aggravation" of the disease in these patients,
the authors concluded that their results confirmed'the relationship
of "active" smoking: with Buerger's disease, but that the "effects
of passive smoking on the disease process were still inconclusive."
A list of the most common weaknesses in, the
epidemiological literature on ETS and cardiovascular disease is
provided below. It will be recognized that these are characteristic
of epidemiological studies of ETS in, general, not simply those
relating to heart and other cardiovascular diseases.
1. Small sample sizes.
2. Lack of statistical significance, or failure to
test for statistical significance.
3. Potential misclassification of the smoking status
of study participants.
4. Inadequate assessment of ETS exposure.
- 7 -
Only five of the 12 epidemiological studies regarding
ETS and heart disease report a statistically significant result at
the 95% level of confidence. These are: (1) He, et al. (1989), a
Chinese language report based on only 34 female heart disease
patients; (2) Helsing, et al. (1988), a study based~ on a Maryland
census in which~the information~regarding spousal smoking (used to
estimate ETS exposure) was from 1963; (3) Hole, et al. (1989), a
Scottish study based on only 84 heart disease deaths; (4) Martin,
et al. (1988), a report based on only 23 women who reported having
a heart attack and which was given at a conference but apparently
not otherwise accepted for publication; and (5) Dobson, et al.
(1991), an Australian study which reported an association with
home exposure for women only and not at all for workplace exposure.
In sum, seven of the 12 studies of ETS exposure and heart
disease have failed to report a statistically significant
association. In the five studies that have claimed a statistically
significant relationship, three were from outside the United States.
Three were very small-scale. All of these studies suffer from a
variety of serious methodological weaknesses.
In addition to the 12 ETS/heart disease reports, there
is also an epidemiological (case-control) study reporting that
spousal smoking was associated with increased stroke risk [relative
risk of 1.7 (95% CI: 1.1-2.6)],13
- 6 -
cardiovascular diseases and the work environment. Thus, the major
reviews were those by Wells in 1988, by Glantz and Parmley in 1991
and by Steenland in 1992. These three reports are discussed further
below.
A. Judson Wells, a consultant to the American Lung
Association, statistically combined the data from several reports
on ETS and heart disease, including both prospective (cohort)i and
case-control studies. He then calculated overall relative risks
(ETS exposed versus nonexposed) for lung cancer (1.44 for females;.
2.1 for males)!, cancers other than lung (1.16 for females; no risk
elevation for males) and heart disease (1.23 for females; 1.31 for
males). Using, various assumptions and statistical manipulations,
Wells calculated' numbers of ETS-related deaths for each disease
category. He claimed that ETS exposure resulted in 46,000 deaths
per year in nonsmokers. Of these, 3,000 are claimed to be fromi
lung, cancer. For cancers other than the lung, he calculated that
ETS exposure results in 11,0001annual deaths. The largest number
of deaths from ETS exposure was claimed to be due to heart disease.
He claimed that 32,000 nonsmoker heart disease deaths per year
stemifrom ETS exposure.
A more widely publicized review of ETS and heart disease
was undertaken by two authors from the Department of Medicine,
University of California, San Francisco. In their 1991 paper,
- 10 -
Stanton Glantz and William Parmley conclude that ETS exposure is
statistically associated~ with an estimated 30% increase (relative
risk of 1.3) in heart disease risk in nonsmokers. They argue,
relying on~ Wells, that this translates into 37, 000 heart disease
deaths in nonsmokers stemming from ETS exposure. Glantz and Parmley
also discuss a number of biochemical and experimental studies which
purportedly support the biological plausibility of such a
relationship.
In evaluating the claims by Wells and by GLantz and
Parmley, it should'be emphasized that meta-analysis, the technique
from which they derive their risk estimates, is appropriately used
only when the underlying studies are highly similar and of high
quality. If the underlying studies are based~ on different
populations and~ procedures and suffer from serious methodological
weaknesses, then~any meta-analysis will consequently be invalidated.
These considerations are directly applicable to an evaluation of
risk claims regarding ETS and~ heart disease. Wells (1988)~ and:
Glantz and Parmley (1991) base their claims on meta-analyses of a
small group of, epidemiological studies reporting a relationship
between ETS exposure and an increased~ risk of heart disease. In
general, these studies deal with spousal smoking and assess heart
disease risk in the nonsmoking spouse. Otherwise, these studies
used widely disparate methodologies, study populations and
endpoints. Several are very weak, preliminary, available only in.
- 11 -
similar to that reported by Wells and'by Glantz and Parmley. This
estimation process involved: positing an overall increase in
relative risk of heart disease associated with ETS exposure; making
adjustments for potential misclassification and for background
exposure; estimating the extent of exposure to ETS; and estimating
the fraction of nonsmoker heart disease deaths attributable to ETS
exposure. These estimates were incorporated into a formula using
data on U.S. heart disease death rates and population estimates,
from which~was derived an estimated number of annual heart disease
deaths attributed to ETS exposure. According to Steenland's
calculations, "the overall estimate of ETS-attributable heart
disease deaths for never-smokers and former smokers is 35000 to
40000." He further commented that these increased risks of death
"are higher than those accepted in regulating environmental toxins."
In a 1992 position statement from the American, Heart
Association,, it was concluded that ETS causes heart disease.
(Taylor, et al.)20
Reviews emphasizing inconclusiveness of the data ("favorable"
reviews)
Reviews such as those by Wells, by Glantz and Parmliey
and by Steenland often receive a great deal of publicity. However,
it is important to recognize that there have been, a number of other
- 13 -
abstract form, or are based on such scanty data that they quite
arguably are not sufficiently reliable or valid
considered seriously in a meta-analysis.
even to be
Kyle Steenland, a National•Institute for Occupational
Safety and Health employee, also performed a risk assessment of
ETS and heart disease. In a 1992 paper, he calculated that 35,000-
40,000 annual U.S. heart disease deaths are attributable to ETS
exposure. He concluded that "heart disease mortality is
contributing the bulk of the public health burden imposed by passive
smoking."
There were two important differences between Steenland's
estimation process and that used by Wells, and later adopted by
Glantz and Parmley. First, Steenland did not do a meta-analysis
to obtain~ a pooled estimate of relative risk for heart disease
mortality associated'with ETS exposure. Instead~, he simply adopted~
the relative risk reported in a single study of a Maryland~ sample
(Helsing, et al., 1988; see endnote ref. 5) and applied~ that to
the entire U.S. population. Second~, he focused only on~ heart
disease and did not attempt to calculate ETS-related deaths from
other diseases.
Other than the above, Stteenland'.'s procedure for
calculating deaths attributable to ETS exposure was generally
- 12 -
are instigated, and some objective measure of
degree of exposure can be devised. (p. 215)24
c. D.F. Weetman presented a similar conclusion at an
indoor air quality conference in~Bangkok, Thailand in November
1991.
It is concluded that too many important
potentially confounding, factors have been~
overlooked to decide if there is an association
between exposure to ETS and cardiovascular
diseases. (p. 275)25'
d. Another scientific review of this literature was
performed! by two physicians from the University of Munich,
Germany and given at an international conference in Hungary in
June 1990. The conclusion was similar..
Taking into account the small increase in
coronary risk in passive smokers as compared
to non-exposed subjects and also the low
validity and small number of epidemiological
studies available and the fact that their
results are at least inconsistent, a
relationship between passive smoking and
cardiovascular diseases cannot be established
on these data. (p. 6)26
e. In a 1991 book discussing a wide range of
issues
involving ETS, the literature on heart disease was reviewed
by Alan Armitage, former director of toxicology of a major
European research laboratory and head of pharmacology at the
- 16 -
scientists have undertaken more balanced and' critical reviews of
the more recent data and have j'udged that it remains inconclusive.
Several of the most significant of these recent reviews, and their
conclusions, are as follows.
a. At a major conference on ETS held~ at McGill
University in 1989,, Lawrence Wexler, of the New York Medical
College, concluded that recent data did not provide a basis
for altering the earlier conclusions by the Surgeon General
and National Research Council concerning ETS and cardiovascular
disease.
Based on the available evidence, it is this
author's opinion that it has not been
demonstrated that exposure to ETS increases
the risk of cardiovascular disease. (p. 139)23
b. A similar evaluation was made by two scientists,
D.F. Weetman and J. Munby, from the School of Pharmacology,.
Sunderland Polytechnic, Sunderland, United Kingdom. They
presented their conclusions fr= a review of the literature
on ETS and heart disease at an international conference on
i_ndoor air quality held'. in Lisbon, Portugal in April 1990.
It is concluded that no increased risk of
cardiovascular disease can be associated
unequivocally with exposure to ETS, and it
seems probable that this will continue to be
the case until specifically designed trials
- 15 -
Tobacco Research Council Laboratories in the United Kingdom.
He judged that the scientific data have not established an
increased heart disease risk in nonsmokers exposed to ETS.
It is clear that the evidence for a harmful
effect of ETS in~enhancing CHD [Icoronary heart
disease) risk in non,smokers is not very
convincing. . . . (p. 114)27
f. In a subsequent review in 1993, Armitage, writing
as a consultant pharmacologist and toxicologist, expressed a
similar evaluation of the ETS/heart disease literature.
On the current evidence a causal relationship
between exposure.to ETS and the development of
CHD has not been proved. (p. 27)28
g.
Armitage's 1993 review appeared in the Journal of
Smoking-Related Diseases. In an~editorial in the same journal
issue, A.D.S. Caldwell, the journal's managing editor,
emphasized that the issue of confounding variables was of
particular importance in the case of heart disease.
This is
because of the hundreds of factors reportedly associated with
the disease. Caldwell observed that the numerous heart disease N
risk factors make it extremely difficult to make confident ~
CJ
statements about a potential role of ETS.
N
W
- 17 -
