Philip Morris
Passive Smoking and Risk of Lung Cancer: the Epidemiologic Evidence
Fields
- Author
- Brown, K.G.
- Type
- PUBL, PUBLICATION, OTHER
- BIBL, BIBLIOGRAPHY
- Area
- PATSKAN,GEORGE/OFFICE
- Site
- R589
- Named Organization
- Epa, Environmental Protection Agency
- Nas, Natl Academy of Sciences
- Named Person
- Hirayama
- Surgeon General
- Trichopoulos
- Surgeon General
- Request
- Stmn/R1-048
- Litigation
- Stmn/Produced
- Master ID
- 2023714085/4177
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- Characteristic
- MARG, MARGINALIA
- Date Loaded
- 05 Jun 1998
- UCSF Legacy ID
- btj78e00
Document Images
securities arc held by universities, pension funds and insurance companies.
Shareholder resolutions on marketing to children and marketing overseas and calls
for divestment have recently appeared. These strategies have met concerted
opposition from the industry, but time is on our side.
Despite enormous efforts on the industry's part, it looks ever more likely that
the Environmental Protection Agency will soon classify tobacco smoke pollution as a
Class A carcinogen. This short list consists of environmental pollutants which are
known human carcinogens.
In late September, a product liability case will come to trial in Philadelphia
involving a stockbroker who developed mcsothclioma after smoking Kent cigarettes
with an asbestos filter. In early October, the Supreme Court will hear an appeal of a
tobacco product liability case. The issue before the court will be whether tobacco
companies are shielded from suit by the government mandate_d warnings which
have been on packs since 1966.
In sum, the industry remains active on a wide variety of fronts, hncreasingiy,
though, it is on the defensive, but an enormous amount of work remains to be done
before we have public policies In place which genuinely meet (he challenges the
tobacco industry poses to the health of our patients, friends and family.
PASSIVE SMOKING AND RISK OF LUNG CANCER:
THE EPIDEMIOLOGIC EVIDENCE
Kenneth G. Brown, Ph.D.
Ten years ago two epidet»iologic studies, one a prospective study conducted in
lapan (Hirayama, 1981) and the other a case-control stutdy from Greece
(Trichopoulos, 1983), reported evidence that passive smoking Increases the risk of
lung cancer in nonsmokers. Both studies estimated the lung cancer Incidence in
nonsmoking women married to smokers reiative to thosc married to nonsmokers,
thus using spousal smoking as a surrogate for exposure to passive smoking.
Although there are other sources of exposure to environmental tobacco smoke (F.TS).
particularly the workplace, the assumption is that women married to smokers arc
more exposed, on average, than women married to a nonsmoker. These two studies,
particularly the prospective study from lapan, evoked considerable critical response,
mueh of it funded by tobacco interests. They also aroused the interest of public
health epidemiologists, who initiated additional studics.
At this time the results of 29 studies have been reported. 25 case-control and
four prospective. Iront ci>;ht countries: China (3). England (I), Greecc (2), Hong Kong
(4), Japan (6). Sweden (2), Scotland (I), and the USA (10). The studies vary widely
in design cxecnlion analysis, and conclusions, but overall the evidence supports
the hypothesis that passive smoking is associated with increased lung cancer
incidence. This conclusion is not new. It is found in the draft F.PA document on this
topic that was made available for external review in May. 1990, and in reports from
the U.S. Surgeon General and the National Academy of Sciences in 1986. The
significance for public health lies in the ubiquity of ETS exposure. Sensilivc
hioassays I'or cotinine, a metabolite of nicotine, indicate that even most nonsmokers
who report not being exposed to tobacco smoke have detectable urina -ry levels. Irl
the absence of information to the contrary, U.S. EPA guidelines for risk assessment
assume that a carcinogen increases the risk of lung cancer at arbitrarily small doses,
i.e., there is no "threshold" dose below which there is no risk.
We partition the lung cancer mortality rate from all causes, a statistic readily
available for most cotmtries, into components attributable to active smoking. to
passive smoking (associated with spousal smoking), and to background (all other
sources) for the countries from which there is study data. This approach leads to
some interesting inter-country differences. The lung cancer mortality rates vary
widely across countries, but it is readily apparent that active smoking is consistently
a lung cancer risk. The lung cancer attributable to active smoking also differs
between countrics, both in absolute terms and as a percentage (the U.S. is high in
both categories). l.ung cancer attributable to passive smoking is, of course, much
lower and may differ between countries. Consequently, study results are mixed an,
qualitative charactcristics of the individual studies need to be considered for
potential sources of bias (a major task of this project). To accomplish this a master
list was constructed against which each study was evaluated for completeness and
rigor. The qualitative characteristics of each study were considered along with
quantitative aspects determined by statistical methods. The results are eauivocal fot
thc ic evid ncc f i k a t d wi a
countdcs_(Asian_and European), where physical environment (e.9 size nf hnmes.
an
DO
of occupants wh_
D-Im41J
and cultural behavior (e.g., where
women
less ant to be exposed to ETS outside the home) mayplay a role.
After adjusting lung cancer mortality rates for active an passive smoking the
remaining backgrotmd, or "baseline" rate, of unexplained etiology in nonsmoking
women is similar across most countries except for Hong Kong and areas of china,
which are about three-fold higher. A number of potential "nonsmoking" risk factors
for lung cancer have been Investigated among the studies evaluated, such as
methods of cooking (e.g.. stir frying and deep frying), sources of fuel for cooking and
heating (e.g., burning wood or straw and use of kerosene), history of lung disease,
hormones (esirogen), and dietary practices (e.g., consumption of fruit, vegetables
and hela-carotene, that might have a protective effect). Aside, perhaps, from sourc
of indoor smoke from burning wood, coal, or straw, which contains known
carcinogens, the evidence is sketchy, more suggestive than conclusive. Further
research in the areas suggested, however, may reveal causal or protective agents
that hnpact the incidence rate of lung cancer, and may improve our knowledge of the
biological mechanisms involved in lung cancer.
Klil'hRI;NCh:S
Ilirayama T. (t0BI) Non smukinG wives of heavy smokers have a higher risk of lung
cancer: A study From lapan. Br Mcd 1282: 183-185.
Trii holonkx, h.; Kal:mdidi, A.; Sparros L. (198:t) Lung cancer and passive smoking:
Conciusion oi t:reek study. (LcIter) I.ancrl 667 668.
U.S. Surgeon General (1-1++6) The hc;dih consequences c+f involuntary smoking. U.S.
Deparunent ol Ihv;dth and Uuman ServicesPuhlic Ilealth Service.
44TV14EZOz
