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Philip Morris

Passive Smoking and Risk of Lung Cancer: the Epidemiologic Evidence

Date: 19900000/P
Length: 1 page
2023714177
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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
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

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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 non•smokers, 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), Greec•c (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 Services„Puhlic Ilealth Service. 44TV14EZOz

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