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Aspects of the epidemiology of lung cancer in smokers and nonsmokers in the United States.

作者信息

Kabat G C

机构信息

Albert Einstein College of Medicine, Bronx, NY, USA.

出版信息

Lung Cancer. 1996 Aug;15(1):1-20. doi: 10.1016/0169-5002(95)00566-8.

DOI:10.1016/0169-5002(95)00566-8
PMID:8865119
Abstract

While it is well-established that smoking is the predominant risk factor for lung cancer, it is clear that factors other than smoking and occupational exposure play a role in some lung cancers, and particularly adenocarcinoma. Data from a large, hospital-based case-control study are used to examine the association of smoking-related risk factors (amount smoked, filter status, mentholation, and differences in smoking habits between blacks and whites) and selected factors other than smoking (environmental tobacco smoke, previous primary cancer and radiotherapy, reproductive and endocrine factors, and body mass index) with lung cancer. Although smoking shows a dose-response relationship with all major lung cancer cell types, the strength of the relationship is weaker for adenocarcinoma, suggesting that other risk factors must play an important role for this cell type. In blacks and whites of both sexes, odds ratios for lung cancer increased with increasing cumulative tobacco tar intake and decreased with years since quitting smoking. Use of mentholated cigarettes was associated with no greater risk for lung cancer than that associated with the use of nonmentholated cigarettes. Exposure to environmental tobacco smoke generally showed little relation to lung cancer risk. In particular, exposure of nonsmoking wives to a husband's smoking showed no increase in risk. A history of a reproductive primary cancer and a history of radiotherapy were each associated with a fourfold increase in risk in female nonsmokers. An association of lean body mass with lung cancer was observed in current smokers, ex-smokers, and female never smokers. These results are discussed in the context of existing studies. In conclusion, variation in lung cancer rates between populations may be due to: (1) differences in effective exposure to tobacco smoke carcinogens; (2) differences in factors which modify the effect of tobacco smoke, including differences in host susceptibility and metabolism of carcinogens, or (3) differences in exposure to other independent risk factors for lung cancer.

摘要

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