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Abstract
This study investigates the relationship of smoking and other factors to risk of different lung cancer cell types in women. 217 Women who were diagnosed with lung cancer between 1969 and 1977 and who had received a multiphasic health checkup (MHC) prior to diagnosis were identified from the records of Northern California Kaiser hospitals. Each case was matched for year of birth, race, and date of MHC to a woman who attended the MHC but did not develop lung cancer. A self-administered questionnaire completed at the MHC provided information on smoking habits and medical and family histories. All pathology specimens were reviewed by a pathologist without knowledge of the initial diagnosis for confirmation of cell type.
The relative odds for the development of lung cancer for women who had ever smoked compared to never-smokers was 6.9 (p < .001). Lung cancer risk was higher for current than ex-smokers, and increased with quantity, duration, and intensity of smoking. The relative odds of developing epidermoid, small cell or large cell carcinoma was 51.0(p < .001); for adenocarcinoma it was 2.7 (p < .01). Both pathology groups exhibited a dose-response relationship with smoking. However, the gradient was much smaller for adenocarcinoma than for other cell types. Light smokers and women smokers age 55 or younger had no increased risk of adenocarcinoma.
Host factors including family history of cancer in first degree relatives, medical history of respiratory disease and history of allergic disease contributed independently to lung cancer risk. After adjusting for smoking and education by multiple logistic analysis, women with a family history of lung cancer experienced an increased risk for lung cancer of 1.9 (p = .22). The relative risk associated with family history of any cancer was 1.8 (p = .05). A significant interaction existed between cigarette smoking and family history of cancer. A past history of bronchitis, pneumonia or emphysema carries an excess adjusted risk of 1.7 (p = 0.09). Women reporting a history of asthma or hay fever were protected against lung cancer; the adjusted odd ratio was (p = .05). These findings suggest an increased host susceptibility in some individuals which may be genetically or environmentally mediated.
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