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We used data from a case-control study conducted in New Jersey between 1980 and 1983 to evaluate race and sex differences in associations of vegetable, fruit, and carotenoid consumption with lung cancer. Cases included 736 White males, 860 White females, 269 Black males, and 86 Black females with incident, histologically confirmed, primary cancer of the trachea, bronchus, or lung. Controls were identified through drivers' license and Health Care Financing Administration files and included 548 White males, 473 White females, 170 Black males, and 47 Black females. Usual intakes of vegetables (predominantly yellow/green) and fruit (predominantly yellow/orange) as well as other food sources of carotenoids were ascertained by a food frequency questionnaire. White females showed significant inverse associations of lung cancer with vegetables, fruit, and carotenoids. White males showed nonsignificant inverse associations with vegetables and carotenoids, and Black females just with vegetables. No inverse associations were found for Black males. Vegetable consumption was associated with risk of all histologic types of lung cancer, but the pattern of increasing risk with decreasing intake was limited to smokers. We infer that consumption of yellow/green vegetables and carotenoids may confer protection from lung cancer to White male and White female smokers. Further studies are needed to clarify the effect in Blacks.

A population-based incident case-control study of lung cancer in white males was conducted during 1980-81 in six high-risk areas of New Jersey. Interviews were completed with 763 cases and 900 controls or with their next of kin. In order to assess whether dietary intake of carotene, preformed retinol, or total vitamin A modified the risk of lung cancer, subjects were asked about their usual frequency of consumption, several years earlier, of 44 food items, which provides 83% of the vitamin A in the American diet, and about their use of vitamin supplements. The men in the lowest quartile of carotene intake had 1.3 the risk (P-value for trend = .05) of those in the highest quartile after adjustment was made for smoking duration and intensity and education. No association was seen for retinol (P-value for trend = .11) or total vitamin A (P-value for trend = .30). The inverse association between carotene intake and lung cancer was most compelling for squamous cell carcinoma, with the smoking-and education-adjusted risk of those in the lowest quartile reaching 1.4 (P-value for trend = .03) the risk of those men in the highest quartile. Risk of lung adenocarcinoma was not related to carotene intake. The reduction in risk of squamous cell lung cancer with increasing carotene intake was noted in pipe and cigar smokers and cigarette smokers of different intensities. Among nonsmokers adenocarcinoma predominated. The inverse association between carotene and risk of squamous cell lung cancer was not especially strong or graded in response; but it was consistent and could be noted in each stratum when the subjects were divided by education, age, or mode of interview (direct vs. next of kin). The results of the other 4 case-control and 3 cohort studies that have looked at diet and risk of lung cancer are not consistent, and the question whether dietary carotene or total vitamin A reduces the risk of lung cancer is not yet resolved.

A population-based incident case-control study of lung cancer in white males was conducted during 1980-1981 in six high-risk areas in New Jersey. Interviews were completed for 763 cases and 900 controls. To assess whether dietary intake of carotenoids, preformed retinol, or total vitamin A influences the risk of lung cancer, the authors asked the respondents about the usual frequency of consumption, approximately four years earlier, of 44 food items which provide 83% of the vitamin A in the US diet and about the use of vitamin supplements. The men in the lowest quartile of carotenoid intake had a relative risk of 1.3 compared with those in the highest quartile after adjusting for smoking. No increase in risk was associated with low consumption of retinol or total vitamin A. Intake of vegetables, dark green vegetables, and dark yellow-orange vegetables showed stronger associations than did the carotenoid index; the smoking-adjusted risks of those in the lowest quartiles of consumption of these food groups reached relative risks of 1.4-1.5 compared with the risks of those in the highest quartiles. The protective effect of vegetables was limited to current and recent cigarette smokers; the smoking-adjusted relative risks for low consumers reached 1.7, 1.8, and 2.2 compared with the risks for high consumers for vegetables, dark green vegetables, and dark yellow-orange vegetables, respectively. The reduction in risk with vegetable intake was most apparent for squamous cell carcinomas, but it extended to adenocarcinomas and most other cell types when only current and recent smokers were analyzed. This protection among current and recent smokers is consistent with the model that vegetable intake prevents a late-stage event of carcinogenesis. Consumption of dark yellow-orange vegetables was consistently more predictive of reduced risk than consumption of any other food group or the total carotenoid index, possibly because of the high content of beta-carotene relative to other carotenoids in this particular food group.

In a population-based case-control study of lung cancer among New Jersey men, usual adult consumption of many vegetables and fruits was included in the interview to assess the protective potential of carotenoids. With data from 900 controls the percentage of New Jersey white men who eat specific vegetables and fruits primarily in certain seasons, the relative importance of in-season and out-of-season consumption, and the median length of season were determined. Although first asking whether a food item was consumed all-year-round or primarily in certain seasons and then asking for the appropriate frequency of consumption facilitated the interview, obtaining out-of-season frequency of consumption and length of season was not necessary. Substituting 0 for reported out-of-season frequencies and 3 mo for reported season lengths reduced slightly the observed associations between diet and lung cancer risk but did not modify the overall pattern noted. Carotenoid intake in winter-fall was estimated to be about two-thirds that in summer-spring.

To evaluate the role of passive smoking in the development of lung cancer among nonsmokers, data were pooled from three large incident case-control interview studies. Ninety-nine lung cancer cases and 736 controls never used any form of tobacco. Overall the adjusted odds ratio for lung cancer among nonsmokers ever living with a smoker was 0.8 (95% confidence interval, 0.5-1.3) rising to 1.2 among those exposed for 40 or more years. Persons living with a spouse who smoked cigarettes were at increased risk (adjusted odds ratio, 1.5; 95% confidence interval, 0.8-2.8). When adjusted for age and gender, there was a significant trend in risk with increasing amounts smoked per week by the spouse (P = 0.05) and with cumulative pack-years of exposure (P = 0.03). This effect was limited to females, especially older women whose husbands were heavy smokers. The elevated risk associated with spouse smoking was restricted to squamous and small cell carcinomas (odds ratio, 2.9; 95% confidence interval, 0.9-9.3), which provides additional evidence linking passive smoking to lung cancer.