a1 = lowest consumption category. The exposure categories of low to high are for summary purposes only and do not correspond to identical categories across studies. AD, adenocarcinoma; F, female; M, male: SCC, squamous cell carcinoma; SM, small cell carcinoma.

prospective studies bolster the evidence supporting the premise that in general, the higher the circulating concentrations of carotenoids (a-carotene, /3-caro-tene, /3-cryptoxanthin, lutein, lycopene, and total carotenoids), the lower the risk of lung cancer. Circulating concentrations of retinol, tocopherol, and selenium have not been associated with a reduced risk of lung cancer in most studies.

Studies of both dietary intake and prediagnostic blood concentrations favor a protective association between provitamin A carotenoids (specifically ^-carotene, a-carotene, and /3-cryptoxanthin) and lung cancer. It is not known, however, if a generally protective association is specific to these carotenoids or whether carotenoid intake merely serves as a marker of the intake of other protective substances or healthier dietary habits in general. The evidence for vitamin C is scant but suggestive of a protective association, whereas the data on vitamin A, vitamin E, and selenium have yielded null findings.

Phytochemicals Phytochemicals are low-molecular-weight molecules produced by plants. Of the many classes of phytochemicals, those studied in relation to lung cancer include phytoestrogens, flavonoids, and glucosinoids.

The tumor-promoting effects of steroid hormones can be blocked by phytoestrogens. Soybeans are a primary source of a specific class of phytoestrogens known as isoflavonoids. The relatively few studies on isoflavonoids in relation to lung cancer have not provided evidence of a link.

Flavonoids exhibit potent antioxidant activity. Flavonoid intake has been at least weakly associated with reduced risk of lung cancer in three out of four studies to date.

Isothiocyanates are metabolites of the class of phy-tochemcials known as glucosinolates. Isothiocyanates could exert anticancer effects by blocking carcinogens via induction of phase II detoxification enzymes, such as glutathione S-tranferase. Cruciferous vegetables contain high concentrations of glucosinolates, and hence consumption leads to higher endogenous iso-thiocyanate levels. As with cruciferous vegetables, lung cancer risk is also consistently lower with higher intakes or urinary levels of isothiocyanates.

A postulated link between isothiocyanates and a common polymorphism in the GSTM1 gene provides an example of a potential gene-diet interaction relevant to lung carcinogenesis. A growing focus in cancer epidemiology is to characterize interindividual susceptibility to cancer by studying polymorphisms in genes involved in DNA repair and in the metabolism and detoxification of potential carcinogens. Of further interest is how such genetic traits interact with environmental exposures to contribute to cancer risk. The role of glutathione S-transferase as a phase II detoxification enzyme has made a common polymorphism in the glutathione S-transferase M1 (GSTM1) gene of interest in relation to lung cancer. Results combined across studies show that compared to people with the GSTM1 present genotype, those with the GSTM1 null genotype had an increased risk of lung cancer.

When isothiocyanates have been studied in combination with GSTM1, the decreased risk of lung cancer associated with isothiocyanates has been especially pronounced in people with the GSTM1 null genotype. This association may represent either the cancer-blocking activity of isothiocyanates playing an enhanced role in GSTM1 null individuals or more efficient metabolism of isothiocyanates in those with the GSTM1 present genotype. Regardless, this is one example of the potential interactions between genetic and dietary factors, an approach that may eventually advance our understanding of the nutritional epidemiology of lung cancer.

Fat and cholesterol Evidence that dietary fat may facilitate tumor growth was reported as early as 1940. Correlation exists between international or regional dietary fat consumption and lung cancer mortality. In case-control studies, total fat intake is consistently associated with lung cancer risk among men and women, but saturated fat, unsaturated fat, and cholesterol intake tend to be associated with lung cancer risk only among men (Table 3). The prospective evidence shows a slightly different picture, with both total fat and saturated fat intake strongly associated with lung cancer in men but not women, and unsaturated fat and cholesterol not consistently associated with lung cancer risk in men or women (Table 3). The equivocal nature of the evidence is reflected in the lack of consistent findings between the sexes and the results of a large, pooled cohort study of both sexes that found lung cancer risk was not strongly associated with fat (total, saturated, or unsaturated) or cholesterol intake.

Regarding cholesterol, there is inconsistency between the dietary data presented previously and serologic data. A review of 33 prospective cohort studies indicated that lower circulating cholesterol levels were predictive of greater lung cancer risk. Similar results were obtained after accounting for the possible preclinical effects of cancer on cholesterol levels by limiting analyses to cases of lung cancer that were diagnosed 5 or more years after the initial cholesterol measurement. This association may be due to a direct effect of cigarette smoking on lipid profiles or to differences in dietary patterns between smokers and non-smokers. The lack of consistency between the serologic

Table 3 Estimated relative risk of lung cancer according to fat intake or cholesterol intakeĀ®

First author (Year)

Sex Total fat

Unsaturated fat

Saturated fat


Goodman (1988) Hinds (1983)

Jain (1990) Swanson (1997)

Bandera (1997)

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