Info

Case-control studies

M/F ______ — — — — — — 1.0 0.9 1.1 2.1 — —

M smokers 1.0 0.7 0.7 0.9 0.5 0.3 1.0 1.1 1.3 0.8 1.2 1.2 — — — — — —

F nonsmokers — — — — — — — — — — — — 1.0 1.0 0.7 — — —

F 1.0 1.0 — — — —(black) 1.0 0.6 — — — — 1.0 0.8 — — — —

F nonsmokers 1.0 0.8 0.6 0.5 — —(green) — — — — — — — — — — — —

F smokers 1.0 1.4 0.6 — — —(green) — — — — — — — — — — — —

M/F 1.0 1.0 1.4 1.6 — — 1.0 1.0 1.2 1.3 — — 1.0 1.6 1.8 — — —(whole)

— — — — — — — — — — — — 1.0 0.8 — — — —(2%)

— — — — — — — — — — — — 1.0 0.6 0.7 — — —(skim)

M, AC 1.0 1.1 1.1 1.3 — — 1.0 0.9 1.2 — — — 1.0 1.0 0.9 0.8 — —

F, AC 1.0 1.0 1.1 1.1 — — 1.0 0.8 0.8 1.3 — — 1.0 0.8 1.0 0.7 — —

M, SCC 1.0 1.0 1.2 1.1 — — 1.0 1.0 1.2 1.6 — — 1.0 0.9 0.8 0.7 — —

— — — — — — — — — — — — 1.0 1.3 0.8 0.8 — —(skim) M/F 1.0 0.9 0.9 1.1 — — 1.0 1.0 0.9 1.3 — — 1.0 1.6 1.6 2.1 — —(whole)

— — — — — — — — — — — — 1.0 0.5 0.7 0.5 — —(2%)

— — — — — — — — — — — — 1.0 0.8 0.5 0.7 — —(skim) M 1.0 0.9 1.2 0.7 — — 1.0 0.9 1.2 1.6 — — 1.0 0.9 1.4 1.7 — —

Prospective studies

— — — — — — — — — — — — 1.0 0.9 0.5 — — —(2%)

— — — — — — — — — — — — 1.0 1.0 0.6 — — —(skim) M smokers 1.0 0.7 — — — — ____________

Brennan (2000) Darby (2001) Mendilaharsu (1998) Kreuzer (2002) Kubik (2002)

Swanson (1997) Takezaki (2001)

Tewes (1990) Yoshiyuki (1995) Mayne (1994) Mettlin (1989)

Axelsson (1996)

Goldbohm (1996) Zheng (1996) Breslow (2000)

Hirvonen (2001) Fraser (1991)

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. AC, adenocarcinoma; F, female; M, male; SCC, squamous cell carcinoma.

drinking and other health behaviors, particularly cigarette smoking, has not been addressed adequately, indicating that much stronger evidence is needed for coffee drinking to be considered a risk factor for lung cancer. Despite numerous in vitro and in vivo studies that have observed potential tumor-inhibitory effects of tea, the epidemiologic evidence does not provide support for a link between tea drinking and the risk of lung cancer (Table 6).

The associations observed between milk drinking and lung cancer depend on milk fat content. Milk drinking is not strongly associated with lung cancer risk when milk fat content is ignored. The associations between whole milk and lung cancer tend to be either null or in the direction of increased risk, whereas the associations for reduced fat or nonfat milk tend to be either null or in the protective direction (Table 6). Perhaps milk consumption, including the type of milk, is merely serving as a marker of fat intake.

Meat and fish Associations have been observed between red meat intake and increased lung cancer risk, but this evidence is counterbalanced by an equal number of null studies. The cooking method may play a role because heterocyclic amines from cooked meat may contribute to an increased lung cancer risk. The evidence does not support a strong link between fish consumption and lung cancer.

Diet and Prevention

Chemoprevention trials Three randomized, doubleblind, placebo-controlled trials were undertaken in the 1980s and 1990s to test whether ^-carotene supplementation protects against lung cancer. All three studies indicated that ^-carotene supplementation in later adulthood does not protect against lung cancer (Table 7). To the contrary, ^-carotene supplementation was associated with an increased risk of lung cancer among the high-risk populations of heavy smokers in the ATBC Cancer Prevention Study and smokers and asbestos-exposed workers in the CARET Study. No beneficial effect was observed for a-tocopherol supplementation in the ATBC Cancer Prevention Study.

These experimental results fail to corroborate the evidence from observational studies that favors a protective association between ^-carotene and lung cancer. In fact, it is possible that ^-carotene may exhibit prooxidant properties. Consistent with the results of observational studies, a protective association was noted when the data from the placebo controls in the ATBC Cancer Prevention Study were analyzed according to baseline serum and dietary ^-carotene.

In interpreting the results of the ATBC and CARET studies, it is important to recognize that the studies enrolled older, high-risk individuals who had high cumulative exposure to tobacco smoke and/or asbestos. The results therefore presumably apply mainly to the latter stages of carcinogenesis. The doses administered were far higher than the normal dietary range, and the dose-response relationship for preventive effects, anticipated from the observational evidence, may not be applicable. Because antioxidant nutrients may exert their protective effect in the earlier stages of carcinogenesis, ^-carotene may have been administered too late to halt the evolution of cellular changes that lead to lung cancer. Alternatively, compounds present in fruits and vegetables other than the micro-nutrients studied in the trials may protect against lung cancer. The protective associations for fruit and vegetable consumption were allied to the micronutrient

Table 7 Summary of randomized chemoprevention trials of micronutrients and lung cancer

Study (year)

Location N

Number of Study cases population

Years of Regimen follow-up

Relative risk

Incidence Mortality

ATBC Finland 29 133 876 (1994)

CARET United 18 314 388 (1996) States

PHS United 22 071 170 (1996) States

Male smokers, age 50-69 years

Asbestos-exposed smokers and heavy smokers Males and females, age 45-69 years Male physicians, age 40-84 years

6 (median)

4 (average)

12 (average)

1. Placebo

1. Placebo

1. Placebo

2. BC (50 mg on alternate days)

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