Lung Cancer Abstracts
Antioxidants & Lung Cancer
Antioxidants & risk
Examined the relation between the dietary intake of vitamins E, C, and A (estimated by a 24-hour recall) and lung cancer incidence. [the First National Health and Nutrition Examination Survey Epidemiologic Followup Study]
The relative risk of lung cancer for subjects in the highest quartile of vitamin C intake compared with those in the lowest quartile was 0.7.
For vitamin A intake, a protective effect was observed only for its fruit and vegetable component (carotenoids) among current smokers but this was modified by the intensity of smoking.
The vitamin E intake-lung cancer relation was modified by the intensity of smoking with a significant protective effect confined to current smokers in the lowest tertile of pack-years of smoking. Overall, there was no additional protective effect of supplements of vitamins E, C, and A beyond that provided through dietary intake. When vitamin E, vitamin C, and carotenoid intakes were examined in combination, a strong protective effect was observed for those in the highest compared with those in the lowest quartile of all 3 intakes.
Data provide support for a protective role of dietary vitamins E and C and of carotenoids against lung cancer risk but with a modification in effects by the intensity of cigarette exposure.
While smoking avoidance is the most important behavior to reduce lung cancer risk, the daily consumption of a variety of fruits and vegetables that provides a combination of these nutrients and other potential protective factors may offer the best dietary protection against lung cancer.
Yong LC et al., Intake of vitamins E, C, and A and risk of lung cancer. The NHANES I epidemiologic followup study. First National Health and Nutrition Examination Survey. Am J Epidemiol, 1997 Aug 1, 146:3, 231-43.
Epidemiology & Lung Cancer
Epidemiology (1)
Epidemiologic evidence on the relationship between nutrition and lung cancer is reviewed.
Observational studies of diet and lung cancer, both prospective and retrospective, continue to suggest strongly that increased vegetable and fruit intake is associated with reduced risk in men and women; in various countries; in smokers, ex-smokers, and never-smokers; and for all histologic types of lung cancer.
Prospective studies of blood beta-carotene levels, arguably the best available biomarker of vegetable and fruit intake, indicate that low levels are predictive of increased lung cancer incidence. However, in a randomized, placebo-controlled clinical trial in male smokers, lung cancer incidence and total mortality were increased significantly among the men receiving beta-carotene supplements. If beta-carotene can prevent lung carcinogenesis, which the trial cannot rule out, then the dosage, duration of use, method of administration, and/or subpopulation are critical. Ongoing clinical trials, some of which include women, will provide much-needed information.
Other carotenoids, other phytochemicals, and associated dietary patterns may explain the beneficial effects of vegetables and fruits and have not been explored adequately in epidemiologic work.
Studies have also indicated that diets high in fat, saturated fat, and cholesterol may increase the risk of lung cancer and that the effect is not mediated through vegetable and fruit intake.
Since beta-carotene can function as an antioxidant, other micronutrients with this potential, specifically vitamins E and C and selenium, also have been proposed to reduce lung cancer risk. However, the totality of the epidemiologic evidence is not, at present, persuasive for any one of these micronutrients.
Ziegler RG et al., Nutrition and lung cancer. Cancer Causes Control, 1996 Jan, 7:1, 157-77.
Epidemiology (2)
Examined patterns and trends in lung cancer and the risk factors associated with development of this disease.
Epidemiological evidence documents that most lung cancer cases could be prevented. With 3 million persons worldwide dying annually from lung cancer attributable to smoking, cigarette smoking remains the number one target for public health action to reduce cancer risk in the general population.
Valanis BG: Epidemiology of lung cancer: a worldwide epidemic. Semin Oncol Nurs, 1996 Nov, 12:4, 251-9.
Mortality & Lung Cancer
Investigated hypotheses that could explain the higher observed lung cancer mortality rates in the smoking cessation (SI) group as compared with the usual care (UC) group. [The Multiple Risk Factor Intervention Trial (MRFIT).]
Rates of mortality from coronary heart (CHD) were examined to explore the possibility that prevention of CHD death may have contributed to greater mortality due to lung cancer in the SI group.
135 SI and 117 UC participants died from lung cancer.
None of the hypotheses proposed to explain the unexpected higher rates of lung cancer mortality among SI as compared with UC subjects were sustained by the data. Thus the difference observed is due to chance, and a longer period of sustained smoking cessation plus follow-up is necessary to detect a reduction in lung cancer mortality as a result of smoking cessation intervention in a randomized clinical trial.
Shaten BJ et al., Lung cancer mortality after 16 years in MRFIT participants in intervention and usual-care groups. Multiple Risk Factor Intervention Trial. Ann Epidemiol, 1997 Feb, 7:2, 125-36.
Passive Smoke & Lung Cancer
This was a population based study evaluating the relationship between passive smoking and lung cancer in 191 patients with confirmed lung cancer who had never smoked, and an equal number of individuals without lung cancer who had never smoked.
Residential histories were taken which included information on environmental tobacco smoke. Smoker years, determined by multiplying the number of years in each residence by the number of smokers, were evaluated. Household exposure to 25 or more smoker year's during childhood and adolescence doubled the risk of lung cancer. About 15% of the subjects who had never smoked reported this exposure.
Less than 25 smoker years exposure during childhood was not associated with an increased risk to lung cancer.
Exposure to passive smoke early in life accounts for approximately 17% of the lung cancers among nonsmokers.
"Lung Cancer and Exposure to Tobacco Smoke in the Household", Janerich, Dwight T., DDS, M.P.H., et al, NEJM. September 6, 1990;323(10):632-636.
Selenium & Lung Cancer
In the Yunnan Tin Corporation in the Peoples Republic of China there is a very high incidence (greater than 1% per year) of lung cancer among the miners [300 ug of selenium in malt cakes or placebo].
Glutathione peroxidase activity was increased 155.7%, where the lipid peroxide levels were reduced 74.5% as compared to placebo. Selenium was safe and effective for humans as a chemoprotective agent and supports a preventive trial against lung cancers.
"Intervention Trial in Selenium For The Prevention of Lung Cancer Among Tin Miners in Yunnan, China", Yu, Shu-Yu, et al, Biological Trace Element Research, 1990;24:105-108.
Vitamin A & Lung Cancer
Vitamin A & Beta-Carotene
It was found that lower consumption of preformed vitamin A and beta-carotene correlated with epidermoid lung cance, confirming the protective role of beta-carotene against lung cancer and preformed vitamin A may also have a protective effect. Vitamin A is suggested to inhibit tumor promotion while beta-carotene inhibits tumor initiation.
"Dietary Vitamin A, Beta-Carotene and Risk of Epidermoid Lung Cancer in Southwestern France", Dartigues, J.F., et al, European Journal of Epidemiology, 1990;6(3):261-265.
Vitamin E & Lung Cancer
It was found vitamin E was lower in hospitalized patients with lung cancer than in matched hospitalized control patients even after adjustment for cholesterol levels. Low serum vitamin E levels may be associated with increased lung cancer risk.
"A Case-Controlled Study of Serum Vitamins A, E and C in Lung Cancer Patients", LeGardeur, BY. et al, Nutrition and Cancer, 1990;14:133-140.
Carcinogens
Diesel Exhaust
While some studies show that diesel exhaust is a probable carcinogen, human evidence of carcinogenicity remains limited. Out of 30 studies conducted on the relationship between diesel exhaust and lung cancer, only 4 have obtained either quantitative data on current exposure or semiquantitative data on historical exposure. There also may be misclassifications of exposure. Most studies in the meta-analysis infer diesel exhaust exposure on the basis of job title rather than individual exposure information. Further study is warranted beyond a meta-analysis to clarify if diesel exhaust is a human carcinogen.
Silverman, Debra T.: Is Diesel Exhaust a Human Lung Carcinogen? Epidemiology, January, 1998;9(1):4-5.
Genistein
Genistein
Genistein, the active metabolite in soy products, may be an effective anti-cancer agent, according to this study. In clinical experiments, this metabolite inhibited the growth of lung cancer cells in vitro. Further experiments demonstrated that genistein may suppress cancerous mutated genes while increasing the expression of the normal genotype.
Lian F, Li Y, Bhuiyan M, Sarkar FH: p53-independent apoptosis induced by genistein in lung cancer cells, Nutr Cancer 1999;33(2):125-31
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