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Background: Epidemiologic studies have suggested that vitamin E and [Bets]-carotene may each influence the development of prostate cancer. In the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, a controlled trial, we studied the effect of [Alpha]-tocopherol (a form of vitamin E) and [Beta]-carotene supplementation, separately or together, on prostate cancer in male smokers. Methods: A total of 29133 male smokers aged 50-69 years from southwestern Finland were randomly assigned to receive [Alpha]-tocopherol (50 mg), [Beta]-carotene (20 mg), both agents, or placebo daily for 5-8 years (median, 6.1 years). The supplementation effects were estimated by a proportional hazards model, and two-sided P values were calculated. Results: We found 246 new cases of and 62 deaths from prostate cancer during the follow-up period. A 32% decrease (95% confidence interval [CI] = -47% to -12%) in the incidence of prostate cancer was observed among the subjects receiving [Alpha]-tocopherol (n = 14564) compared with those not receiving it (n = 14 569). The reduction was evident in clinical prostate cancer but not in latent cancer. Mortality from prostate cancer was 41% lower (95% CI = -65% to -1%) among men receiving [Alpha]-tocopherol. Among subjects receiving [Beta]-carotene (n = 14560), prostate cancer incidence was 23% higher (95% CI = -4%-59%) and mortality was 15% higher (95% CI = -30%-89%) compared with those not receiving it (n = 14573). Neither agent had any effect on the time interval between diagnosis and death. Conclusions: Long-term supplementation with [Alpha]-tocopherol, substantially reduced prostate cancer incidence and mortality in male smokers. Other controlled trials are required to confirm the findings. [J Natl Cancer Inst 1998;90:440-6]

Background: Cigarette smoking is responsible for at least one third of all cancer deaths annually in the United States. Few sources exist in the peer-reviewed literature documenting state and regional differences in smoking behavior, despite the fact that cancer prevention and control efforts are increasingly being implemented below the national level. Purpose: Our goals were to determine smoking prevalence rates among men and women, by region, and for each of the 50 states and the District of Columbia from census survey data collected in 1992 and 1993 and to compare these rates with rates determined in 1985. Methods: Every month, the U.S. Bureau of the Census collects labor force statistics on more than 100 000 individuals on its Current Population Survey (CPS). For the September 1992, January 1993, and May 1993 CPS, the National Cancer Institute sponsored a 40-item Tobacco Use Supplement. The definition of a current smoker changed slightly between 1985 and 1992-1993. For the 1985 CPS, individuals were considered current smokers if they had smoked 100 cigarettes in their lifetime and were smoking at the time of interview; for the 1992-1993 CPS, current smokers included anyone who had smoked 100 cigarettes and was currently smoking every day or just on some days. We calculated current smoking rates (every day and some days combined) based on more than a quarter million adults (n = 266 988) interviewed in 1992-1993. Results: Substantial geographic variation exists in rates of current cigarette use among adults within the United States. In general, adults in the southern United States have higher rates of smoking and adults in the western states have lower rates of smoking than adults in the rest of the country, although differences in smoking behavior between men and women and among various racial and ethnic populations strongly influence these patterns. Only two states, Kentucky and West Virginia, exhibited adult smoking rates (men and women combined) of 30% or higher in 1992-1993; in contrast, in 1985, such rates were reported from 20 states. The only states in which the prevalence was below 20% in 1992-1993 were Utah (17.1%) and California (19.5%). Rates approaching 20% were reported from New Jersey (20.7%), Massachusetts (21.5%), and Nebraska, New York, and Hawaii (22.0% each) in 1992-1993. Rhode Island experienced the greatest relative decline in smoking prevalence from 1985 to 1992-1993, with a calculated relative change of -30.7% (based on a change in rate from 33.5% to 23.2%), followed by Delaware (-25.9%), the District of Columbia and New Jersey (-23.9% each), Connecticut (-23.2%), California (-22.9%), Alaska (-22.8%), Georgia (-22.6%), Massachusetts (-22.1%), and New York (-22.0%). Conclusions: Smoking rates are not uniform in the United States but vary considerably from state to state, even within the same region of the country. The CPS is the only mechanism currently capable of simultaneously monitoring smoking trends nationally, regionally, and on a state-by-state basis.

Background: Experimental and epidemiologic investigations suggest that [alpha]-tocopherol (the most prevalent chemical form of vitamin E found in vegetable oils, seeds, grains, nuts, and other foods) and [beta]-carotene (a plant pigment and major precursor of vitamin A found in many yellow, orange, and dark-green, leafy vegetables and some fruit) might reduce the risk of cancer, particularly lung cancer. The initial findings of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study) indicated, however, that lung cancer incidence was increased among participants who received [beta]-carotene as a supplement. Similar results were recently reported by the Beta-Carotene and Retinol Efficacy Trial (CARET), which tested a combination of [beta]-carotene and vitamin A. Purpose: We examined the effects of a-tocopherol and [beta]-carotene supplementation on the incidence of lung cancer across subgroups of participants in the ATBC Study defined by base-line characteristics (e.g., age, number of cigarettes smoked, dietary or serum vitamin status, and alcohol consumption), by study compliance, and in relation to clinical factors, such as disease stage and histologic type. Our primary purpose was to determine whether the pattern of intervention effects across subgroups could facilitate further interpretation of the main ATBC Study results and shed light on potential mechanisms of action and relevance to other populations. Methods: A total of 29 133 men aged 50-69 years who smoked five or more cigarettes daily were randomly assigned to receive [alpha]-tocopherol (50 mg), [beta]-carotene (20 mg), [alpha]-tocopherol and [beta]-carotene, or a placebo daily for 5-8 years (median, 6.1 years). Data regarding smoking and other risk factors for lung cancer and dietary factors were obtained at study entry, along with measurements of serum levels of [alpha]-tocopherol and [beta]-carotene. Incident cases of lung cancer (n = 894) were identified through the Finnish Cancer Registry and death certificates. Each lung cancer diagnosis was independently confirmed, and histology or cytology was available for 94% of the cases. Intervention effects were evaluated by use of survival analysis and proportional hazards models. All P values were derived from two-sided statistical tests. Results: No overall effect was observed for lung cancer from [alpha]-tocopherol supplementation (relative risk [RR] = 0.99; 95% confidence interval [CI] = 0.87-1.13; P = .86, logrank test). [beta]-Carotene supplementation was associated with increased lung cancer risk (RR = 1.16; 95% CI = 1.02-1.33; P = .02, logrank test). The 13-carotene effect appeared stronger, but not substantially different, in participants who smoked at least 20 cigarettes daily (RR = 1.25; 95% CI = 1.07-1.46) compared with those who smoked five to 19 cigarettes daily (RR = 0.97; 95% CI = 0.76-1.23) and in those with a higher alcohol intake ([greater than or equal to]11 g of ethanol/day just under one drink per day]; RR = 1.35; 95% CI = 1.01-1.81) compared with those with a lower intake (RR = 1.03; 95% CI = 0.85-1.24). Conclusions: Supplementation with [alpha]-tocopherol or [beta]-carotene does not prevent lung cancer in older men who smoke. [beta]-Carotene supplementation at pharmacologic levels may modestly increase lung cancer incidence in cigarette smokers, and this effect may be associated with heavier smoking and higher alcohol intake. Implications: While the most direct way to reduce lung cancer risk is not to smoke tobacco, smokers should avoid high-dose [beta]-carotene supplementation.