CancerCausesand Control,3,
361 - 369
Alcohol consumption and lung cancer in White males Elisa V. Bandera, Jo L. Freudenheim, Saxon Graham, James R. Marshall, Brenda P. Haughey, Mya Swanson, John Brasure, and Gregg Wilkinson (Received 25 February 1992; accepted in revisedform 16 April 1992) Experimental and epidemiologic investigations in alcoholic and nonalcoholic populations have suggested a role of alcohol in lung carcinogenesis. The association between alcohol consumption and lung cancer was investigated among 280 White males with histologically confirmed, primary lung cancer and 564 White male controls, participants in the Western New York Diet Study (United States). Among heavy smokers (over 40 pack-years), total alcohol consumption was associated with an increased risk of lung cancer with adjustment for age, years of education, pack-years of cigarette smoking, and intake of carotenoids and fat. In this group, the odds ratio for drinkers of more than 24 drinks per month was 1.6 compared with those who drank less. Drinkers of more than 12 beers per month were 1.6 times more likely to develop lung cancer than nondrinkers of beer after controlling for age, years of education, and cigarette smoking (95 percent confidence interval = 1.0-2.4, P for trend =0.003). Occupational and dietary factors did not seem to explain these findings. Although cigarette smoking is the major cause of lung cancer, the role of alcohol, independent or in interaction with cigarette smoking, deserves further investigation.
Key words: Alcohol, B-carotene, diet, fat, lung cancer, United States.
Introduction Although the role of cigarette smoking in lung cancer etiology is well accepted, it does not explain all the variation in disease distribution. Other factors, such as diet and alcohol, also may play a role. Mortality studies on alcoholic cohorts suggest an association between alcohol consumption and lung cancer. All of these studies ~-s have reported increased lung cancer mortality among alcoholics. There is some indication from epidemiologic investigations in nonalcoholic populations that alcohol may play an etiologic role in lung cancer.
Correlation,9.n case-control,12,~and cohort 14-~sstudies have reported a relationship between alcohol consumption and lung cancer. However, these findings were not consistent.19-~This discrepancy in results may derive at least in part from issues such as small sample size2°and the choice of comparison group. "~° Further, the assessment of alcohol intake varied from one study to another. Many investigators queried subjects only about their frequency of intake, and some only about their intensity of intake. This could introduce severe
Drs Bandera, Freudenheim, Graham, and Marshall, Ms Swanson, and Mr Brasure are with the Department of Socialand Preventive Medicine, State University of New York at Buffalo, Buffalo, NY, USA. Dr Haughey is with the School of Nursing, State University of New York at Buffalo, Buffalo, NY, USA. Dr Wilkinson is with Department of Preventive Medicine and Community Health, University of Texas Medical Branch, Galveston, TX, USA. Address correspondence to Dr Bandera, Department of Social and Preventive Medicine, State University of New York at Buffalo, 270 Father Hall, Buffalo, N Y 14214, USA. This investigation was supported in part by US Public Health Service Grants CA 09051 and CA 11535, and American Cancer Society Grant PD T-434. These data werepresented, in part, at the AnnuaI Meeting of the Federation of American Societies of Experimental Biology, Atlanta, GA, USA, 1991;and at the Annual Meeting of the Societyfor Epidemiologic Research, Buffalo, NY, USA, 1991. © 1992 Rapid Communications of Oxford Ltd
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misclassification of alcohol exposure; e.g., a person drinking heavily once a week would be classified as a light drinker if only frequency were assessed. Another important issue confronted by investigations of the relationship between lung cancer and alcohol consumption has been the adjustment for cigarette smoking, given the positive correlation of alcohol drinking and cigarette smoking. Finally, the majority of previous studies of this association did not take into account dietary and occupational factors. The objective of this investigation was to examine further the role of total alcohol, and of wine, beer, and hard liquor consumption on lung cancer risk, taking into account the effects of cigarette smoking and other confounding variables in a population of White male residents of western New York State (United States).
Materials and methods The methods utilized in this case-control study have been described in detail elsewhere. 22Briefly, during the period from August 1980 to July 1984, cases between the ages of 35 and 79 years were identified from pathology records in all major hospitals in Erie, Niagara, and Monroe counties in western New York State. All lung cancer cases were incident, primary, and histologically confirmed. Those cases with a history of lung cancer at another site were excluded to minimize the possibility that the lung cancer might be, in fact, metastatic disease. Interviews were conducted approximately three months after diagnosis. Of the 1,663 lung cancer cases (males and females) initially identified, 273 died before the interview could be scheduled and 174 were too ill to be interviewed (approximate duration 2.5 h). Physician permission to contact the case could not be obtained for 461 cases; 237 cases refused to participate; 28 could not be located; and 40 had language or hearing problems that precluded their interview. A total of 450 cases were interviewed successfully. Controls were between the ages of 35 and 79 and residents of the same counties as the cases, who had participated as controls in a series of case-control studies of gastrointestinal tract cancer. All of these controls selected between August 1980 and July 1984 were pooled to form a single control group for this investigation. Controls for these studies were selected following a standardized protocol requiring interviewers to visit systematically those residences closest to the home of the case. In these studies, controls were matched to cases on age (within five years), sex, and neighborhood. Controls with a history of cancer were excluded. All potential controls were informed of the interview's length; 42 percent agreed to participate. Because of our inability to interview a portion of both 362
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the cases and controls, this study cannot be considered a population-based study; rather it must be viewed as a series of cases and controls whom we were able to interview successfully. The implications of this are outlined in detail in the Discussion section below. Because of the relatively small number of females interviewed (154 cases and 315 controls) and their limited alcohol consumption (median consumption of wine, beer, and hard liquor in drinks per month was 1, 0, and 1, respectively), this investigation was restricted to males. After excluding females and those males with missing values for the study variables, 280 cases and 564 controls remained. All subjects were interviewed in their homes by carefully trained interviewers. Usual dietary and drinking habits were ascertained for one year prior to the onset of symptoms of cancer for cases and up to the time of interview for controls. The reliability of alcohol consumption was evaluated among a 10 percent random sample of the total group participating in the Western New York Diet Study (a series of case-control studies of cancer). They were recontacted by phone between one and three months after the initial interview and asked to respond to some of the questions regarding alcohol consumption in the original questionnaire, including frequency and quantity of wine and beer intake. Spearman correlation coefficients between answers to the original and repeated questions for beer and wine (in drinks/ month) were 0.7 and 0.6, respectively. The level of agreement was very similar in cases and controls. The reliability of the food frequency questionnaire also was tested and results are reported elsewhere.22 Subjects were questioned about their consumption of beer, wine, and hard liquor. When asked, for example, "Do you drink beer?", only those responding "yes, presently" were considered current drinkers of beer. Those answering "yes, but not presently, ~ that is, ex-drinkers, were grouped with nondrinkers. Because we were concerned about the appropriateness of this comparison group (a mixture of never drinkers and exdrinkers), analyses also were performed excluding exdrinkers. Current drinkers of beer were then asked to report their frequency of consumption in one of five categories: times per week (daily, 6, 5, 4, 3, 2, or 1); times per month (3, 2, or 1); less than once per month but more than once per year; once per year; or less than once per year. They were asked also to report the quantity of intake. These questions were repeated for wine and hard liquor. Consumption of wine, beer, and hard liquor (in drinks per month) was calculated by multiplying the self-reported frequency of consumption per month of each type of alcoholic beverage by the number of glasses consumed per occasion. Since the alcohol contents of standard drinks of beer, wine, and
Alcohol and lung cancer
hard liquor are approximately equivalent, total alcohol consumption was computed by adding the number of drinks of beer, wine, and liquor consumed per month. A lifetime history of cigarette smoking was obtained. Subjects also were asked to report their current smoking status (never smoker, ex-smoker, or smoker). The number of years of cigarette smoking was ascertained by querying subjects about the years when they smoked, and taking into account periods of time in which they quit smoking for more than a year. Smokers and ex-smokers then were asked to report the number of packs per day of cigarettes (>2; 1-2; 1; 0.5-1;
361 - 369
Alcohol consumption and lung cancer in White males Elisa V. Bandera, Jo L. Freudenheim, Saxon Graham, James R. Marshall, Brenda P. Haughey, Mya Swanson, John Brasure, and Gregg Wilkinson (Received 25 February 1992; accepted in revisedform 16 April 1992) Experimental and epidemiologic investigations in alcoholic and nonalcoholic populations have suggested a role of alcohol in lung carcinogenesis. The association between alcohol consumption and lung cancer was investigated among 280 White males with histologically confirmed, primary lung cancer and 564 White male controls, participants in the Western New York Diet Study (United States). Among heavy smokers (over 40 pack-years), total alcohol consumption was associated with an increased risk of lung cancer with adjustment for age, years of education, pack-years of cigarette smoking, and intake of carotenoids and fat. In this group, the odds ratio for drinkers of more than 24 drinks per month was 1.6 compared with those who drank less. Drinkers of more than 12 beers per month were 1.6 times more likely to develop lung cancer than nondrinkers of beer after controlling for age, years of education, and cigarette smoking (95 percent confidence interval = 1.0-2.4, P for trend =0.003). Occupational and dietary factors did not seem to explain these findings. Although cigarette smoking is the major cause of lung cancer, the role of alcohol, independent or in interaction with cigarette smoking, deserves further investigation.
Key words: Alcohol, B-carotene, diet, fat, lung cancer, United States.
Introduction Although the role of cigarette smoking in lung cancer etiology is well accepted, it does not explain all the variation in disease distribution. Other factors, such as diet and alcohol, also may play a role. Mortality studies on alcoholic cohorts suggest an association between alcohol consumption and lung cancer. All of these studies ~-s have reported increased lung cancer mortality among alcoholics. There is some indication from epidemiologic investigations in nonalcoholic populations that alcohol may play an etiologic role in lung cancer.
Correlation,9.n case-control,12,~and cohort 14-~sstudies have reported a relationship between alcohol consumption and lung cancer. However, these findings were not consistent.19-~This discrepancy in results may derive at least in part from issues such as small sample size2°and the choice of comparison group. "~° Further, the assessment of alcohol intake varied from one study to another. Many investigators queried subjects only about their frequency of intake, and some only about their intensity of intake. This could introduce severe
Drs Bandera, Freudenheim, Graham, and Marshall, Ms Swanson, and Mr Brasure are with the Department of Socialand Preventive Medicine, State University of New York at Buffalo, Buffalo, NY, USA. Dr Haughey is with the School of Nursing, State University of New York at Buffalo, Buffalo, NY, USA. Dr Wilkinson is with Department of Preventive Medicine and Community Health, University of Texas Medical Branch, Galveston, TX, USA. Address correspondence to Dr Bandera, Department of Social and Preventive Medicine, State University of New York at Buffalo, 270 Father Hall, Buffalo, N Y 14214, USA. This investigation was supported in part by US Public Health Service Grants CA 09051 and CA 11535, and American Cancer Society Grant PD T-434. These data werepresented, in part, at the AnnuaI Meeting of the Federation of American Societies of Experimental Biology, Atlanta, GA, USA, 1991;and at the Annual Meeting of the Societyfor Epidemiologic Research, Buffalo, NY, USA, 1991. © 1992 Rapid Communications of Oxford Ltd
Cancer Causes and Control. Vol 3. 1992
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E. V. Bandera et al
misclassification of alcohol exposure; e.g., a person drinking heavily once a week would be classified as a light drinker if only frequency were assessed. Another important issue confronted by investigations of the relationship between lung cancer and alcohol consumption has been the adjustment for cigarette smoking, given the positive correlation of alcohol drinking and cigarette smoking. Finally, the majority of previous studies of this association did not take into account dietary and occupational factors. The objective of this investigation was to examine further the role of total alcohol, and of wine, beer, and hard liquor consumption on lung cancer risk, taking into account the effects of cigarette smoking and other confounding variables in a population of White male residents of western New York State (United States).
Materials and methods The methods utilized in this case-control study have been described in detail elsewhere. 22Briefly, during the period from August 1980 to July 1984, cases between the ages of 35 and 79 years were identified from pathology records in all major hospitals in Erie, Niagara, and Monroe counties in western New York State. All lung cancer cases were incident, primary, and histologically confirmed. Those cases with a history of lung cancer at another site were excluded to minimize the possibility that the lung cancer might be, in fact, metastatic disease. Interviews were conducted approximately three months after diagnosis. Of the 1,663 lung cancer cases (males and females) initially identified, 273 died before the interview could be scheduled and 174 were too ill to be interviewed (approximate duration 2.5 h). Physician permission to contact the case could not be obtained for 461 cases; 237 cases refused to participate; 28 could not be located; and 40 had language or hearing problems that precluded their interview. A total of 450 cases were interviewed successfully. Controls were between the ages of 35 and 79 and residents of the same counties as the cases, who had participated as controls in a series of case-control studies of gastrointestinal tract cancer. All of these controls selected between August 1980 and July 1984 were pooled to form a single control group for this investigation. Controls for these studies were selected following a standardized protocol requiring interviewers to visit systematically those residences closest to the home of the case. In these studies, controls were matched to cases on age (within five years), sex, and neighborhood. Controls with a history of cancer were excluded. All potential controls were informed of the interview's length; 42 percent agreed to participate. Because of our inability to interview a portion of both 362
Cancer Causes and Control. Vol 3. 1992
the cases and controls, this study cannot be considered a population-based study; rather it must be viewed as a series of cases and controls whom we were able to interview successfully. The implications of this are outlined in detail in the Discussion section below. Because of the relatively small number of females interviewed (154 cases and 315 controls) and their limited alcohol consumption (median consumption of wine, beer, and hard liquor in drinks per month was 1, 0, and 1, respectively), this investigation was restricted to males. After excluding females and those males with missing values for the study variables, 280 cases and 564 controls remained. All subjects were interviewed in their homes by carefully trained interviewers. Usual dietary and drinking habits were ascertained for one year prior to the onset of symptoms of cancer for cases and up to the time of interview for controls. The reliability of alcohol consumption was evaluated among a 10 percent random sample of the total group participating in the Western New York Diet Study (a series of case-control studies of cancer). They were recontacted by phone between one and three months after the initial interview and asked to respond to some of the questions regarding alcohol consumption in the original questionnaire, including frequency and quantity of wine and beer intake. Spearman correlation coefficients between answers to the original and repeated questions for beer and wine (in drinks/ month) were 0.7 and 0.6, respectively. The level of agreement was very similar in cases and controls. The reliability of the food frequency questionnaire also was tested and results are reported elsewhere.22 Subjects were questioned about their consumption of beer, wine, and hard liquor. When asked, for example, "Do you drink beer?", only those responding "yes, presently" were considered current drinkers of beer. Those answering "yes, but not presently, ~ that is, ex-drinkers, were grouped with nondrinkers. Because we were concerned about the appropriateness of this comparison group (a mixture of never drinkers and exdrinkers), analyses also were performed excluding exdrinkers. Current drinkers of beer were then asked to report their frequency of consumption in one of five categories: times per week (daily, 6, 5, 4, 3, 2, or 1); times per month (3, 2, or 1); less than once per month but more than once per year; once per year; or less than once per year. They were asked also to report the quantity of intake. These questions were repeated for wine and hard liquor. Consumption of wine, beer, and hard liquor (in drinks per month) was calculated by multiplying the self-reported frequency of consumption per month of each type of alcoholic beverage by the number of glasses consumed per occasion. Since the alcohol contents of standard drinks of beer, wine, and
Alcohol and lung cancer
hard liquor are approximately equivalent, total alcohol consumption was computed by adding the number of drinks of beer, wine, and liquor consumed per month. A lifetime history of cigarette smoking was obtained. Subjects also were asked to report their current smoking status (never smoker, ex-smoker, or smoker). The number of years of cigarette smoking was ascertained by querying subjects about the years when they smoked, and taking into account periods of time in which they quit smoking for more than a year. Smokers and ex-smokers then were asked to report the number of packs per day of cigarettes (>2; 1-2; 1; 0.5-1;
