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Nutritional Epidemiology

Lung Cancer in Humans Is Not Associated with Lifetime Total Alcohol Consumption or with Genetic Variation in Alcohol Dehydrogenase 3 (ADH₃)^1,2

Jo L. Freudenheim^*,3, Malathi Ram, Jing Nie^*, Paola Muti^*, Maurizio Trevisan^*, Peter G. Shields, Elisa V. Bandera, Lucy A Campbell, Susan E. McCann^*, Holger J. Schunemann^*,, Anne Marie Carosella^*, Dominica Vito^*, Marcia Russell^#, Thomas H. Nochajski^** and Radoslav Goldman

Departments of ^* Social and Preventive Medicine, School of Public Health and Health Professions and Department of Medicine and the ^** School of Social Work, University at Buffalo, State University of New York, Buffalo, NY, 14260; Department of International Health, Johns Hopkins School of Public Health, Baltimore, MD, 21205; Lombardi Cancer Center, Georgetown University, Washington, D.C. 20057-1421; The Cancer Institute of New Jersey, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ 08903; and ^# Prevention Research Center, Pacific Institute for Research and Evaluation, Berkeley, CA 94704

³To whom correspondence should be addressed. E-mail: jfreuden{at}buffalo.edu.

Although there is clear evidence that smoking is the primary risk factor for lung cancer, not all variation in disease risk is understood. There is some evidence that alcohol may contribute to risk. We examined lifetime and recent (12–24 mo previous) alcohol consumption in relation to risk of lung cancer in a case-control study in western New York. In addition we examined the alcohol dehydrogenase 3 (ADH₃) genotype in relation to lung cancer risk; ADH₃ is rate limiting in alcohol metabolism and has a functional polymorphism. We interviewed incident, primary, histologically confirmed lung cancer cases (n = 111) in two counties. Controls were randomly selected from among those residing in the counties, frequency-matched to cases for age and race (n = 1546). Lifetime and recent total alcohol and beverage-specific alcohol consumption as well as relevant confounders were assessed by interview. ADH₃ genotype was evaluated by a PCR-restriction fragment length polymorphism assay. Because of the small sample size, power was limited and CI were wide. Residual confounding by smoking remains a concern. Although we found a significant trend for increased risk for beer consumption in the recent period (odds ratio 1.67, 95% CI 0.96–2.92, P for trend = 0.05), chance cannot be ruled out as an explanation. We found no evidence of risk related to lifetime alcohol consumption nor evidence that alcohol dehydrogenase genotype modifies risk related to alcohol and lung cancer.

KEY WORDS: • alcohol consumption • alcohol dehydrogenase • epidemiology • humans • lung cancer

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