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ORIGINAL RESEARCH COMMUNICATION |
1 From the Department of Social and Preventive Medicine, University at Buffalo, State University of New York, Buffalo, NY (JLF); the Departments of Biostatistics (JR), Nutrition (SAS-W, ER, WCW, and DJH), and Epidemiology (SAS-W, GC, ER, WCW, and DJH), Harvard School of Public Health, Boston, MA; the Cancer Prevention Studies Branch, Division of Clinical Sciences, National Cancer Institute, Bethesda, MD (DA); the Cancer Institute of New Jersey, UMDNJ–Robert Wood Johnson Medical School, New Brunswick, NJ (EVB); the Department of Epidemiology, Maastricht University, Maastricht, Netherlands (PAB); Harvard Center for Cancer Prevention, Boston, MA (GC, WCW, and DJH); the Channing Laboratory, Harvard Medical School/Brigham and Women's Hospital, Boston, MA (GC, DF, WCW, and DJH); the Department of Epidemiology, TNO Nutrition and Food Research Institute, Zeist, Netherlands (RAG); the Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, MN (LH); the Department of Public Health Sciences, Faculty of Medicine, University of Toronto, Toronto, Canada (ABM); the Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY (TER); Cancer Prevention and Control, H Lee Moffitt Cancer Center and Research Institute, Tampa, FL (TAS); and the Department of Epidemiology and Health Promotion, National Public Health Institute, Helsinki, Finland (JV)
Background: Although smoking is the primary cause of lung cancer, much is unknown about lung cancer etiology, including risk determinants for nonsmokers and modifying factors for smokers.
Objective: We hypothesized that alcohol consumption contributes to lung cancer risk.
Design: We conducted a pooled analysis using standardized exposure and covariate data from 7 prospective studies with 399 767 participants and 3137 lung cancer cases. Study-specific relative risks (RRs) and CIs were estimated and then combined to calculate pooled multivariate RRs by using a random-effects model.
Results: We found a slightly greater risk for the consumption of 
30 g alcohol/d than for that of 0 g alcohol/d in men (RR: 1.21; 95% CI: 0.91, 1.61; P for trend = 0.03) and in women (RR: 1.16; 95% CI: 0.94, 1.43; P for trend = 0.03). In male never smokers, the RR for consumption of 15 g alcohol/d rather than 0 g alcohol/d was 6.38 (95% CI: 2.74, 14.9; P for trend < 0.001). In women, there were few never-smoking cases and no evidence of greater risk (RR: 1.35; 95% CI: 0.64, 2.87). Because of possible residual confounding by smoking, we performed sensitivity analyses by reclassifying the never smokers in the highest drinking category as former smokers. Resulting associations for alcohol consumption were somewhat attenuated, but P for trend = 0.05 for men, which was near the original P = 0.03.
Conclusions: A slightly greater risk of lung cancer was associated with the consumption of 30 g alcohol/d than with no alcohol consumption. Alcohol consumption was strongly associated with greater risk in male never smokers. Residual confounding by smoking may explain part of the observed relation.
Key Words: Alcohol consumption • diet • epidemiology • lung neoplasms • meta-analysis
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