Alcohol consumption and risk of lung cancer: a pooled analysis of cohort studies

被引:82
|
作者
Freudenheim, JL
Ritz, J
Smith-Warner, SA
Albanes, D
Bandera, EV
van den Brandt, PA
Colditz, G
Feskanich, D
Goldbohm, RA
Harnack, L
Miller, AB
Rimm, E
Rohan, TE
Sellers, TA
Virtamo, J
Willett, WC
Hunter, DJ
机构
[1] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14214 USA
[2] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA
[3] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA
[4] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA
[5] NCI, Canc Prevent Studies Branch, Div Clin Sci, Bethesda, MD 20892 USA
[6] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Canc Inst New Jersey, New Brunswick, NJ USA
[7] Maastricht Univ, Dept Epidemiol, Maastricht, Netherlands
[8] Harvard Univ, Ctr Canc Prevent, Boston, MA 02115 USA
[9] Harvard Univ, Channing Lab, Brigham & Womens Hosp, Boston, MA 02115 USA
[10] TNO, Nutr & Food Res Inst, Dept Epidemiol, NL-3700 AJ Zeist, Netherlands
[11] Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA
[12] Univ Toronto, Fac Med, Dept Publ Hlth Sci, Toronto, ON, Canada
[13] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA
[14] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA
[15] Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, Helsinki, Finland
来源
关键词
alcohol consumption; diet; epidemiology; lung neoplasms; meta-analysis;
D O I
10.1093/ajcn/82.3.657
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
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 3 137 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 alcohol/d than for that of 0 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.
引用
收藏
页码:657 / 667
页数:11
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