Martínez M E, McPherson R S, Annegers J F, Levin B
University of Texas-Houston Health Science Center, School of Public Health, USA.
J Natl Cancer Inst. 1995 Feb 15;87(4):274-9. doi: 10.1093/jnci/87.4.274.
Results of epidemiologic studies suggest that there is limited evidence for the association between cigarette smoking and risk of colorectal cancer. Cigarette smoking has been shown to increase the risk of colorectal adenomatous polyps, which are recognized as precursors of colorectal cancer, while few studies have examined the association between alcohol consumption and the development of adenomatous polyps.
We examined the association between cigarette smoking, alcohol consumption, and the presence of colorectal adenomatous polyps.
Analyses were based on data from a case-control study of dietary and other lifestyle factors for colorectal adenomatous polyps. We assessed the risk of adenomatous polyps associated with total number of years of smoking, number of cigarettes smoked per day, and pack-years of smoking for past and current smokers separately. We also assessed the joint association between cigarette smoking and alcohol consumption on the risk of adenomatous polyps.
Current smokers who smoked more than 20 pack-years were at significantly higher risk of adenomatous polyps compared with never smokers (odds ratio [OR] = 2.56; 95% confidence interval [CI] = 1.28-5.14). Past smokers also had an increased risk of having adenomatous polyps, but no clear trend was observed for pack-years of smoking. Alcohol consumption was positively associated with risk of adenomatous polyps. Compared with nondrinkers, the strongest risk was observed for individuals who consumed 2.31-9.46 g alcohol per day (OR = 2.23; 95% CI = 1.29-3.83), and a decrease in risk was observed for individuals who consumed 9.47-67.36 g alcohol per day (OR = 1.63; 95% CI = 0.92-2.88). Among current smokers, a joint effect was observed for individuals who smoked and drank compared with those who never smoked and were not current drinkers (OR = 4.21; 95% CI = 1.88-9.41). For past smokers, a significant joint effect of smoking and current alcohol consumption was also observed, but the risk was not as strong as that for current smokers (OR = 2.61; 95% CI = 1.40-4.87).
These data provide further evidence of the positive association between cigarette smoking and the development of colorectal adenomatous polyps. The combination of cigarette smoking and alcohol consumption increased the risk of adenomatous polyps.
Future research should focus on the understanding of the role of cigarette smoking and alcohol consumption as these two factors relate to the evolution of colorectal adenomatous polyps and subsequent carcinogenesis.
流行病学研究结果表明，吸烟与结直肠癌风险之间的关联证据有限。吸烟已被证明会增加结直肠腺瘤性息肉的风险，而结直肠腺瘤性息肉被认为是结直肠癌的前体，不过很少有研究探讨饮酒与腺瘤性息肉发生之间的关联。
我们研究了吸烟、饮酒与结直肠腺瘤性息肉存在情况之间的关联。
分析基于一项关于结直肠腺瘤性息肉的饮食及其他生活方式因素的病例对照研究数据。我们分别评估了过去和现在吸烟者的吸烟总年数、每日吸烟量以及吸烟包年数与腺瘤性息肉相关的风险。我们还评估了吸烟与饮酒对腺瘤性息肉风险的联合关联。
与从不吸烟者相比，当前吸烟超过20包年的人患腺瘤性息肉的风险显著更高（优势比[OR]=2.56；95%置信区间[CI]=1.28 - 5.14）。既往吸烟者患腺瘤性息肉的风险也有所增加，但未观察到吸烟包年数的明显趋势。饮酒与腺瘤性息肉风险呈正相关。与不饮酒者相比，每日摄入2.31 - 9.46克酒精的个体风险最高（OR = 2.23；95% CI = 1.29 - 3.83），而每日摄入9.47 - 67.36克酒精的个体风险降低（OR = 1.63；95% CI = 0.92 - 2.88）。在当前吸烟者中，与从不吸烟且不饮酒者相比，吸烟且饮酒的个体存在联合效应（OR = 4.21；95% CI = 1.88 - 9.41）。对于既往吸烟者，也观察到吸烟与当前饮酒的显著联合效应，但风险不如当前吸烟者那么强（OR = 2.61；95% CI = 1.40 - 4.87）。
这些数据进一步证明了吸烟与结直肠腺瘤性息肉发生之间存在正相关。吸烟与饮酒的结合增加了腺瘤性息肉的风险。
未来的研究应专注于理解吸烟和饮酒这两个因素在结直肠腺瘤性息肉演变及后续致癌过程中的作用。
