ARE RACIAL-DIFFERENCES IN SQUAMOUS-CELL ESOPHAGEAL CANCER EXPLAINED BY ALCOHOL AND TOBACCO USE
ARE RACIAL-DIFFERENCES IN SQUAMOUS-CELL ESOPHAGEAL CANCER EXPLAINED BY ALCOHOL AND TOBACCO USE
复制标题
DOI：
10.1093/jnci/86.17.1340
复制
发表时间：
1994-09-07
期刊：
影响因子：
--
通讯作者：
POTTERN, LM
中科院分区：
文献类型：
--
作者：
BROWN, LM;HOOVER, RN;POTTERN, LM
背景资料：在美国，鳞状细胞食管癌的发病率在黑人男性中比在白色男性中高五倍以上。人们正在寻找可能解释这种巨大种族差异的原因。目的：我们评估了酒精和烟草的不同使用是否可以完全解释美国黑人中鳞状细胞食管癌的过量。研究方法：我们进行了一项基于人群的病例对照研究，对来自美国三个地理区域的373例鳞状细胞食管癌病例患者（124例白色男性和249例黑人男性）和1364例对照受试者（750例白色男性和614例黑人男性）进行了面对面访谈。纳入了1986年8月1日至1989年4月30日在年龄30-79岁的白色和黑人男性中新诊断的经组织学证实的鳞状细胞食管癌病例。结果如下：每天饮酒超过一杯和/或目前每天吸烟至少一包的占92.7%（95%置信区间[CI] = 86.8%-98.5%），而黑人鳞状细胞食管癌的95%置信区间[CI]= 86.3%（95% CI = 75.5%-97.1%），黑人和白色人之间的年发病率差异为93%。在logistic回归分析中，种族和持续饮酒/吸烟变量之间的相互作用具有统计学显著性（双侧，P = .02）。对照组在所有酒精和烟草使用水平下的暴露率在黑人中略高，占发病率种族差异的一小部分。结论：尽管我们的数据中绝大多数黑人和白人的食管癌都可以通过使用酒精和烟草来解释，但目前尚不清楚为什么大量饮酒和/或吸烟会导致黑人每年每10万人中有14.9例鳞状细胞食管癌病例比白人多。比值比的差异似乎比单独暴露于酒精和烟草的患病率更能解释发病率的种族差异。相同水平的酒精和烟草使用的致癌风险存在明显种族差异的原因尚不清楚，但可能包括酒精消费的质的差异，与酒精和/或烟草相互作用以改变风险的其他环境暴露的差异，或对这些因素的敏感性差异。
Background: In the United States, incidence rates of squamous cell esophageal cancer are more than five times higher among black men than among white men. Reasons that might explain this large racial disparity are being sought. Purpose: We evaluated whether differential use of alcohol and tobacco can fully account for the excess of squamous cell esophageal cancer among U.S. blacks. Methods: We conducted a population-based, case-control study with in-person interviews with 373 squamous cell esophageal cancer case patients (124 white males and 249 black males) and 1364 control subjects (750 white males and 614 black males) from three U.S. geographic areas. Histologically confirmed cases of squamous cell esophageal cancer newly diagnosed from August 1, 1986, through April 30, 1989, among white and black men aged 30-79 years were included. Results: Alcohol use of more than one drink per day and/or current cigarette use of at least one pack per day accounted for 92.7% (95% confidence interval [CI] = 86.8%-98.5%) of the squamous cell esophageal cancers in blacks, versus 86.3% (95% CI = 75.5%-97.1%) in whites, and for 93% of the difference between the black and white annual incidence rates. The interaction between race and the continuous drinking/smoking variable in a logistic regression analysis a-as statistically significant (two-sided, P = .02). Exposure rates among controls at all levels of combined alcohol and tobacco use examined were slightly higher among blacks and accounted for a small portion of the racial differences in incidence rates. Conclusion: Although the vast majority of esophageal cancers in both blacks and whites in our data can be explained by use of alcohol and tobacco, it is not clear why heavy consumption of alcohol and/or tobacco is responsible for 14.9 per 100 000 per year more cases of squamous cell esophageal cancer among blacks than among whites. The differences in the odds ratios appear to account for more of the racial differences in incidence rates than do the prevalences of exposure to alcohol and tobacco alone. The reasons for this apparent racial difference in carcinogenic risk from the same level of alcohol and tobacco use are unknown, but they may include qualitative differences in alcohol consumption, differences in other environmental exposures that interact with alcohol and/or tobacco to modify risks, or differences in susceptibility to these factors.