Lee Chien-Hung, Lee Jang-Ming, Wu Deng-Chyang, Hsu Hon-Ki, Kao Ein-Long, Huang Hsiao-Ling, Wang Tsu-Nai, Huang Meng-Chuan, Wu Ming-Tsang
Graduate Institute of Public Health, Kaohsiung Medical University, Kaohsiung, Taiwan.
Int J Cancer. 2005 Jan 20;113(3):475-82. doi: 10.1002/ijc.20619.
A multicenter case-control study was conducted in northern and southern Taiwan to clarify the independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer. A total of 513 patients with newly diagnosed and histopathologically confirmed squamous cell carcinoma of the esophagus and 818 gender, age and study hospital-matched controls were included. We found a significant dose-response relationship between the duration and intensity of consumption of the 3 substances and the development of this neoplasm in this site. Although the amount of alcohol consumed had a stronger effect on the risk of esophageal cancer than the number of years it was consumed, however, the number of years one smoked had a stronger effect on the risk than the amount of cigarettes consumed. The strongest risk factor of esophageal cancer was alcohol intake, with highest risk (OR = 13.9) being for those who consumed more than 900 g/day-year. Combined exposure to any 2 of 3 substances brought the risks up to 8.8-19.7 fold and, to all 3 substances, to 41.2-fold. A multiplicative interaction effect for alcohol drinkers who smoked on cancer risk was detected, whereas an additive interaction effect was found among drinkers who chewed. The combined effect of all 3 substances accounted for 83.7% of the attributable fraction of contracting esophageal cancer in this population. In conclusion, these results suggest that the intensity and the length of time alcohol and tobacco are used play different roles in the etiology of esophageal cancer. Alcohol separately interacts with tobacco and betel quid in a differently synergistic way in determining the development of this site of cancer.
在台湾北部和南部开展了一项多中心病例对照研究,以阐明饮酒、吸烟和嚼食槟榔对食管癌风险的独立影响及联合影响。该研究共纳入了513例新诊断且经组织病理学确诊的食管鳞状细胞癌患者以及818例性别、年龄与研究医院相匹配的对照者。我们发现,这三种物质的消费持续时间和强度与该部位肿瘤的发生之间存在显著的剂量反应关系。尽管饮酒量对食管癌风险的影响比对饮酒年限的影响更强,然而,吸烟年限对风险的影响比对吸烟量的影响更强。食管癌最强的风险因素是饮酒,对于那些每年饮酒超过900克的人,风险最高(比值比=13.9)。三种物质中任意两种的联合暴露使风险增加至8.8 - 19.7倍,而三种物质全部暴露则使风险增加至41.2倍。检测到饮酒且吸烟的人群对癌症风险存在相乘交互作用,而在饮酒且嚼食槟榔的人群中发现存在相加交互作用。这三种物质的联合作用占该人群食管癌归因分数的83.7%。总之,这些结果表明,饮酒和吸烟的强度及持续时间在食管癌病因学中发挥着不同作用。在决定该部位癌症的发生方面,酒精分别与烟草和槟榔以不同的协同方式相互作用。