Interaction Effects and Population-attributable Risks for Smoking and Alcohol on Laryngeal Cancer and Its Subsites
Interaction Effects and Population-attributable Risks for Smoking and Alcohol on Laryngeal Cancer and Its Subsites
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吸烟和饮酒对喉癌及其亚部位的相互作用影响和人群归因风险
DOI：
10.1055/s-0038-1633906
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发表时间：
2004
影响因子：
1.7
通讯作者：
Heiko Becher
中科院分区：
文献类型：
--
作者：
H. Ramroth;Andreas Dietz;Heiko Becher
目的：评估吸烟和饮酒对肿瘤亚部位喉部风险的联合影响。研究方法：在德国西南部开展的基于人群的病例对照研究，纳入257例组织学确诊病例（236例男性，21例女性），年龄37 - 80岁，769例人群对照（702例男性，67例女性），按年龄和性别匹配的频率为1：3。结果：声门及声门下肿瘤占50.6%，声门上占17.5%。31.9%的肿瘤由于分期较晚，不能明确定位。随着烟草消费量的增加，风险显著增加，重度吸烟（>80包年（py））的比值比（OR）为59.8（95%置信区间（CI）21.3-167.3）。与目前吸烟者相比，戒烟（>2年）的癌症风险降低，OR=0.36，95% CI 0.24-0.53。声门上肿瘤的风险高于声门和声门下肿瘤。酒精的影响并不强烈。75-100 g乙醇/天仅对声门和声门下肿瘤产生显著增加的比值比2.0，95% CI（1.0-3.9）。OR从100-150 g乙醇/天的2.2，95% CI（1.1-4.3）上升到超过150 g乙醇/天的4.3，95% CI（1.4-13.2）（所有模型均针对教育进行调整）。吸烟和饮酒的联合效应表现为亚乘法但超加法。几乎90%的肿瘤可以归因于这两个因素。结论：与早期的调查相反，我们观察到吸烟和饮酒的亚倍增效应。酒精和烟草消费都很高的人的风险极高，这表明干预的重要性。
Summary Objectives: To assess the joint effect of smoking and alcohol consumption on laryngeal risk on tumor subsites. Methods: Population-based case-control study in South-West Germany with 257 histologically confirmed cases (236 males, 21 females), age 37 to 80 years, and 769 population controls (702 males, 67 females), 1:3 frequency matched by age and sex. Results: Half of the tumors (50.6%) were glottic or subglottic, 17.5% were supraglottic. Due to advanced stage, the subsite of 31.9% of the tumors could not be determined clearly. There is a strong increase in risk with increasing tobacco consumption with an odds ratio (OR) of 59.8 (95% confidence interval (CI) 21.3-167.3) for heavy smoking (>80 packyears (py)), all cases combined. In comparison to current smokers, cancer risk is reduced for ex-smoking (>2 years) OR=0.36, 95% CI 0.24-0.53. The risks were higher for supraglottic than for glottic and sub-glottic tumors. The effect of alcohol is not as strong. A significantly increased odds ratio of 2.0, 95% CI (1.0-3.9) results for 75-100 g ethanol/day only for glottic and subglottic tumors. The OR rises from 2.2, 95% CI (1.1-4.3) for 100-150 g ethanol/day to 4.3, 95% CI (1.4-13.2) for more than 150 g ethanol/day (all models adjusted for education). The joint effect of smoking and alcohol results appears sub-multiplicative but super-additive. Almost 90% of the tumors can be attributed to both factors. Conclusion: Contrary to earlier investigations we observed a sub-multiplicative effect of smoking and alcohol. The risk for persons with both high alcohol and tobacco consumption is extremely high which indicates the importance of intervention.