Cigarette smoking and lung cancer - Modeling effect modification of total exposure and intensity
Cigarette smoking and lung cancer - Modeling effect modification of total exposure and intensity
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DOI：
10.1097/ede.0b013e31812717fe
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发表时间：
2007-09-01
期刊：
影响因子：
5.4
通讯作者：
Alavanja, Michael C. R.
中科院分区：
文献类型：
--
作者：
Lubin, Jay H.;Caporaso, Neil;Alavanja, Michael C. R.
背景资料：最近的一项分析表明，吸烟导致肺癌的超额比值比由一个函数描述，该函数在包年中是线性的，在吸烟强度的对数及其平方中是指数的（Cancer Epidemiol Biomarkers Prev.二○ ○六年; 15：517 i，s i，52他的模型表明，低于每天15-20支香烟，存在直接暴露率效应，即，高强度（和较短持续时间）吸烟者每包-年的超额比值比大于低强度（和较长持续时间）吸烟者。超过每天20支香烟，有一个“反向暴露率”的影响，即，高强度吸烟者每包年的超额优势比小于低强度吸烟者。研究方法：使用来自2个大型肺癌病例对照研究（欧洲吸烟与健康研究和德国氡研究）的汇总数据，我们评估了吸烟与肺癌之间相关性的影响修饰。结果：交互作用效应具有特异性。肺癌风险随戒烟年限、年龄、吸入方法和香烟类型的变化是由于吸烟强度的相互作用，而不是总包年数。相比之下，风险变化的性别结果与总包年的相互作用，而强度效应是同质的。开始吸烟的年龄的风险变化与总包年和强度的相互作用。所有强度相互作用在研究中均是均匀的。结论：这些相互作用的特异性可能为吸烟与肺癌关系的分子基础提供线索。
Background: A recent analysis indicates that the excess odds ratio for lung cancer by smoking is described by a function that is linear in pack-years and exponential in the logarithm of smoking intensity and its square (Cancer Epidemiol Biomarkers Prev. 2006;15:517i, s i, 52 he model suggests that below 15-20 cigarettes per day there a direct exposure rate" effect, ie, the excess odds ratio per pack-year for higher intensity (and shorter duration) smokers is greater than for lower-intensity (and longer duration) smokers. Above 20 cigarettes per day, there is an "inverse-exposure-rate" effect, ie, the excess odds ratio per pack-year for higher intensity smokers is smaller than for lower-intensity smokers. Methods: Using pooled data from 2 large case-control studies of lung cancer (the European Smoking and Health Study and the German Radon Study), we evaluated effect modification of the association between smoking and lung cancer. Results: Interaction effects are very specific. Variations in risk of lung cancer with years since cessation of smoking, age, method of inhalation, and type of cigarette result from interactions with smoking intensity, and not total pack-years. In contrast, risk variations by sex result from the interaction with total pack-years, while intensity effects are homogeneous. Risk variations by age at which smoking started result from interactions with both total pack-years and intensity. All intensity interactions are homogeneous across studies. Conclusions: The specificity of the interactions may provide clues for the molecular basis of the smoking and lung cancer relationship.