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吸烟与肺癌:总暴露量和强度的效应修正建模

Cigarette smoking and lung cancer: modeling effect modification of total exposure and intensity.

作者信息

Lubin Jay H, Caporaso Neil, Wichmann H Erich, Schaffrath-Rosario Angelika, Alavanja Michael C R

机构信息

Biostatistics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland 20852, USA.

出版信息

Epidemiology. 2007 Sep;18(5):639-48. doi: 10.1097/EDE.0b013e31812717fe.

DOI:10.1097/EDE.0b013e31812717fe
PMID:17700253
Abstract

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;15:517-523). The model suggests that below 15-20 cigarettes per day there is 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.

摘要

背景

最近的一项分析表明,吸烟导致肺癌的超额比值比可由一个在吸烟包年数上呈线性、在吸烟强度及其平方的对数上呈指数形式的函数来描述(《癌症流行病学、生物标志物与预防》。2006年;15:517 - 523)。该模型表明,每天吸烟低于15 - 20支时存在“直接暴露率”效应,即高强度(且吸烟持续时间短)吸烟者每吸烟包年的超额比值比大于低强度(且吸烟持续时间长)吸烟者。每天吸烟超过20支时,存在“反向暴露率”效应,即高强度吸烟者每吸烟包年的超额比值比小于低强度吸烟者。

方法

利用两项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关联中的效应修饰。

结果

交互作用效应非常特异。肺癌风险随戒烟时间、年龄、吸入方式和香烟类型的变化是由与吸烟强度的交互作用导致的,而非总吸烟包年数。相比之下,按性别划分的风险变化是由与总吸烟包年数的交互作用导致的,而强度效应是一致的。开始吸烟时的年龄导致的风险变化是由与总吸烟包年数和强度两者的交互作用引起的。所有强度交互作用在各项研究中都是一致的。

结论

这些交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。

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