Associated Links Among Smoking, Chronic Obstructive Pulmonary Disease, and Small Cell Lung Cancer: A Pooled Analysis in the International Lung Cancer Consortium

作者:Huang, Ruyi; Wei, Yongyue; Hung, Rayjean J.; Liu, Geoffrey; Su, Li; Zhang, Ruyang; Zong, Xuchen; Zhang, Zuo-Feng; Morgenstern, Hal; Brueske, Irene; Heinrich, Joachim; Hong, Yun-Chul; Kim, Jin Hee; Cote, Michele; Wenzlaff, Angela; Schwartz, Ann G.; Stucker, Isabelle; Mclaughlin, L. John; Marcus, Michael W.; Davies, Michael P. A.; Liloglou, Triantafillos; Field, John K.; Matsuo, Keitaro; Barnett, Matt; Thornquist, Mark; Goodman, Gary; Wang, Yi; Chen, Size; Yang, Ping; Duell, Eric J.
来源:EBioMedicine, 2015, 2(11): 1677-1685.
DOI:10.1016/j.ebiom.2015.09.031

摘要

Background: The high relapse and mortality rate of small-cell lung cancer (SCLC) fuels the need for epidemiologic study to aid in its prevention. @@@ Methods: We included 24 studies from the ILCCO collaboration. Random-effects panel logistic regression and cubic spline regression were used to estimate the effects of smoking behaviors on SCLC risk and explore their non-linearity. Further, we explored whether the risk of smoking on SCLC was mediated through COPD. @@@ Findings: Significant dose-response relationships of SCLC risk were observed for all quantitative smoking variables. Smoking pack-years were associated with a sharper increase of SCLC risk for pack-years ranged 0 to approximately 50. The former smokers with longer cessation showed a 43%(quit_for_5-9 years) to 89%(quit_for_>= 20 years) declined SCLC risk vs. subjects who had quit smoking <5 years. Compared with non-COPD subjects, smoking behaviors showed a significantly higher effect on SCLC risk among COPD subjects, and further, COPD patients showed a 1.86-fold higher risk of SCLC. Furthermore, smoking behaviors on SCLC risk were significantly mediated through COPD which accounted for 0.70% to 7.55% of total effects. @@@ Interpretation: This is the largest pooling study that provides improved understanding of smoking on SCLC, and further demonstrates a causal pathway through COPD that warrants further experimental study.