Lubin Jay H, Albanes Demetrius, Hoppin Jane A, Chen Honglei, Lerro Catherine C, Weinstein Stephanie J, Sandler Dale P, Beane Freeman Laura E
Biostatistics Branch, Division of Cancer Epidemiology and Genetics, US National Cancer Institute, National Institutes of Health, Bethesda, MD.
Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, US National Cancer Institute, National Institutes of Health, Bethesda, MD.
Nicotine Tob Res. 2017 Jul 1;19(7):817-825. doi: 10.1093/ntr/ntw290.
Relative risks (RRs) for coronary heart disease (CHD) by cigarettes/day exhibit a concave pattern, implying the RR increase with each additional cigarette/day consumed decreases with greater intensity. Interpreting this pattern faces limitations, since cigarettes/day alone does not fully characterize smoking-related exposure. A more complete understanding of smoking and CHD risk requires a more comprehensive representation of smoking.
Using Poisson regression, we applied a RR model in pack-years and cigarettes/day to analyze two diverse cohorts, the US Agricultural Health Study, with 4396 CHD events and 1 425 976 person-years of follow-up, and the Finnish Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, with 5979 CHD events and 486 643 person-years.
In both cohorts, the concave RR pattern with cigarettes/day was consistent with cigarettes/day modifying a linear RR association for CHD by pack-years within categories of cigarettes/day, indicating that strength of the pack-years association depended on cigarettes/day (p < .01). For example, at 50 pack-years (365 000 total cigarettes), estimated RRs of CHD were 2.1 for accrual at 20 cigarettes/day and 1.5 for accrual at 50 cigarettes/day.
RRs for CHD increased with pack-years with smoking intensities affecting the strength of association. For equal pack-years, smoking fewer cigarettes/day for longer duration was more deleterious than smoking more cigarettes/day for shorter duration. We have now observed inverse smoking intensity effects in multiple cohorts with differing smoking patterns and other characteristics, suggesting a common underlying phenomenon.
Risk of CHD increases with pack-years of smoking, but accrual intensity strongly influences the strength of the association, such that smoking fewer cigarettes/day for longer duration is more deleterious than smoking more cigarettes/day for shorter duration. This observation offers clues to better understanding biological mechanisms, and reinforces the importance of cessation rather than smoking less to reduce CHD risk.
冠心病(CHD)的相对风险(RR)与每日吸烟量呈现出一种凹形模式,这意味着随着每日吸烟量每增加一支,RR的增加幅度会以更大的强度减小。对这种模式的解读存在局限性,因为仅每日吸烟量并不能完全表征与吸烟相关的暴露情况。要更全面地理解吸烟与冠心病风险之间的关系,需要对吸烟情况进行更全面的描述。
我们使用泊松回归,在吸烟包年数和每日吸烟量方面应用RR模型,分析了两个不同的队列,即美国农业健康研究队列(有4396例冠心病事件,随访1425976人年)和芬兰α-生育酚、β-胡萝卜素癌症预防研究队列(有5979例冠心病事件,随访486643人年)。
在两个队列中,每日吸烟量呈现的凹形RR模式与每日吸烟量在各分类中修正吸烟包年数与冠心病之间的线性RR关联一致,这表明吸烟包年数关联的强度取决于每日吸烟量(p <.01)。例如,在50吸烟包年(总共365000支香烟)时,每日吸烟20支累积的冠心病估计RR为2.1,每日吸烟50支累积的冠心病估计RR为1.5。
冠心病的RR随着吸烟包年数增加,吸烟强度影响关联强度。对于相同的吸烟包年数,长时间少吸烟比短时间多吸烟更有害。我们现在已经在多个具有不同吸烟模式和其他特征的队列中观察到了相反的吸烟强度效应,这表明存在一个共同的潜在现象。
冠心病风险随吸烟包年数增加,但累积强度强烈影响关联强度,以至于长时间少吸烟比短时间多吸烟更有害。这一观察结果为更好地理解生物学机制提供了线索,并强化了戒烟而非减少吸烟以降低冠心病风险的重要性。