Cox Associates.
Dose Response. 2012;10(2):219-32. doi: 10.2203/dose-response.11-038.Cox. Epub 2011 Oct 14.
Some recent discussions of adverse human health effects of active and passive smoking have suggested that low levels of exposure are disproportionately dangerous, so that "The effects of even brief (minutes to hours) passive smoking are often nearly as large (averaging 80% to 90%) as chronic active smoking" (Barnoya and Glantz, 2005). Recent epidemiological evidence (Teo et al., 2006) suggests a more linear relation. This paper reexamines the empirical relation between self-reported low levels of active smoking and risk of coronary heart disease (CHD) in public-domain data from the National Health and Nutrition Examination Survey (NHANES). Consistent with biological evidence on J-shaped and U-shaped relations between smoking-associated risk factors and CHD risks, we find that low levels of active smoking do not appear to be associated with increased CHD risk. Several methodological challenges in epidemiology may explain how model-derived estimates can predict low-dose linear or concave dose-response estimates, even if the empirical (i.e., data-based) relation does not show a clear increased risk at the lowest doses.
一些最近关于主动和被动吸烟对人体健康的不良影响的讨论表明，低水平的暴露是不成比例的危险，因此“即使是短暂的（几分钟到几个小时）被动吸烟的影响也往往与慢性主动吸烟相当（平均 80%到 90%）”（Barnoya 和 Glantz，2005）。最近的流行病学证据（Teo 等人，2006）表明存在更线性的关系。本文重新审视了来自国家健康和营养检查调查（NHANES）的公共领域数据中自我报告的低水平主动吸烟与冠心病（CHD）风险之间的经验关系。与吸烟相关的风险因素与 CHD 风险之间存在 J 形和 U 形关系的生物学证据一致，我们发现低水平的主动吸烟似乎与增加的 CHD 风险无关。流行病学中的一些方法学挑战可能解释了为什么模型衍生的估计可以预测低剂量线性或凹剂量反应估计，即使经验（即基于数据）关系在最低剂量下没有显示出明显的增加风险。
