Department of Epidemiology and Public Health, University College London, London, United Kingdom.
J Am Coll Cardiol. 2010 Jun 29;56(1):18-23. doi: 10.1016/j.jacc.2010.03.032.
The aim of this study was to examine the association between objectively measured secondhand smoke (SHS) exposure and incident cardiovascular disease (CVD) death and assess the extent to which this association can be explained through novel circulating markers of inflammation and hemostasis.
Existing evidence suggests there is an association between SHS and CVD risk, although the mechanisms remain poorly understood.
In a prospective study of 13,443 participants living in England and Scotland (age 53.5 +/- 12.6 years, 52.3% women), we measured salivary cotinine (an objective marker of SHS exposure) and novel CVD biomarkers (C-reactive protein, fibrinogen) at baseline.
Of the sample, 20.8% had high SHS exposure on the basis of elevated levels of salivary cotinine (range 0.71 to 14.99 ng/ml). During a mean follow-up of 8 years, there were 1,221 all-cause deaths and 364 CVD deaths. High SHS was associated with all-cause (age-adjusted hazard ratio [HR]: 1.25, 95% confidence interval [CI]: 1.02 to 1.53) and CVD death (age-adjusted HR: 1.21, 95% CI: 0.85 to 1.73). High SHS was also associated with elevated CRP, which explained 48% of the association between SHS and CVD death. The excess risk of CVD associated with active smoking was exaggerated in relation to self report (age-adjusted HR: 3.27, 95% CI: 2.48 to 4.31) compared with objective assessment (age-adjusted HR: 2.44, 95% CI: 1.75 to 3.40).
Among a large representative sample of British adults we observed elevated levels of low-grade inflammation in otherwise healthy participants exposed to high SHS, and this partly explained their elevated risk of CVD death.
本研究旨在探讨二手烟(SHS)暴露与心血管疾病(CVD)死亡的关系,并评估新型循环炎症和止血标志物在多大程度上可以解释这种关系。
现有证据表明,SHS 与 CVD 风险之间存在关联,但机制仍知之甚少。
在一项对居住在英格兰和苏格兰的 13443 名参与者(年龄 53.5 +/- 12.6 岁,52.3%为女性)的前瞻性研究中,我们在基线时测量了唾液可替宁(SHS 暴露的客观标志物)和新型 CVD 生物标志物(C 反应蛋白、纤维蛋白原)。
在样本中,根据唾液可替宁水平升高(范围为 0.71 至 14.99ng/ml),有 20.8%的人暴露于高水平的 SHS。在平均 8 年的随访期间,共有 1221 例全因死亡和 364 例 CVD 死亡。高 SHS 与全因死亡(年龄调整后的危险比 [HR]:1.25,95%置信区间 [CI]:1.02 至 1.53)和 CVD 死亡(年龄调整后的 HR:1.21,95% CI:0.85 至 1.73)相关。高 SHS 还与 CRP 升高相关,CRP 解释了 SHS 与 CVD 死亡之间 48%的关联。与自我报告相比(年龄调整后的 HR:3.27,95% CI:2.48 至 4.31),与客观评估相比(年龄调整后的 HR:2.44,95% CI:1.75 至 3.40),与主动吸烟相关的 CVD 风险增加更为明显。
在英国成年人的大型代表性样本中,我们观察到暴露于高水平 SHS 的健康参与者存在低度炎症水平升高,这在一定程度上解释了他们 CVD 死亡风险升高的原因。