Turner Michelle C, Cohen Aaron, Burnett Richard T, Jerrett Michael, Diver W Ryan, Gapstur Susan M, Krewski Daniel, Samet Jonathan M, Pope C Arden
McLaughlin Centre for Population Health Risk Assessment, University of Ottawa, Ottawa, Canada; Barcelona Institute for Global Health (ISGlobal), Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain; CIBER Epidemiología y Salud Pública (CIBERESP), Madrid, Spain.
Health Effects Institute, Boston, USA.
Environ Res. 2017 Apr;154:304-310. doi: 10.1016/j.envres.2017.01.024. Epub 2017 Jan 28.
Associations between long-term exposure to ambient fine particulate matter (PM) and all-cause and cardiovascular mortality are well documented however less is known regarding possible interactions with cigarette smoking. We previously reported a supra-additive synergistic relationship between PM and cigarette smoking for lung cancer mortality. Here we examine interactions for all-cause and cardiovascular mortality among 429,406 current or never smoking participants in the prospective American Cancer Society Cancer Prevention Study-II with modeled PM concentrations. Cox proportional and additive hazards models were used to estimate mortality associations and interactions on the multiplicative and additive scales. A total of 146,495 all-cause and 64,339 cardiovascular (plus diabetes) deaths were observed. The hazard ratio (HR) (95% confidence interval (CI)) for cardiovascular mortality for high vs. low PM exposure (>14.44µg/m vs ≤10.59µg/m, 75th vs 25th percentile) was 1.09 (95% CI 1.05, 1.12) in never smokers. The HR for cigarette smoking was 1.89 (95% CI 1.82, 1.96) in those with low PM. The HR for both high PM and cigarette smoking was 2.08 (95% CI 2.00, 2.17). A small significant excess relative risk due to interaction (0.10; 95% CI 0.02, 0.19) was observed. Quantification of the public health burden attributed to the interaction between PM and cigarette smoking indicated a total of 32 (95% CI -6, 71) additional cardiovascular deaths per 100,000 person-years due to this interaction. In conclusion, PM was associated with all-cause and cardiovascular mortality in both smokers and never smokers, with some evidence for a small additive interaction with cigarette smoking. Reductions in cigarette smoking will result in the greatest impact on reducing all-cause and cardiovascular death at the levels of PM observed in this study. However, reductions in PM will also contribute to preventing a proportion of mortality attributed to cigarette smoking.
长期暴露于环境细颗粒物(PM)与全因死亡率和心血管死亡率之间的关联已有充分记录,但关于其与吸烟可能的相互作用却知之甚少。我们之前报道了PM与吸烟在肺癌死亡率方面存在超相加协同关系。在此,我们对美国癌症协会癌症预防研究II前瞻性队列中429,406名当前吸烟者或从不吸烟者,结合模拟的PM浓度,研究全因死亡率和心血管死亡率的相互作用。采用Cox比例风险模型和相加风险模型来估计死亡率关联以及乘法尺度和加法尺度上的相互作用。共观察到146,495例全因死亡和64,339例心血管(加糖尿病)死亡。从不吸烟者中,高PM暴露(>14.44µg/m³与≤10.59µg/m³,第75百分位数与第25百分位数)与低PM暴露相比,心血管死亡率的风险比(HR)(95%置信区间(CI))为1.09(95%CI 1.05, 1.12)。低PM人群中吸烟的HR为1.89(95%CI 1.82, 1.96)。高PM且吸烟人群的HR为2.08(95%CI 2.00, 2.17)。观察到因相互作用导致的相对风险有小的显著超额(0.10;95%CI 0.02, 0.19)。对PM与吸烟相互作用所致公共卫生负担的量化表明,每10万人年因这种相互作用额外增加32例(95%CI -6, 71)心血管死亡。总之,PM与吸烟者和从不吸烟者的全因死亡率和心血管死亡率均相关,有证据表明与吸烟存在小的相加相互作用。在本研究观察到的PM水平下,减少吸烟对降低全因死亡和心血管死亡的影响最大。然而,降低PM水平也将有助于预防一部分归因于吸烟的死亡。