Pinault Lauren L, Weichenthal Scott, Crouse Daniel L, Brauer Michael, Erickson Anders, Donkelaar Aaron van, Martin Randall V, Hystad Perry, Chen Hong, Finès Philippe, Brook Jeffrey R, Tjepkema Michael, Burnett Richard T
Health Analysis Division, Statistics Canada, Ottawa, ON, Canada.
McGill University, Montreal, QC, Canada; Air Health Science Division, Health Canada, Ottawa, ON, Canada.
Environ Res. 2017 Nov;159:406-415. doi: 10.1016/j.envres.2017.08.037. Epub 2017 Sep 18.
Large cohort studies have been used to characterise the association between long-term exposure to fine particulate matter (PM) air pollution with non-accidental, and cause-specific mortality. However, there has been no consensus as to the shape of the association between concentration and response.
To examine the shape of this association, we developed a new cohort based on respondents to the 2001 Canadian census long-form. We applied new annual PM concentration estimates based on remote sensing and ground measurements for Canada at a 1km spatial scale from 1998 to 2011. We followed 2.4 million respondents who were non-immigrants aged 25-90 years and did not reside in an institution over a 10 year period for mortality. Exposures were assigned as a 3-year mean prior to the follow-up year. Income tax files were used to account for residential mobility among respondents using postal codes, with probabilistic imputation used for missing postal codes in the tax data. We used Cox survival models to determine hazard ratios (HRs) for cause-specific mortality. We also estimated Shape Constrained Health Impact Functions (a concentration-response function) for selected causes of death.
In models stratified by age, sex, airshed, and population centre size, and adjusted for individual and neighbourhood socioeconomic variables, HR estimates for non-accidental mortality were HR = 1.18 (95% CI: 1.15-1.21) per 10μg/m increase in concentration. We observed higher HRs for cardiovascular disease (HR=1.25; 95% CI: 1.19-1.31), cardio-metabolic disease (HR = 1.27; 95% CI: 1.21-1.33), ischemic heart disease (HR = 1.36; 95% CI: 1.28-1.44) and chronic obstructive pulmonary disease (COPD) mortality (HR = 1.24; 95% CI: 1.11-1.39) compared to HR for all non-accidental causes of death. For non-accidental, cardio-metabolic, ischemic heart disease, respiratory and COPD mortality, the shape of the concentration-response curve was supra-linear, with larger differences in relative risk for lower concentrations. For both pneumonia and lung cancer, there was some suggestion that the curves were sub-linear.
Associations between ambient concentrations of fine particulate matter and several causes of death were non-linear for each cause of death examined.
大型队列研究已被用于描述长期暴露于细颗粒物(PM)空气污染与非意外及特定病因死亡率之间的关联。然而,关于浓度与反应之间关联的形状尚未达成共识。
为了研究这种关联的形状,我们基于2001年加拿大人口普查长表的受访者建立了一个新的队列。我们应用了基于1998年至2011年加拿大遥感和地面测量数据的新的年度PM浓度估计值,空间尺度为1公里。我们追踪了240万年龄在25至90岁之间的非移民受访者,他们在10年期间不住在机构中,以观察死亡率。暴露被指定为随访年份之前的3年平均值。所得税文件用于根据邮政编码来考虑受访者之间的居住流动性,对于税务数据中缺失的邮政编码使用概率插补法。我们使用Cox生存模型来确定特定病因死亡率的风险比(HRs)。我们还估计了选定死因的形状受限健康影响函数(浓度 - 反应函数)。
在按年龄、性别、空气流域和人口中心规模分层并针对个人和邻里社会经济变量进行调整的模型中,每增加10μg/m³浓度,非意外死亡率的HR估计值为HR = 1.18(95%CI:1.15 - 1.21)。与所有非意外死因的HR相比,我们观察到心血管疾病(HR = 1.25;95%CI:1.19 - 1.31)、心脏代谢疾病(HR = 1.27;95%CI:1.21 - 1.33)、缺血性心脏病(HR = 1.36;95%CI:1.28 - 1.44)和慢性阻塞性肺疾病(COPD)死亡率(HR = 1.24;95%CI:1.11 - 1.39)的HR更高。对于非意外、心脏代谢、缺血性心脏病、呼吸系统和COPD死亡率,浓度 - 反应曲线的形状是超线性的,较低浓度时相对风险差异更大。对于肺炎和肺癌,有迹象表明曲线是次线性的。
在所研究的每种死因中,细颗粒物的环境浓度与几种死因之间的关联都是非线性的。