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Associations between fine particulate matter and mortality in the 2001 Canadian Census Health and Environment Cohort

机译:2001年加拿大人口普查健康与环境队列中的细颗粒物与死亡率之间的关联

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Background: Large cohort studies have been used to characterise the association between long-term exposure to fine particulate matter (PM2.5) 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. Methods: 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 PM2.5 concentration estimates based on remote sensing and ground measurements for Canada at a 1 km 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. Results: 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 10 µg/m~3 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. Conclusions: Associations between ambient concentrations of fine particulate matter and several causes of death were non-linear for each cause of death examined.
机译:背景:大型队列研究已用于表征长期暴露于细颗粒物(PM2.5)空气污染与意外事故和特定原因死亡率之间的关系。然而,关于浓度与反应之间的联系形式尚无共识。方法:为了检查这种关联的形状,我们根据2001年加拿大人口普查长篇问卷的受访者建立了一个新的队列。从1998年到2011年,我们基于加拿大的遥感和地面测量,以1 km为空间比例,应用了基于PM2.5的新年度浓度估算。我们追踪了240万被调查者,他们是25-90岁的非移民,并且没有居住在加拿大机构在10年内的死亡率。暴露被指定为随访年之前的3年平均值。所得税档案被用来解释使用邮政编码的受访者的居住流动性,而概率归因法则被用于税务数据中缺失的邮政编码。我们使用Cox生存模型来确定特定原因死亡率的危险比(HRs)。我们还为选定的死亡原因估计了形状受约束的健康影响函数(浓度响应函数)。结果:在按年龄,性别,气隙和人口中心规模进行分层并针对个人和社区社会经济变量进行调整的模型中,非偶然死亡率的HR估计值为HR = 1.18(95%CI:1.15-1.21)每10 µg / m〜3浓度增加。我们观察到心血管疾病(HR = 1.25; 95%CI:1.19-1.31),心血管疾病(HR = 1.27; 95%CI:1.21-1.33),缺血性心脏病(HR = 1.36; 95%CI)的HRs较高: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),与所有非偶然死亡原因的HR相比。对于非偶然的,心脏代谢性的,缺血性心脏病,呼吸道疾病和COPD死亡率,浓度-反应曲线的形状呈超线性,较低浓度的相对风险差异较大。对于肺炎和肺癌,有人认为曲线是亚线性的。结论:对于所检查的每种死亡原因,细颗粒物的周围环境浓度与几种死亡原因之间的关系都是非线性的。

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