Department of Environmental Medicine, New York University School of Medicine, New York, NY, USA.
Atomic Energy Centre, Dhaka, Bangladesh.
Int J Epidemiol. 2021 Aug 30;50(4):1172-1183. doi: 10.1093/ije/dyab037.
Fine-particulate-matter (i.e. with an aerodynamic diameter of ≤2.5 µm, PM2.5) air pollution is commonly treated as if it had 'equivalent toxicity', irrespective of the source and composition. We investigate the respective roles of fossil-fuel- and biomass-combustion particles in the PM2.5 relationship with cardiovascular morbidity and mortality using tracers of sources in Dhaka, Bangladesh. Results provide insight into the often observed levelling of the PM2.5 exposure-response curve at high-pollution levels.
A time-series regression model, adjusted for potentially confounding influences, was applied to 340 758 cardiovascular disease (CVD) emergency-department visits (EDVs) during January 2014 to December 2017, 253 407 hospital admissions during September 2013 to December 2017 and 16 858 CVD deaths during January 2014 to October 2017.
Significant associations were confirmed between PM2.5-mass exposures and increased risk of cardiovascular EDV [0.27%, (0.07% to 0.47%)] at lag-0, hospitalizations [0.32% (0.08% to 0.55%)] at lag-0 and deaths [0.87%, (0.27% to 1.47%)] at lag-1 per 10-μg/m3 increase in PM2.5. However, the relationship of PM2.5 with morbidity and mortality effect slopes was less steep and non-significant at higher PM2.5 concentrations (during crop-burning-dominated exposures) and varied with PM2.5 source. Fossil-fuel-combustion PM2.5 had roughly a four times greater effect on CVD mortality and double the effect on CVD hospital admissions on a per-µg/m3 basis than did biomass-combustion PM2.5.
Biomass burning was responsible for most PM2.5 air pollution in Dhaka, but fossil-fuel-combustion PM2.5 dominated the CVD adverse health impacts. Such by-source variations in the health impacts of PM2.5 should be considered in conducting ambient particulate-matter risk assessments, as well as in prioritizing air-pollution-mitigation measures and clinical advice.
细颗粒物(即空气动力学直径≤2.5μm 的颗粒物,PM2.5)空气污染通常被视为具有“等效毒性”,而不论其来源和成分如何。我们使用孟加拉国达卡的来源示踪剂来研究化石燃料和生物质燃烧颗粒在 PM2.5 与心血管发病率和死亡率之间的各自作用。结果为经常观察到的 PM2.5 暴露-反应曲线在高污染水平下趋于平稳提供了一些见解。
采用时间序列回归模型,调整了潜在的混杂因素影响,对 2014 年 1 月至 2017 年 12 月期间的 340758 例心血管疾病(CVD)急诊就诊(EDV)、2013 年 9 月至 2017 年 12 月期间的 253407 例住院治疗和 2014 年 1 月至 2017 年 10 月期间的 16858 例 CVD 死亡进行了分析。
PM2.5 质量暴露与心血管 EDV 风险增加显著相关[0.27%(0.07%至 0.47%)],在 lag-0 时增加;住院治疗[0.32%(0.08%至 0.55%)],在 lag-0 时增加;死亡率[0.87%(0.27%至 1.47%)],在 lag-1 时增加,每增加 10μg/m3 的 PM2.5。然而,PM2.5 与发病率和死亡率的关系斜率在较高的 PM2.5 浓度下(在以作物燃烧为主的暴露期间)变得较不陡峭且不显著,并且因 PM2.5 来源而异。在每微克/立方米的基础上,化石燃料燃烧产生的 PM2.5 对 CVD 死亡率的影响大约是生物质燃烧产生的 PM2.5 的四倍,对 CVD 住院治疗的影响是其两倍。
生物质燃烧是达卡 PM2.5 空气污染的主要来源,但化石燃料燃烧产生的 PM2.5 对心血管不良健康影响占主导地位。在进行环境颗粒物风险评估时,以及在优先考虑空气污染缓解措施和临床建议时,应考虑 PM2.5 健康影响的这种按来源的差异。