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首页> 外文期刊>Environmental health perspectives. >An Estimate of the Global Burden of Anthropogenic Ozone and Fine Particulate Matter on Premature Human Mortality Using Atmospheric Modeling
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An Estimate of the Global Burden of Anthropogenic Ozone and Fine Particulate Matter on Premature Human Mortality Using Atmospheric Modeling

机译:利用大气模型估算人为臭氧和精细颗粒物对人类早产全球负担的总和

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Background Ground-level concentrations of ozone (O3) and fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM2.5)] have increased since preindustrial times in urban and rural regions and are associated with cardiovascular and respiratory mortality. Objectives We estimated the global burden of mortality due to O3 and PM2.5 from anthropogenic emissions using global atmospheric chemical transport model simulations of preindustrial and present-day (2000) concentrations to derive exposure estimates. Methods Attributable mortalities were estimated using health impact functions based on long-term relative risk estimates for O3 and PM2.5 from the epidemiology literature. Using simulated concentrations rather than previous methods based on measurements allows the inclusion of rural areas where measurements are often unavailable and avoids making assumptions for background air pollution. Results Anthropogenic O3 was associated with an estimated 0.7 ± 0.3 million respiratory mortalities (6.3 ± 3.0 million years of life lost) annually. Anthropogenic PM2.5 was associated with 3.5 ± 0.9 million cardiopulmonary and 220,000 ± 80,000 lung cancer mortalities (30 ± 7.6 million years of life lost) annually. Mortality estimates were reduced approximately 30% when we assumed low-concentration thresholds of 33.3 ppb for O3 and 5.8 μg/m3 for PM2.5. These estimates were sensitive to concentration thresholds and concentration–mortality relationships, often by > 50%. Conclusions Anthropogenic O3 and PM2.5 contribute substantially to global premature mortality. PM2.5 mortality estimates are about 50% higher than previous measurement-based estimates based on common assumptions, mainly because of methodologic differences. Specifically, we included rural populations, suggesting higher estimates; however, the coarse resolution of the global atmospheric model may underestimate urban PM2.5 exposures.
机译:背景自工业化以来,城市和农村地区的臭氧(O 3 )和细颗粒物[空气动力学直径≤2.5μm(PM 2.5 )]的地面浓度有所增加地区,并与心血管和呼吸道疾病相关。目的我们使用工业化前和现今(2000年)浓度的全球大气化学迁移模型模拟,估算了人为排放中由O 3 和PM 2.5 引起的全球死亡负担。得出暴露估计。方法根据流行病学文献中O 3 和PM 2.5 的长期相对风险估计,使用健康影响函数估算归因死亡率。使用模拟浓度而不是基于测量的先前方法,可以将无法进行测量的农村地区包括在内,并且避免对背景空气污染进行假设。结果人为的O 3 每年与估计的0.7±30万人的呼吸道死亡(6.3±300万人的生命损失)相关。每年人为引起的PM 2.5 与3.5±90万心肺和220,000±80,000例肺癌死亡(30±760万年生命损失)相关。当我们假设O 3 的低浓度阈值为33.3 ppb,PM 2.5 的低浓度阈值为5.8μg/ m 3 时,死亡率估计降低了约30%。 。这些估计值对浓度阈值和浓度-死亡率关系敏感,通常大于50%。结论人为原因的O 3 和PM 2.5 对全球过早死亡具有重要作用。 PM 2.5 死亡率估计值比以前基于共同假设的基于测量的估计值高约50%,这主要是由于方法上的差异。具体来说,我们纳入了农村人口,这表明估计值较高;然而,全球大气模型的粗略分辨率可能会低估城市PM 2.5 的暴露量。

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