An estimate of the global burden of anthropogenic ozone and fine particulate matter on premature human mortality using atmospheric modeling.
An estimate of the global burden of anthropogenic ozone and fine particulate matter on premature human mortality using atmospheric modeling.
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DOI：
10.1289/ehp.0901220
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发表时间：
2010-09
影响因子：
10.4
通讯作者：
West JJ
中科院分区：
文献类型：
--
作者：
Anenberg SC;Horowitz LW;Tong DQ;West JJ
城市和农村地区的臭氧（O3）和细颗粒物[空气动力学直径≤ 2.5 μm（PM2.5）]的地面浓度自工业化前以来一直在增加，并与心血管和呼吸道死亡率有关。我们估计全球的死亡率负担，由于O3和PM2.5的人为排放使用全球大气化学传输模型模拟工业化前和现在（2000年）的浓度，以获得暴露估计。使用基于流行病学文献中O3和PM2.5的长期相对风险估计的健康影响函数估计归因死亡率。使用模拟浓度而不是以前基于测量的方法，可以将通常无法获得测量结果的农村地区包括在内，并避免对背景空气污染作出假设。据估计，每年人为O3与70万± 30万例呼吸道死亡（630万± 300万年寿命损失）相关。人为PM2.5每年与350万± 90万心肺和220，000 ± 80，000肺癌死亡率（3000 ± 760万年寿命损失）相关。当我们假设O3和PM2.5的低浓度阈值分别为33.3 ppb和5.8 μg/m3时，死亡率估计值降低了约30%。这些估计值对浓度阈值和浓度-死亡率关系敏感，通常超过50%。人为O3和PM2.5对全球过早死亡率的贡献很大。PM2.5死亡率估计值比以前基于共同假设的测量估计值高出约50%，主要是因为方法上的差异。具体而言，我们包括农村人口，这表明估计值较高;然而，全球大气模型的粗分辨率可能低估了城市PM2.5暴露。
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. 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. 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. 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%. 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.
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影响因子：
4.4
作者：
Horowitz, LW;Walters, S;Brasseur, GP
通讯作者：
Brasseur, GP
影响因子：
11.4
作者：
Roman, Henry A. .;Walker, Katherine D.;Kinney, Patrick L.
通讯作者：
Kinney, Patrick L.
DOI：
10.1097/ede.0b013e3181812bb7
发表时间：
2008-09
期刊：
Epidemiology (Cambridge, Mass.)
影响因子：
--
作者：
Franklin M;Koutrakis P;Schwartz P
通讯作者：
Schwartz P
影响因子：
4.4
作者：
Horowitz, Larry W.
通讯作者：
Horowitz, Larry W.
影响因子：
10.4
作者：
Ostro B;Lipsett M;Reynolds P;Goldberg D;Hertz A;Garcia C;Henderson KD;Bernstein L
通讯作者：
Bernstein L