Health Effects of Fine Particulate Air Pollution: Lines that Connect
Health Effects of Fine Particulate Air Pollution: Lines that Connect
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DOI：
10.1080/10473289.2006.10464484
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发表时间：
2006-06
影响因子：
2.7
通讯作者：
J. Chow
中科院分区：
文献类型：
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作者：
J. Chow
S颗粒物（PM）对能见度、1气候、2生态系统、3、4以及沿着其他污染物对人类健康产生不利影响。5 -11在这些影响中，人类健康是最重要的，在以前的重要审查中已经得到了解决。5 -11这个主题在2006年特别重要，因为美国环境保护署（EPA）12这些修订将保留PM2.5的年平均水平（空气动力学直径小于2.5 m的颗粒）为15 g/m，3年平均值，13，但将24小时PM2.5水平从65 g/m 3降至35 g/m（3年平均98百分位数）。PM10（空气动力学直径小于10米的颗粒）年平均值为50克/米、24小时平均值为150克/米的标准14将被仅适用于人口超过100 000的城市地区的粗颗粒指标（PM10-2.5，PM10和PM2.5质量浓度之差）所取代。该提案的理由是，有足够的证据表明再悬浮的城市铺装道路灰尘，建筑灰尘和工业灰尘对健康有不利影响，但没有足够的证据表明其他来源的PM10-2.5的不利影响。该提案明确将农业和采矿业的贡献排除在减排战略之外。24小时平均PM10-2.5不允许超过70 g/m（3年平均98个百分点）。PM10-2.5合规性监测将仅在相对较大的城市的人口密集地区进行。EPA的建议与EPA的清洁空气科学咨询委员会（CASAC）建议的PM2.5年平均值在13-14 g/m3范围内以及在城市和农村社区进行PM10-2.5监测的建议不一致。人体接触、剂量和相关健康终点。第36次年度A&WMA批判性评论16，17讨论了PM对人类健康指标影响的流行病学证据，特别是疾病（发病率）和死亡（死亡率）。本次审查确定并建立在以前和最近的审查，特别是EPA标准文件18和工作人员文件19用于证明NAAQS修订。该审查记录了自1997年批判性审查以来在所有认识领域取得的重大进展，在以下领域取得了显著进展：1）短期接触和死亡率; 2）长期接触和死亡率; 3）接触的时间尺度; 4）浓度-反应函数的形状; 5）心血管疾病;和6）生物相容性。作者Arden Pope和道格拉斯多克里博士观察到，过去10年发表的100多项研究，使用许多不同的研究设计和数据分析方法，一致显示心肺死亡率与每日PM10或PM2.5浓度之间存在统计学显著相关性。在所有研究中，长期暴露的影响都比短期暴露的影响大。PM对健康的影响似乎取决于浓度和暴露时间，多年重复暴露于高水平比较不频繁的短期暴露于较高浓度更严重。他们指出，设定一个标准意味着有一个“阈值”，低于这个阈值就不会观察到任何效应，而且估计的浓度-反应函数似乎是线性的，没有证据表明存在一个没有观察到任何效应的下限。早期的研究主要集中在PM暴露对呼吸系统的影响上，而过去十年在与心血管疾病的关系上取得了很大进展。现在有一个明确的联系之间的发病心脏病发作或心脏不规则和PM吸入。其中一些可能是由于PM2.5质量监测器无法很好地量化的颗粒数量或表面积（超细颗粒）过多。他们描述了在理解导致PM对公众健康产生不利影响的生物和化学机制方面的实质性进展。现有肺部疾病的加重、氧化应激和炎症、心脏自主功能的变化、脉管系统改变、PM穿过内部生物屏障的易位、防御机制降低和肺损伤都与不同水平的PM暴露以及不同的颗粒尺寸和组成相关。Pope和Dockery博士确定了未来需要解决的几个知识差距：（1）更好地定义易感人群，目前认为是年轻人，老年人以及患有呼吸道和心血管疾病的人;（2）确定特定Judith C的相对影响。周梁
S particulate matter (PM) has adverse effects on visibility,1 climate,2 ecosystems,3,4 and, along with other pollutants, human health.5–11 Of these effects, human health is of greatest importance and has been addressed in previous critical reviews.5–11 This topic is of special interest in 2006 because the U.S. Environmental Protection Agency (EPA) has proposed revisions to the PM National Ambient Air Quality Standards (NAAQS).12 These revisions would retain the annual average level for PM2.5 (particles with aerodynamic diameters less than 2.5 m) of 15 g/m, averaged over 3 yr,13 but lower the 24-hr PM2.5 level from 65 g/m 3 to 35 g/m (98 percentile averaged over 3 yr). The PM10 (particles with aerodynamic diameters less than 10 m) standards of 50 g/m annual average and 150 g/m 24-hr average14 would be replaced by a coarse particle indicator (PM10–2.5, the difference between collocated PM10 and PM2.5 mass concentrations) applicable only in urban areas with populations exceeding 100,000. The proposal reasons that there is sufficient evidence to implicate resuspended urban paved road dust, construction dust, and industrial dust in adverse health effects, but there is insufficient evidence of adverse effects from other sources of PM10–2.5. The proposal explicitly excludes agricultural and mining contributions from emission reduction strategies. Twenty-four-hour average PM10–2.5 would not be allowed to exceed 70 g/m (98 percentile averaged over 3 yr). PM10–2.5 compliance monitoring would only be pursued in highly populated areas in relatively large cities. EPA’s proposal is at odds with EPA’s Clean Air Science Advisory Committee’s (CASAC) recommendation of a PM2.5 annual average in the range of 13–14 g/m 3 and PM10–2.5 monitoring in both urban and rural communities.15 This disagreement highlights the controversy that often accompanies air quality standards owing to uncertainties in measuring size-specific PM and its chemical components, PM toxicity, human exposure, dosage, and relevant health end points. The 36 Annual A&WMA Critical Review16,17 addresses the epidemiological evidence for the effects of PM on human health indicators, specifically sickness (morbidity) and death (mortality). This review identifies and builds on previous and recent reviews, especially the EPA criteria document18 and staff paper19 used to justify NAAQS revisions. The review documents substantial progress since the 1997 critical review11 in all areas of understanding, with notable advances in the areas of: 1) short-term exposure and mortality; 2) long-term exposure and mortality; 3) time-scales of exposure; 4) the shape of the concentration-response function; 5) cardiovascular disease; and 6) biological plausibility. The authors, Drs. Arden Pope and Douglas Dockery, observe that more than 100 studies published over the past 10 yr, using many different study designs and data analysis methods, consistently show statistically significant associations between cardiopulmonary mortality and daily PM10 or PM2.5 concentrations. Long-term exposures show larger effects than short-term exposures across all of the studies. PM health effects appear to depend on both the concentrations and the length of exposure, with repeated exposures to high levels over many years being more serious than less frequent short-term exposures to higher concentrations. They note that setting a standard implies that there is a “threshold” below which no effects are observed, and that estimated concentration-response functions appear to be linear with no evidence of a lower limit at which no effects are observed. Whereas earlier research focused on the respiratory effects of PM exposure, the last decade has seen much progress on relationships with cardiovascular disease. There is now a definite link between the onset of heart attacks or heart irregularities and PM inhalation. Some of this may be due to excessive particle number or surface area (ultrafine particles) that are not well quantified by PM2.5 mass monitors. They describe substantial progress in understanding the biological and chemical mechanisms that cause PM to adversely affect public health. Exacerbation of existing pulmonary disease, oxidative stress and inflammation, changes in cardiac autonomic functions, vasculature alterations, translocation of PM across internal biological barriers, reduced defense mechanisms, and lung damage have all been related to different levels of PM exposure, as well as to different particle sizes and compositions. Despite this additional science, Drs. Pope and Dockery identify several knowledge gaps that need to be addressed in the future: (1) better defining susceptible populations, currently believed to the young, the elderly, and people with existing respiratory and cardiovascular disease; (2) determining the relative effects of specific Judith C. Chow