From Olympians to mere mortals: the indiscriminate, global challenges of air pollution.
From Olympians to mere mortals: the indiscriminate, global challenges of air pollution.
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从奥运选手到凡人：空气污染的全球性挑战。
DOI：
10.1164/rccm.201209-1594ed
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发表时间：
2012
影响因子：
24.7
通讯作者：
Pope3rd,CArden
中科院分区：
文献类型：
--
作者：
VanHee,VictorC;Pope3rd,CArden
北京赢得了2008年奥运会的主办权，同时承诺大幅改善空气质量，花费超过100亿美元实施污染控制措施（1）。基于大量和越来越多的证据表明空气污染会影响心脏和呼吸系统健康，奥运会运动员和公众担心北京臭名昭著的空气质量可能会对运动员产生不利影响。即使在2008年奥运会期间个别空气污染物浓度大幅降低（13-60%）后，正如本期《华尔街日报》所报道的那样。1150-1159）（3），北京细颗粒物等污染物的日平均水平仍然比同期美国大城市高4至9倍（4）。运动员仍然担心潜在的健康影响，一些人推迟了奥运会的比赛（5），奥运代表团在北京以外的地方建立了训练营，以避免强烈的空气污染暴露（6）。在2008年奥运会之前的几年里，流行病学研究报告说，细颗粒物空气污染和原因特异性死亡率之间的关联模式与空气污染暴露导致肺和全身氧化应激，炎症以及相关的动脉粥样硬化和缺血性心血管疾病和阻塞性肺疾病风险增加的假设一致（2，7）。最近对不断扩大的文献（8）和来自动脉粥样硬化多种族研究（9）的新证据的综述表明，可能存在将空气污染与心肺疾病联系起来的多个，复杂的，相互依赖的机制途径，但也提供了越来越多的证据表明肺部和全身氧化应激和炎症起着重要作用。在此背景下，在本期《华尔街日报》中，黄和同事们（第100页）。1150-1159）报告了一项基于北京奥运会的研究结果，该研究调查了空气污染和呼出气体与肺部和全身氧化应激和炎症的尿液生物标志物之间的关系（3）。这项准实验研究评估了125名年轻健康的医学生在2008年北京奥运会之前，期间和之后。Huang和他的同事证明，随着空气污染的减少，这些生物标志物的跟踪大幅减少，随后在北京恢复到典型的空气污染水平后，这些生物标志物随后增加。这些结果增加了先前报道的证据，来自同一研究小组，这些奥运会相关的北京空气污染变化也与全身炎症，血栓形成，血压和心率的变化有关。此外，第三项研究利用北京奥运会相关的空气污染变化（重点是炭黑）发现，空气污染的减少也与呼出的一氧化氮有关，一氧化氮是急性呼吸道炎症的生物标志物（11）。这些研究有几个重要的优势。例如，Huang及其同事（3）利用了奥运会期间通过严格限制北京地区的工业运营和交通而实现的污染物水平的急剧下降，然后在奥运会之后迅速恢复到通常的做法和更典型的奥运前污染物浓度。在这个小组研究中使用准实验设计来估计空气污染对结果的影响，减少了长期健康趋势造成混淆的可能性。随着时间的推移，受关注的健康结果和空气污染水平趋势的这种混淆一直是空气污染领域的共同挑战。
Beijing won its bid to host the 2008 Olympics while promising to substantially improve its air quality, spending in excess of 10 billion dollars to implement pollution control measures (1). Based on substantial and growing evidence that air pollution impacts cardiac and respiratory health (2), Olympic athletes and the public were concerned that notoriously poor air quality in Beijing might have detrimental impacts on athletes. Even after substantive (13–60%) reductions in individual air pollutant concentrations during the 2008 Games as reported in this issue of the Journal (pp. 1150–1159) by Huang and colleagues (3), daily average levels of pollutants such as fine particulate matter in Beijing remained four to nine times higher than in large metropolitan cities in the United States during the same time period (4). Athletes remained concerned about potential health impacts, some deferred competing in the Games (5), and Olympic teams set up training camps away from Beijing to avoid intense air pollution exposures (6). Over several years just prior to the 2008 Olympics, epidemiological studies reported that patterns of associations between fine particulate air pollution and cause-specific mortality were consistent with the hypothesis that air pollution exposure contributes to pulmonary and systemic oxidative stress, inflammation, and associated increased risk of atherosclerosis and ischemic cardiovascular and obstructive pulmonary diseases (2, 7). Recent reviews of the expanding literature (8) and emerging evidence from the Multi-Ethnic Study of Atherosclerosis (9) suggest that there are likely multiple, complex, interdependent mechanistic pathways linking air pollution to cardiopulmonary disease, but also provide growing evidence that pulmonary and systemic oxidative stress and inflammation play important roles. Against this backdrop, in this issue of the Journal, Huang and coworkers (pp. 1150–1159) report results of a Beijing Olympics–based study investigating the relationship between air pollution and exhaled breath and urinary biomarkers of pulmonary and systemic oxidative stress and inflammation (3). This quasiexperimental study evaluated 125 young and healthy medical students before, during, and after the 2008 Beijing Olympics. Huang and colleagues demonstrated substantial decreases in these biomarkers tracking with reductions in air pollution, followed by subsequent increases in these biomarkers after return toward typical levels of air pollution in Beijing. These results add to previously reported evidence, from the same research team, that these Olympics-related changes in air pollution in Beijing were also associated with changes in systemic inflammation, thrombosis, blood pressure, and heart rate (10). Also, a third study using the Beijing Olympics–related changes in air pollution (with a focus on black carbon) found that the reductions in air pollution were also associated with exhaled nitric oxide, a biomarker of acute respiratory inflammation (11). These studies have several important strengths. For example, Huang and colleagues (3) took advantage of the sharp reductions in pollutant levels achieved through intense restrictions on industrial operations and traffic in the Beijing area during the Olympics, followed by a rapid return to usual practices and more typical pre-Olympic pollutant concentrations after the Games. The use of quasiexperimental design in this panel study to estimate the effect of air pollution on the outcomes reduces the potential for confounding by long-term trends in health. Such confounding by trends in both the health outcomes of interest and air pollution levels over time has been a common challenge in air pollution …