Department of Epidemiology, School of Medicine, University of California-Irvine, Irvine, California 92617-7555, USA.
Environ Health Perspect. 2011 Feb;119(2):196-202. doi: 10.1289/ehp.1002372. Epub 2010 Oct 21.
Air pollutants have not been associated with ambulatory electrocardiographic evidence of ST-segment depression ≥ 1 mm (probable cardiac ischemia). We previously found that markers of primary (combustion-related) organic aerosols and gases were positively associated with circulating biomarkers of inflammation and ambulatory blood pressure in the present cohort panel study of elderly subjects with coronary artery disease.
We specifically aimed to evaluate whether exposure markers of primary organic aerosols and ultrafine particles were more strongly associated with ST-segment depression of ≥ 1 mm than were secondary organic aerosols or PM2.5 (particulate matter with aerodynamic diameter ≤ 2.5 µm) mass.
We evaluated relations of air pollutants to ambulatory electrocardiographic evidence of cardiac ischemia over 10 days in 38 subjects without ST depression on baseline electrocardiographs. Exposures were measured outdoors in retirement communities in the Los Angeles basin, including daily size-fractionated particle mass and hourly markers of primary and secondary organic aerosols and gases. Generalized estimating equations were used to estimate odds of hourly ST-segment depression (≥ 1 mm) from hourly air pollution exposures and to estimate relative rates of daily counts of ST-segment depression from daily average exposures, controlling for potential confounders.
We found significant positive associations of hourly ST-segment depression with markers of combustion-related aerosols and gases averaged 1-hr through 3-4 days, but not secondary (photochemically aged) organic aerosols or ozone. The odds ratio per interquartile increase in 2-day average primary organic carbon (5.2 µg/m3) was 15.4 (95% confidence interval, 3.5-68.2). Daily counts of ST-segment depression were consistently associated with primary combustion markers and 2-day average quasi-ultrafine particles < 0.25 µm.
Results suggest that exposure to quasi-ultrafine particles and combustion-related pollutants (predominantly from traffic) increase the risk of myocardial ischemia, coherent with our previous findings for systemic inflammation and blood pressure.
空气中的污染物与 1 毫米（可能的心肌缺血）以上的动态心电图 ST 段压低的间歇性心电图证据无关。我们之前发现，在本研究中，与冠心病老年患者队列的研究中，主要（燃烧相关）有机气溶胶和气体的标志物与循环炎症生物标志物和间歇性血压呈正相关。
我们特别评估了主要有机气溶胶和超细颗粒的暴露标志物是否与 1 毫米以上的 ST 段压低比二次有机气溶胶或 PM2.5（空气动力学直径≤2.5µm 的颗粒物质）质量更密切相关。
我们评估了在洛杉矶盆地的退休社区中，在没有基线心电图 ST 段压低的 38 名患者中，10 天内的间歇性心电图心肌缺血的证据与大气污染物的关系。在退休社区中，通过每日大小分级的颗粒质量和每小时主要和次要有机气溶胶和气体的标志物来测量室外暴露。使用广义估计方程来估计每小时大气污染暴露与每小时 ST 段压低（≥1 毫米）的几率，并估计每日平均暴露与每日 ST 段压低的每日计数的相对率，同时控制潜在的混杂因素。
我们发现，与燃烧相关的气溶胶和气体的每小时 ST 段压低与标记物有显著的正相关，从 1 小时到 3-4 天的平均时间，而不是二次（光化学老化）有机气溶胶或臭氧。每增加一个四分位距的 2 天平均主要有机碳（5.2µg/m3）的比值比为 15.4（95%置信区间，3.5-68.2）。每日 ST 段压低的计数与主要燃烧标记物和 2 天平均准超细颗粒<0.25µm 始终相关。
结果表明，暴露于准超细颗粒和燃烧相关的污染物（主要来自交通）会增加心肌缺血的风险，这与我们之前关于系统性炎症和血压的发现是一致的。
