Department of Social and Environmental Health Research, London School of Hygiene and Tropical Medicine, London, UK.
Department of Non-Communicable Disease Epidemiology, London School of Hygiene and Tropical Medicine, London, UK.
Heart. 2014 Jul;100(14):1093-8. doi: 10.1136/heartjnl-2013-304963. Epub 2014 Jun 4.
To inform potential pathophysiological mechanisms of air pollution effects on cardiovascular disease (CVD), we investigated short-term associations between ambient air pollution and a range of cardiovascular events from three national databases in England and Wales.
Using a time-stratified case-crossover design, over 400,000 myocardial infarction (MI) events from the Myocardial Ischaemia National Audit Project (MINAP) database, over 2 million CVD emergency hospital admissions and over 600,000 CVD deaths were linked with daily mean concentrations of carbon monoxide (CO), nitrogen dioxide (NO2), particulate matter less than 10 μm in aerodynamic diameter (PM10), particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5) and sulfur dioxide (SO2), and daily maximum of 8-hourly running mean of O3 measured at the nearest air pollution monitoring site to the place of residence. Pollutant effects were modelled using lags up to 4 days and adjusted for ambient temperature and day of week.
For mortality, no CVD outcome analysed was clearly associated with any pollutant, except for PM2.5 with arrhythmias, atrial fibrillation and pulmonary embolism. With hospital admissions, only NO2 was associated with a raised risk: CVD 1.7% (95% CI 0.9 to 2.6), non-MI CVD 2.0% (1.1 to 2.9), arrhythmias 2.9% (0.6 to 5.2), atrial fibrillation 2.8% (0.3 to 5.4) and heart failure 4.4% (2.0 to 6.8) for a 10th-90th centile increase. With MINAP, only NO2 was associated with an increased risk of MI, which was specific to non-ST-elevation myocardial infarction (non-STEMIs): 3.6% (95% CI 0.4 to 6.9).
This study found no clear evidence for pollution effects on STEMIs and stroke, which ultimately represent thrombogenic processes, though it did for pulmonary embolism. The strongest associations with air pollution were observed with selected non-MI outcomes.
为了探究空气污染对心血管疾病（CVD）影响的潜在病理生理学机制，我们从英格兰和威尔士的三个国家数据库中调查了短期环境空气污染与一系列心血管事件之间的关联。
使用时间分层病例交叉设计，将超过 40 万例心肌梗死（MI）事件纳入心肌缺血国家审计项目（MINAP）数据库，超过 200 万例 CVD 急症住院和超过 60 万例 CVD 死亡与每日一氧化碳（CO）、二氧化氮（NO2）、小于 10μm 空气动力学直径的颗粒物（PM10）、小于 2.5μm 空气动力学直径的颗粒物（PM2.5）和二氧化硫（SO2）的日平均浓度以及居住地附近空气污染监测点每日最大 8 小时平均臭氧（O3）进行关联。使用滞后 4 天的模型来模拟污染物的影响，并调整环境温度和星期几的影响。
对于死亡率，除了 PM2.5 与心律失常、心房颤动和肺栓塞有关外，没有任何 CVD 结局与任何污染物明显相关。对于住院，只有二氧化氮与风险升高有关：CVD 1.7%（95%CI 0.9 至 2.6），非-MI CVD 2.0%（1.1 至 2.9），心律失常 2.9%（0.6 至 5.2），心房颤动 2.8%（0.3 至 5.4），心力衰竭 4.4%（2.0 至 6.8），这是第 10 至 90 百分位的增加。在 MINAP 中，只有二氧化氮与非 ST 段抬高心肌梗死（非 STEMI）的 MI 风险增加有关：3.6%（95%CI 0.4 至 6.9）。
本研究未发现空气污染对 STEMI 和中风的明显影响，这些疾病最终代表血栓形成过程，但对肺栓塞有影响。与空气污染的最强关联是观察到某些非-MI 结局。
