Despite increasing epidemiological evidence of an association between air pollution and adverse health outcomes, the detailed mechanisms underlying the adverse effects of air pollution on medical conditions remain unclear. We evaluated the effects of short- and long-term exposure to ambient air pollution on key inflammatory markers in non-smoking subjects. Serum fibrinogen, C-reactive protein, ferritin, and white blood cell counts were repeatedly measured 3 times in 6589 subjects at the Samsung Medical Center (Seoul, South Korea) between 2010 and 2016. Both short- (≤8-day averages) and long-term (annual averages) exposure measures of 6 air pollutants (particles < 2.5 μm, particles < 10 μm, nitrogen dioxide, sulfur dioxide, ozone, and carbon monoxide) were estimated for each subject based on available residential addresses. Linear mixed-effects models were used to relate interquartile range increases in pollutant concentrations to inflammatory marker levels. Short-term exposure to air pollution was associated with increased fibrinogen and ferritin levels. Long-term exposure to air pollution was associated with increased fibrinogen levels and white blood cell counts. The largest short- and long-term associations were observed for ferritin in response to nitrogen dioxide exposure (1.4%, 95% confidence interval [CI] 0.3–2.5) and fibrinogen exposed to particles < 2.5 μm (3.4%, 95% CI 3.0–3.8), respectively. Significantly higher associations were observed among subjects with elevated levels of inflammatory markers (upper 25th percentile), including C-reactive protein, and those with cardiac infarction, chronic obstructive pulmonary disease, cerebral infarction, or diabetes. We found clear associations between short- and long-term exposure to air pollution and inflammatory markers, especially among vulnerable subgroups. Our findings provide evidence in support of the hypothesis that air pollution increases systemic inflammation, particularly among susceptible subgroups.

尽管越来越多的流行病学证据表明空气污染与不良健康后果之间存在关联，但仍不清楚空气污染对医疗条件不利影响的详细机制。我们评估了短期和长期暴露于环境空气污染对非吸烟受试者关键炎症标志物的影响。在2010年至2016年之间，在三星医学中心（韩国首尔）对6589名受试者进行了3次重复的血清纤维蛋白原，C反应蛋白，铁蛋白和白细胞计数测量。短期（≤8天平均值）和六种空气污染物的长期（年度平均值）暴露措施（颗粒<2.5μm，颗粒<10μm，二氧化氮，二氧化硫，臭氧和一氧化碳）是根据可用的住所地址估算出来的。使用线性混合效应模型来关联污染物浓度的四分位数间距增加炎症标记物水平。短期暴露于空气污染与纤维蛋白原和铁蛋白水平升高有关。长期暴露于空气污染与纤维蛋白原水平和白细胞计数增加有关。观察到最大的短期和长期关联是铁蛋白响应二氧化氮暴露（1.4％，95％置信区间[CI] 0.3-2.5）和纤维蛋白原暴露于<2.5μm的颗粒（3.4％，95％CI 3.0） –3.8）。在炎症标志物水平升高（25％以上）（包括C反应蛋白）的受试者以及患有心肌梗塞，慢性阻塞性肺疾病的受试者中，观察到更高的相关性，脑梗塞或糖尿病。我们发现短期和长期暴露于空气污染与炎症标记之间有明确的关联，尤其是在脆弱人群中。我们的发现提供了证据支持空气污染增加全身炎症的假说，尤其是在易感亚组中。