Air pollution is associated with increased risk of cardiovascular disease, possibly through chronic systemic inflammation that promotes the progression of atherosclerosis and the risk of cardiovascular events. This study aimed to investigate the associations between air pollution and established biomarkers of inflammation and cardiovascular disease. The Cardiovascular Subcohort of the Malmö Diet and Cancer cohort includes 6103 participants from the general population of Malmö, Sweden. The participants were recruited 1991–1994. Annual mean residential exposure to particulate matter < 2.5 and < 10 μm (PM2.5 and PM10), and nitrogen oxides (NOx) at year of recruitment were assigned from dispersion models. Blood samples collected at recruitment, including blood cell counts, and biomarkers (lymphocyte- and neutrophil counts, C-reactive protein (CRP), soluble urokinase-type plasminogen activator receptor (suPAR), lipoprotein-associated phospholipase A2 (Lp-PLA2), ceruloplasmin, orosomucoid, haptoglobin, complement-C3, and alpha-1-antitrypsin) were analyzed. Multiple linear regression models were used to investigate the cross-sectional associations between air pollutants and biomarkers. The mean annual exposure levels in the cohort were only slightly or moderately above the new WHO guidelines of 5 μg/m3 PM2.5 (10.5 μg/m3 PM2.5). Residential PM2.5 exposure was associated with increased levels of ceruloplasmin, orosomucoid, C3, alpha-1-antitrypsin, haptoglobin, Lp-PLA2 and the neutrophil-lymphocyte ratio. Ceruloplasmin, orosomucoid, C3 and alpha-1-antitrypsin were also positively associated with PM10. There were no associations between air pollutants and suPAR, leukocyte counts or CRP. The associations between particles and biomarkers were still significant after removing outliers and adjustment for CRP levels. The associations were more prominent in smokers. Long-term residential exposure to moderate levels of particulate air pollution was associated with several biomarkers of inflammation and cardiovascular disease. This supports inflammation as a mechanism behind the association between air pollution and cardiovascular disease.

中文翻译：

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马尔默饮食和癌症队列中的空气污染和心血管疾病和炎症的生物标志物

空气污染与心血管疾病风险增加有关，可能是通过促进动脉粥样硬化进展和心血管事件风险的慢性全身炎症。本研究旨在调查空气污染与已建立的炎症和心血管疾病生物标志物之间的关联。马尔默饮食和癌症队列的心血管亚群包括来自瑞典马尔默普通人群的 6103 名参与者。参与者是在 1991-1994 年招募的。从分散模型中分配了招募年份的年平均住宅暴露于 < 2.5 和 < 10 微米（PM2.5 和 PM10）和氮氧化物 (NOx) 的颗粒物。招募时采集的血样，包括血细胞计数和生物标志物（淋巴细胞和中性粒细胞计数，分析了 C 反应蛋白 (CRP)、可溶性尿激酶型纤溶酶原激活物受体 (suPAR)、脂蛋白相关磷脂酶 A2 (Lp-PLA2)、铜蓝蛋白、口腔粘蛋白、触珠蛋白、补体-C3 和 α-1-抗胰蛋白酶)。多元线性回归模型用于研究空气污染物和生物标志物之间的横截面关联。该队列的平均年暴露水平仅略高于 WHO 新指南 5 μg/m3 PM2.5（10.5 μg/m3 PM2.5）。住宅 PM2.5 暴露与铜蓝蛋白、口腔粘蛋白、C3、α-1-抗胰蛋白酶、触珠蛋白、Lp-PLA2 和中性粒细胞-淋巴细胞比值水平升高有关。铜蓝蛋白、口腔粘蛋白、C3 和 α-1-抗胰蛋白酶也与 PM10 呈正相关。空气污染物与 suPAR 之间没有关联，白细胞计数或 CRP。在去除异常值并调整 CRP 水平后，颗粒和生物标志物之间的关联仍然显着。这种关联在吸烟者中更为突出。长期住宅暴露于中等水平的颗粒物空气污染与炎症和心血管疾病的几种生物标志物有关。这支持炎症作为空气污染与心血管疾病之间关联背后的一种机制。