四分位间距
超细粒子
微粒
纤维蛋白原
血清淀粉样蛋白A
污染物
医学
环境化学
内科学
化学
炎症
有机化学
作者
Megi Vogli,Annette Peters,Kathrin Wolf,Barbara Thorand,Christian Herder,Wolfgang Köenig,Josef Cyrys,Elena Maestri,Nelson Marmiroli,Stefan Karrasch,Siqi Zhang,Regina Pickford
标识
DOI:10.1016/j.scitotenv.2023.169416
摘要
Previous studies consistently showed an association between fine atmospheric particulate matter (PM2.5) and cardiovascular diseases. Concerns about adverse health effects of ultrafine particles (UFP) are growing but long-term studies are still scarce. In this study, we examined the association between long-term exposure to ambient air pollutants and blood biomarkers of inflammation and coagulation, including fibrinogen, high-sensitivity C-reactive protein (hs-CRP), serum amyloid A (SAA) adiponectin and interleukin-6 (IL-6), measured in the German KORA-S4 cohort study (1999–2001). IL-6 was available for older participants only, who were therefore considered as a subsample. Annual mean concentrations of UFP (as particle number concentration), particulate matter in different particles sizes (PM10, PMcoarse, PM2.5, PM2.5 absorbance), ozone (O3), and nitrogen oxides (NO2, NOX) were estimated by land-use regression models and assigned to participants' home addresses. We performed a multiple linear regression between each pollutant and each biomarker with adjustment for confounders. Per 1 interquartile range (IQR, 1945 particles/cm3) increase of UFP, fibrinogen increased by 0.70 % (0.04; 1.37) and hs-CRP increased by 3.16 % (−0.52; 6.98). Adiponectin decreased by −2.53 % (−4.78; −0.24) per 1 IQR (1.4 μg/m3) increase of PM2.5. Besides, PM2.5 was associated with increased IL-6 in the subsample. In conclusion, we observed that long-term exposure to air pollutants, including both fine and ultrafine particles, was associated with higher concentrations of pro-inflammatory and lower concentrations of an anti-inflammatory blood biomarkers, which is consistent with an increased risk for cardiovascular disease observed for long-term exposure to air pollutants.
科研通智能强力驱动
Strongly Powered by AbleSci AI