Yanping Ruana, Ruijuan Liangb, Hui Liana, Xiaoyi Zhaoa, Xiaole Liua and Zhongjie Fan
Association of particulate matter with endothelial function Current evidence has confirmed the definite correlation between air pollution and cardiovascular disease. One of the mechanisms was the adverse effect on endothelial function. However, there is heterogeneity between the air pollution and endothelial function in different studies. We performed a meta-analysis to determine the direction and strength of the association. PubMed, EMBASE, Cochrane library and Web of Science were searched for a combination of keywords related to major air pollutants and to the indexes of endothelial function, including reactive hyperemia, flow-mediated dilation and nitroglycerin-mediated dilatation. Thirteen of reviewed articles with sufficient details met inclusion criteria. Descriptive and quantitative information was extracted from the included studies. A pooled estimate in a random effects model was computed, and change in endothelial function (95% CIs) were calculated for each increment of 10 μg/m3 in PM2.5, and 1 μg/ m3 scaled for black carbon. A 0.27% decrease in flow-mediated dilation was marginally associated with per 1 μg/m3 increase in PM2.5 in overall risk estimate analysis, with the greatest effect occurred in PM2.5 exposure for 1-day lag. Subgroup analyses have shown that the effect was modified by the factors as follows: American, subjects aged less than 55 years old, the proportion of female less than 50%, and the panel design. A 0.07 mm decrease in brachial artery diameter and 2.46% decrease in nitroglycerin-mediated dilation for per 1 μg/m3 increment in BC were observed in the pooled analysis from two studies(P=0.005 and P=0.043, respectively). No significant association was found between black carbon and flow-mediated dilation. Short-term exposure to PM2.5 and black carbon was associated with endothelial function, which provided the evidence for the increased risk of cardiovascular disease due to air pollution
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