Endothelial function and chronic exposure to air pollution in normal male subjects
Endothelial function and chronic exposure to air pollution in normal male subjects
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DOI：
10.1161/hypertensionaha.107.095844
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发表时间：
2007-11-01
期刊：
影响因子：
8.3
通讯作者：
Boutouyrie, Pierre
中科院分区：
文献类型：
--
作者：
Briet, Marie;Collin, Cedric;Boutouyrie, Pierre
暴露于城市空气污染，超细颗粒或气体，与急性心血管疾病的死亡率和发病率。我们调查了法国巴黎40名自发呼吸环境空气的健康白色男性不吸烟者的环境空气污染对内皮功能的影响。空气污染物水平（氮，硫和碳氧化物，颗粒物）的平均值在5天前动脉测量。以2周为间隔，使用基于射频的回声跟踪装置测量肱动脉内皮依赖性血流介导的扩张和手部缺血诱导的反应性充血以及内皮素依赖性三硝酸甘油扩张。血流介导的扩张与二氧化硫（P < 0.001）和一氧化氮（P < 0.01）的平均水平呈独立负相关。二氧化硫水平解释了19%的流量介导的扩张的方差。相隔2周，气体污染物的增加与血流介导的扩张的减少显著相关。未发现空气污染物与硝酸甘油诱导的血管舒张之间存在关联。反应性充血与空气动力学直径< 10 μ m和< 2.5 μ m的颗粒物（分别为P < 0.0001和P < 0.001）和二氧化氮（P < 0.01）显著正相关。间隔2周的颗粒物增加与反应性充血增加显著相关。内皮功能受损的普通水平的污染在健康的年轻男性，在城市地区，并可能减少50%之间的最少和最污染的一天。气态污染物影响大动脉内皮功能，而颗粒物则会夸大小动脉对缺血的舒张反应。
Exposure to urban air pollution, ultrafine particles or gases, is associated with acute cardiovascular mortality and morbidity. We investigated the effect of ambient air pollution on endothelial function in 40 healthy white male nonsmokers spontaneously breathing ambient air in Paris, France. Air pollutant levels (nitrogen, sulfur and carbon oxides, and particulate matter) were averaged during the 5 days preceding arterial measurements. Brachial artery endothelium-dependent flow-mediated dilatation and reactive hyperemia induced by hand ischemia and endotheliumin-dependentglyceryl trinitrate dilatation were measured using a radiofrequency-based echo-tracking device at 2-week intervals. Flow-mediated dilatation was independently and negatively correlated with the average levels of sulfur dioxide (P < 0.001) and nitrogen monoxide (P < 0.01). Sulfur dioxide levels explained 19% of the variance of flow-mediated dilatation. An increase in gaseous pollutants, 2 weeks apart, was significantly associated with a decreased in flow-mediated dilatation. No association was found between air pollutants and glyceryl trinitrate-induced vasodilatation. Reactive hyperemia was significantly and positively correlated with particulate matter with aerodynamic diameters < 10 mu m and < 2.5 mu m (P < 0.0001 and P < 0.001, respectively) and nitrogen dioxide (P < 0.01). An increase in particulate matter, 2 weeks apart, was significantly correlated with an increase in reactive hyperemia. Endothelial function was impaired by ordinary levels of pollution in healthy young males, in an urban area, and may be reduced by 50% between the least and the most polluted day. Gaseous pollutants affect large artery endothelial function, whereas particulate matter exaggerates the dilatory response of small arteries to ischemia.