Briet Marie, Collin Cédric, Laurent Stéphane, Tan Alice, Azizi Michel, Agharazii Mohsen, Jeunemaitre Xavier, Alhenc-Gelas François, Boutouyrie Pierre
Faculté de Médecine René Descartes, Université Paris-Descartes, INSERM, UMR872, Paris, France.
Hypertension. 2007 Nov;50(5):970-6. doi: 10.1161/HYPERTENSIONAHA.107.095844. Epub 2007 Sep 17.
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 endothelium-independent glyceryl 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 microm and <2.5 microm (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.
暴露于城市空气污染、超细颗粒物或气体中与急性心血管疾病的死亡率和发病率相关。我们在法国巴黎对40名健康的白人男性非吸烟者进行了研究，这些人在自然呼吸环境空气的情况下，调查了环境空气污染对其内皮功能的影响。在进行动脉测量前的5天内，对空气污染物水平（氮氧化物、硫氧化物、碳氧化物和颗粒物）进行了平均。使用基于射频的回声跟踪装置，每隔2周测量一次肱动脉内皮依赖性血流介导的舒张功能以及手部缺血诱导的反应性充血和非内皮依赖性硝酸甘油介导的舒张功能。血流介导的舒张功能与二氧化硫平均水平（P<0.001）和一氧化氮平均水平（P<0.01）呈独立负相关。二氧化硫水平解释了血流介导舒张功能变化的19%。间隔2周的气态污染物增加与血流介导舒张功能下降显著相关。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微米和<2.5微米的颗粒物（分别为P<0.0001和P<0.001）以及二氧化氮（P<0.01）呈显著正相关。间隔2周的颗粒物增加与反应性充血增加显著相关。在城市地区，健康年轻男性的内皮功能会因普通污染水平而受损，在污染最轻和最重的日子之间，内皮功能可能会降低50%。气态污染物影响大动脉内皮功能，而颗粒物会增强小动脉对缺血的扩张反应。
