Brook Robert D, Brook Jeffrey R, Rajagopalan Sanjay
University of Michigan, 3918 Taubman Center, 1500 East Medical Center Drive, Ann Arbor, MI 48109, USA.
Curr Hypertens Rep. 2003 Feb;5(1):32-9. doi: 10.1007/s11906-003-0008-y.
Air pollution exposure is associated with an increased risk of acute and chronic cardiovascular mortality. Recent observations have implicated fine particulate matter (PM(2.5)) as one of the most important pollutants. Inhalation of PM(2.5) causes acute pulmonary inflammation and oxidative stress. The subsequent generation of a systemic inflammatory response could link air pollution exposure with the development of cardiovascular disease. Human experiments have demonstrated pro-arrhythmic alterations in cardiac autonomic tone, increased blood pressure, higher serum C-reactive protein levels, and alterations in blood rheology favoring coagulation following controlled pollution exposures or in relation to elevated ambient PM(2.5) levels. Recent studies have also uncovered several harmful impacts on the systemic vasculature, including the triggering of acute vasoconstriction and the enhanced development of atherosclerosis. Many questions, however, remain unanswered and future studies will be required to clarify the relevant biologic mechanisms and to identify the specific constituents responsible for mediating the adverse health impacts.
接触空气污染与急性和慢性心血管疾病死亡风险增加相关。最近的观察表明，细颗粒物（PM2.5）是最重要的污染物之一。吸入PM2.5会导致急性肺部炎症和氧化应激。随后产生的全身炎症反应可能将接触空气污染与心血管疾病的发展联系起来。人体实验表明，在受控污染暴露后或与环境PM2.5水平升高相关时，心脏自主神经张力会出现促心律失常改变、血压升高、血清C反应蛋白水平升高以及血液流变学改变有利于凝血。最近的研究还发现了对全身血管系统的几种有害影响，包括引发急性血管收缩和加速动脉粥样硬化的发展。然而，许多问题仍未得到解答，未来需要进行研究以阐明相关的生物学机制，并确定介导不良健康影响的具体成分。
