Henning Robert J
University of South Florida, Tampa, FL.
Curr Probl Cardiol. 2024 Jan;49(1 Pt B):102094. doi: 10.1016/j.cpcardiol.2023.102094. Epub 2023 Sep 20.
Air pollution is responsible worldwide for 9-12 million deaths annually. The major contributor to air pollution is particulate matter ≤2.5 µg per cubic meter of air (PM2.5) from vehicles, industrial emissions, and wildfire smoke. United States ambient air standards recommend annual average PM2.5 concentrations of ≤12 μg/m³ while European standards allow an average annual PM2.5 concentration of ≤20 μg/m. However, significant PM2.5 cardiovascular and pulmonary health risks exist below these concentrations. Chronic PM2.5 exposure significantly increases major cardiovascular and pulmonary event risks in Americans by 8 to more than 20% for each 10-μg/m increase in PM2.5. PM2.5-induced increases in lipid peroxidation, induction of vascular inflammation and endothelial cell injury initiate and propagate respiratory diseases, coronary and carotid atherosclerosis. PM2.5 can cause atherosclerotic vascular plaque rupture and myocardial infarction and stroke by activating metalloproteinases. This article discusses PM2.5 effects on the cardiovascular and pulmonary systems, specific PM2.5 pathophysiologic mechanisms contributing to cardiopulmonary disease, and preventive measures to limit the cardiovascular and pulmonary effects of PM2.5.
空气污染在全球范围内每年导致900万至1200万人死亡。造成空气污染的主要因素是每立方米空气中直径小于等于2.5微米的颗粒物(PM2.5),其来源包括车辆尾气、工业排放和野火烟雾。美国环境空气质量标准建议PM2.5的年平均浓度应小于等于12微克/立方米,而欧洲标准允许的PM2.5年平均浓度为小于等于20微克/立方米。然而,在这些浓度之下,PM2.5依然会对心血管和肺部健康构成显著风险。在美国,长期接触PM2.5会显著增加主要心血管和肺部疾病的发病风险,PM2.5每增加10微克/立方米,发病风险就会上升8%至20%以上。PM2.5会导致脂质过氧化增加、引发血管炎症以及造成内皮细胞损伤,从而引发并加剧呼吸系统疾病、冠状动脉和颈动脉粥样硬化。PM2.5可通过激活金属蛋白酶导致动脉粥样硬化斑块破裂,进而引发心肌梗死和中风。本文将探讨PM2.5对心血管和肺部系统的影响、导致心肺疾病的具体病理生理机制,以及限制PM2.5对心血管和肺部影响的预防措施。