Progress in research on effect of PM2.5 on occurrence and development of atherosclerosis

Fine particulate matter ≤2.5 μm (PM2.5) air pollution is regarded as one of the prominent risk factors that contributes to morbidity and mortality globally, among which cardiovascular disease (CVD) has been strongly associated with PM2.5 exposure and is a leading cause of death. Atherosclerosis (AS), the common pathological basis of many CVDs, is a progressive syndrome characterized by the accumulation of lipids and fibrous plaque in the arteries. Recent epidemiological and toxicological studies suggest that PM2.5 may also contribute to the development of AS, even at levels below the current air quality standards. In this paper, the complete pathological process of atherosclerotic plaque from occurrence to rupture leading to CVD was elaborated. Then, the growing epidemiological evidence linking PM2.5 to AS in humans was reviewed and summarized. Furthermore, the potential mechanisms of PM2.5‐mediated AS were discussed, including oxidative stress, inflammation, endothelial dysfunction, abnormal lipid metabolism, disturbance of the autonomic nervous system, and abnormal coagulation function. This paper aimed to provide a comprehensive view of the effect of PM2.5 on the occurrence and development of AS for better prevention and mitigation of adverse health impacts due to PM2.5 air pollution. Atherosclerotic cardiovascular disease (CVDs) has been strongly associated with PM2.5 exposure. The promoting effect of PM2.5 on arteriosclerosis runs through the whole development process from lesion initiation to plaque rupture. The main mechanisms are oxidative stress, inflammation, endothelial dysfunction, abnormal lipid metabolism, disturbance of the autonomic nervous system and abnormal coagulation function.