Potential Harmful Effects of PM2.5 on Occurrence and Progression of Acute Coronary Syndrome: Epidemiology, Mechanisms, and Prevention Measures

Abstract

The harmful effects of particulate matter with an aerodynamic diameter of <2.5 µm (PM2.5) and its association with acute coronary syndrome (ACS) has gained increased attention in recent years. Significant associations between PM2.5 and ACS have been found in most studies, although sometimes only observed in specific subgroups. PM2.5-induced detrimental effects and ACS arise through multiple mechanisms, including endothelial injury, an enhanced inflammatory response, oxidative stress, autonomic dysfunction, and mitochondria damage as well as genotoxic effects. These effects can lead to a series of physiopathological changes including coronary artery atherosclerosis, hypertension, an imbalance between energy supply and demand to heart tissue, and a systemic hypercoagulable state. Effective strategies to prevent the harmful effects of PM2.5 include reducing pollution sources of PM2.5 and population exposure to PM2.5, and governments and organizations publicizing the harmful effects of PM2.5 and establishing air quality standards for PM2.5. PM2.5 exposure is a significant risk factor for ACS, and effective strategies with which to prevent both susceptible and healthy populations from an increased risk for ACS have important clinical significance in the prevention and treatment of ACS.

Potential injurious effects of the fine particulate PM2.5 on the progression of atherosclerosis in apoE-deficient mice by activating platelets and leukocytes

“…Much epidemiological and experimental study of the fine particulate PM2.5 suggests that it is a risk factor for atherosclerotic progression, and therefore has acquired considerable attention worldwide. PM2.5 exerts atherogenic effects by inducing endothelial damage, mitochondrial injury, genotoxicity, inflammatory responses and oxidative stress [14]. Furthermore, many toxic compounds are adsorbed to fine particles in air pollutants, especially PM2.5.…”

Aerobic training reduces oxidative stress in skeletal muscle of rats exposed to air pollution and supplemented with chromium picolinate

“…Moreover, our study was performed using healthy animals. In contrast, studies using different experimental models of diseases have demonstrated that an underlying condition represents the greatest risk after ROFA exposure, as once oxidants and inflammatory migration occur at sites where there is a pre-established inflammation; this is not observed in healthy animals [44][45][46].…”

A Review of Recent Advances in Research on PM2.5 in China

“…Measles incidence was found to be associated with exposure to ambient PM 2.5 [ 143 ]. Significant associations between PM 2.5 and acute coronary syndrome (ACS) have also been found in most studies [ 144 ]. PM 2.5 may induce oxidative stress and inflammatory responses in human nasal epithelial cells, thereby leading to nasal inflammatory diseases [ 145 ].…”