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.

Highlights

  • The Great Smog event in London [1] resulted in an estimated death toll in excess of 4000 people because of the significant short-term increase in the concentration of particles in ambient air

  • The Global Burden of Diseases, Injuries, and Risk Factors Study 2010 indicated that particulate matter with an aerodynamic diameter (AD) of

  • A recent study in China reported that fluffy soot particles play a key role in enhancing the toxicity of PM2.5 because of their high intrinsic adhesive capability to stick to toxic matter with different chemical components, generating more complicated compositions of ambient fine particulate matter [12]

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Summary

Introduction

The Great Smog event in London [1] resulted in an estimated death toll in excess of 4000 people because of the significant short-term increase in the concentration of particles in ambient air. Natural combustion processes are far from efficient, and products of combustion mainly include organic carbon species (such as polyaromatic hydrocarbons and dioxins) and trace metals (e.g., lead and arsenic), which are toxic substances that remain in the ambient atmosphere for days, weeks, or even longer [8]. PM10 , PM2.5 , and PM0.1 are termed thoracic particles, fine particles, and ultrafine particles, respectively These categories are generally used as essential indicators of ambient air quality management because of their known effects on human health. A recent study in China reported that fluffy soot particles play a key role in enhancing the toxicity of PM2.5 because of their high intrinsic adhesive capability to stick to toxic matter with different chemical components, generating more complicated compositions of ambient fine particulate matter [12]. Research on the health impacts of airborne particulate matter has traditionally focused on PM2.5

Basic Mechanisms of ACS
Acute Myocardial Infarction
Sudden Coronary Death
Elevated Incidence of ACS
Promoting Progression of ACS
Potential Cellular and Molecular Biology Mechanisms
Pulmonary and Systemic Inflammatory Response
Endothelial Dysfunction of the Coronary Artery
Direct Injury of Cells
Nitric Oxide-Related Mechanisms
Endothelin-1 Involved Mechanisms
Other Factors
Oxidative Stress and Nitrative Stress
Autonomic Dysfunctions
Mitochondrial Damages
Genotoxic Effects
Coronary Artery Atherosclerosis
Elevation of Blood Pressure
Imbalance between Energy Demand and Supply to Heart Tissue
Hypercoagulable State
Perspectives and Significance
Findings
Conclusions

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