Chronic obstructive pulmonary disease (COPD), a heterogeneous disease, is the leading cause of death worldwide. In recent years, air pollution, especially particulate matter (PM), has been widely studied as a contributing factor to COPD. As an essential component of PM, PM2.5 is associated with COPD prevalence, morbidity, and acute exacerbations. However, the specific pathogenic mechanisms were still unclear and deserve further research. The diversity and complexity of PM2.5 components make it challenging to get its accurate effects and mechanisms for COPD. It has been determined that the most toxic PM2.5 components are metals, polycyclic aromatic hydrocarbons (PAHs), carbonaceous particles (CPs), and other organic compounds. PM2.5-induced cytokine release and oxidative stress are the main mechanisms reported leading to COPD. Nonnegligibly, the microorganism in PM 2.5 may directly cause mononuclear inflammation or break the microorganism balance contributing to the development and exacerbation of COPD. This review focuses on the pathophysiology and consequences of PM2.5 and its components on COPD.
Keywords: DNA methylation; chronic obstructive lung disease; inflammation; microorganisms; oxidative stress; particulate matter 2.5.
© 2023 Wang and Liu.