The Effects and Pathogenesis of PM2.5 and Its Components on Chronic Obstructive Pulmonary Disease

Abstract

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.

Graphical Abstract

Keywords:

• particulate matter 2.5
• chronic obstructive lung disease
• oxidative stress
• inflammation
• DNA methylation
• microorganisms

Abbreviations

AT1, Alveolar epithelial type I cell; AT2, Alveolar epithelial type II cell; BC, black carbon; CB, carbon black; CPs, carbonaceous particles; COPD, Chronic obstructive pulmonary disease; CRP, C-reactive protein; CS, cigarette smoke; DALYs, Disability-adjusted life years; DCs, dendritic cells; EC, Elemental carbon; EGFR, epidermal growth factor receptor; EVs, Extracellular vesicles; IFN-γ, interferon-gamma; MAD, malondialdehyde; NF-κB, nuclear factor kappa B; OC, Organic carbon; OGG1, 8-oxoguanine DNA glycosylase 1; PAHs, polycyclic aromatic hydrocarbons; PM, particulate matter; ROS, reactive oxygen species; TLRS, toll-like receptors; TRPM2, Transient Receptor Potential Melastatin2 WBC, white blood cells.

Acknowledgments

We appreciate Prof. Tan Xiaowu’s work on the article revision.

Disclosure

The authors declare no conflicts of interest in this work.

Additional information

Funding

The study was funded by National Natural Science Foundation of China (81900044, to Dr. S. Liu), Natural Science Foundation of Hunan Province (2021JJ40484, to Dr. S. Liu), The Key project of Science and Technology Plan of Health Commission of Hunan Province (20201922, to Prof. X. Tan).