Chronic obstructive pulmonary disease (COPD) continues to be a leading cause of mortality worldwide. Emerging evidence increasingly identifies exposure to fine particulate matter (PM2.5) as a significant risk factor, in addition to cigarette smoking, highlighting a critical gap in available treatment options. This review synthesizes epidemiological and experimental data that documents the correlation between airborne PM2.5 and the incidence and exacerbations of COPD. Numerous studies have demonstrated that PM2.5 exposure exacerbates COPD, manifesting in reduced lung function, lung and systemic inflammation, oxidative stress, mitochondrial dysfunction, cell death, emphysema, and small airway remodeling, all of which involve complex molecular pathways. Understanding the cellular and molecular mechanisms underlying these effects may inform the development of potential therapeutic interventions, mainly including reactive oxygen species scavengers, anti-inflammatory agents, specific pathway regulators, and traditional Chinese medicine. Future research should prioritize longitudinal exposure assessments and the development of personalized mitigation strategies to address the increasing burden of COPD in regions with high-pollution levels. This review serves as a stark reminder of the urgent necessity for substantive measures to combat air pollution, with the aim of reducing the associated health burden on our expanding global population.
Dong et al. (Mon,) studied this question.
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