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Air pollution-induced airway epithelial barrier dysfunction in COPD: a narrative review of mechanisms and therapeutic implications
Summary
Breathing polluted air—from smoke, car exhaust, ozone, and even tiny microplastic particles—can damage the protective lining of your airways, making it easier for irritants and germs to get in and worsen lung disease like COPD. This review pulls together existing research showing that this damage doesn't just stay in the lungs; it can also disrupt gut bacteria in ways that further harm lung health. The encouraging news is that scientists are exploring treatments—like antioxidants, natural compounds, and probiotics—that might help repair this airway lining and protect people who live in heavily polluted areas.
Air pollution is particularly harmful to people with chronic obstructive pulmonary disease (COPD). Exposure to air pollution from sources such as biomass burning leads to a unique COPD phenotype. This phenotype mainly shows airway damage, with less emphysema than typical smoking-related phenotypes. Across various COPD phenotypes, airway epithelial barrier dysfunction is a basic pathological mechanism. This narrative review summarises the current available evidence on how different types of airborne pollutants, including particulate matter (PM), ozone (O 3 ), diesel exhaust and microplastics, damage the airway epithelial barrier. The toxicity of fine PM with a diameter of ≤2.5 µm, one of its main constituents, largely depends on its chemical composition. Some metals or organic chemicals with redox properties can initiate oxidation reactions and induce pathologic responses. The main injury mechanisms are direct physical damage to apical junctional complexes, serious impairment of mucociliary clearance and induction of oxidative stress. Apart from these immediate harms, pollutants also create epigenetic modifications and disturbed epithelium–immune cell cross-talk, which breaks down the equilibrium of the airway epithelial barrier. These system-wide effects are exacerbated through the gut–lung axis, which aggravates local lung damage via microbiome dysregulation. We evaluate emerging therapeutic strategies that aim to restore barrier integrity, including antioxidants, natural compounds, inhibitors directing specific pathways ( e.g. epidermal growth factor receptor (EGFR), NLR family pyrin domain containing 3 (NLRP3)) and microbiome modulation via probiotics. Protection and repair of the airway epithelial barrier offer a promising approach to reducing the onset and progression of pollution-related COPD in populations vulnerable to highly polluted environments.