Particulate matter (PM) pollution significantly impacts airway injury and epithelial plasticity, contributing to chronic airway diseases such as asthma and chronic obstructive pulmonary disease (COPD). PM, a complex mixture of solid and liquid particles, can penetrate deep into the lungs, causing mucociliary dysfunction, epithelial barrier disruption, and airway inflammation. PM exposure impairs ciliary function, increases epithelial permeability, and modulates the proliferation and death of airway epithelial cells. It also affects epithelial plasticity, which involves epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET), playing a central role in airway remodeling. PM induces the production of inflammatory mediators such as interleukin (IL)-1β, -6, -8, tumor necrosis factor (TNF)-α, and granulocyte macrophage-colony stimulating factor (GM-CSF), leading to increased airway inflammation and remodeling. PM exposure disrupts tight junction proteins, leading to decreased epithelial barrier integrity and increased paracellular permeability. PM also activates inflammatory pathways such as the TGF-β, NF-κB, and MAPK pathways, contributing to oxidative stress and fibrosis. PM induces EMT by activating ROS production and mitochondrial dysfunction, leading to changes in apical-basal polarity and increased expression of mesenchymal markers. PM exposure can also lead to the differentiation of progenitor cells into secretory and mucus-producing cells, affecting epithelial plasticity. PM exposure is associated with increased airway remodeling in asthma and COPD, characterized by goblet cell hyperplasia, ECM deposition, and increased airway smooth muscle mass. PM exposure disrupts the balance of oxidant/antioxidant systems, leading to chronic airway inflammation and remodeling. PM exposure is linked to increased levels of inflammatory cytokines such as IL-6, IL-8, and TGF-β1, contributing to airway remodeling and fibrosis. PM exposure also activates the Wnt/β-catenin pathway, promoting epithelial plasticity and airway remodeling. Overall, PM exposure plays a significant role in the pathogenesis of chronic airway diseases by impairing epithelial function, inducing inflammation, and promoting airway remodeling.Particulate matter (PM) pollution significantly impacts airway injury and epithelial plasticity, contributing to chronic airway diseases such as asthma and chronic obstructive pulmonary disease (COPD). PM, a complex mixture of solid and liquid particles, can penetrate deep into the lungs, causing mucociliary dysfunction, epithelial barrier disruption, and airway inflammation. PM exposure impairs ciliary function, increases epithelial permeability, and modulates the proliferation and death of airway epithelial cells. It also affects epithelial plasticity, which involves epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET), playing a central role in airway remodeling. PM induces the production of inflammatory mediators such as interleukin (IL)-1β, -6, -8, tumor necrosis factor (TNF)-α, and granulocyte macrophage-colony stimulating factor (GM-CSF), leading to increased airway inflammation and remodeling. PM exposure disrupts tight junction proteins, leading to decreased epithelial barrier integrity and increased paracellular permeability. PM also activates inflammatory pathways such as the TGF-β, NF-κB, and MAPK pathways, contributing to oxidative stress and fibrosis. PM induces EMT by activating ROS production and mitochondrial dysfunction, leading to changes in apical-basal polarity and increased expression of mesenchymal markers. PM exposure can also lead to the differentiation of progenitor cells into secretory and mucus-producing cells, affecting epithelial plasticity. PM exposure is associated with increased airway remodeling in asthma and COPD, characterized by goblet cell hyperplasia, ECM deposition, and increased airway smooth muscle mass. PM exposure disrupts the balance of oxidant/antioxidant systems, leading to chronic airway inflammation and remodeling. PM exposure is linked to increased levels of inflammatory cytokines such as IL-6, IL-8, and TGF-β1, contributing to airway remodeling and fibrosis. PM exposure also activates the Wnt/β-catenin pathway, promoting epithelial plasticity and airway remodeling. Overall, PM exposure plays a significant role in the pathogenesis of chronic airway diseases by impairing epithelial function, inducing inflammation, and promoting airway remodeling.