Air pollution, particularly particulate matter (PM), is a significant contributor to the mortality and morbidity of chronic airway diseases such as asthma and chronic obstructive pulmonary disease (COPD). PM, a complex mixture of solid and liquid particles, can cause airway inflammation and injury by impairing mucociliary function, deteriorating epithelial barrier integrity, and inducing inflammatory responses. The airway epithelium, which forms the first line of defense against inhaled toxicants, plays a crucial role in clearing irritants and orchestrating the inflammatory response. PM can modulate epithelial plasticity and airway remodeling, which are central to the pathogenesis of chronic airway diseases. The review focuses on the effects of PM on airway injury and epithelial plasticity, and the underlying mechanisms involving mucociliary activity, epithelial barrier function, airway inflammation, epithelial-mesenchymal transition (EMT), mesenchymal-epithelial transition (MET), and airway remodeling. PM can impair ciliary function, induce epithelial permeability, and lead to inflammatory changes, while modulating the proliferation and death of airway epithelial cells. It can also affect epithelial plasticity, causing changes in cell morphology, intercellular connections, and increased production of α-smooth muscle actin (α-SMA) and collagen I. PM exposure can disrupt tight junction proteins, leading to increased epithelial permeability and decreased transepithelial electrical resistance. In terms of inflammation, PM exposure can increase the production of inflammatory mediators such as interleukins (ILs), tumor necrosis factor (TNF)-α, and granulocyte-macrophage colony-stimulating factor (GM-CSF). It can also alter the balance of Th1 and Th2 cytokines, leading to increased immune cell recruitment and activation of inflammatory pathways. PM can induce EMT and MET, contributing to the progression of chronic airway diseases. For example, PM can activate the TGF-β, Wnt/β-catenin, and Notch pathways, leading to the expression of transcription factors that promote mesenchymal characteristics and the secretion of matrix metalloproteases (MMPs). Airway remodeling, characterized by changes in the composition and organization of the airway wall, is a common feature of chronic respiratory diseases. PM exposure can lead to airspace enlargement, thickening of the airway walls, and increased deposition of extracellular matrix components. It can also activate pathways involved in ROS production and mitochondrial dysfunction, promoting epithelial cell invasion and remodeling. Despite the extensive research, there are limitations in the current understanding of PM's effects on airway diseases. In vitro studies often use different cell lines and methods, and the impact of PM on primary cells and in vivo models needs further investigation. Additionally, the use of organoid and 3D cell culture systems may provide better insights into the in vivo effects of air pollutants onAir pollution, particularly particulate matter (PM), is a significant contributor to the mortality and morbidity of chronic airway diseases such as asthma and chronic obstructive pulmonary disease (COPD). PM, a complex mixture of solid and liquid particles, can cause airway inflammation and injury by impairing mucociliary function, deteriorating epithelial barrier integrity, and inducing inflammatory responses. The airway epithelium, which forms the first line of defense against inhaled toxicants, plays a crucial role in clearing irritants and orchestrating the inflammatory response. PM can modulate epithelial plasticity and airway remodeling, which are central to the pathogenesis of chronic airway diseases. The review focuses on the effects of PM on airway injury and epithelial plasticity, and the underlying mechanisms involving mucociliary activity, epithelial barrier function, airway inflammation, epithelial-mesenchymal transition (EMT), mesenchymal-epithelial transition (MET), and airway remodeling. PM can impair ciliary function, induce epithelial permeability, and lead to inflammatory changes, while modulating the proliferation and death of airway epithelial cells. It can also affect epithelial plasticity, causing changes in cell morphology, intercellular connections, and increased production of α-smooth muscle actin (α-SMA) and collagen I. PM exposure can disrupt tight junction proteins, leading to increased epithelial permeability and decreased transepithelial electrical resistance. In terms of inflammation, PM exposure can increase the production of inflammatory mediators such as interleukins (ILs), tumor necrosis factor (TNF)-α, and granulocyte-macrophage colony-stimulating factor (GM-CSF). It can also alter the balance of Th1 and Th2 cytokines, leading to increased immune cell recruitment and activation of inflammatory pathways. PM can induce EMT and MET, contributing to the progression of chronic airway diseases. For example, PM can activate the TGF-β, Wnt/β-catenin, and Notch pathways, leading to the expression of transcription factors that promote mesenchymal characteristics and the secretion of matrix metalloproteases (MMPs). Airway remodeling, characterized by changes in the composition and organization of the airway wall, is a common feature of chronic respiratory diseases. PM exposure can lead to airspace enlargement, thickening of the airway walls, and increased deposition of extracellular matrix components. It can also activate pathways involved in ROS production and mitochondrial dysfunction, promoting epithelial cell invasion and remodeling. Despite the extensive research, there are limitations in the current understanding of PM's effects on airway diseases. In vitro studies often use different cell lines and methods, and the impact of PM on primary cells and in vivo models needs further investigation. Additionally, the use of organoid and 3D cell culture systems may provide better insights into the in vivo effects of air pollutants on