Effects of PM2.5 exposure on lung histology: Cellular, molecular, and pathophysiological mechanisms

Abstract

Particulate matter smaller than 2.5 μm in aerodynamic diameter (PM2.5) is one of the most harmful environmental pollutants affecting respiratory health worldwide. Due to its ultrafine size and complex chemical composition, PM2 1 .5 can penetrate deeply into the respiratory tract, accumulate within alveolar regions, and trigger multiple pathological processes in lung tissue. Increasing evidence from experimental and clinical studies demonstrates that PM2.5 exposure induces oxidative stress, mitochondrial dysfunction, inflammatory signaling, epithelial injury, extracellular matrix remodeling, and pulmonary fibrosis. This review comprehensively evaluates the histopathological and molecular alterations induced by PM2.5 exposure in lung tissue. Experimental findings from animal models and cellular studies are comparatively discussed to better integrate histological observations with molecular mechanisms and clinical outcomes. Particular emphasis is placed on oxidative stress pathways, NF-κB-mediated inflammation, mitochondrial damage, and TGF-β-associated fibrotic remodeling. Furthermore, current challenges, research limitations, and future perspectives regarding PM2.5-associated lung injury are highlighted. Understanding these mechanisms is essential for developing preventive strategies and novel therapeutic approaches against air pollution-related respiratory diseases.