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Inhalable airborne pollutants, including particulate matter, ozone, cigarette smoke, and emerging microparticles and nanoparticles can initiate or exacerbate various lung diseases. Their toxicological impact depends not only on their chemical composition, but also on the host's capacity for clearance and post-injury repair mechanisms. Studies have identified region-specific stem cells within the lung epithelial-mucosal barrier, which are pivotal for mucosal repair after damage. This review delineates the roles of airway and alveolar key stem cells in lung epithelial mucosal repair, details how traditional and emerging airborne pollutants affect their regenerative capabilities. Additionally, it discusses the transformative contributions of organoids and single-cell sequencing technologies to advance our understanding of how inhaled pollutants affect lung tissue toxicity. A tissue regeneration perspective on the interplay between inhaled pollutants and lung stem cells is crucial for developing comprehensive strategies to prevent and control lung diseases associated with exposure to airborne pollutants.
Wu et al. (Thu,) studied this question.