Lung hazards of microplastics and their toxicological mechanisms

Microplastics (MPs), as ubiquitous environmental pollutants, pose significant risks to pulmonary health through inhalation exposure. Due to their small size, large surface area, and high permeability, MPs evade respiratory clearance mechanisms upon entering the airways and deposit in the lungs, triggering a range of multifaceted toxicological effects. Drawing upon extensive research, this review summarizes eight key mechanisms by which MPs induce lung injury including (1) Oxidative stress: MPs promote the generation of reactive oxygen species (ROS), disrupting pulmonary antioxidant defenses and damaging cellular macromolecules; (2) Inflammatory response: MPs induce inflammatory cell infiltration and upregulate pro-inflammatory cytokines (e.g., IL-6, TNF-α), leading to pulmonary inflammation; (3) Apoptosis and autophagy: MPs trigger apoptosis and autophagy in lung cells, with their interplay exacerbating pulmonary tissue damage; (4) Microbial dysbiosis: MPs alter the lung microbiota, aggravating immune dysfunction; (5) Lung surfactant inhibition: MPs adsorb proteins and other components of lung surfactant, impairing alveolar structure and function; (6) Suppressed cell proliferation: MPs hinder lung cell repair, worsening tissue injury; (7) Pulmonary fibrosis: chronic MPs exposure induces epithelial-mesenchymal transition (EMT), promoting collagen deposition and scar formation; (8) Synergistic toxicity: MPs adsorb co-pollutants (e.g., heavy metals), amplifying lung injury. Prolonged MPs exposure is associated with pneumoconiosis, asthma, and lung cancer. Despite the insights gained into the mechanisms of MPs on lung injury, the effects and exact mechanisms of long-term exposure to MPs on lung disease remain unclear, and further research into their causes is the need of time.