Polystyrene nanoplastics induced lung injury in mice: Insights into lung metabolic disorders

Micro- and nanoplastics have attracted increasing attention to their potential health hazards. However, the impacts of plastic particles in the air on the respiratory system were largely neglected, and the mechanisms by which micro- and nanoplastics elicit toxicity to the lung have not been clearly recognized. This study aims to clarify the pulmonary toxicity of polystyrene nanoplastics (PSNPs) with or without surface modification and explore the underlying mechanisms via metabolomics technology. After exposure to bare PSNPs (PSNP-B) or aminated PSNPs (PSNP-NH₂) via intratracheal instillation at the dose within real-world nanoplastic inhalation levels in humans, the accumulation of PSNPs in lung tissues of mice was observed, accompanied by aberrant histological structure and remarkable oxidative stress and inflammation. Metabolomics analysis revealed that PSNP exposure disturbed the levels of lung metabolites, and the significantly differential metabolites were mainly enriched in purine metabolism and arachidonic acid metabolism pathways. PSNP-NH₂ elicited more diverse impacts on lung metabolism compared to PSNP-B. Further in vitro studies identified that PSNP-NH₂ could enter human lung epithelial BEAS-2B cells and induce oxidative stress, inflammatory responses and key metabolic enzyme alterations in BEAS-2B cells. Together, these results revealed disorder of lung metabolism as an essential mechanism of PSNP-induced lung injury. This study provides new insights into the health impacts of airborne nanoplastics.