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Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Environmental Sources Human Health Effects Nanoplastics Sign in to save

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

Ecotoxicology and Environmental Safety 2025 3 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Zhe Wang, Ning Wang, Shuo Jiang, R. S. Shi, Rui Wang, Weidong Wu

Summary

Researchers exposed mice to polystyrene nanoplastics through the airway and found that the particles caused lung inflammation and tissue damage. Using metabolomics analysis, they discovered that the nanoplastics disrupted multiple metabolic pathways in lung tissue, with surface-modified particles causing more severe effects. The study provides evidence that inhaled nanoplastics can alter lung metabolism in ways that may contribute to respiratory health problems.

Polymers
Models
Study Type In vitro

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.

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