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Pulmonary toxicity of polymethyl methacrylate nanoplastics via intratracheal intubation in mice

Scientific Reports 2026
Changsic Youn, Yujin Jo, Jeongwoo Kwon, Seung-Bin Yoon, Hyeong-Ju You, Ji-Su Kim, Ji-Su Kim

Summary

Researchers exposed mice to polymethyl methacrylate nanoplastics through inhalation over 28 days to study their lung effects. The exposed mice experienced weight loss, nanoplastic accumulation in the lungs, increased inflammatory cell counts, and elevated inflammatory cytokines. The findings demonstrate that inhaling these common nanoplastics can induce lung inflammation, tissue damage, and changes in protein and RNA expression.

Polymers
Models
Study Type In vivo

Plastics, ubiquitous in daily life and industry, are released into the environment in substantial quantities. Instead of complete biodegradation, plastic waste fragments into smaller particles, accumulating as nanoplastics (NPs; < 1 μm). Humans are exposed to NPs through inhalation and ingestion of contaminated water and food, which can induce cytotoxicity through physical and chemical pathways. Polymethyl methacrylate (PMMA), commonly used in implants and artificial bones, has been identified in human lungs and associated with pulmonary embolism. While PMMA NP toxicity has been reported in vitro, their in vivo effects, as well as the underlying mechanism, remain poorly understood. In this study, we investigated the pulmonary effects of inhaled PMMA NPs in mice. Mice received 20 or 100 μg of PMMA NPs (25 nm) via intratracheal intubation for 28 days. PMMA-NP preparation and characterization are described in the Methods section. Exposed mice exhibited body weight loss and pulmonary accumulation of PMMA NPs. Bronchoalveolar lavage fluid (BALF) analysis revealed increased cell count and elevated inflammatory cytokines in serum and BALF. Histopathology (H&E staining) revealed abnormalities in lung tissue and alterations in protein and RNA expression. The findings demonstrate that respiratory exposure to PMMA NPs induces lung inflammation, tissue damage, and molecular dysregulation.

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