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Inhaled polystyrene nanoparticles may cause fibrotic lesions via immune dysregulation and energy metabolism disturbance
Summary
Mice received polystyrene nanoparticles via pharyngeal instillation for 90 days and were assessed for local lung and systemic toxicity. The nanoparticles accumulated in lungs and hearts, caused immune dysregulation, disrupted energy metabolism, and induced fibrotic lesions at higher doses, suggesting that chronic inhalation of nanoplastics may contribute to pulmonary fibrosis.
Microplastics have emerged as a major risk to human health. In this study, we dosed polystyrene nanoparticles (PS-NPs) via the pharynx for 90 days and assessed local and systemic toxicity. PS-NPs increased white blood cell counts and decreased blood potassium levels, and they were widely distributed in the lungs and hearts. The total count of pulmonary cells increased with dose, whereas the proportion of macrophages decreased. Levels of immune regulation-related cytokines increased markedly in the lungs of male and female mice exposed to PS-NPs, accompanied by infiltration of inflammatory cells and the aggregation of foamy macrophages. Collagen fiber-and lamellar body-like structures were notably observed in the lungs and hearts of PS-NP-treated mice, accompanied by elevations in both blood total cholesterol and pulmonary IL-11 levels. We also investigated cellular responses in alveolar macrophages (MH-S cells), bronchial epithelial cells (BEAS-2B), and cardiomyocytes (H9C2), which are considered primary target organs for inhaled PS-NPs. PS-NPs inhibited the proliferation of H9C2 cells but not that of BEAS-2B or MH-S cells. In addition, PS-NPs disrupted the expression of energy metabolism-related genes, including those involved in oxidative phosphorylation and respiratory electron transport, across all three cell types, inducing a proteotoxic stress response that involved both mitochondrial and endoplasmic reticulum stress. Based on these results, we propose that chronic inhalation of PS-NPs may lead to fibrotic lesions via immune dysregulation and energy metabolism dysfunction.
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