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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. Detection Methods Human Health Effects Nanoplastics Sign in to save

Nanoplastics Penetrate Human Bronchial Smooth Muscle and Small Airway Epithelial Cells and Affect Mitochondrial Metabolism

International Journal of Molecular Sciences 2024 21 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 65 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Ewa Winiarska, Ewa Winiarska, Monika Chaszczewska-Markowska, Marek Jutel Magdalena Zemelka‐Wiącek, Daniel Ghete, Marek Jutel Magdalena Zemelka‐Wiącek, Marek Jutel Marek Jutel

Summary

When human lung cells were exposed to 25 and 50 nanometer polystyrene nanoplastics in the lab, the particles penetrated both airway lining cells and the smooth muscle cells underneath, including cells from asthmatic donors. The nanoplastics disrupted the cells' energy-producing mitochondria, impairing both normal oxygen-based metabolism and backup energy pathways -- demonstrating a direct mechanism by which inhaled nanoplastics could harm respiratory health.

Polymers
Study Type In vitro

Micro- and nanoplastic particles, including common forms like polyethylene and polystyrene, have been identified as relevant pollutants, potentially causing health problems in living organisms. The mechanisms at the cellular level largely remain to be elucidated. This study aims to visualize nanoplastics in bronchial smooth muscle (BSMC) and small airway epithelial cells (SAEC), and to assess the impact on mitochondrial metabolism. Healthy and asthmatic human BSMC and SAEC in vitro cultures were stimulated with polystyrene nanoplastics (PS-NPs) of 25 or 50 nm size, for 1 or 24 h. Live cell, label-free imaging by holotomography microscopy and mitochondrial respiration and glycolysis assessment were performed. Furthermore, 25 and 50 nm NPs were shown to penetrate SAEC, along with healthy and diseased BSMC, and they impaired bioenergetics and induce mitochondrial dysfunction compared to cells not treated with NPs, including changes in oxygen consumption rate and extracellular acidification rate. NPs pose a serious threat to human health by penetrating airway tissues and cells, and affecting both oxidative and glycolytic metabolism.

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