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Nanoplastics Penetrate Human Bronchial Smooth Muscle and Small Airway Epithelial Cells and Affect Mitochondrial Metabolism
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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.
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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Researchers exposed human HeLa cells (grown in the lab) to polystyrene nanoplastics and measured effects on mitochondria, the cell's energy-producing structures. The nanoplastics disrupted mitochondrial energy production, increased oxidative stress markers, and interfered with communication between mitochondria and another cell structure called the endoplasmic reticulum.
Internalization and toxicity: A preliminary study of effects of nanoplastic particles on human lung epithelial cell
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Researchers studied the effects of polystyrene nanoplastic particles on human lung cells and found that the particles were internalized by the cells and caused dose-dependent toxicity. The nanoplastics triggered oxidative stress, inflammation, and disrupted normal cell function. The findings suggest that inhaling airborne nanoplastics may pose risks to respiratory health.
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This review examines how micro- and nanoplastics can damage mitochondria, the energy-producing structures inside cells that are critical for metabolism and cell survival. Researchers found that plastic particle exposure can trigger oxidative stress, disrupt mitochondrial membrane function, and interfere with energy production pathways. Since mitochondrial dysfunction is linked to numerous health conditions, the study suggests this may be a key mechanism through which plastic pollution affects human health.
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