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Size-dependent toxicity of polystyrene microplastics in lung cells: An in vivo and in vitro study
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Researchers investigated the size-dependent toxicity of polystyrene microplastics in lung cells using both mouse and cell culture models. The study found that smaller 1-micrometer particles accumulated more in lung tissue than larger particles and identified epithelial-mesenchymal transition as a key toxic mechanism, driven by ECM-MMP signaling cascades that contribute to lung injury.
Microplastics (MPs) are emerging pollutants with pervasive respiratory exposure routes, yet their lung-specific toxicity mechanisms remain poorly defined. This study aims to investigate the size-dependent detrimental effects on pulmonary systems using in vivo (mice) and in vitro (coculture) models, simulating acute (single dose) and subchronic (28-day) exposures. Crucially, we identify epithelial-mesenchymal transition (EMT) as a novel cytotoxic mechanism and delineate the ECM-MMP signaling cascade as the primary driver of PS-MP-induced lung injury. In vivo, acute intratracheal exposure to 12 mg/kg PS-MPs (with 1 µm particles) resulted in weight loss (9.09 % vs. controls). PS-MPs accumulated dominantly in lungs, with 1 µm particles depositing 1.38-fold higher than 10 µm particles (quantitative result). Subchronic exposure (8 mg/kg) triggered particle-size-dependent pathology. 1 µm PS-MPs increased lung injury scores by 2.5-fold vs. 10 µm. Myeloperoxidase (MPO) and malondialdehyde (MDA) rose by 2.13-fold (1 µm) vs. 1.81-fold (10 µm). In vitro, 1 µm PS-MP-exposed lung cells induced mitochondrial depolarization (ΔΨm loss: 50 %) and apoptosis (17 % increase). Critically, 1 µm PS-MPs potently activated MMPs (MMP-2↑180 %, MMP9↑250 %) via ECM-MMP dysregulation. Our findings reveal that PS-MPs drive lung injury through oxidative stress, cell apoptosis, and mitochondrial dysfunction in a strict size-dependent manner (1 µm > 5 µm > 10 µm), with the ECM-MMP axis as a central pathway. The signaling pathway activated by PS-MPs in lung injury suggested that PS-MPs induced proliferation inhibition, oxidative stress, and EMT via activating the ECM-MMP signaling cascade. In addition, EMT activation suggested a novel mechanism for the cytotoxicity of PS-MPs, hinting at the potential carcinogenic effect of these pollutants.
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Microplastics and nanoplastics, emerging pollutants, increased the risk of pulmonary fibrosis in vivo and in vitro: A comparative evaluation of their potential toxicity effects with different polymers and size
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Researchers compared the lung toxicity of microplastics and nanoplastics made from polystyrene, polyethylene, and polypropylene in mice and human lung cells. They found that all particle types induced signs of pulmonary fibrosis, inflammation, and tissue remodeling, with polystyrene nanoplastics causing the most severe effects. The study suggests that smaller nanoplastic particles and certain polymer types may pose greater risks to lung health.
Unveiling the Pulmonary Toxicity of Polystyrene Nanoplastics: A Hierarchical Oxidative Stress Mechanism Driving Acute–Subacute Lung Injury
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Researchers investigated the pulmonary toxicity of polystyrene nanoplastics smaller than 100 nm in lung epithelial cells and macrophages, finding that exposure triggered a hierarchical oxidative stress mechanism that drove acute to subacute lung injury through lipid peroxidation and inflammation.
Toxic effects of nanoplastics with different sizes and surface charges on epithelial-to-mesenchymal transition in A549 cells and the potential toxicological mechanism
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Researchers exposed human lung cells to polystyrene nanoplastics of different sizes and surface charges and found they triggered a process called epithelial-to-mesenchymal transition, which is associated with the early stages of lung fibrosis. Smaller particles and those with positive surface charges caused the strongest effects, activating oxidative stress and inflammatory pathways. The study suggests that inhaled nanoplastics could contribute to respiratory health risks by promoting tissue scarring in the lungs.
Inhalation of Environmental Polystyrene Micro/Nanoplastics Induces Pulmonary Toxicity and Synergistically Exacerbates Acute Lung Injury in Male Mice
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Breathing in tiny plastic particles—like those found in air pollution—caused lung inflammation and breathing problems in mice, even without any other health issues. Even more concerning, mice that had already inhaled these plastic particles got much sicker when exposed to a bacterial infection afterward, suggesting that everyday plastic pollution in the air we breathe could make our lungs more vulnerable to future illness. Smaller "microplastic" particles (as opposed to even tinier "nanoplastics") seemed to cause the most damage, highlighting that size matters when it comes to how harmful these particles are.
Size-dependent pulmonary toxicity of inhaled micro- and nano-polystyrene and initial identification of microplastics in human lung cancer tissue
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This study evaluated the carcinogenic potential of inhaled micro- and nano-polystyrene particles in mice over 12 weeks of repeated inhalation at environmentally relevant doses, finding that micro-polystyrene (mPS) caused greater pulmonary toxicity than nano-polystyrene, including lung volume reduction, impaired exercise capacity, and stronger EGFR pathway activation. Transcriptomic profiling identified AREG and MAP3K13 as key mediators, and human lung cancer tissue was also surveyed, providing early evidence linking airborne microplastic exposure to lung carcinogenesis molecular pathways.
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