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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.
This study evaluated the carcinogenic potential of inhaled micro-polystyrene (mPS) and nano-polystyrene (nPS) using a murine exposure model. Repeated inhalation of environmentally relevant doses for up to 12 weeks resulted in marked pulmonary toxicity, most prominently in the mPS group. mPS exposure led to greater reductions in lung volume, impaired exercise capacity, and stronger induction of EGFR expression. Transcriptomic profiling further identified AREG and MAP3K13 as key mediators, indicating activation of EGFR-dependent MAPK signalling. Overall, these findings demonstrate that polystyrene (PS) particles exert size-dependent toxic effects, with mPS showing greater pathogenicity than nPS, and provide evidence linking airborne MP exposure to molecular pathways relevant to lung carcinogenesis.
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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 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.
Size-Dependent PulmonaryToxicity and Whole-Body Distributionof Inhaled Micro/Nanoplastic Particles in Male Mice from Chronic Exposure
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Researchers used a whole-body inhalation exposure system to chronically expose male mice to polystyrene micro- and nanoplastics at environmental concentrations and tracked particle distribution and lung toxicity. Nanoplastics (80 nm) showed greater tissue transport than microplastics (1 µm), with highest accumulation in lungs followed by blood and spleen, and both sizes disrupted oxidative balance and antioxidant defenses.
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.
Intratracheal Administration of Polystyrene Micro(nano)plastics with a Mixed Particle Size Promote Pulmonary Fibrosis in Rats by Activating TGF-β1 Signaling and Destabilizing Mitochondrial Dynamics and Mitophagy in a Dose- and Time-Dependent Manner.
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SD rats exposed to mixed polystyrene micro(nano)plastics via intratracheal administration at escalating doses over time developed pulmonary fibrosis and mitochondrial dysfunction, with severity linked to dose. The findings demonstrated a clear biological pathway connecting inhaled microplastic exposure to lung injury.
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