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Size-dependent pulmonary toxicity of inhaled micro- and nano-polystyrene and initial identification of microplastics in human lung cancer tissue
Summary
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.