ScholarWorks@중앙대학교

초록

Microplastics enter the human body primarily through inhalation and ingestion, circulate in the bloodstream, and are ultimately excreted in urine; however, this transient residence is often misinterpreted as biological harmlessness. Here, we demonstrate that the physicochemical diversity of microplastics critically determines their biological fate and toxicity along the circulation-to-excretion axis. Biosphere-mimicked fragments of alkyl polypropylene (PP) and aromatic polyethylene terephthalate (PET) were exposed to whole human blood. Due to π–π interactions involving carbonyl and benzene moieties, PET adsorbed approximately three times more serum proteins and red blood cells than PP, forming a dense protein corona. The protein-coated PET preferentially adhered to human umbilical vein endothelial cells and urine-derived epithelial cells, inducing elevated intracellular reactive oxygen species and apoptosis markers (p < 0.01 vs. PP). These cell-type-specific disruptions reveal an overlooked risk pathway linking vascular injury to urinary bladder stress during excretion. Our findings highlight the necessity of exposure models that reflect realistic microplastic chemistries and demonstrate that aromatic surfaces, even during brief systemic transit, can initiate both renal and vascular dysfunction.

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