Microplastics, nanoplastics, and thrombogenesis

Microplastics and nanoplastics (MNPs) are generated through mechanical, chemical, and ultraviolet-mediated plastic degradation and may enter the human bloodstream through ingestion, inhalation, dermal exposure, and iatrogenic sources. Their detection in human blood, atheromas, and thrombi has raised concern that they may contribute to thrombogenesis. We conducted a structured narrative review of English-language studies indexed in PubMed, Embase, and Scopus over the preceding 15 years, up to 31 March 2026. The search identified 981 database records and 39 additional manually identified articles; after duplicate removal and screening, 72 articles were included. Evidence was synthesized according to Virchow's triad, focusing on endothelial injury, altered blood flow, hypercoagulability, cellular uptake, polymer type, surface charge, weathering, and protein corona formation. MNPs may contribute to all three components of Virchow's triad. Proposed mechanisms include oxidative endothelial injury, glycocalyx disruption, monocyte adhesion, foam-cell formation, plaque instability, immune-cell-mediated microvascular obstruction, platelet activation, NETosis, von Willebrand factor interactions, factor XII activation, thrombin generation, and fibrin-rich clot stabilization. These effects appear modified by particle size, polymer composition, surface charge, and environmental weathering. However, much mechanistic evidence derives from polystyrene nanoparticle models, whereas human thrombus and atheroma studies more commonly detect polyethylene and polyvinyl chloride. MNPs are biologically plausible contributors to thrombogenesis, but clinical relevance remains uncertain. Prospective human studies, standardized contamination-controlled detection methods, and dose-response experiments using clinically relevant particles and concentrations are required.