Microplastics, nanoplastics, and thrombogenesis

Micro- and nanoplastics (MNPs) are produced through mechanical, chemical, and ultraviolet-mediated degradation of plastics and may enter the human bloodstream via ingestion, inhalation, dermal exposure, and iatrogenic sources. Their detection in human blood, atheromas, and thrombi has raised concerns 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 March 31, 2026. The search identified 981 database records and 39 additional manually identified articles; after removing duplicates 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 3 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 to vary with particle size, polymer composition, surface charge, and environmental weathering. However, mechanistic evidence largely comes 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 their clinical relevance remains uncertain. Prospective human studies, standardized contamination-controlled detection methods, and dose-response experiments using clinically relevant particles and concentrations are required.