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Microplastics, Nanoplastics, and the Cardiovascular Exposome: Emerging Evidence for Vascular Deposition, Thrombotic Pathways, and Cardiovascular Risk
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This review pulls together existing studies on tiny plastic particles found in blood vessels and artery plaque, some of which link their presence to higher rates of heart attack, stroke, and death. However, these studies show a connection, not proof that plastics cause these problems. Scientists say more research is needed before doctors should test for plastics or change how they treat heart disease.
ABSTRACT Microplastics and nanoplastics (MNPs) are increasingly detected in human biological matrices, including blood and cardiovascular tissues, but their causal contribution to cardiovascular disease remains unresolved. This narrative review draws on literature identified through PubMed/MEDLINE and Europe PMC, supplemented by citation chaining, with human and experimental evidence considered separately. Human cardiovascular evidence now includes cross‐sectional blood and tissue studies, procedure‐related exposure studies, thrombus and plaque investigations, and prospective associations. In a carotid endarterectomy cohort, plaque MNP detection was associated with myocardial infarction, stroke, or all‐cause death (hazard ratio 4.53, 95% CI 2.00–10.27); a later myocardial‐infarction cohort reported a logistic‐regression association between coronary‐blood polyvinyl chloride concentration (mg/kg) and major adverse cardiac events (odds ratio 1.090 per 1 mg/kg increase, 95% CI 1.032–1.1523; p = 0.002). Neither study establishes causality. Experimental studies directly demonstrate effects on endothelial biology, macrophage lipid handling, fibrinogen interactions, inflammatory signaling, and myocardial injury or remodeling within defined models, but translation is limited by frequent use of pristine polystyrene, uncertain delivered dose, and poor comparability with human internal dosimetry. Analytical heterogeneity, contamination, incomplete particle‐size characterization, co‐exposures, reverse causality, and procedure‐related particle introduction remain major barriers. We therefore propose a staged framework that separates external exposure, systemic detection, tissue deposition, cellular response, organ dysfunction, prospective association, causal triangulation, and intervention evidence. The current balance of evidence supports an emerging cardiovascular hazard signal that warrants rigorous causal research, but it does not justify routine MNP testing, risk‐score modification, or MNP‐specific treatment.
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