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Microplastic and Nanoplastic Exposure and Cardiovascular Disease: A Narrative Review of Mechanistic Evidence, Candidate Epigenetic Pathways and Current Evidence Gaps
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This review paper summarizes existing research on whether microplastics and nanoplastics affect heart and blood vessel health. Studies in cells, mice and fish found signs of oxidative stress, inflammation and altered DNA activity after plastic particle exposure, and one human study linked plastics found in neck artery plaque to higher rates of heart attack, stroke or death. The authors conclude a clear biological pathway remains unproven.
Microplastics (MPs; particles 1 μm–5 mm) and nanoplastics (NPs; <1 μm) are ubiquitous environmental contaminants and have been detected in human blood, placenta, lung tissue and carotid atherosclerotic plaque. They do not constitute a uniform exposure: polymer composition, particle size, shape, surface chemistry and charge, chemical additives and leachates, adsorbed co-contaminants and weathering state all vary and may each modify biological effects. Experimental studies, most of which have used pristine polystyrene spheres, link MP/NP exposure to oxidative stress, mitochondrial dysfunction and vascular inflammation. Epigenetic regulation has been proposed as a mechanism by which a transient exposure could produce persistent cardiovascular effects, but the strength of the supporting evidence has not been systematically appraised. To summarise the experimental, translational and human evidence concerning the cardiovascular effects of MP/NP exposure, and to appraise candidate epigenetic pathways — DNA methylation, RNA and histone modifications, and non-coding RNAs — while explicitly separating mechanisms demonstrated after defined MP/NP exposure from those extrapolated from general cardiovascular biology. In cultured cells and rodent models, polystyrene particles of approximately 1–10 μm induce endothelial activation, oxidative stress, mitochondrial dysfunction, and cardiac hypertrophic and fibrotic remodelling. Direct evidence that MP/NP exposure alters epigenetic marks derives mainly from fish studies — global DNA hypomethylation on re-exposure in zebrafish after early-life exposure to 9.5–11.5 μm polystyrene at 50 mg/L, and sex-dependent liver methylome changes in fathead minnow exposed to 150–500 μm polyethylene at 100–2000 particles/L — together with one mouse study reporting altered cardiac N6-methyladenosine (m6A) RNA methylation after chronic polystyrene exposure. No study identified in this review measured histone modifications, long non-coding RNAs or circular RNAs in cardiovascular tissue after MP/NP exposure; these links remain hypothetical extensions of general cardiovascular epigenetics. In humans, polyethylene (58.4% of plaques) and polyvinyl chloride (12.1%) detected in carotid plaque were associated with a higher composite rate of myocardial infarction, stroke or death (hazard ratio 4.53, 95% CI 2.00–10.27) in a single observational cohort of 257 patients, in which epigenetic markers were not assessed. An epigenetically mediated pathway from MP/NP exposure to cardiovascular injury is biologically plausible but largely unproven, and existing findings cannot be generalised across polymer types, particle sizes or dose ranges. Standardised particle characterisation, environmentally relevant exposure models and longitudinal human cohorts combining exposure assessment with multi-omic cardiovascular phenotyping are required before epigenetic dysregulation can be regarded as an established mechanism of plastic-related cardiovascular disease.
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