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A review of the literature on microplastics exposure and cardiovascular disease was recently published in the journal Cardiovascular Toxicology, concluding that microplastics and nanoplastics (MNPs) cross biological barriers, accumulate and cause damage in vascular and myocardial tissues, and should be recognized as cardiovascular toxins, requiring strategies for prevention, risk stratification, and targeted intervention.
Perhaps most notable was the prospective, multicenter, observational study published in the New England Journal of Medicine in which carotid artery plaque from over 250 patients undergoing carotid endarterectomy was examined for MNPs. Nearly 60% contained polyethylene and 12% had measurable polyvinyl chloride. Among patients who had MNPs detected in their plaques, the risk for the primary endpoint, a composite of myocardial infarction, stroke, or death from any cause, was 4.53 times higher at 34 months of follow-up. Similarly, the Journal of Advanced Research published the first study detailing the evidence of microparticles in thrombi. Twenty-six patients undergoing cardiovascular surgery had a total of 87 environmental microparticles detected in their thrombi, comprised of microparticles and microplastics, with between 1 to 15 microparticles per thrombus (an average of 5).
The authors review the pathways by which MNPs induce harm, including oxidative stress, endothelial dysfunction, innate immune activation, and mitochondrial injury. MNPs also induce cellular senescence, with all of the above pathways associated with cardiovascular disease development. Preclinical models have demonstrated enhanced expression of inflammatory cytokines and adhesion molecules, resulting in endothelial inflammation and structural damage to vascular endothelial cells. In addition to oxidative stress and inflammation, MNPs appear to cause both genetic and epigenetic changes. For example, in a 2024 systematic review published in Chemosphere, MNPs were predicted to make epigenetic modifications that “may lead to disruptions in key metabolic and immune pathways, including glucose balance, apoptosis, cell proliferation, and angiogenesis.” Similarly, specific modifications (N6-methyladenosine (m6A)) have been linked to cardiotoxicity, and immunotoxicity associated with histone modifications, both a result of microplastic exposure.
MNPs directly cause mitochondrial damage and dysfunction, including damage to both nuclear and mitochondrial DNA. Polystyrene microplastics have been shown to damage kidney cells in vitro as well as in animal models, marked by mitochondrial dysfunction, endoplasmic reticulum stress, inflammation, and autophagy, implicating their role in kidney dysfunction. Multiple models indicate that MNPs easily cross the intestinal epithelium, accumulate in the gut mucosa, disrupt the intestinal barrier, and adversely affect the microbiome. In one specific example of the gut-heart axis: bisphenol F (found in the urine of ~90% of adults) is metabolized to N-acetylputrescine (NAP), which both impairs the intestinal barrier and induces cardiomyocyte hypertrophy (potentially mitigated by Akkermansia muciniphila), in part by activating the p53 protein, a recognized biomarker of cardiovascular system injury.
The recent review in Cardiovascular Toxicology points out that the annual global production of (non-biodegradable) plastic is over 400 million tons per year, expected to double by 2050, indicating the need to urgently develop biomarkers of exposure and injury, longitudinal studies, and clinical trials, etc. Food and water intake are the leading sources of MNP exposure, with plastics used in mulching films, biosolids, etc., not visibly obvious sources of microplastics. Certainly, avoiding bottled water, packaging, food processing, etc. is a good first step, though effective policies are needed on a much larger scale to address the problem.
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