In a 2024 observational study of patients undergoing carotid endarterectomy, researchers detected polyethylene in the excised plaque of 150 of 257 patients who completed follow-up; 31 of those 150 also had detectable polyvinyl chloride. Over a mean follow-up of about 34 months, the group with detected microplastics and nanoplastics had a higher rate of heart attack, stroke or death from any cause than the group without detected particles (hazard ratio 4.53). The study did not establish that the particles caused those outcomes.
The study was published in the New England Journal of Medicine in March 2024.
The number nobody expected
Raffaele Marfella and his team at the University of Campania had set out to do something modest: recruit patients scheduled for carotid endarterectomy — a routine procedure to clear plaque from the neck arteries — and see whether the debris they pulled out contained any of the microplastic contamination that had been showing up in oceans, soil, and, more recently, human blood.
They expected to find some. They did not expect to find it in 58% of patients. And they certainly did not expect the follow-up numbers.
Of the 150 patients with detected microplastics and nanoplastics, 30 had a heart attack, non-fatal stroke or death from any cause during follow-up, compared with eight of the 107 patients without detected particles. The adjusted hazard ratio was 4.53, with a 95% confidence interval of 2.00 to 10.27. The association remained after adjustment for the risk factors included in the study, but residual confounding and measurement limitations cannot be excluded.
That is a large association in this cohort, but its size should not be treated as a causal effect estimate.
What the plastic was doing there
The mechanism, insofar as anyone understands it, tracks with the way atherosclerosis already works. Arterial plaque begins as a slow-motion failure of the endothelium — the single-cell lining that keeps blood on one side of the vessel wall and everything else on the other. Low-density lipoprotein particles slip through, get oxidised, and summon monocytes that mature into macrophages and gorge themselves on lipid until they turn into foam cells. Foam cells die. Their debris forms a necrotic core. A fibrous cap grows over the top. When the cap thins and breaks, the contents spill into the bloodstream and a clot forms. That clot is what a heart attack or stroke is, mechanically speaking. The Nature Research Intelligence summary of plaque vulnerability lays out the cascade in detail.
The study found higher levels of inflammatory markers in participants whose plaque contained detected particles. Those findings are compatible with several possible mechanisms, but they do not show how the particles entered the plaque or whether they caused the inflammation or later clinical events.
Whether microplastics and nanoplastics accelerate atherosclerosis remains an open research question.
Naples was not a fluke
The obvious question after any single study is whether anyone can replicate it. In April 2025, Ross Clark, a vascular surgeon-scientist at the University of New Mexico, presented data at the American Heart Association’s Vascular Discovery Scientific Sessions in Baltimore. His team had built on the Italian work with a smaller cohort — fewer than 50 patients — and compared three groups: people with healthy carotid arteries, people with plaque but no symptoms, and people who had already suffered a stroke, transient ischaemic attack, or temporary vision loss.
The gradient was steep. According to ScienceDaily’s reporting on the Baltimore presentation, plaque from symptomatic patients contained roughly 51 times more micronanoplastic material than the arteries of the healthy control group. Plaque from asymptomatic patients sat in between.
Karen Furie, chair of neurology at Brown University’s Warren Alpert Medical School, noted in a statement that plastic exposure has not traditionally been considered a modifiable stroke risk factor. Furie suggested the finding could represent a new avenue for stroke prevention research. Furie was not involved in the New Mexico work.
Clark himself was more cautious. His team’s method — pyrolysis gas chromatography-mass spectrometry — burns tissue samples down to their molecular signatures, and lipids in arterial plaque can produce signatures that look uncomfortably like polyethylene. Clark told the conference that his team’s methods are designed to address concerns about lipid interference in the analysis, according to News Tribune coverage. Clark acknowledged that future discoveries could alter interpretation of the findings.
The exposure math
The headline figure that circulated after the WWF-commissioned 2019 study — that the average person swallows about 5 grams of plastic a week, roughly the weight of a credit card — has been picked apart by other researchers and does not hold up to close scrutiny. But the direction of travel is not in dispute. Plastic particles have now been documented in human blood, breast milk, placental tissue, testicular tissue, and, most recently, brain tissue.
The researchers stopped short of claiming causation. Higher concentrations in diseased tissue may reflect cause, consequence, exposure differences or measurement effects; further work is needed to distinguish among those explanations.
Clark, in Baltimore, noted that consumers often mistakenly believe microplastics primarily come from direct contact with plastic items like utensils and packaging. He explained that the particles are actually already present in food and water supplies before packaging.
Why cardiology is nervous
Cardiovascular disease is a leading cause of death worldwide. The field has spent four decades identifying modifiable risk factors — smoking, LDL cholesterol, hypertension, diabetes, obesity, sedentary behaviour — and building interventions around each one.
A hazard ratio above 4 in a single observational cohort is a strong signal for follow-up, but it is not enough to classify exposure as a causal or modifiable cardiovascular risk factor.
The problem is that nobody yet knows what a clinical intervention would look like. You cannot prescribe less plastic the way you prescribe less salt. Regulatory action on plastic production is negotiated at international levels, but binding agreements on production caps remain elusive. The petrochemical industry, which supplies the feedstock for plastic production, has resisted upstream limits and pushed the conversation toward recycling and waste management instead.
For now, the finding supports better measurement, replication and prospective research rather than a clinical prescription.
The gap between signal and proof
The honest scientific position, in 2026, is that association is not causation and 257 patients from a single Italian hospital is not a global cohort. Marfella’s team acknowledged as much in the original paper. Clark repeats the caveat every time he presents his own data. It is possible that microplastics in plaque are a marker of some other exposure that is doing the actual harm — that they are the fingerprint at the crime scene rather than the weapon.
What has changed is the burden of proof. For decades, the assumption behind consumer plastic — that it was inert, that it passed through, that whatever fragments did stick around were biologically irrelevant — sat on no particular evidence base. It was simply the default. That default is now being tested against tissue samples, and the tissue samples keep failing to cooperate.
Silicon Canals has previously covered how occupational psychology research keeps upending intuitive assumptions about health, and the microplastics story is following a similar arc: a background variable that everyone treated as neutral turns out, on inspection, to be doing something.
What follows the finding
The Marfella paper prompted follow-up research, but replication in larger cohorts and agreement on measurement methods remain necessary before the association can guide clinical care.
Longer follow-up and independent replication will help show whether the association persists and whether unmeasured confounding or analytical artefacts explain part of it.
Neither outcome changes what is already true about the 150 patients whose plaque contained plastic. Something got inside them. It found a place to settle. It is still there.
Correction, 17 September 2026: This article previously described an observational association as though microplastics had been shown to accelerate atherosclerosis and constitute a modifiable cardiovascular risk factor. The study found an association but did not establish causation. The relevant passages have been corrected and the primary paper linked.
