Microplastics in artery plaque: what the 2024 NEJM study found
Patients whose carotid plaque contained plastics had a higher rate of heart attack, stroke or death. It is an association in 257 people, not proof of cause.
| Group | Value (µg/mg) |
|---|---|
| Polyethylene | 21.7 |
| Polyvinyl chloride | 5.2 |
In March 2024 the New England Journal of Medicine published the first study to link plastics inside human artery plaque to later cardiovascular events. Patients whose excised carotid plaque contained microplastics and nanoplastics had a markedly higher rate of heart attack, stroke or death over the following three years. The finding is important and widely misread: it is an association in a few hundred people, and the study was not built to show that the plastics caused the events.
What was done
The study enrolled patients undergoing carotid endarterectomy — surgical removal of plaque from the neck arteries — for asymptomatic carotid disease [s1]. A total of 304 patients were enrolled, and 257 completed a mean follow-up of 33.7 months [s1]. The removed plaque was analysed for plastics using pyrolysis–gas chromatography–mass spectrometry, stable-isotope analysis and electron microscopy [s1].
Polyethylene was detected in the plaque of 150 patients, 58.4% of the group, at a mean level of 21.7 micrograms per milligram of plaque [s1]. Polyvinyl chloride was measurable in 31 patients, 12.1%, at a mean of 5.2 micrograms per milligram [s1]. Electron microscopy showed jagged-edged foreign particles among the macrophages — immune cells — in the plaque, and some particles contained chlorine [s1].
The study did not stop at counting plastics. It also assessed inflammatory biomarkers in the plaque using enzyme-linked immunosorbent assay and immunohistochemistry [s1]. That the particles were found sitting among macrophages, alongside markers of inflammation, is the mechanistic thread the authors pull on — a picture consistent with plastics feeding the inflammatory process that destabilises plaque [s1]. It is a picture, though, captured in the same tissue at the same moment as the outcome was measured, not a mechanism tested over time.
What was found
The primary endpoint was a composite of myocardial infarction, stroke or death from any cause, compared between patients with plastics in their plaque and those without [s1]. Patients in whom plastics were detected were at higher risk of that composite endpoint, with a hazard ratio of 4.53 (95% confidence interval, 2.00 to 10.27; P<0.001) [s1].
A hazard ratio of 4.53 is large. Taken at face value it says the plastics-positive group had well over four times the rate of events. That is why the study drew the attention it did, and why the caveats matter as much as the headline number.
Why it is an association, not a verdict
The authors describe the study as observational, and its own accompanying commentary in Cardiovascular Research calls microplastics a "potential" cardiovascular threat rather than an established one [s2]. Several limits sit between this result and a causal claim.
The people with plastics in their plaque may differ from those without in ways the study could not fully account for — diet, occupation, where they live, other exposures. A marker of plastic burden may travel with some other risk factor that is doing the real damage. The confidence interval, running from 2.00 to 10.27, is wide, which is what a few hundred patients and a modest number of events produce [s1]. And detecting plastic inside plaque does not establish that it drove the inflammation or the rupture; it establishes that it was there.
There is also a measurement dimension. Plastics are everywhere, including in laboratories, and distinguishing plastic that was in the tissue from plastic introduced during handling is one of the hardest problems in this field. The study used multiple analytical methods partly to guard against that, but no single study settles a question this contamination-prone on its own.
What would move it forward
The result did not arrive from nowhere. As the study's own follow-up commentary in Cardiovascular Research notes, microplastics had already emerged as a candidate cardiovascular risk factor in preclinical work — animal and laboratory studies suggesting the particles can promote inflammation and vascular damage [s2]. What the 2024 study added was the first direct human link, which is why it mattered, and why its observational design is the ceiling on what it can claim. Preclinical plausibility plus one human association is a strong reason to keep looking, not a closed case.
A causal reading needs more: replication in other cohorts, a dose-response relationship — more plastic, more events — and a plausible mechanism confirmed in humans rather than inferred. The plaque in this study showed inflammatory changes around the particles, which is a mechanistic hint, but a hint measured in the same cross-section as the outcome, not tested prospectively [s1].
The honest summary is the one the data support: in 257 people, plastics in carotid plaque marked a group at higher cardiovascular risk over three years [s1]. Whether the plastics caused that risk, or flagged something else that did, is the question the next studies have to answer — and it is a different question from the one the headline implies.
This article is informational and is not medical advice.
Sources
- Microplastics and Nanoplastics in Atheromas and Cardiovascular Events — New England Journal of Medicine , March 6, 2024
- Microplastics and nanoplastics: tiny threats for cardiovascular diseases? — Cardiovascular Research , August 21, 2025
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