A 2024 study in Italy examined artery plaque from patients undergoing surgery and asserted the presence of microplastics was associated with subsequent cardiovascular events.
- The Marfella et al. study is observational and exploratory: it reports an association in a small, high-risk patient group but does not establish that microplastics cause heart disease.
- Well-known cardiovascular risk factors could explain the findings: patients with detectable plastics were more likely to smoke and have high cholesterol, diabetes, and existing heart disease, and the study does not adequately separate these effects from any potential role of plastics.
- The evidence is not sufficient to support broad health or policy conclusions: methodological uncertainties, limited sample size, and short follow-up mean the results should be interpreted cautiously and not treated as proof of a new cardiovascular risk.
Why this 2024 Study Does Not Establish that microplastics cause heart disease
In March 2024, Marfella et al. published a study in the New England Journal of Medicine that generated global headlines by suggesting that microplastics found in artery plaque could increase the risk of heart attacks, strokes, and death.1 The findings quickly entered public and policy discussions, often framed as evidence that plastics may be causing cardiovascular disease.
A closer look at the study, however, shows that its conclusions are far more limited than many headlines suggest. For policymakers and reporters, understanding what the study does and does not demonstrate is essential before drawing broader implications.
What the Study Reported
Researchers examined artery plaque removed from 257 patients in Italy undergoing surgery for carotid artery disease. They reported that patients whose plaques contained detectable microplastics or nanoplastics experienced a higher rate of a combined outcome that included heart attack, stroke, or death from any cause over roughly three years of follow-up compared with patients whose plaques did not contain detectable particles.
Importantly, the authors explicitly state “our results do not prove causality (emphasis added).” The study was observational and cannot determine whether plastics played any role in causing disease.
Why the Findings Require Caution
1. Traditional risk factors could explain the results
Patients with detectable plastics in their plaques were more likely to smoke and to have high cholesterol, diabetes, and pre-existing cardiovascular disease. These are among the strongest and best-established predictors of heart attack and stroke.
The study does not adequately disentangle whether plastics contributed anything beyond these known risks. As a result, the observed differences in outcomes may simply reflect the fact that one group was already sicker at baseline.
In practical terms, the study may be measuring the effects of long-recognized cardiovascular risk factors rather than identifying a new hazard.
2. Correlation is not the same as causation
As the saying goes, correlation does not imply causation. A correlation is an observable relationship between exposure and a disease, while causation means the exposure directly produces the disease in question.
For example, when there is an increase in ice cream sales at the beach there is also an increase in shark attacks. The increase in both events are correlated with each other, but one does not cause the other.
There is another factor that causes these increases at the same time (i.e., it is hot outside). Such associations may be due to chance, confounding factors (e.g., drinking, diet, exercise, etc.), or bias, whereas causation requires strict evidence of temporality (i.e., does disease follow exposure), strength (i.e., weight of evidence), and biological plausibility (i.e., are the results consistent with current medical knowledge and explains how the exposure causes a specific effect in the body).
Significantly, this study did not evaluate the individual patient’s exposure to microplastics (i.e., dose) to determine if there is an association between increased exposure and adverse events, control or measure patient behavior (e.g., whether the person smoked, exercised, or drank alcohol), or rule out alternative explanations. It simply observed outcomes in patients who already had advanced cardiovascular disease.
Decades of epidemiology show that early studies in emerging research areas frequently produce associations that fail to hold up under more rigorous testing.2 Without replication, stronger study designs and consistency across populations, single observational studies should be treated as exploratory.
3. The outcome measure blurs meaningful distinctions
The researchers combined heart attacks, strokes, and death from any cause into a single “composite endpoint.” Including deaths unrelated to cardiovascular disease, such as cancer or infection, weakens the interpretation of the results.
The paper does not report what participants actually died from, and with only 38 adverse events in total, this approach risks exaggerating associations rather than clarifying them.
4. Measurement and contamination issues remain unresolved
The study acknowledges that laboratory conditions were not plastic-free, raising the possibility that some detected particles originated from the lab environment rather than from artery plaque.
The analytical method, Pyr-GC-MS (i.e., pyrolysis–gas chromatography–mass spectrometry) used, is a highly complex method involving heating samples and analyzing chemical residues. Importantly, drawing conclusions from the results is highly dependent upon what type of data is obtained and how it is analyzed. While Pyr-GC-MS is a powerful tool, when used for biological tissue samples it necessitates additional methodological steps. First and foremost, biological tissue from the sample needs to be completely removed prior to measurement because some plastics have a similar “signal” as lipids (i.e., fats) found in tissue samples.3,4 It can be difficult or impossible to distinguish certain plastics from lipid rich tissues, like the plaques analyzed in this study.
Unfortunately, the researchers did not take any steps to remove the tissue from the sample, meaning the plastic “signal” may be due to lipids. From the data provided, the distinction between the two is impossible to make.
These uncertainties make it difficult to determine whether the reported findings reflect true exposure or methodological artefacts.
Putting the Findings in Broader Context: Microplastics and Cardiovascular Mortality Trends
The study population was small, geographically limited, and already suffering from severe cardiovascular disease. Follow-up lasted less than three years, which is short in the context of heart disease research.
At the population level, long-term trends run counter to the study’s implied narrative. Plastic use has increased substantially over the past half-century, while cardiovascular mortality in countries like Italy has fallen by more than 80 percent. The authors themselves acknowledge this disconnect.
How the Study Was Covered in the Media
Despite the study’s limitations, many news stories framed the findings as evidence that plastics cause heart disease. Examples included:
- Microplastics in blood linked with stroke, heart attack and early death (Sky News)Microscopic plastics could raise risk of stroke and heart attack (The Guardian)
- Nanoplastics linked to heart attack, stroke and early death (CNN)
Some coverage contained factual errors, including claims that plastics were found in blood rather than artery plaque. More importantly, most reports gave little attention to the role of smoking, cholesterol, diabetes, and other confounding factors that could fully explain the results.
This matters because overstated interpretations can shape public concern and policy debates in ways not supported by the evidence.
The Bottom Line for Policymakers and Reporters
The Marfella et al. study is exploratory. It raises questions that may encourage future research, but it does not demonstrate that microplastics cause cardiovascular disease.
Strong public health conclusions require multiple, well-designed studies that consistently point in the same direction. At present, the evidence does not meet that standard. Careful reporting and measured policy responses are essential to avoid confusing preliminary observations with established scientific conclusions.
References
- Marfella et al., (2024). Microplastics and nanoplastics in atheromas and cardiovascular events. N. Engl. J. Med., 390 (10), pp. 900-910. DOI: 10.1056/NEJMoa2309822.
- Ioannidis JP. Why most published research findings are false. PLoS Med. 2005 Aug;2(8):e124. doi: 10.1371/journal.pmed.0020124. Epub 2005 Aug 30. Erratum in: PLoS Med. 2022 Aug 25;19(8):e1004085. doi: 10.1371/journal.pmed.1004085.
- Rauert C, Charlton N, Bagley A, Dunlop SA, Symeonides C, Thomas KV. Assessing the Efficacy of Pyrolysis-Gas Chromatography-Mass Spectrometry for Nanoplastic and Microplastic Analysis in Human Blood. Environ Sci Technol. 2025 Feb 4;59(4):1984-1994. doi: 10.1021/acs.est.4c12599.
- Monikh, F., Materić, D., Valsami-Jones, E. et al. Challenges in studying microplastics in human brain. Nat Med 31, 4034–4035 (2025). https://doi.org/10.1038/s41591-025-04045-3