Summary: A new study found dramatically higher concentrations of micronanoplastics—tiny plastic particles originating from degraded plastics in the environment—in the carotid arteries of people with plaque-related stroke symptoms compared with those who had healthy arteries. Individuals with symptomatic carotid plaque showed plastic levels up to 51 times greater than age-matched artery samples from donors without plaque. These particles were linked to changes in immune cell gene activity inside plaque, which could influence plaque stability and long-term stroke risk, though causation has not been established.
Researchers analyzed carotid artery samples to evaluate how micronanoplastics associate with inflammation and immune responses inside atherosclerotic plaque. While the study did not find a clear association between plastic levels and acute inflammation, it did detect altered gene expression in macrophages and progenitor cells that help stabilize plaque. The findings raise concern that plastic accumulation in arteries may represent a previously unrecognized factor in vascular disease and stroke risk, warranting further investigation.
Key findings:
- Micronanoplastics concentrated in plaque: Carotid plaque from people who experienced stroke, transient ischemic attack (mini-stroke) or temporary vision loss contained up to 51× more micronanoplastics than artery samples from age-matched donors without plaque.
- Biological effects on immune cells: High plastic concentrations were associated with changes in gene activity of macrophages and other plaque-stabilizing cells, including reduced expression of some anti-inflammatory genes.
- Uncertain causal role: The study cannot prove that micronanoplastics caused symptoms; they may be a marker of other processes. Additional research is needed to determine mechanisms and whether reducing exposure would lower risk.
Micronanoplastics refer to a range of small plastic fragments that come from industrial processes or the breakdown of larger plastic items in soils, waterways and oceans. The term covers both microplastics (particles up to a few millimeters) and nanoplastics (submicron particles typically measured in nanometers). Because nanoplastics are extremely small, they can disperse widely and penetrate biological tissues and cells, which is why many researchers now emphasize the term “nanoplastics” when studying health effects.
Lead author Ross Clark, M.D., M.B.A., a vascular surgeon-scientist at the University of New Mexico, noted that environmental plastics accumulate in water, soil and the food chain over time. Although common sources of everyday exposure include packaging, bottles and utensils, the study authors emphasize that food and drinking water are key routes through which micronanoplastics enter the human body.
Previous work in Italy detected micronanoplastics in carotid plaque removed from people without symptoms. That earlier study also reported worse outcomes over following years among patients whose plaques contained micronanoplastics. Building on that work, the current analysis sought to compare plastic levels across groups with different clinical presentations and to explore effects on inflammation and immune gene activity.
In this study, researchers examined 48 carotid artery samples collected in 2023–2024. Samples came from three groups: people with symptomatic carotid plaque (who had stroke, mini-stroke or temporary vision loss), people with plaque but no symptoms, and age-matched tissue donors who had no carotid blockage. Using pyrolysis gas chromatography–mass spectrometry to measure plastics, the team compared plastic concentrations and performed RNA sequencing on plaques with the highest versus lowest plastic amounts to assess gene expression differences.
Key quantitative results included:
- Plaque from people without symptoms contained about 16 times more micronanoplastics (895 µg/g) than artery walls from age-matched donors without plaque (57 µg/g).
- Plaque from people with stroke-related symptoms contained about 51 times more micronanoplastics (2,888 µg/g) than artery tissue from donors without plaque (57 µg/g).
When comparing high-plastic versus low-plastic plaques, the investigators did not observe a direct link between micronanoplastic amount and markers of acute inflammation (measured by TNF-α and IL-6). However, RNA sequencing revealed shifts in immune and progenitor cell gene expression, notably less activity in some anti-inflammatory pathways of macrophages—cells that play a central role in plaque stability and the vascular immune response.
The study has several important limitations. It cannot demonstrate causation—micronanoplastics might simply be associated with other biological processes that cause plaque instability. The analytical method (pyrolysis GC-MS) can detect nanoplastics but may also register signals from biological molecules such as lipids that break down into similar compounds, making separation of plastics from tissue-derived signals technically challenging. The research team reports ongoing efforts to improve sample preparation to reduce lipid interference. Researchers also lacked complete demographic data for tissue donors, including sex and race/ethnicity, which limits interpretation across populations.
Researchers emphasized that these early findings are concerning and merit further study. Understanding how environmental micronanoplastics interact with vascular tissues and immune cells will be important before considering public health recommendations or potential interventions. As Karen L. Furie, M.D., M.P.H., FAHA, noted, if confirmed, plastic accumulation in arteries could represent a novel, modifiable target for preventing stroke—but more evidence is needed.
Study details and design:
- 48 carotid artery samples from 48 adults collected at the University of New Mexico and the Office of the Medical Investigator (2023–2024).
- Approximately one-third of samples from symptomatic patients (stroke, transient ischemic attack, or amaurosis fugax) who had carotid plaque removed surgically.
- Approximately one-third from people of similar age with asymptomatic plaque identified during screening and removed surgically.
- Approximately one-third from age-matched tissue donors who had died of various causes and had no carotid blockage.
- Inflammation was measured by TNF-α and IL-6 levels; RNA sequencing focused on samples with the highest and lowest plastic concentrations to evaluate immune cell gene expression.
About this neurology research news
Author: Karen Astle
Source: AHA (American Heart Association)
Contact: Karen Astle – AHA
Image: The image is credited to Neuroscience News
Original presentation: Findings presented at the American Heart Association’s Vascular Discovery 2025 Scientific Sessions: From Genes to Medicine in Baltimore, April 22–25, 2025.