# Micro- and Nanoplastics as a Potential Risk Factor for Stroke: A Systematic Review

**Authors:** Jakub Kufel, Miłosz Korbaś, Julita Janiec, Zofia Pankowska, Marta Młynek, Aleksandra Gaweł, Adam Mitręga

PMC · DOI: 10.3390/jox16010034 · Journal of Xenobiotics · 2026-02-14

## TL;DR

This study reviews evidence linking micro- and nanoplastics to increased stroke risk and suggests they may be a modifiable risk factor.

## Contribution

The paper systematically reviews the association between micro- and nanoplastics and stroke risk, identifying MNPs in human stroke-related tissues.

## Key findings

- MNPs, especially polyethylene and polyvinyl chloride, were found in human stroke thrombi and atherosclerotic plaques.
- MNP presence in plaques was linked to a 4.5-fold higher risk of cardiovascular events and death.
- Animal studies suggest MNPs may cause cerebral microembolization and worsen ischemic injury.

## Abstract

Environmental pollution with micro- and nanoplastics (MNPs) is an escalating global health concern. Despite growing evidence of MNPs’ presence in the human body, their impact on cerebrovascular diseases remains poorly understood. This study aimed to systematically assess the presence of MNPs in the vascular system and their association with the risk and progression of stroke. A systematic review was conducted in accordance with PRISMA 2020 guidelines and registered in PROSPERO (CRD420251272759). PubMed, Scopus, Web of Science, and Embase databases were searched for original research articles published in the last 10 years. Five studies were included (2 human observational, 3 animal in vivo), comprising 287 patients and rodent models. Methodological quality was assessed using ROBINS-E and SYRCLE’s RoB tools. The analysis confirmed the presence of MNPs, particularly polyethylene and polyvinyl chloride, in key human pathological structures, including carotid atherosclerotic plaques and stroke thrombi. Notably, the presence of MNPs in plaques was associated with a 4.5-fold increase in the risk of major cardiovascular events and death. Animal model studies provided a biological rationale for these observations, demonstrating that MNP exposure may lead to microembolization in cerebral circulation, blood–brain barrier disruption, and exacerbated ischemic injury. Importantly, MNP burden may reflect cumulative environmental exposure and vascular disease severity rather than a direct causal factor in stroke pathogenesis. Nevertheless, MNPs may still represent a novel, modifiable risk factor for stroke through their association with adverse vascular outcomes. Available evidence confirms their accumulation in the cardiovascular system and suggests an association with adverse clinical outcomes. Due to the limited number of studies, further standardized research on larger populations is required to establish whether a causal relationship exists.

## Linked entities

- **Diseases:** stroke (MONDO:0005098), atherosclerosis (MONDO:0005311)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Diseases:** ischemic stroke (MESH:D002544), Ischemic Injury (MESH:D017202), GCI (MESH:D002545), endothelial dysfunction (MESH:D014652), cardiovascular disease (MESH:D002318), PVC (MESH:C536210), myocardial infarction (MESH:D009203), behavioral disturbances (MESH:D001523), neuroinflammation (MESH:D000090862), anxiety (MESH:D001007), toxicity (MESH:D064420), vascular harm (MESH:D057772), cerebrovascular disease (MESH:D002561), BBB damage (MESH:C536830), deep vein thrombosis (MESH:D020246), thrombosis (MESH:D013927), internal carotid artery occlusion (MESH:D002340), fibrosis (MESH:D005355), hippocampal damage (MESH:D000092223), Inflammation (MESH:D007249), injury to (MESH:D014947), atherosclerotic (MESH:D050197), brain damage (MESH:D001925), death (MESH:D003643), brain injury (MESH:D001930), occlusion (MESH:D001157), demyelination (MESH:D003711), necrotic (MESH:D009336), microtubule and myelin damage (MESH:D020279), ischemia (MESH:D007511), neurological and behavioral abnormalities (MESH:D009461), atheromas (MESH:D058226), Chronic Vascular Disease (MESH:D002908), disability (MESH:D009069), depressive (MESH:D003866), infarct (MESH:D007238), transient ischemic attack (MESH:D002546), Stroke (MESH:D020521), myocardial damage (MESH:D009202), neurobehavioral deficits (MESH:D019954)
- **Chemicals:** polyester (MESH:D011091), PVC (MESH:D011143), polymer (MESH:D011108), Fluoro-Jade B (MESH:C435731), FJB (-), salt (MESH:D012492), PS (MESH:D010758), sugar (MESH:D000073893), MP (MESH:D000080545), PE (MESH:D020959), polystyrene (MESH:D011137), lipid (MESH:D008055)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12922052/full.md

## References

24 references — full list in the complete paper: https://tomesphere.com/paper/PMC12922052/full.md

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Source: https://tomesphere.com/paper/PMC12922052