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Micro-and Nano-Plastic Exposure as an Emerging Risk for Atherosclerotic Cardiovascular Disease
Summary
Tiny plastic particles from our food, water, and even the air we breathe are showing up in human blood and blood vessels—including in the fatty buildup that causes heart attacks and strokes. This review pulls together existing research suggesting these particles may fuel heart disease by triggering inflammation and damaging blood vessels, though scientists haven't yet proven direct cause-and-effect. It's a wake-up call: everyday exposure to plastics, especially through household dust, packaged food, and synthetic textiles, may be a hidden and preventable risk to your heart health.
PURPOSE OF REVIEW: This review examines micro- and nanoplastic (MNP) exposure as an emerging risk factor for atherosclerotic cardiovascular disease, focusing on how individual-level exposures shaped by behaviours, micro-environments, and lifestyle factors contribute to cumulative internal dose and cardiovascular risk. RECENT FINDINGS: Micro- and nanoplastic (MNP) exposure occurs through multiple, continuous pathways, including inhalation of airborne particles, ingestion via food and drinking water, and contact with consumer products. Dietary intake varies substantially, with high concentrations reported in fruits, vegetables, and seafood. Indoor environments represent a dominant exposure setting due to elevated microplastic levels in household dust, synthetic textiles, and personal care products, while urban roadside environments further contribute to inhalation exposure. Marked global disparities are evident, with populations in low- and middle-income countries disproportionately affected due to concentrated plastic production, occupational exposures, and transboundary waste flows. Emerging biomonitoring and clinical evidence confirms the presence of MNPs in human blood, vascular tissues, and atherosclerotic plaques, indicating systemic exposure with potential cardiovascular implications. MNP exposure is a plausible contributor to CVD via inflammation, oxidative stress, and endothelial dysfunction. Despite limited causal evidence, findings highlight the need for improved exposure assessment, prevention strategies, and policy action.