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Environmental Exposure to Micro- and Nanoplastics: Linking Cardiovascular Disease and Cancer Through Shared Biological Pathways—A Critical Review

Original title: Environmental Exposure to Micro- and Nanoplastics: Linking Cardiovascular Disease and Cancer Through Shared Biological Pathways—A Critical Review

Antioxidants 2026
Andrea Borghini, Mariangela Palazzo, Alessandro Tonacci, Fabrizio Minichilli, H. Wu, Francesca Gorini

Summary

Tiny plastic particles from our air, food, and water are showing up inside the human body, and this review pulls together existing research suggesting they may trigger inflammation, cell damage, and other harmful processes linked to both heart disease and cancer. The catch: most of this evidence comes from lab and animal studies so far, not large human studies, so scientists can't yet say for certain that microplastics cause these diseases in people. Still, given how common plastic exposure is in daily life, this is a strong signal that more research—and possibly more caution—is warranted.

Models
Study Type In vitro

Micro- and nanoplastics (MPs/NPs) are ubiquitous environmental contaminants increasingly detected in air, food, drinking water, and human tissues, raising concerns about their potential long-term health effects. Accumulating evidence indicates that these particles can enter the human body, cross biological barriers, and elicit cellular and molecular responses relevant to disease development. This review synthesizes current mechanistic evidence linking MP/NP exposure to cardiovascular disease (CVD) and cancer, two leading global causes of morbidity and mortality that share interconnected pathogenic pathways. Key mechanisms include chronic inflammation, oxidative stress, gut microbiota dysbiosis, genotoxicity, and epigenetic alterations, all of which are widely implicated in both conditions. However, the available evidence is still largely derived from in vitro and animal studies, with limited human epidemiological data. Important uncertainties remain regarding real-world exposure characterization, dose–response relationships, and long-term clinical outcomes, underscoring the need for standardized analytical approaches, validated exposure and effect biomarkers, and large-scale longitudinal studies to clarify causal associations for both cancer and CVD. Taken together, current evidence suggests that MPs/NPs may represent emerging environmental contributors to shared pathogenic pathways linking CVD and cancer; however, establishing causality in humans will require well-designed longitudinal studies that integrate exposure assessment and clinical outcomes.

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