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Environmental Exposure to Micro- and Nanoplastics: Linking Cardiovascular Disease and Cancer Through Shared Biological Pathways
Summary
Tiny plastic particles from our environment—found in air, food, and water—may get into our bodies and trigger inflammation and cell damage linked to both heart disease and cancer, according to this review of existing research. While the studies so far are mostly from labs and animals rather than large human trials, the findings suggest these plastics could be a hidden contributor to two of the world's biggest killers. More research on real-world exposure and long-term effects in people is still needed before we know for sure how much risk they pose.
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 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 integrating exposure assessment and clinical outcomes.