Microplastics and nanoplastics are ubiquitous environmental contaminants increasingly implicated in cardiovascular disease, the leading cause of global mortality. These synthetic particles enter the human body primarily through ingestion, inhalation, and dermal contact, interact with epithelial and immune barriers, and accumulate within critical organs and vascular tissues. Once internalized, they trigger oxidative stress, systemic inflammation, endothelial dysfunction, and prothrombotic cascades, collectively promoting atherogenesis and vascular injury which are central to cardiovascular disease pathogenesis. Recent human tissue–based studies have detected microplastics within atherosclerotic plaques and demonstrated associations between higher plaque microplastic burden and adverse cardiovascular events. Emerging data further suggest epigenetic dysregulation and extracellular vesicle–mediated signaling as potential mechanisms by which microplastics alter gene expression relevant to cardiometabolic disease. Populations with greater occupational or dietary exposure, such as industrial workers, high-seafood consumers, and frequent bottled-water users, may bear disproportionate risk. While experimental interventions, including enzymatic degradation and antioxidant therapy, show preliminary promise, major knowledge gaps persist, including limited longitudinal data, undefined dose–response relationships, uncertainty regarding optimal biological compartments for exposure assessment, and nonstandardized detection methodologies. This review integrates current mechanistic, clinical, and epidemiologic evidence linking plastics exposure to cardiovascular pathology, highlighting the urgent need for public education, health policy, continued research, and coordinated multidisciplinary strategies to mitigate risk.
Gu et al. (Sun,) studied this question.