Environmental Pollutant–Induced Cardiopathogenesis Through Immune Dysfunction: The Emerging Role of Micro- and Nanoplastics

Exposure to environmental pollutants and toxicants is increasingly recognized as a major determinant of cardiovascular disease (CVD). Beyond direct toxic effects, these agents profoundly alter immune homeostasis, thereby contributing to endothelial dysfunction, atherogenesis, arrhythmogenesis, and impaired myocardial repair. Among emerging pollutants, micro- and nanoplastics (MNPs) have recently gained attention due to their ubiquity and potential cardiovascular impact. This narrative review synthesizes mechanistic, translational, and clinical evidence on pollutant-induced cardiovascular injury mediated by immune dysfunction. We integrate data from experimental models, human tissue studies, and clinical observations to delineate shared and pollutant-specific immunoinflammatory pathways, with a particular focus on MNPs. Environmental toxicants, including particulate matter, heavy metals, endocrine disruptors, and MNPs, promote chronic innate immune activation, mitochondrial stress responses, NLRP3 inflammasome signaling, and maladaptive epigenetic reprogramming of myeloid cells. MNPs have been detected in human cardiovascular tissues and are associated with adverse cardiovascular events. Experimental evidence indicates that MNPs accumulate within vascular and cardiac compartments, disrupt endothelial barrier integrity, enhance macrophage pro-inflammatory polarization, and amplify oxidative and nitrosative stress. These converging mechanisms foster plaque vulnerability, microvascular instability, and increased susceptibility to ischemic and arrhythmic complications. Environmental cardiopathogenesis represents a rapidly expanding frontier in cardioimmunology. Elucidating the immune-mediated mechanisms linking pollutant exposure-particularly MNPs-to cardiovascular injury may improve risk stratification and inform targeted preventive and therapeutic strategies in increasingly polluted environments.