Microplastics and nanoplastics are widespread environmental pollutants that have been detected in human cardiovascular tissues, including the heart, arterial plaques, and bloodstream—highlighting their systemic bioavailability.

Evidence from clinical and experimental studies suggests a growing association between micro-/nanoplastics and increased cardiovascular disease (CVD) risk, particularly through their role in accelerating atherogenesis.

In vitro and in vivo models show that these particles cause endothelial toxicity, oxidative stress, foam cell formation, and lipid metabolism disruption, contributing to the progression of atherosclerosis.

Micro- and nanoplastics activate inflammatory signaling and impair vascular barrier function. They also influence coagulation dynamics, increasing the potential for thrombus formation by altering clotting cascade components.

These particles induce haemolysis, alter red blood cell morphology, and disrupt immune cell functions, including cytokine secretion and macrophage/lymphocyte activity, indicating broad immunovascular implications.

Recognition of micro- and nanoplastics as emerging cardiovascular risk factors underscores the need for heightened awareness, further research, and the integration of environmental risk assessments into public health strategies.

The accumulating evidence linking micro- and nanoplastics to cardiovascular pathology highlights a critical and emerging area of investigation. These particles not only infiltrate cardiovascular tissues but also contribute to atherogenesis through endothelial toxicity, lipid dysregulation, inflammation, and thrombogenic effects. Further mechanistic studies and longitudinal clinical research are urgently needed to elucidate causal pathways, quantify exposure thresholds, and inform regulatory and public health interventions aimed at mitigating cardiovascular risk associated with plastic pollution.