Interaction of nanoplastics with platelets: activation and fibrin clot formation

Environmental exposure to micro- and nanoplastics (NPs) is an emerging toxicological concern, with recent evidence demonstrating their presence in human blood and vascular tissues. Although plastic-associated chemicals are known to induce oxidative stress and mitochondrial dysfunction, the direct impact of circulating NPs on blood cell function and redox-sensitive vascular processes remains poorly defined. Therefore, this study investigated the interaction between 100 nm carboxylated polystyrene nanoplastics (PS-NPs) and human platelets, which are key regulators of vascular homeostasis and thromboinflammation.

The interaction and uptake of PS-NPs by human platelets were assessed using flow cytometry and fluorescence microscopy. To evaluate platelet activation, we measured cytoskeletal remodeling (via side scatter) and dense granule secretion (via CD63 externalization). Additionally, whole blood assays were conducted under calcium-permissive conditions to determine the impact of PS-NPs on the formation and structure of fibrin networks.

PS-NPs rapidly associated with human platelets in a time- and concentration-dependent manner, reaching near-maximal uptake within 10 minutes. Exposure to PS-NPs induced marked platelet activation, evidenced by significant cytoskeletal remodeling and concentration-dependent CD63 externalization at levels comparable to those induced by thrombin stimulation. Furthermore, in whole blood, PS-NPs promoted the formation of dense fibrin networks and were actively incorporated into the resulting fibrin matrix.

The rapid nature of PS-NP-platelet interactions suggests high-capacity physicochemical adsorption, potentially mediated by membrane lipid microdomains and protein corona formation. Notably, the observed procoagulant phenotype is consistent with the perturbation of redox-sensitive platelet activation pathways. Collectively, these findings identify platelets as direct cellular targets of nanoplastics and demonstrate that circulating particulate matter can acutely promote prothrombotic responses. These data support a model in which nanoplastic exposure contributes to cardiovascular risk through the dysregulation of redox-dependent vascular signaling.