PB1066 - The Effects of Polystyrene Microplastics on Thrombosis

Background: Micro-plastic particles (MPs) are now ubiquitous in nature; being found in aquatic and terrestrial environments and have been shown to be ingested by animals and have entered the human food chain. Human exposure to MPs occurs through numerous routes since plastic usage is widespread and recent landmark studies have identified MPs in human tissues, blood and thrombi surgically removed from patients. However, the health effects are yet to be fully investigated. MP research in thrombosis focuses mostly on commercial polystyrene beads, our study provides a novel insight on natural “rough and ready” MPs.

Aims: Determine the effects of MPs exposure on endothelial cells and thrombus formation.

Methods: MP particles were generated by cryomilling of Polystyrene (PS) powder to produce irregular PS-MPs < 5 µm diameter. To determine the impact on endothelial cell function, Human Umbilical vein endothelial cells (HUVECS) were exposed to PS-MPs for 24 hours and the expression of endothelial activation markers measured using qPCR. Thrombus formation was analysed by spiking PS-MPs into whole blood at reported plasma concentrations and perfused over collagen coated surfaces. Turbidity assays were used to measure fibrin clot formation.

Results: HUVECS incubated with PS-MPs demonstrated significant upregulation of ICAM-1 and VCAM-1 expression indicating MPs may possess the ability to activate the endothelium. As shown in figure A and B 1.6µg/ml and 3.2 µg/ml PS-MPs significantly enhanced platelet deposition to collagen and resulted in the formation of larger, denser thrombi. It was also observed that at higher PS-MPs concentrations thrombi became very unstable and embolic. Additionally, turbidity assay revealed that PS-MPs reduce the lag time to fibrin formation and maximal turbidity indicating denser clot formation.

Conclusion(s): Our data indicates that PS-MP particles closely mimicking those found in the bloodstream can enhance thrombus formation and can alter the phenotype of the endothelium to become potentially more pro-inflammatory and prothrombotic.