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Background/Hypothesis:Widespread use of plastic has created a world where exposure to microplastics is inevitable leading to their presence in our circulatory system. This raises questions about microplastics impact on thrombosis. Aminated polystyrene (aPS) plastics have been shown to increase platelet aggregation and thrombus formation in animal models. Given this, we hypothesized that aPS administration will increase the rate of fibrin clot formation in a simple thrombin-fibrinogen clot model. Project Methods:We evaluated how concentrations of 25-200 μg/mL of 100 nm aPS particles affect fibrin clot formation using turbidity assays. To determine the effect of surface charge, experiments were also performed with non-modified polystyrene (nPS) particles. Microplastics were pre-incubated either with physiological concentrations of fibrinogen or thrombin and the clot formation was measured using turbidity at 405 nm every 10 seconds over 45-minutes. Clotting parameters such as maximum turbidity (TurbMax), time to 90% maximum turbidity (TurbTime), and clot formation rate (Vmax) were determined and compared to controls without microplastics. Results:When increasing concentrations of aPS were preincubated with thrombin or fibrinogen, there was less than a 2-fold change in Vmax, TurbMax, and TurbTime. When increasing concentrations of nPS were preincubated with thrombin, there was up to a 27-fold decrease in Vmax, 2.4-fold decrease in TurbMax, and 4.36-fold increase in TurbTime compared to the control. Whereas preincubation of nPS with fibrinogen resulted in 1.86-fold decrease in Vmax, 1.63-fold decrease in TurbMax, and 2.30-fold increase in TurbTime. Potential Impact:In this simplified clotting model, it was surprising to find inhibitory effects on clot formation and that they were more pronounced with nPS than with aPS. However, these results align with increase prothrombin time observed in literature in presence of aPS. Therefore, future studies with more complex clotting models need to be performed before claims can be made on the impact of microplastics on thrombosis. 

Micro/nanoplastics, whether manufactured or resulting from environmental degradation, can enter the body through ingestion, inhalation, or dermal pathways. Previous research has found that nanoplastics with diameters of ≤100 nm can translocate into the circulatory system in a dose-dependent manner and potentially impact thrombosis and hemostasis. To investigate the direct effects of microplastics on fibrin clot formation, a simplified ex vivo human thrombin/fibrinogen clot model was utilized. The 100 nm polystyrene particles (non-functionalized [nPS] and aminated [aPS]) were preincubated (0–200 µg/mL) with either thrombin or fibrinogen, and fibrin clot formation was characterized via turbidity and thromboelastography (TEG). When the particles were preincubated with fibrinogen, little effect was observed for aPS or nPS on turbidity or TEG up through 100 µg/mL. TEG results demonstrated a significant impact on clot formation rate and strength, in the case of nPS preincubated with thrombin exhibiting a significant dose-dependent inhibitory effect. In conclusion, the presence of microplastics can have inhibitory effects on fibrin clot formation that are dependent upon both particle surface charge and concentration. Negatively charged nPS exhibited the most significant impacts to clot strength, turbidity, and rate of fibrin formation when first incubated with thrombin, with its impact being greatly diminished when preincubated with fibrinogen in this simplified fibrin clot model.