Effect of Perfluorooctanesulfonic Acid on Fibrin Clot Properties and Thrombin Generation: Linking Environmental Pollution with Cardiovascular Diseases

Perfluorooctanesulfonic acid (PFOS) is a persistent organic pollutant linked in epidemiological studies to increased coronary artery disease (CAD) risk, higher LDL-cholesterol, hypertension, and other adverse outcomes. However, the mechanisms by which PFOS affects cardiovascular physiology, particularly coagulation, remain insufficiently understood. We evaluated the ex vivo effects of PFOS on fibrin clot structure and thrombin generation in platelet-poor plasma (PPP) and citrated whole blood from ten healthy volunteers (five women, aged 27–32 years; mean serum PFOS: 2.63 ± 0.85 μg/L). PPP samples were incubated with PFOS at 50, 200, and 400 μg/L. Assays included calibrated automated thrombogram, clot permeability (Ks), clot lysis time (CLT), thromboelastography (400 μg/L), and scanning electron microscopy (SEM). PFOS did not significantly modify endogenous thrombin potential or peak thrombin. In contrast, it reduced Ks and prolonged CLT at 200 and 400 μg/L, indicating impaired fibrinolysis. SEM images confirmed the formation of thinner, tightly packed fibrin fibers with reduced pore size at higher PFOS concentrations. These findings were consistent across dilution models, with only minimal changes observed in low-dilution protocols. Overall, PFOS appears to disrupt fibrin polymerization, generating denser and more fibrinolysis-resistant clots without major effects on thrombin generation. Such alterations may promote a prothrombotic state and predispose exposed individuals to clinically relevant thrombotic events, including myocardial infarction and stroke. Further studies are required to define the clinical consequences of PFOS-related coagulation abnormalities in exposed populations.