Acrylamide and Bisphenol A: Two Plastic Additives Increase Platelet Activation, via Oxidative Stress

Carlos Felipe Burgos¹Diego Mendez²Santiago Quintana¹Slawomir Gonkowski³Andrés Trostchansky^4*Marcelo Alarcon^2*

• ¹University of Concepcion, Concepción, VIII Biobío Region, Chile
• ²University of Talca, Talca, Chile
• ³University of Warmia and Mazury in Olsztyn, Olsztyn, Warmian-Masurian, Poland
• ⁴Facultad de Medicina, Universidad de la República, Montevideo, Uruguay

With the rise of plastic use in the mid-20th century, the slow degradation and environmental accumulation of its components have introduced new health risks. Acrylamide (AA) and bisphenol A (BPA), common byproducts of plastic, are now widespread environmental pollutants found in human tissues, yet their impact on human health remains only partially understood. This study focuses on how AA and BPA influence platelet function, which plays a central role in cardiovascular diseases (CVD) by facilitating blood clot formation. Our findings reveal that both compounds trigger platelet activation and aggregation, signaling increased thrombotic risk and highlighting potential cardiovascular implications. Through bioinformatic analysis, we identified around 1,230 proteins as possible targets of AA and BPA, with significant effects on 191 and 429 proteins in platelets, respectively. These proteins include key players in oxidative stress and apoptosis, with AA and BPA impacting molecular pathways mediated by PKC, P38α-MAPK, and SOD. Molecular simulations show stable complexes form between these compounds and the enzymes they inhibit, further impairing platelet function. Our results underscore the need for greater awareness around AA and BPA exposure, as these pollutants contribute to enhanced platelet aggregation and may increase CVD risk.