Benzo[a]pyrene (BaP), a major environmental pollutant and component of cigarette smoke, is both carcinogenic and atherogenic in experimental models, as platelet play critical roles in atherothrombogenesis, we studied the effect of BaP on platelet activation and its underlying mechanisms.BaP dose-dependently enhances platelet aggregation induced by ADP.It augmented ADP-induced platelet P-selectin expression and fibrinogen binding.Under an arterial shear rate of 1000 s-1, BaP increased platelet adhesion on collagen surfaces by 20%.Western blot analysis showed that BaP could increase P38MAPK phosphorylation in the model of ADP-induced platelet aggregation, which have become the focus of research into platelet signaling pathways.The in vitro findings were further evaluated in the mouse model of arterial thrombosis induced by FeCI3, in which BaP increased the carotid arterial occlusion time in wild-type mice by 25%,P < 0.01.BaP augment platelet activation via the up-regulation of P38MAPK in the model of ADP-induced platelet aggregation, and enhanced arterial thrombus formation in vivo.Our data suggest that BaP may be related to atherothrombogenesis via platelet signaling pathways.