Summary. Background: There is a proven link between exposure to traffic-derived particulate air pollution and the incidence of platelet-driven cardiovascular diseases. It is suggested that inhalation of small, nanosized particles increases cardiovascular risk via toxicological and inflammatory processes and translocation of nanoparticles into the bloodstream has been shown in experimental models. We therefore investigated the ability of diesel exhaust particles (DEP) to interact physically and functionally with platelets.
Methods: The interaction of DEP and carbon black (CB) with platelets was examined by transmission electron microscopy (TEM), whereas the functional consequences of exposure were assessed by measuring in vitro and in vivo platelet aggregation via established methods.
Results: Both DEP and CB were internalized and seen in proximity with the open canalicular system in platelets. DEP induced platelet aggregation in vitro whereas CB had no effect. DEP induced Ca2+ release, dense granule secretion and surface P-selectin expression, but not toxicologic membrane disruption. Low concentrations of DEP potentiated agonist-induced platelet aggregation in vitro and in vivo.
Conclusions: DEP associate physically with platelets in parallel with a Ca2+-mediated aggregation response displaying the conventional features of agonist-induced aggregation. The ability of DEP to enhance the aggregation response to platelet stimuli would be expected to increase the incidence of platelet-driven cardiovascular events should they be inhaled and translocate into the blood. This study provides a potential mechanism for the increased thrombotic risk associated with exposure to ambient particulate air pollution.