• Microparticles
• Particulate matter

Background: Particulate airborne pollution is associated with increased cardiopulmonary morbidity. Microparticles are extracellular vesicles shed by cells upon activation or apoptosis involved in physiological processes such as coagulation and inflammation. We investigated the hypothesis that particulate matter causes the shedding of microparticles by human mononuclear and endothelial cells.
Methods: Cells were isolated from the blood and the umbilical cords of normal donors with standard techniques and cultured in the presence of particulate from a standard reference. Microparticles were assessed in the conditioned medium as posphatidylserine concentration. Microparticle-associated tissue factor was assessed by a one-stage clotting assay. Nanosight technology was used to confirm the main results.
Results: Particulate matter induces a dose- and time- dependent, rapid (1 h) increase in microparticle generation in both cells. These microparticles express functional tissue factor. Particulate matter increases intracellular calcium concentration and phospholipase C inhibition reduces microparticle generation. Nanosight analysis confirmed that upon exposure to particulate matter both cells express particles with a size range consistent with the definition of microparticles (50-100 nm).
Conclusions: Exposure of mononuclear and endothelial cells to particulate matter upregulates the generation of microparticles at least partially mediated by calcium mobilization from intracellular storage pools. This observation might provide a further link between airborne pollution and cardiopulmonary morbidity.