Epidemiology studies have linked exposure to pollutant particles to increased cardiovascular mortality and morbidity, but the mechanisms remain unknown. The study tested the hypothesis that the ultrafine fraction of ambient pollutant particles would cause endothelial cell dysfunction. The gene expression of human pulmonary artery endothelial cells (HPAEC) were profiled after exposure to ultrafine particles (UFPs ; 100 µg/mL). UFPs may induce vascular endothelial cells to express genes related to clotting. The results indicate that PM may cause adverse cardiovascular health effects by activating coagulation-inflammation circuitry.

URL: http://www.ehponline.org/members/2007/9556/9556.pdf