关键词：大气；环境污染；健康
摘 要：Previous work by us and others demonstrates induction of a systemic pro-inflammatory and pro-coagulant state in response to inhalation of environmental particulate matter. Our work demonstrated PM exposure activated platelets to a enhanced state of reactivity and suggested this could be a key factor in adverse cardiovascular events. This project evaluated pulmonary inflammation and systemic inflammatory and platelet responses to fine and ultrafine (PM2.5) ambient particulate matter collected from an urban (Sacramento) and rural (Davis) location. The objective of these experiments was to determine whether prior chelation of transition metals with deferoxamine mesylate (DFM) or binding of bacterial source endotoxin by polymyxin B reduced pulmonary and systemic responses to PM2.5. We hypothesized those inflammatory responses to a more transition metal rich urban source PM2.5 would be inhibited more by metal chelation while rural source PM2.5 would be more affected by endotoxin binding. Adult mice were given intratracheal instillations of collected PM2.5 and pulmonary pathology, systemic cytokine concentrations, and platelet activation were evaluated 24 hours later. To better assess contributions of aromatic hydrocarbons, oxidants or pro-inflammatory responses to biologically active material like endotoxin, we used laser capture microscopy to probe specific anatomic locations in lung for gene responses associated with each of these components.