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EFFECTS OF CARBON ULTRAFINE PARTICLES ON HUMAN AIRWAY EPITHELIAL CELLS
Impact/Purpose:
Specifically, this work will support efforts to (1) Identify mechanisms of toxicity for particulate matter (PM) constituents/sources; (2) Describe the role of PM size in causing health effects in pulmonary cells; and (3) Define the molecular basis of carbon ultrafine-particle effects in human lung cells.
Description:
One of the leading theories concerning the toxicology of ambient particulate matter (PM) attributes health effects associated with PM inhalation to ultrafine particles (UF). UF numbers dwarf those of fine and coarse particles present in the ambient air as a result of fossil fuel combustion processes. They are extremely small particles that have infinitesimal mass but enormous surface areas. Multiple theories propose that the large numbers of UF particles present a particle overload stress on or link UF surface areas to various metrics of toxicity. Our lab has shown that elemental carbon UF particles induce strong IL-8 expression in cultured human airway epithelial cells (HAEC). Initial attempts at identifying the signaling mechanism responsible for this effect were unsuccessful as one signaling parameter after another was found to be negative for activation by EC exposure. Very recently we detected activation of NFkB and P38 in HAEC after prolonged exposure (8 hours and longer). We are now confident that we will elucidate the mechanism through which EC exposure activates HAEC to induce IL-8 synthesis and thereby contributes to inflammatory lung injury in response to EC inhalation.