| Studies were initiated to characterize the acute and sub-chronic pulmonary responses to inhaled Jet-Propulsion Fuel 8 (JP-8) aerosol. At 24 to 30 hours following JP-8 exposure, physiological, biochemical, cellular, and morphological techniques were used to assay for lung injury. In addition, C57BL/6 and B6.A.D.(;The pulmonary clearance of JP-8 following inhalation exposures was determined indirectly by analysis for tetradecane content within lung homogenates from exposed mice. Clearance of JP-8 following acute exposure was determined to have a half-life of 43 minutes and increased by 14 minutes following a toxic sub-chronic exposure. The relatively rapid pulmonary clearance of JP-8 following either acute or sub-chronic exposure implies that JP-8 induced lung injury was independent of pulmonary retention.;Studies were also performed to determine if non-cytotoxic concentrations of JP-8 or tetradecane could decrease bronchial epithelial barrier function. Studies showed that one hour of exposure to JP-8 or tetradecane could significantly enhance paracellular permeability to mannitol in the BEAS-2B human bronchial epithelial cell line, at two hours after exposure. Bronchial epithelial permeability appeared to be more sensitive to tetradecane than JP-8. Subsequent recovery studies determined that JP-8 and tetradecane-induced decreases in barrier function reach a maximum at 12 hours and barrier function returns to control by 48 hours post-exposure. These results indicate that JP-8 induced lung injury may be initiated by changes in airway barrier function. |
