ACUTE PULMONARY RESPONSE TO INHALED JP-8 JET FUEL AEROSOL IN MICE

Abstract

The pulmonary response to JP-8 jet fuel inhalation was investigated by characterizing biomarkers of lung injury, respiratory permeability, pulmonary function, and lung morphology. C57BL/6 and B6.A.D. (Ahrd/Nats) mice, aryl hydrocarbon hydroxylase nonresponsive and slow N -acetylator, were exposed to atmospheres ranging from 0 to 113 mg/m 3 of aerosolized JP-8 jet fuel for 1 h. At 24-30 h after the exposure, pulmonary function testing was performed on anesthetized animals. Respiratory permeability was measured by monitoring the pulmonary clearance of instilled 99 m Tc-labeled diethylenetriamine pentaacetate and then lungs were assigned for bronchoalveolar lavage or histopathology. Bronchoalveolar lavage fluid (BALF) was analyzed for total protein, lactate dehydrogenase (LDH), and N -acetyl--D-glucosaminidase (NAG) as well as cell number and type. Pulmonary responses to JP-8 were similar in both strains of mice. JP-8 exposure between 50 and 113 mg/m 3 caused an increase in respiratory permeability, which was accompanied by BALF increases of total protein, LDH, NAG, and alveolar macrophages. There was also a small increase in BALF neutrophils in the C57BL/6 strain. JP-8 exposures did not have an effect on pulmonary function even though histopathology showed evidence of terminal bronchiole lesions. These results indicate that the acute pulmonary response to permissible exposure levels of aerosolized JP-8 jet fuel can cause changes in respiratory permeability and BALF markers of lung injury. These changes in biochemical, cellular, and pathological parameters following JP-8 exposure provide evidence that occupational exposure to hydrocarbon fuel aerosol is more detrimental than vapor exposure.