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

The pulmonary response to JP-8 jet fuel inhalation was investigated by characterizing biomarkers of lung injury, respiratory permeability, p ulmonary function, and lung morphology. C57BL/6 and B6.A.D. (Ahr(d)/Na t(s)) mice, aryl hydrocarbon hydroxylase nonresponsive and slow N-acet ylator, were exposed to atmospheres ranging from 0 to 113 mg/m(3) of a erosolized JP-8 jet fuel for 1 h. At 24-30 h after the exposure, pulmo nary function testing was performed on anesthetized animals. Respirato ry permeability was measured by monitoring the pulmonary clearance of instilled Tc-99m-labeled diethylenetriamine pentaacetate and then lung s were assigned for bronchoalveolar lavage or histopathology. Bronchoa lveolar lavage fluid (BALF) was analyzed for total protein, lactate de hydrogenase (LDH), and N-acetyl-beta-D-glucosaminidase (NAG) as well a s cell number and type. Pulmonary responses to JP-8 were similar in bo th strains of mice. JP-8 exposure between 50 and 113 mg/m(3) caused an increase in respiratory permeability, which was accompanied by BALF i ncreases of total protein, LDH, NAG, and alveolar macrophages. There w as 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 r esults indicate that the acute pulmonary response to permissible expos ure levels of aerosolized JP-8 jet fuel can cause changes in respirato ry permeability and BALF markers of lung injury. These changes in bioc hemical, cellular, and pathological parameters following JP-8 exposure provide evidence that occupational exposure to hydrocarbon fuel aeros ol is more detrimental than vapor exposure.