A 90-day continuous vapor inhalation toxicity study of JP-8 jet fuel followed by 20 or 21 months of recovery in Fischer 344 rats and C57BL/6 mice

• Published in: Toxicologic pathology Vol. 19; no. 2; p. 77
• Main Authors: Mattie, D R, Alden, C L, Newell, T K, Gaworski, C L, Flemming, C D
• Format: Journal Article
• Language: English
• Published: United States 01-01-1991
• Subjects: Administration, Inhalation; Animals; Dose-Response Relationship, Drug; Female; Hydrocarbons - administration & dosage; Hydrocarbons - toxicity; Kidney - drug effects; Kidney - pathology; Kidney - ultrastructure; Kidney Diseases - chemically induced; Kidney Diseases - mortality; Kidney Diseases - pathology; Kidney Tubules - drug effects; Kidney Tubules - pathology; Kidney Tubules - ultrastructure; Male; Mice; Mice, Inbred C57BL; Microscopy, Electron; Organ Size; Petroleum - toxicity; Rats; Rats, Inbred F344; Sex Characteristics; Time Factors
• ISSN: 0192-6233
• DOI: 10.1177/019262339101900201

The kerosene-type jet fuel, JP-8, consists of a complex mixture of aliphatic and aromatic hydrocarbons. Because of the utility of JP-8, studies have been conducted to identify the potential long-term consequence of occupational inhalation exposure. Fischer 344 rats and C57BL/6 mice of both sexes were exposed to JP-8 vapors at 0, 500, and 1,000 mg/m3 on a continuous basis for 90 days, then followed by recovery until approximately 24 months of age. Occurrence of necrotizing dermatitis associated with fighting resulted in an increase in mortality in mice (male greater than female) during the 2 week to 9 month post-exposure recovery period. The male rat kidney developed a reversible ultrastructural increase in size and propensity for crystalloid changes of phagolysosomal proteinic reabsorption droplets in the proximal convoluted tubular epithelium. A specific triad of persisting light microscopic renal lesions occurred but functional change was limited to a decrease in urine concentration compared to controls that persisted throughout the recovery period. The response is comparable to the chronic effect of lifetime exposure of the male rat to unleaded gasoline, d-limonene, and p-dichlorobenzene, except for the absence of tubular tumorigenesis. The active toxicologic response presumably must occur over a greater proportion of the male rat's life span for the tumor component of this male rat hydrocarbon nephropathy syndrome. The predictiveness for humans must be questioned, since the pathologic response to JP-8 involved only one tissue in one sex of one species, and since the male rat response appears to be linked to an inherent renal protein peculiarity.