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JP-5, JP-8, and Jet A are kerosene-based jet fuels. They are refined by a straight distillation of crude or

shale oil, or a distillation of crude or shale oil in the presence of a catalyst. The jet fuels are, however, refined under more stringent conditions and contain various additives not found in kerosene; Jet A serves as the base fuel for JP-8. The performance-enhancing additives found in JP-5, JP-8, and Jet A include antioxidants (including phenolic antioxidants), static inhibitors, corrosion inhibitors, fuel system icing inhibitors, lubrication improvers, biocides, and thermal stability improvers. These additives are used in specified amounts as governed by commercial and military specifications. Jet fuels are composed of more than 200 aliphatic and aromatic hydrocarbons (C6-C17+); the exact composition of a jet fuel is also dependent upon the crude oil from which it is refined. Because of this inherent variability, little information exists on the exact chemical and physical properties of jet fuels.

Many of the constituents of JP-5, JP-8, and Jet A fuels are volatile and will evaporate into the air when jet fuels are spilled accidentally onto soils or surface waters. Other components of these jet fuels are more likely to dissolve in water following spills to surface waters or leaks from underground storage tanks.

Some of the chemicals in jet fuels may slowly move down through the soil to the groundwater. The chemicals that evaporate will undergo photodegradation by atmospheric oxidants such as hydroxyl radicals. The photooxidation half-life range for a group of representative chemicals of kerosene, JP-5, JP-8, and Jet A was reported as 0.2–1.1 days. In soil and water, the constituents of JP-5, JP-8, and Jet A fuels are biodegraded at varying rates. Exposure to JP-5, JP-8, and Jet A fuels by the general population is expected to be low and could occur through atmospheric, soil, or groundwater contamination. Military or civilian personnel who are employed in jet fuel storage or re-fueling activities will have the greatest exposure via inhalation and dermal routes to these substances. Occupational exposure could involve exposure to raw fuel, vapor phase, aerosol phase, a mixture of vapors and aerosols, or fuel combustion exhaust. General population exposure is most likely to occur in populations living near military installations using JP-5 or JP-8 or commercial airports using Jet A. Airborne exposure to jet fuel vapors and/or aerosols can result from fuel spillage, engine cold starts, and high-altitude fuel jettisoning. Jet fuel spills can also result in exposure via contaminated groundwater or soil.

Because JP-5, JP-8, and Jet A fuels are complex mixtures of both aliphatic and aromatic hydrocarbons, exposure is typically measured by monitoring the total hydrocarbon concentration (THC) and the levels of

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certain aromatic substances, such as benzene, toluene, ethylbenzene, xylene, and naphthalene, that are present in jet fuels. Since there are multiple sources of these components in the environment, exposure studies usually include a control population that has had little or no exposure to jet fuels in order to establish a baseline level of these substances that would exist in the absence of jet fuel exposure. In a study of Air Force personnel exposed to JP-8 during regular work shifts, the geometric mean concentration of THC in the breathing zone of a high exposure group was 4.4 mg/m3, while that of a low exposure group was 0.9 mg/m3. The geometric mean concentrations of naphthalene were reported as

4.8 and 0.7 µg/m3 for the high and low exposure groups, respectively. See Chapter 6 for more information on levels of exposure and environmental fate of JP-5 and JP-8.


Although JP-5 and Jet A fuels have been used for over 60 years and JP-8 was identified by the Department of Defense as its single military fuel over 30 years ago, there are very little data on the toxicity of kerosene-based jet fuels in humans. Most of the studies focused on the potential neurotoxicity of JP-8 fuel. Single studies in humans exposed to JP-8 fuel reported increases in white blood cell neutrophil and monocyte levels with no change in lymphocyte subpopulations and an inverse association between aliphatic hydrocarbons in exhaled breath and serum levels of luteinizing hormone (LH).

However, exposure to JP-8 was not associated with higher odds of menstrual disorders. Limited information is available on the carcinogenic potential of jet fuels in humans. Studies in laboratory animals have examined the toxicity of JP-5, JP-8, and Jet A fuels following inhalation, oral, or dermal exposure and have reported a number of targets of toxicity, including the lungs, liver, skin, immunological system, nervous system, and developing organism. Although renal effects have also been observed in male rats exposed to JP-5 or JP-8, the lesions are considered to be characteristic of alpha2u­ globulin nephropathy, which is only observed in male rats and is not considered to be toxicologically relevant to humans. JP-5 was not carcinogenic in mice in a 2-year dermal bioassay. Increases in skin tumors were observed in mice dermally exposed to Jet A for 52–62 weeks; however, tumors were only observed at concentrations resulting in significant skin damage (inflammation and necrosis). Similarly, increased numbers of skin tumors were observed in mice that received applications of undiluted kerosene on the skin for 2 years, but this occurred only in the presence of moderate-to-marked skin damage. No inhalation or oral studies evaluated the carcinogenicity of JP-5, JP-8, or Jet A in laboratory animals; no increases in tumor incidences were observed in rats administered kerosene by gavage for 2 years.

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Neurological Effects. Studies in subjects occupationally exposed to JP-8 have reported alterations in balance associated with cumulative exposure to benzene, a component of JP-8, and alterations in neuropsychological test results in workers with daily exposures to 10 mg/m3 JP-8. Another study of workers did not find an association between daily exposures to JP-8 and balance. A study of veterans found alterations in reaction time on divided attention tests following 3 weekly 7-minute exposures to

0.00057 ppm JP-8 vapor. Kerosene induces neurological effects in humans, as evidenced in many reports of acute accidental ingestion of this fuel. Neurological effects noted most frequently reported in these cases included unconsciousness or semiconsciousness, drowsiness, restlessness, and irritability. There are limited data that suggest that the central nervous system effects following ingestion of kerosene are due to hypoxia from kerosene-induced respiratory impairment. In laboratory animals, JP-5 and JP-8 caused alterations in performance in a battery of tests in rats exposed to 1,200 mg/m3 JP-5 vapor or 1,000 mg/m3 JP-8 vapor in intermediate-duration inhalation studies. Exposure to 1,000 mg/m3 JP-8 vapor also resulted in impaired performance on higher cognitive tests, but not on simple memory tests. Another study found hyperlocomotive activity and increased arousal levels in rats exposed to aerosolized JP-8 for 4 weeks. In contrast, lethargy was observed in mice administered Jet A gavage doses of 100 mg/kg/day and was observed once in most rats exposed to 500 mg/kg/day. In addition to the central nervous system effects, exposure to JP-8 can result in auditory effects. Acute- and intermediate-duration exposure to JP-8 followed by exposure to noise resulted in alterations in the peripheral auditory system and the central auditory processing area.

Respiratory Effects. No human studies have examined the potential of JP-5, JP-8, or Jet A to induce respiratory effects. Respiratory effects are a common finding in humans ingesting kerosene; the observed effects include bronchopneumonia, bronchitis, pneumonitis, lung infiltrates and effusions, cough, dyspnea, and tachypnea. However, these effects are likely attributable to aspiration of the kerosene. The results of studies in laboratory animals suggest that the respiratory tract is a target for airborne JP-8. Most of this information comes from a series of studies conducted at the University of Arizona in which rats and mice were exposed to aerosolized JP-8 1 hour/day for 1 or 7 days. There are several limitations to these studies: the primary limitation being that only the aerosol component of the test atmosphere was measured, resulting in a large underestimation of the JP-8 exposure (the studies’ limitations are discussed in greater detail in Section 3.2.1). These studies reported an increase in respiratory permeability, increased lung resistance, and terminal bronchiole lesions. These effects were usually accompanied by increased biomarkers of inflammation in broncheoalveolar lavage fluid (BALF). In contrast, an acuteduration study in which rats were exposed to Jet A aerosols and vapors and most intermediate-duration inhalation studies involving exposure to JP-5 or JP-8 vapor did not report respiratory effects. The

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exception is the finding of enlarged alveolar capillaries in rats exposed to 500 mg/m3 JP-8 vapor 6 hours/day for 90 days; the no-observed-adverse-effect level (NOAEL) was 250 mg/m3. No histological alterations were observed in the respiratory tracts of rats exposed to ≤1,980 mg/m3 Jet A aerosols and vapors 4 hours/day, 5 days/week for 14 days, in rats continuously exposed to ≤1,000 mg/m3 JP-8 vapor for 90 days, or in rats, mice, and dogs continuously exposed to ≤750 mg/m3 JP-5 vapor for 90 days. One possible explanation for the conflicting results between studies is the differences in the composition of the test atmosphere. For example, a vapor test atmosphere could contain a higher percentage of low molecular weight, more volatile compounds than the raw fuel and aerosolizing the jet fuel could generate liquid droplets enriched in higher molecular weight n-alkanes.

Hepatic Effects. Several studies in laboratory animals provide evidence that the liver is a sensitive target of jet fuel toxicity; however, the findings are not consistent across studies, which may be due to species or strain differences or differences in the physical properties of the fuel (e.g., aerosols versus vapor). Continuous exposure to ≥150 mg/m3 JP-5 vapor resulted in hepatocellular fatty changes and vacuolization in mice. In similarly exposed rats and dogs, exposure to 750 mg/m3 JP-5 vapor resulted in no effects in rats and mild diffuse hepatocellular swelling in dogs. Dilated sinusoids and fatty hepatocytes were observed in rats exposed to ≥500 mg/m3 JP-8 vapor for 91 days; another 90-day study found no histological alterations in rats exposed to 1,000 mg/m3 JP-8 vapor. A 14-day exposure to 1,980 mg/m3 Jet A vapor and aerosol also did not result in histological alterations or changes in alanine aminotransferase (ALT) levels. In acute-duration gavage studies, increases in ALT and aspartate aminotransferase (AST) levels were observed in rats administered a single gavage dose of 19 mg/kg JP-5 or single or repeated gavage doses of 18,000 mg/kg JP-5. Intermediate-duration gavage administration of ≥750 mg/kg/day JP-8 for 90 days in rats resulted in non-dose-related increases in ALT and AST; this study also found an increase in total bilirubin levels at ≥750 mg/kg/day, but no histological alterations. A 90-day gavage exposure to 500 mg/kg/day Jet A also did not result in histological alterations in the livers of rats or mice; the exposure did result in an increase liver weight and enlarged livers in rats. Chronic dermal exposure to 500 mg/kg/day JP-5 resulted in liver amyloidosis in mice.

Dermal Effects. Studies in rats, mice, rabbits, and pigs demonstrate the dermal toxicity of topically applied JP-5, JP-8, and Jet A. Similar effects have been observed for all three fuel types, although the results of one study suggests that Jet A may be slightly more irritating than JP-8 in pigs exposed for 5 hours. Single 1-hour exposures to low concentrations did not result in visible damage to the skin;

however, evidence of inflammation (increased granulocyte infiltration and increased levels of inflammatory biomarkers) was observed. Additionally, ultrastructural changes suggest that jet fuel

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exposure alters the epidermal-dermal barrier, which could result in increased absorption. Overt signs of dermal toxicity have been observed following repeated exposures; effects ranged from erythema and edema to dermatitis to ulceration. The severity of the lesions increased with duration and concentration.

Other factors that can affect the dermal toxicity include the test vehicle and whether the application site is occluded. At a given dose, undiluted jet fuel resulted in more severe erythema and desquamation, as compared to jet fuel diluted in mineral oil or acetone:olive oil. Occluding the application site resulted in moderate-to-severe erythema and moderate edema as compared to slight erythema when the application site was not occluded.

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