Toxicologic and Oncogenic Potential of JP-4 Vapor: 90-Day Continuous Inhalation Exposure

Kinkead, E.R.; Wolfe, R. E.; Flemming, Carlyle D.; Solomon, Richard A.; Mattie, David R.; Grabau, John H.; Marit, Gary B.

doi:10.3109/08958379509029096

Cited by 7 publications

(6 citation statements)

References 11 publications

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“…Employ- Petroleum-Related Risk Factors and Soil Screening Levels ing an uncertainty factor of 1,000 (HAD), the oral RiD s was estimated herein at 1.07 mg/kg/d. These findings are supported by the data presented in the final report of the work initially reported in the MacEwen and Vernot, 1984 study (Kinkead et al, 1995). Male and female Fischer 344 rats (225 animals per sex), female C57BL/6 mice (450 animals), and male and female beagle dogs (9 animals per sex) were exposed almost continuously (23 hr/d, 7 d/wk) for 90 days to JP-4 vapor at concentrations of 0,500, and 1,000 mg/m 3 .…”

Section: Jp-4supporting

confidence: 91%

Petroleum‐related risk factors and soil screening levels

Staats¹,

Mattie²,

Fisher³

1997

Human and Ecological Risk Assessment: An International Journal

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In an effort to develop risk-based Soil Screening Levels (SSLs) for Total Petroleum Hydrocarbons (TPH) in weathered soils, literature reviews were conducted to identify information regarding toxicology and previously developed oral risk factors for neat petroleum products and their potential surrogates, in particular, long chain petroleum hydrocarbons (LCPHs). Oral reference doses (RfDs) were identified in the literature for hexane; nonane; gasoline; JE-4; JP-5; marine diesel fuel; and mineral oil. Alternative RfDs s are proposed for these previously developed oral RfDs and new oral RfDs s were developed for other petroleum-related chemicals where sufficient toxicological information was available. RfDs s were developed for hexane; nonane; decane; C 10 -C 11 isoparaffinic hydrocarbon; dearomatized white spirit C 11 -C 12 ; gasoline; JP-4; JP-5; JP-7; JP-8; marine diesel fuel; mineral oil; and for petroleum wax. Then risk-based SSLs were estimated for each of these compounds using the oral RfDs and the child resident soil ingestion pathway. Finally, a general SSL of 25,000 mg/kg is proposed for LCPHs.

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Section: Jp-4supporting

confidence: 91%

Petroleum‐related risk factors and soil screening levels

Staats¹,

Mattie²,

Fisher³

1997

Human and Ecological Risk Assessment: An International Journal

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“…While certain neurotoxicity and neurobehavioral consequences appear to be unique to specific fuel formulations, a number of effects appear to result, as a function of dose and duration, from exposure to any of a number of hydrocarbon fuel formulations. For example, a number of animal studies of repeated inhalation exposure or oral gavage ingestion of hydrocarbon fuels have reported reductions in weight gain during the period of exposure (Kinkead et al, 1974(Kinkead et al, , 1995Bruner et al, 1993;Cooper & Mattie, 1996). Typically, a difference in mean weight between fuel-exposed and control groups will occur within 3-10 d of the initial exposure, as a function of fuel type and dose, and will persist throughout, and up to 14 d following the exposure.…”

Section: Neurotoxicity Of Selected Hydrocarbon Fuelsmentioning

confidence: 94%

“…A recently published study (Hong et al, 1999) provides excellent dermal absorption profiles for Jet-A, JP-8, and JP-8(100) jet fuels, empha- sizing differences that may occur as a function of fuel aging. Prolonged JP-8 contact with the skin may induce irritation, contact dermatitis, and sensitizat ion (Kinkead et al, 1992(Kinkead et al, , 1995Wolfe et al, 1997;Ullrich, 1999), although the potential for systemic toxicity was not estimated. In 4-h static diffusion cell experiments using rabbit skin, McDougal et al (1999McDougal et al ( , 2000 indicated that dermal penetration of JP-8 jet fuel across rabbit skin is very limited (74 ng/cm 2 /h), but that diethylene glycol monomethyl ether (DiEGME), an anti-icing additive, accounted for over 60% of the dermal absorption (weight/weight), although accounting for only about 0.1% of the applied JP-8.…”

Section: Hydrocarbon Fuel Exposure Scenariosmentioning

confidence: 97%

“…Repeated exposure to hydrocarbon fuel has been shown to result in greatly increased liver transcription of a protein known as alpha-2-microglobulin (alpha-2-mu). The increased alpha-2-mu clearance through the kidneys results in hyaline droplet formation in proximal tubular epithelial cells, incidence of granular protein casts in medullary tubules, and development of chronic progressive nephrosis Gaworski et al, 1985;Alden, 1986;Mattie et al, 1991Mattie et al, , 1995Bruner et al, 1993;Kinkead et al, 1995), limiting the ability of the kidneys to clear potential neurotoxicants. Additionally, it is thought that alpha-2-mu is responsible for transporting low-molecular-weight hydrophobic molecules (Swenberg et al, 1989), with limited evidence that cleavage products of alpha-2-mu may be capable of transporting toxicants such as lead (Fowler & DuVal, 1991), possibly related to their cellular toxicity in the brain.…”

Section: Neurological Consequences As Secondary Toxicity Effectsmentioning

confidence: 97%

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A Review of the Neurotoxicity Risk of Selected Hydrocarbon Fuels

Ritchie¹

2001

Journal of Toxicology and Environmental Health, Part B

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Over 1.3 million civilian and military personnel are occupationally exposed to hydrocarbon fuels, emphasizing gasoline, jet fuel, diesel fuel, or kerosene. These exposures may occur acutely or chronically to raw fuel, vapor, aerosol, or fuel combustion exhaust by dermal, respiratory inhalation, or oral ingestion routes, and commonly occur concurrently with exposure to other chemicals and stressors. Hydrocarbon fuels are complex mixtures of 150-260+ aliphatic and aromatic hydrocarbon compounds containing varying concentrations of potential neurotoxicants including benzene, n-hexane, toluene, xylenes, naphthalene, and certain n-C9-C12 fractions (n-propylbenzene, trimethylbenzene isomers). Due to their natural petroleum base, the chemical composition of different hydrocarbon fuels is not defined, and the fuels are classified according to broad performance criteria such as flash and boiling points, complicating toxicological comparisons. While hydrocarbon fuel exposures occur typically at concentrations below permissible exposure limits for their constituent chemicals, it is unknown whether additive or synergistic interactions may result in unpredicted neurotoxicity. The inclusion of up to six performance additives in existing fuel formulations presents additional neurotoxicity challenge. Additionally, exposures to hydrocarbon fuels, typically with minimal respiratory or dermal protection, range from weekly fueling of personal automobiles to waist-deep immersion of personnel in raw fuel during maintenance of aircraft fuel tanks. Occupational exposures may occur on a near daily basis for from several months to over 20 yr. A number of published studies have reported acute or persisting neurotoxic effects from acute, subchronic, or chronic exposure of humans or animals to hydrocarbon fuels, or to certain constituent chemicals of these fuels. This review summarizes human and animal studies of hydrocarbon fuel-induced neurotoxicity and neurobehavioral consequences. It is hoped that this review will support ongoing attempts to review and possibly revise exposure standards for hydrocarbon fuels.

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“…Parton et al [18] reported significant increases in mean liver weights, without tissue lesions or changes in ALT activity, in male Fischer-344 rats exposed for only 1 h per day for 7 days to aerosolized JP-8 at 500 mg/m 3 . Kinkead et al [42], exposing dogs, mice and rats to 500 or 1000 mg/m 3 JP-4 vapor, failed to find significant differences in liver weights, or in TB, AST or ALR serum levels throughout 90-day continuous exposures.…”

Section: Introductionmentioning

confidence: 99%

Toxicity of chemical mixtures:Proteomic analysis of persisting liver and kidney protein alterations induced by repeated exposure of rats to JP-8 jet fuel vapor

et al. 2000

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Male Sprague-Dawley rats were exposed by whole body inhalation to 1000 mg/m3 +/- 10% JP-8 jet fuel vapor or room air control conditions for 6 h/day, 5 days/week for six consecutive weeks. Following a rest period of 82 days rats were sacrificed, and liver and kidney tissues examined by proteomic methods for both total protein abundance and protein charge modification. Kidney and lung samples were solubilized and separated via large scale, high resolution two-dimensional electrophoresis (2-DE) and gel patterns scanned, digitized and processed for statistical analysis. Through the use of peptide mass fingerprinting, confirmed by sequence tag analysis, three altered proteins were identified and quantified. Numerical, but not significantly different increases were found in total abundance of lamin A (NCBI Accession No. 1346413) in the liver, and of 10-formyltetrahydrofolate dehydrogenase (10-FTHF DH, #1346044) and glutathione-S-transferase (GST; #2393724) in the kidneys of vapor-exposed subjects. Protein charge modification index (CMI) analysis indicated significant alterations (P< 0.001) in expressed lamin A and 10-FTHF DH. These persisting changes in liver and kidney proteins are discussed in terms of possible alterations in the functional capacity of exposed subjects.

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Toxicologic and Oncogenic Potential of JP-4 Vapor: 90-Day Continuous Inhalation Exposure

Cited by 7 publications

References 11 publications

Petroleum‐related risk factors and soil screening levels

Petroleum‐related risk factors and soil screening levels

A Review of the Neurotoxicity Risk of Selected Hydrocarbon Fuels

Toxicity of chemical mixtures:Proteomic analysis of persisting liver and kidney protein alterations induced by repeated exposure of rats to JP-8 jet fuel vapor

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