TOXICOLOGICAL PROFILE FOR
 

JET FUELS JP-4 AND JP-7
 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
 

Public Health Service
 

Agency for Toxic Substances and Disease Registry
 

June 1995 
JET FUELS JP-4 AND JP-7 ii 

DISCLAIMER 

The use of company or product name(s) is for identification only and does not imply endorsement by 

the Agency for Toxic Substances and Disease Registry. 
JET FUELS JP-4 AND JP-7 iii 

UPDATE STATEMENT 

Toxicological profiles are revised and republished as necessary, but no less than once every three 

years. For information regarding the update status of previously released profiles contact ATSDR at: 

Agency for Toxic Substances and Disease Registry
 

Division of Toxicology/Toxicology Information Branch
 

1600 Clifton Road NE, E-29
 

Atlanta, Georgia 30333
 



JET FUELS JP-4 AND JP-7 vii 

CONTRIBUTORS 

CHEMICAL MANAGER(S)/AUTHORS(S): 

Obaid Faroon, Ph.D.
 

ATSDR, Division of Toxicology, Atlanta, GA
 

Diane Mandell, Ph.D.
 

Clement International Corp., Fairfax, VA
 

Hernan Navarro, Ph.D.
 

Research Triangle Institute, Research Triangle Park, NC
 

THE PROFILE HAS UNDERGONE THE FOLLOWING ATSDR INTERNAL REVIEWS: 

1. Green Border Review. Green Border review assures consistency with ATSDR policy. 

2. Health Effects Review. The Health Effects Review Committee examines the health effects 

chapter of each profile for consistency and accuracy in interpreting health effects and 

classifying end points. 

3. Minimal Risk Level Review. The Minimal Risk Level Workgroup considers issues relevant to 

substance-specific minimal risk levels (MRLs), reviews the health effects database of each 

profile, and makes recommendations for derivation of MRLs. 

4. Quality Assurance Review. The Quality Assurance Branch assures that consistency across 

profiles is maintained, identifies any significant problems in format or content, and establishes 

that Guidance has been followed. 

JET FUELS JP-4 AND JP-7 ix 

PEER REVIEW
 

A peer review panel was assembled for JP-4 and JP-7. The panel consisted of the following members: 

1. Dr. William Nick Norton, Professor, Biology Department, Southeastern Louisiana University, 

Hammond, Louisiana; 

2.	 Dr. Laurence Martin Holland, Private Consultant, 215 Rio Bravo, Los Alamos, New Mexico; 

3. Dr. Arthur Gregory, Private Consultant, Techto Enterprises, Sterling, Virginia; 

4. Dr. Tim Borges, Technical Information Analyst, Oak Ridge National Laboratory, Oak Ridge, 

Tennessee; and 

5. Dr. Bruce Jacobs, Environmental Health Engineering Services Manager, General Physics 

Corporation, Edgewood, Maryland. 

These experts collectively have knowledge of JP-4’s and JP-7’s physical and chemical properties, 

toxicokinetics, key health end points, mechanisms of action, human and animal exposure, and 

quantification of risk to humans. All reviewers were selected in conformity with the conditions for 

peer review specified in Section 104(i)(13) of the Comprehensive Environmental Response, 

Compensation, and Liability Act, as amended. 

Scientists from the Agency for Toxic Substances and Disease Registry (ATSDR) have reviewed the 

peer reviewers’ comments and determined which comments will be included in the profile. A listing 

of the peer reviewers’ comments not incorporated in the profile, with a brief explanation of the 

rationale for their exclusion, exists as part of the administrative record for this compound. A list of 

databases reviewed and a list of unpublished documents cited are also included in the administrative 

record. 

The citation of the peer review panel should not be understood to imply its approval of the profile’s 

final content. The responsibility for the content of this profile lies with the ATSDR. 









JET FUELS JP-4 AND JP-7 1 

1. PUBLIC HEALTH STATEMENT 

This statement was prepared to give you information about jet fuels JP-4 and JP-7 and to 

emphasize the human health effects that may result from exposure to them. The 

Environmental Protection Agency (EPA) has identified 1,397 hazardous waste sites as the 

most serious in the nation. These sites make up the National Priorities List (NPL) and are the 

sites targeted for long-term federal clean-up activities. JP-4 has been found in at least 4 of 

these sites. JP-7 has not been found in any NPL site. However, the number of NPL sites 

evaluated for JP-4 and JP-7 is not known. As EPA evaluates more sites, the number of sites 

at which JP-4 and JP-7 are found may increase. This information is important for you to 

know because JP-4 and JP-7 may cause harmful health effects and because these sites are 

potential or actual sources of human exposure to JP-4 and JP-7. 

When a chemical is released from a large area, such as an industrial plant, or from a 

container, such as a drum or bottle, it enters the environment as a chemical emission. This 

emission, which is also called a release, does not always lead to exposure. You can be 

exposed to a chemical only when you come into contact with the chemical. You may be 

exposed to it in the environment by breathing, eating, or drinking substances containing the 

chemical or from skin contact with it. 

If you are exposed to a hazardous chemical such as JP-4 or JP-7, several factors will 

determine whether harmful health effects will occur and what the type and severity of those 

health effects will be. These factors include the dose (how much), the duration (how long), 

the route or pathway by which you are exposed (breathing, eating, drinking, or skin contact), 

the other chemicals to which you are exposed, and your individual characteristics such as age, 

sex, nutritional status, family traits, lifestyle, and state of health. 

1.1 WHAT ARE JET FUELS JP-4 AND JP-7? 

JP-4 and JP-7 (jet propellant-4 and jet propellant-7) are substances that are used by the U.S. 

Air Force as aircraft fuels. They are also called jet fuel-4 and jet fuel-7. JP-4 is a colorless 
JET FUELS JP-4 AND JP-7 2 

1. PUBLIC HEALTH STATEMENT 

to straw-colored liquid. It smells like gasoline and/or kerosene. JP-7 is also a liquid, usually 

colorless. It smells like kerosene. Both JP-4 and JP-7 are flammable. JP-4 can be made by 

refining either crude petroleum oil or shale oil. JP-7 is made by refining kerosene, a product 

of refined crude petroleum. Both JP-4 and JP-7 are blends of other chemicals made according to 

standards specified by the U.S. Air Force for each fuel. Both JP-4 and JP-7 are liquids at room 

temperature, but they can also change into vapor. 

In this profile, JP-4 and JP-7 are discussed together. See Chapter 3 for more information on 

the chemical and physical properties of JP-4 and JP-7. More information on the production 

and use of JP-4 and JP-7 is found in Chapter 4. 

1.2 WHAT HAPPENS TO JET FUELS JP-4 AND JP-7 WHEN THEY ENTER THE

 ENVIRONMENT? 

We have information about what happens to JP-4 or its components in the environment. 

Although JP-7 is similar, there is not much information about what happens to it in the 

environment. JP-4 enters the environment when it spills or leaks into water or soil. It can 

enter the air during manufacturing, by evaporation of spills, and when it is discarded or 

jettisoned from jets during flight. JP-4 is a mixture of many chemicals. After it is released, 

the mixture spreads out in the atmosphere, and the component chemicals behave differently 

than they did in the liquid mixture. The behavior of each component in the environment 

depends on its individual chemical and physical properties. When JP-4 enters the air from 

flying jets as unburned fuel, some of the constituent chemicals fall back to the earth and land 

on water or soil. Other chemicals stay in the air and may change to different compounds 

when they react with light or other chemicals. Most of the chemicals in JP-4 evaporate when 

JP-4 spills into water. Some of the chemicals that do not evaporate as fast may dissolve in 

the water. If the water is very rough when the spill occurs, more JP-4 components will 

dissolve in the water. The chemicals that dissolve in the water are broken down further by 

microorganisms or become attached to the solid materials, called sediment, in the water. The 

chemicals that bind to this sediment may settle to the bottom of the water and stay there for a 
JET FUELS JP-4 AND JP-7 3 

1. PUBLIC HEALTH STATEMENT 

long time. When JP-4 spills or leaks to soil, some of the chemicals evaporate, but many of 

them are broken down by microorganisms. Some of them may also stick to the soil. 

Components that do not break down easily and components that stick to soil particles may 

stay in the soil for a long time. Currently, no information is available about what happens to 

JP-7 or its components in the environment, but it is similar in composition to JP-4 so it would 

probably act like JP-4 when it enters the environment. 

We know that many chemicals found in JP-4 can break down in the atmosphere to other 

chemicals, but we do not know what many of these breakdown products are. We have some 

information on several chemicals found in jet fuel (for example, benzene, toluene, hexane, xylene, 

and lead). We know more about what happens to them when they enter the environment as individual 

chemicals. When they enter the environment as part of jet fuel, they may behave the same way as 

when they are released alone. You can find more information on several individual components of jet 

fuel in the ATSDR toxicological profiles for these chemicals. See Chapters 4 and 5 for more 

information on what happens to JP-4 when it enters the environment. 

1.3 HOW MIGHT I BE EXPOSED TO JET FUELS JP-4 AND JP-7? 

It is unlikely that you would be exposed to JP-4 unless you work with jet fuel or live very 

close to where it is used or spilled. Exposure to JP-4 can occur if you touch soil or water 

contaminated from a spill or leak. If you drink water contaminated with JP-4 you will be 

exposed to the chemicals in the mixture. You might breathe in some of the chemicals 

evaporating from a spill or leak site if you stay in the area where an accident has occurred. 

Exposure to some components might occur from air releases if the components settle to the 

ground near populated areas. 

Workers involved in making or transporting JP-4 or in refueling military aircraft that use JP-4 

might breathe air containing it. They might also spill some on their skin. Occupational data 

from 1981 to 1983 show that about 4,866 workers employed in 633 plants might have been 

exposed to JP-4. See Chapter 5 for more information on how exposure to JP-4 might occur. 
JET FUELS JP-4 AND JP-7 4 

1. PUBLIC HEALTH STATEMENT 

No information is available specifically on exposure of individuals to JP-7. However, it is 

similar in composition to JP-4 and it is reasonable to assume that you could be exposed to it

 in the same way as described above for JP-4. 

1.4 HOW CAN JET FUELS JP-4 AND JP-7 ENTER AND LEAVE MY BODY? 

JP-4 and JP-7 can enter your bloodstream when you breathe them in, when you drink water containing 

them, or when your skin comes in contact with them. This can occur in the workplace or if you live 

near a manufacturing facility or an Air Force base. We do not know how much of the compounds your 

body might take up if you breathe them, drink them, or get them on your skin. We have no information 

on what happens to these chemical mixtures once they enter your body. We do not know if they 

remain in any tissues in the body. We also do not know whether these compounds leave the body in 

the urine or feces. See Chapter 2 for further discussion. 

1.5 HOW CAN JET FUELS JP-4 AND JP-7 AFFECT MY HEALTH? 

We know very little about the human health effects caused by JP-4 and JP-7. Breathing in 

large amounts of JP-4 would cause you to feel suffocated and breathing would be painful. 

Animal studies showed that breathing in extremely high levels of JP-4 and JP-7 does not 

cause death. We do not know if breathing in large amounts could cause death in people. 

Breathing in high levels of JP-4 has caused harmful effects on the nervous system. Some of the 

nervous system effects in people include headache, dizziness, nausea, depression, anxiety, memory 

loss, and irritability. Nervous system effects have occurred in people exposed to vapor from jet fuels 

like JP-4 for short and long periods in their jobs. Laboratory animals that breathed very high levels of 

JP-4 vapor for a short time developed nervous system effects, including poor coordination and 

convulsions. In lower doses, JP-4 vapor has caused animals to have a depressed level of activity 

compared with animals that were not exposed. Experimental animals have also had decreased numbers 

of white blood cells after breathing JP-4 vapor. Changes in liver cells have also been seen in animals 

exposed to either JP-4 or JP-7 vapor. Studies in animals show that both JP-4 and JP-7 can cause skin 

and eye 
JET FUELS JP-4 AND JP-7 5 

1. PUBLIC HEALTH STATEMENT 

irritation. JP-4 may cause skin cancer in mice or rats after exposure by skin contact. The 

data about cancer effects from breathing in JP-4 or JP-7 are not clear-cut. No data about 

cancer effects exist for exposure to JP-4 or JP-7 by eating or drinking. We do not know if 

JP-4 or JP-7 causes cancer in people. We do not have any information on whether JP-4 or 

JP-7 can cause birth defects or if they affect reproduction. For more information on the 

health effects of JP-4 and JP-7, see Chapter 2. 

1.6 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN 

EXPOSED TO JET FUELS JP-4 AND JP-7? 

There is no medical test that shows if you have been exposed to JP-4 or JP-7. For
 

information on tests for measuring exposure to some individual components of jet fuels, see the
 

ATSDR toxicological profiles on benzene, toluene, xylene, and polycyclic aromatic hydrocarbons.
 

See Chapters 2 and 6 for more information on medical tests.
 

1.7 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO 

PROTECT HUMAN HEALTH? 

The government has developed regulations and guidelines for JP-4 and JP-7 and the 

chemicals in them. These are designed to protect the public from the possible harmful health effects of 

the chemicals. The Occupational Safety and Health Administration (OSHA) and the Air Force Office 

of Safety and Health (AFOSH) regulate levels of petroleum products in the workplace. The maximum 

allowable amount of petroleum distillates in workroom air during an 8-hour workday, 40-hour 

workweek, is 500 parts per million (ppm). For more information on regulations and guidelines, see 

Chapter 7. 
JET FUELS JP-4 AND JP-7 6 

1. PUBLIC HEALTH STATEMENT 

1.8 WHERE CAN I GET MORE INFORMATION? 

If you have any more questions or concerns, please contact your community or state health or 

environmental quality department or: 

Agency for Toxic Substances and Disease Registry
 

Division of Toxicology
 

1600 Clifton Road, E-29
 

Atlanta, GA 30333
 

Phone 404-639-6000
 

This agency can also provide you with information on the location of the nearest occupational 

and environmental health clinic. These clinics specialize in the recognition, evaluation, and 

treatment of illnesses resulting from exposure to hazardous substances. 
JET FUELS JP-4 AND JP-7 7 

2. HEALTH EFFECTS 

2.1 INTRODUCTION 

The primary purpose of this chapter is to provide public health.officials, physicians, toxicologists, and 

other interested individuals and groups with an overall perspective of the toxicology of jet fuels JP-4 

and JP-7 and a depiction of significant exposure levels associated with various adverse health effects. 

It contains descriptions and evaluations of studies and presents levels of significant exposure for JP-4 

and JP-7 based on toxicological studies and epidemiological investigations. 

A glossary and list of acronyms, abbreviations, and symbols can be found at the end of this profile. 

2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 

To help public health professionals address the needs of persons living or working near hazardous 

waste sites, the information in this section is organized first by route of exposure- inhalation, oral, 

and dermal-and then by health effect-death, systemic, immunological, neurological, developmental, 

reproductive, genotoxic, and carcinogenic effects. These data are discussed in terms of three exposure 

periods-acute (14 days or less), intermediate (15-364 days), and chronic (365 days or more). 

Levels of significant exposure for each route and duration are presented in tables and illustrated in 

figures. The points in the figures showing no-observed-adverse-effect levels (NOAELs) or lowest 

observed-adverse-effect levels (LOAELs) reflect the actual doses (levels of exposure) used in the 

studies. LOAELs have been classified into “less serious” or “serious” effects. These distinctions are 

intended to help the users of the document identify the levels of exposure at which adverse health 

effects start to appear. They should also help to determine whether or not the effects vary with dose 

and/or duration, and place into perspective the possible significance of these effects to human health. 

The significance of the exposure levels shown in the tables and figures may differ depending on the 

user’s perspective. For example, physicians concerned with the interpretation of clinical findings in 

exposed persons may be interested in levels of exposure associated with “serious” effects. Public 

health officials and project managers concerned with appropriate actions to take at hazardous waste 
JET FUELS JP-4 AND JP-7 8 

2. HEALTH EFFECTS
 

sites may want information on levels of exposure associated with more subtle effects in humans or 

animals (LOAEL) or exposure levels below which no adverse effects (NOAEL) have been observed. 

Estimates of levels posing minimal risk to humans (Minimal Risk Levels, MRLs) may be of interest to 

health professionals and citizens alike. 

The jet fuels JP-4 and JP-7 are liquid military aviation turbine fuels whose composition varies slightly 

with the nature of the crude petroleum from which they were derived (Dukek 1978). Jet fuels derived 

from crude oil, the common name for liquid petroleum, are referred to as petroleum-derived jet fuels. 

Jet fuels derived from an organic material found in shale that can be converted by heat to shale oil are 

called shale-derived jet fuels. JP-4 is a wide-cut fuel; this is a refinery term indicating that it is 

distilled from crude oil using a broad temperature range and consists of hydrocarbons in a wide range 

of chain-lengths (4 to 16 carbons long) (Air Force 1989b; CONCAWE 1985). It was developed by 

the U.S. Air Force in order to ensure fuel availability in times of war (Dukek 1978; ITC 1985). JP-7 

is a kerosene with a high flash point and is used in advanced supersonic aircraft. The jet fuels are 

blends of various hydrocarbons, including alkanes (paraffins) and cycloalkanes (naphthenes), 

aromatics, and olefins, as well as small amounts of compounds such as benzene, n-hexane, and 

polycyclic aromatic hydrocarbons. 

The purpose of this chapter is to consider the toxicological effects of exposure to the mixture JP-4 or 

JP-7. Exposure to jet fuel components, exhaust, or combustion products will not be discussed. For 

information concerning the possible toxicity associated with exposure to some of the individual 

components of jet fuels, the reader is referred to the ATSDR toxicological profiles for benzene 

(ATSDR 1991a), toluene (ATSDR 1990), total xylenes (ATSDR 1991c), and polycyclic aromatic 

hydrocarbons (ATSDR 1991b). In addition, because of the variable composition of the jet fuels, the 

molecular weights are unknown (Kinkead et al. 1974). 

2.2.1 Inhalation Exposure 

2.2.1 .I Death 

No studies were located regarding death in humans after inhalation exposure to JP-4 or JP-7. 
JET FUELS JP-4 AND JP-7 9 

2. HEALTH EFFECTS
 

Exposure of Sprague-Dawley rats to concentrations as high as 5,000 mg/m3 shale- or petroleum 

derived JP-4 for 4 hours did not result in any mortality or apparent toxic signs during the 2-week 

post exposure holding period (Clark et al. 1989). 

Intermediate-duration exposure of rats and mice to concentrations of JP-4 as high as 5,000 mg/m3 

resulted in death in 1 of 40 exposed mice and 1 of 50 exposed rats, between 4 and 6 months after the 

exposure was begun (Air Force 1974). It was concluded that exposure to the test substance was 

probably not responsible for the deaths of these animals since two unexposed mice and one unexposed 

rat also died and because there were no abnormal histological findings in the rat. No deaths occurred 

when dogs or monkeys were exposed to similar JP-4 concentrations for 8 or 6 months, respectively 

(Air Force 1974). 

No increase in mortality was seen in chronic studies in which mice and rats were exposed 

intermittently (6 hours/day, 5 days/week) to as much as 5,000 mg/m3

 JP-4 (Air Force 1981i; Bruner et 

al. 1993) or in studies where rats were exposed to 750 mg/m3

 JP-7 (Air Force 19828, 1983e, 1991). 

Additionally, no increase in mortality was observed in rats or mice 12 months after chronic 

intermittent exposure (6 hours/day, 5 days/week) to 5,000 mg/m3

 JP-4 (Bruner et al. 1993). 

2.2.1.2 Systemic Effects 

No studies were located regarding cardiovascular, gastrointestinal, musculoskeletal, dermal or ocular 

effects in humans or animals after inhalation exposure to JP-7. No studies were located regarding 

gastrointestinal, musculoskeletal, dermal or ocular effects in humans after inhalation exposure to JP-4. 

No studies were located regarding musculoskeletal or dermal effects in animals after inhalation 

exposure to JP-4. 

The highest NOAEL values and all reliable LOAEL values for systemic effects for each study and end 

point are recorded in Table 2-l and plotted in Figure 2-l. 

Respiratory Effects. No studies were located regarding respiratory effects in humans after 

inhalation exposure to JP-7. 









JET FUELS JP-4 AND JP-7 19 

2. HEALTH EFFECTS
 

A pilot who was exposed to high levels of JP-4 vapor had symptoms of intoxication, but pulmonary 

function appeared normal upon clinical examination. Lungs were clear to percussion and auscultation, 

and respirations were normal (Davies 1964). The authors estimated that the exposure levels were 

between 3,000 and 7,000 ppm, based on the degree of the pilot’s neurological impairment. 

Intermediate-duration studies in rats revealed normal pulmonary mechanics (lung volume, 

pressurevolume relationships), pulmonary dynamics (airway resistance, lung compliance), and gas 

distribution and transfer in anesthetized rats exposed to 1,000 mg/m3 shale-derived JP-4 (Air Force 

1985c; Newton et al. 1991). The effects of intermittent exposure to 1,000 or 5,000 mg/m3

 JP-4 were 

determined in dogs, rats, and mice with up to a 12-month postexposure period (Air Force 1974, 1976, 

1984b) indicated that JP-4 did not cause adverse respiratory clinical signs or lung histopathology. 

Chronic exposure (12 months) to 1,000 or 5,000 mg/m3

 JP-4 did not cause respiratory tract irritation or 

pulmonary lesions in rats at the end of the exposure period or 12 months postexposure (Bruner et al. 

1993). Differing effects were observed in mice exposed to JP-4 under an identical study design 

(Bruner et al. 1993). At the end of the 12-month exposure period, mild pulmonary inflammation was 

seen only in treated females, and hyperplasia of the nasolacrimal duct epithelium was detected only in 

treated males. However, those effects had disappeared by the end of the 12-month postexposure 

period. 

Cardiovascular Effects. A pilot who was exposed to estimated concentrations of 3,000-7,000 ppm 

JP-4 did not show any adverse effects on blood pressure or heart sounds (Davies 1964). 

Dogs exposed for 90 days to 1,000 mg/m3 JP-4 did not experience cardiac histopathological changes 

(Air Force 1984b). 

Gastrointestinal Effects. Exposure to 5,000 mg/m3

 JP-4 for 8 months caused emesis in male and 

female dogs (Air Force 1974), but no emesis was seen at 2,500 mg/m3

 JP-4. 
JET FUELS JP-4 AND JP-7 20 

2. HEALTH EFFECTS
 

Hematological Effects. No studies were located regarding hematological effects in humans after 

inhalation exposure to JP-7. 

Accidental exposure of a pilot to a high concentration of JP-4 during a leak in the jet’s fuel system did 

not result in any abnormalities in hematological or clinical chemistry tests during a physical 

examination performed after an unspecified period of time had passed since the exposure (Davies 

1964). 

Hematological parameters have been measured on a routine basis during exposure of animals to JP-4 

and JP-7 in intermediate- and chronic-duration studies. Such measurements have included red and 

white blood cell counts, methemoglobin concentration, mean corpuscular volume, mean corpuscular 

hemoglobin, mean corpuscular hemoglobin concentration, hematocrit, and hemoglobin concentration. 

Exposure for 90 days to 1,000 mg/m3

 JP-4 caused increased white blood cell counts and increased the 

mean corpuscular hemoglobin in Fischer 344 rats (Air Force 1984d). In the same study, increased 

white blood cell counts and decreased hematocrit and hemoglobin concentrations were observed in 

Osborne-Mendel rats. In contrast, continuous exposure (24 hours/day) of rats to 1,000 mg/m3

 JP-4 

vapor for 90 days did not affect white blood cell and red blood cell counts in males or females (Air 

Force 1980). 

Treatment for 12 months, 5 days/week, 6 hours/day with 0, 1,000, or 5,000 mg/m3

 JP-4 revealed a 

treatment-related decrease in white blood cell count and blood glucose levels in exposed male and 

female rats at the conclusion of the exposure period (Bruner et al. 1993). Histopathological evaluation 

of various tissues in the exposed rats did not reveal a definitive cause for the decreases in white blood 

cells. However, bone marrow cytopenia was reported to be of borderline statistical significance 

(significance level not specified) in the treated animals. The incidence in males of this finding was 0%, 

1%, and 4% for the control, low, and high concentrations, respectively. Incidence in females was 0%, 

0%, and 2%, respectively. These findings may have contributed to the decreases in white blood cell 

count. The LOAEL for this effect was 1,000 mg/m3

. 

The results of hematological tests conducted in monkeys and dogs following intermediate-duration 

(Air Force 1974, 1984c) or chronic-duration exposures (Air Force 1981i) revealed no significant 

effects that were dose dependent or out of the range of normal biological variation. 
JET FUELS JP-4 AND JP-7 21 

2. HEALTH EFFECTS
 

Intermediate-duration exposure of animals to 2,500 or 5,000 mg/m3

 JP-4 was tested in combination 

with 12.5 or 25 ppm benzene, respectively (Air Force 1974). Benzene was administered in 

combination with the jet fuel because benzene is sometimes a contaminant of jet fuels and exposure to 

benzene is associated with hematological effects. Both air-exposed controls and a positive control 

group were used for comparison. Three species of animals were exposed to 25 ppm benzene so that 

the level would not exceed that equivalent to a 6-hour time-weighted average concentration of 10 ppm 

(Air Force 1974, 1976). For further information on the hematological effects of benzene, refer to the 

ATSDR toxicological profile for benzene (ATSDR 1991a). In this study, the myeloid/erythroid ratio 

in rats and the hematocrit, hemoglobin, and red blood cell counts in monkeys were not different from 

those of the air-exposed control group after 6 months of exposure to JP-4 (Air Force 1974). However, 

between weeks 12 and 24 of this study, red blood cell fragility was abnormally high in female dogs 

exposed to 5,000 mg/m3

 JP-4 (Air Force 1974). This effect was transient, since red blood cell fragility 

was normal at the end of the exposure. No concomitant hemolytic changes occurred in these animals, 

and the mechanisms and significance, if any, of these findings are unclear. In a 90-day continuous 

exposure (24 hours/day) of male and female dogs (3 per group) to 500 or 1,000 mg/m3

, there was no 

increase in red blood cell fragility (Air Force 1980). 

Rats chronically exposed to 750 mg/m3

 JP-4 did not exhibit any abnormal hematology, but alkaline 

phosphatase and blood urea nitrogen were elevated at 150 mg/m3

 (Air Force 1991). 

Hepatic Effects. No studies were located regarding hepatic effects in humans after inhalation 

exposure to JP-4 or JP-7. 

Hepatocellular fatty change occurred in the livers of 88-89% of JP-4-exposed C57BL/6 mice (50 

females/group) after 90 days of continuous exposure (24 hours/day) to 500 or 1,000 mg/m3

 (Air Force 

1984b). The lesions in mice were described as multiple, discrete vacuoles of varying sizes within the 

hepatocytes. They occurred primarily in the centrilobular region of the liver and were regarded as 

reversible degenerative processes. The incidence of these lesions immediately after the exposure 

period was 3/49 for controls, 42/48 (87%) for 500 mg/m3

, and 40145 (88%) for 1,000 mg/m3 JP-4. A 

LOAEL of 500 mg/m3

 was identified for fatty changes in the liver. The incidence of sinusoidal 

hematopoiesis also increased with increasing exposure concentration; however, statistical significance 

was only achieved in the 1,000-mg/m3

 group. Rats and dogs, also included in that study, did not 

develop histopathological liver changes. In contrast, intermediate exposure to 500 or 1,000 mg/m3 
JET FUELS JP-4 AND JP-7 22 

2. HEALTH EFFECTS
 

JP-4 has been shown to increase (Air Force 1980, 1984c, 1984d) male rat liver weight, but doses as 

high as 1,000 mg/m3

 JP-4 apparently have no effect on female rat liver weight (Air Force 1980, 

1984c). 

Chronic (12 months), intermittent exposure (5 days/week, 6 hours/day) to 1,000 or 5,000 mg/m3

 JP-4 

caused no liver toxicity in rats that were examined at the end of the 12-month exposure period (Bruner 

et al. 1993). However, in a subset of the exposed animals examined 12 months after the end of the 

exposure period, the same doses caused non-dose-related decreases in male, but not female, rat liver 

weight (Bruner et al. 1993). In mice exposed to JP-4 under an identical study design, there was an 

increase in lymphocytic inflammatory infiltrates in the livers of high-dose female mice, but not males, 

at the end of the 12-month exposure period (Bruner et al. 1993). However, that effect was no longer 

evident 12 months after the end of the exposure period. 

Chronic exposure of C57BW6 mice to 0 (control), 150, or 750 mg/m3

 JP-7 resulted in an increased 

incidence of hepatic inflammation in female mice exposed to 750 mg/3

 after a l-year postexposure 

period (Air Force 1991). One year after the end of the exposure period, hepatic inflammation was 

discovered in females from both the 150 and 750 mg/m3

 groups. Hepatic inflammation was not 

observed in the exposed males. A LOAEL of 150 mg/m3

 was identified for hepatic inflammation in 

female mice. 

Renal Effects. No studies were located regarding renal effects in humans after inhalation exposure to 

JP-4 or JP-7. 

Blood urea nitrogen was elevated, but considered to be within normal limits, in Fischer 344 rats 

exposed continuously (24 hours/day) for 90 days to 500 or 1,000 mg/m3

 shale- or petroleum-derived 

JP-4 (Air Force 1980, 1984c). In a subsequent l-year study using an intermittent exposure protocol (6 

hours/day, 5 days/week) and a higher concentration of JP-4 (5,000 mg/m3

), blood urea nitrogen was 

increased only in female rats (Air Force 1981i). Thus, no consistent effect was seen in this parameter 

with JP-4 exposure. 

The effects of intermediate (24 hours/day for 90 days) exposure to 500 or 1,000 mg/m3

 shale-derived 

JP-4 was determined in rats (Air Force 1984c). Increased kidney weight was observed in male rats at 

500 mg/m3

, but no effect on kidney weight was seen in females at either dose of JP-4. Urinalysis 
JET FUELS JP-4 AND JP-7 23 

2. HEALTH EFFECTS
 

conducted in the male rats revealed a 50-70% decrease in osmolality at termination of exposure and 2 

weeks postexposure. Urine pH was not affected. The decreased osmolality was also found when 

comparing the renal effects in four strains of male rats (Fischer 344, Sprague-Dawley, Wistar, and 

Osborne-Mendel) after 90 days of continuous exposure (24 hours/day) to 1,000 mg/m3

 JP-4 (Air Force 

1984d). In this study, rats from all four strains were killed midway through the exposure period (45 

days) and at the end of the exposure period. No effect on urine osmolality was observed at the 45-day 

interim kill. But after 90 days, urine osmolality.was statistically decreased in all except the Wistar 

strain of rats. Urine osmolality was decreased in the Wistar rats, but the variability in the treated group 

prevented statistical significance from being reached. Blood urea nitrogen was transiently elevated in 

the Fischer 344 and Sprague-Dawley strains at 45 days of exposure. That effect was not detected in 

any strain at the end of the dosing period. Similarly, blood creatinine levels were elevated after 45 

days of exposure in the Fischer 344 and Wistar rats, but that effect was also transient as no differences 

were found in blood creatinine in any strain after 90 days of exposure. Kidney weight was increased in 

all strains at the end of the 90-day exposure period. The methods section in the report states that 

additional animals were allowed to live for 6 or 12 months postexposure, but there is no mention of 

those animals in any other section of the report. Consequently, it is not known if the renal effects 

persisted after dosing had concluded. 

Absolute kidney weight was increased in male Fischer 344 rats exposed continuously (24 hours/day) 

for 90 days (Air Force 1980) to 500 or 1,000 mg/kg JP-4 and Sprague-Dawley rats exposed 

intermittently (6 hours/day, 5 days/week) for 8 months (Air Force 1976) to 5,000 mg/m3 JP-4. Chronic 

(12 months) intermittent exposure to 1,000 or 5,000 mg/m3

 JP-4 decreased kidney weight in male and 

female rats 12 months after the end of the exposure period (Bruner et al. 1993). 

Histopathological changes have also been observed following intermediate- and chronic-duration 

exposure to JP-4 treatment (Air Force 1984b; Bruner et al. 1993) or chronic JP-7 treatment (Air Force 

1991). Microscopic examination of the kidneys revealed hyaline droplet formation in renal proximal 

tubular epithelium in both dose groups; this effect was more severe in high dose animals, indicating a 

dose-response relationship in male rats exposed to 1,000 or 5,000 mg/m3

 JP-4 (Air Force 1984b). In 

addition, there were intratubular casts of necrotic debris in the outer renal medulla. Mild progressive 

kidney neuropathies and medullary mineral deposits were observed in male, but not female, rats 

exposed to 5,000 mg/m3

 JP-4 for 12 months, 6 hours/day, 5 days/week (Bruner et al. 1993). Twelve 

months after the conclusion of the exposure period, medullary mineral deposits were still present in 

the 
JET FUELS JP-4 AND JP-7 24 

2. HEALTH EFFECTS 

5,000 mg/m3

 group. Moreover, those changes were also seen in the kidneys of rats exposed to 

1,000 mg/m3

 JP-4 (Bruner et al. 1993). Similar effects were observed in rats after 1 year of 

intermittent exposure to 150 or 750 mg/m3

 JP-7 (Air Force 1991). No nephrotoxicity was observed in 

mice following chronic (12 months), intermittent exposure to 1,000 or 5,000 mg/m3

 JP-4 (Bruner et 

al.1993). 

The histopathological changes described above are characteristic of a syndrome of nephropathy unique 

to male rats following intermediate- or chronic-duration inhalation exposure to hydrocarbons (Bruner 

et al. 1993). These changes have also been found to increase with age (Air Force 1991). This 

syndrome was not induced in female rats (Air Force 1976, 1984b, 1991; Bruner et al. 1993), mice of 

either sex (Air Force 1976, 1980, 1984b; Bruner et al. 1993), or dogs of either sex (Air Force 1984b) 

when exposed to JP-4 or JP-7. This type of nephropathy appears to be unique to male rats and is 

most likely not relevant to humans (EPA 1991) (see Section 2.4); therefore, this end point was not 

used for MRL derivation. 

Endocrine Effects. Chronic (12 months) intermittent exposure to 5,000 mg/m3

 JP-4 in rats caused 

an increase in cystic degeneration of the prostate 12 months postexposure (Bruner et al. 1993). No 

effects were observed in female rats, or in mice of both sexes, under identical exposure conditions 

(Bruner et al. 1993). 

Ocular Effects. Chronic (1 year, 5 days/week) exposure to 750 mg/m3

 did not cause any 

histopathological changes in the eyes of male or female rats (Air Force 1991). 

Body Weight Effects. The effects of intermediate exposure to between 500 and 1,000 mg/m3

 JP-4 

on body weight has not been consistent. Intermediate-duration exposure of rats to JP-4 decreased the 

body weight of male (Air Force 1980, 1984b) and female (Air Force 1980, 1984b, 1984c) rats. 

However, similar doses and dosing models produced no effect on rat body weight (Air Force 1984d). 

Additionally, doses of JP-4 as high as 5,000 mg/m3

 did not affect the body weight of dogs (Air Force 

1974) or monkeys (Air Force 1974). 

Chronic (1 year, 5 days/week, 6 hours/day) exposure to 750 mg/m3

 JP-4 had no effect on rat body 

weight (Air Force 1991). Similarly, chronic exposure to 1,000 or 5,000 mg/m3

 JP-4 did not adversely 

affect body weight in rats immediately after a 12-month exposure period (Bruner et al. 1993). 
JET FUELS JP-4 AND JP-7 25 

2. HEALTH EFFECTS
 

However, 1,000 mglm3

 caused minor body weight reductions (3-4%) in both female and male rats 

12 months postexposure (Bruner et al. 1993). This statistically significant decrease in body weight is 

not considered to be biologically significant. Mice exposed to 1,000 or 5,000 mg/m3

 JP-4 for 1 year 

did not exhibit adverse body weight effects either at the end of the exposure period or 12 months 

postexposure (Bruner et al. 1993). 

Other Systemic Effects. Histological exammation of rat lymph nodes after the intermediate 

exposure to 1,000 mg/m3

 JP-4 did not reveal any abnormalities (Air Force 1984b). Chronic exposure 

to 5,000 mg/m3

 JP-4 in rats increased the incidence of cystic hyperplasia of the mammary glands 

12 months after a l-year intermittent exposure period (Bruner et al. 1993). 

2.2.1.3 Immunological and Lymphoreticular Effects 

No studies were located regarding immunological and lymphoreticular effects in humans after 

inhalation exposure to JP-4 or JP-7. Additionally, no studies were found regarding immunological and 

lymphoreticular effects in animals after inhalation exposure to JP-7. 

Chronic (12 months) intermittent exposure to 1,000 mg/m3

 JP-4 was found to increase spleen weight 

in female rats at the end of the dosing period (Bruner et al. 1993). However, no effect on spleen 

weight was observed at the higher dose of 5,000 mg/m3

 or at either dose 12 months after the end of 

the exposure period. 

2.2.1.4 Neurological Effects 

No studies were located regarding neurological effects in humans or animals after inhalation exposure 

to JP-7. 

Acute exposure to a high level of JP-4 (3,000-7,000 ppm) from a fuel leak on a routine flight 

produced a groggy, weak, intoxicated state in the pilot (Davies 1964). Neurological examination 

revealed that the mild intoxication was accompanied by normal cardiovascular and respiratory 

function. The pilot had a staggering gait, mild muscular weakness, decreased sensitivity to painful 

stimuli, slight slurring of speech, and a positive Romberg; these effects were no longer evident 

36 hours postexposure. 
JET FUELS JP-4 AND JP-7 26 

2. HEALTH EFFECTS
 

Animals acutely exposed by inhalation to very high concentrations of JP-4 (38,000 mg/m3

) exhibited 

neurotoxic effects including poor coordination and convulsions (Air Force 1974). Dogs (4 males, 

2 females/exposure level), monkeys (1 male, 3 females/exposure level), rats (50 males/exposure level), 

and mice (40 females/exposure level) were exposed to 0, 2,500, or 5,000 mg/m3

 JP-4, 6 hours/day, 

5 days/week for 6 months (rats, mice, and monkeys) or 8 months (dogs) (Air Force 1974). During the 

initial 3 weeks of exposure, dogs were reported to have decreased activity compared to control 

animals. When the animals were not sleeping, they were reported to be “quiescent and prostrate” 

during exposure periods. Monkeys in both JP-4 groups also demonstrated decreased activity, but to a 

lesser extent than the dogs. Rats and mice did not exhibit neurological signs at either dose of JP-4. 

No long-term epidemiological studies were located regarding exposure to JP-4. 

No NOAEL values for neurological effects of JP-4 were recorded in Table 2-l or plotted in 

Figure 2-l. The case study (Davies 1964) has inadequately characterized exposure conditions and the 

intermediate animal exposure studies lacked presentation of important experimental details. 

2.2.1.5 Reproductive Effects 

No studies were located regarding reproductive effects in humans after inhalation exposure to JP-4 or 

JP-7. Additionally, no studies were found regarding reproductive effects in animals after inhalation 

exposure to JP-7. 

Chronic (12 months) exposure to 1,000 or 5,000 mg/m3

 of JP-4 did not adversely affect the testis in 

rats, but did cause testicular atrophy in mice 12 months after the end of exposure period (Bruner et al. 

1993). 

2.2.1.6 Developmental Effects 

No studies were located regarding developmental effects in humans or animals after inhalation 

exposure to JP-4 or JP-7. 
JET FUELS JP-4 AND JP-7 27 

2. HEALTH EFFECTS 

2.2.1.7 Genotoxic Effects 

No studies were located regarding genotoxic effects in humans or animals after in vivo inhalation 

exposure to JP-4 or JP-7. Genotoxicity studies are discussed in Section 2.4. 

2.2.1.8 Cancer 

No studies were located regarding carcinogenic effects in humans after inhalation exposure to JP-4 or 

JP-7. 

Long-term animal studies were conducted to investigate the potential of JP-4 or JP-7 to induce cancer 

in laboratory animals. Groups of 50 male Sprague-Dawley rats and 40 female CF-1 mice were 

exposed to JP-4 intermittently (6 hours/day, 5 days/week) for 8 months. Interim sacrifices were 

performed immediately after exposure and at 12 months postexposure (Air Force 1976). No increase 

in the incidence of tumors was seen in any group following gross and histopathologic examination of 

tissues from either rats or mice. 

Fischer-344 rats exposed chronically to JP-4 for 12 months at 5,000 mg/m3

 had an increased incidence 

of interstitial cell tumors in the testis 12 months after the termination of the exposure period (Bruner et 

al. 1993). Under an identical exposure regimen, no effect on the incidence of neoplastic lesions was 

seen in mice (Bruner et al. 1993). A l-year JP-7 exposure produced no toxicologically significant 

treatment-related neoplastic lesions in mice or rats except for a small increase in the incidence of 

C-cell adenomas and kidney adenomas in male rats exposed to 750 mg/m3

 of JP-7 (Air Force 1991). 

The exposure period in the above carcinogenicity studies was only 1 year compared to the 2 years 

(lifetime) of exposure normally included in standard carcinogenicity assays. This less-than-lifetime 

exposure was chosen because the authors believed it is more typical of military occupational exposure 

to jet fuels. Nevertheless, the results from the above studies suggest that jet fuels JP-4 and JP-7 are 

not carcinogenic to humans. 
JET FUELS JP-4 AND JP-7 28 

2. HEALTH EFFECTS 

2.2.2 Oral Exposure 

2.2.2.1 Death 

No studies were located regarding death in humans after oral exposure to JP-4 or JP-7, or in animals 

after oral exposure to JP-7. 

The acute oral administration of 5,000 mg/kg (Clark et al. 1989) or 8,000 mg/kg (Air Force 1974) 

shale-derived JP-4 to rats did not result in treatment-related mortality. Two of three mice died after 

administration of 500 mg/kg JP-4; one of three mice died after administration of 1,000 mg/kg (Air 

Force 1974). However, no histopathology was performed on these animals and the numbers of mice 

dosed in this study were so small that the reported deaths are not necessarily relevant. 

2.2.2.2 Systemic Effects 

No studies were located regarding respiratory, cardiovascular, gastrointestinal, hematological, 

musculoskeletal, hepatic, renal, dermal, ocular, or body weight effects in humans or animals after oral 

exposure to JP-4 or JP-7. 

No studies were located regarding the following health effects in humans or animals after oral 

exposure to JP-4 or JP-7: 

2.2.2.3 Immunological and Lymphoreticular Effects 

2.2.2.4 Neurological Effects 

2.2.2.5 Reproductive Effects 

2.2.2.6 Developmental Effects 
JET FUELS JP-4 AND JP-7 29 

2. HEALTH EFFECTS 

2.2.2.7 Genotoxic Effects 

No studies were located regarding genotoxic effects in humans after oral exposure to JP-4 or JP-7, or 

in animals after oral exposure to JP-7. 

Two dominant lethal studies were found in the literature where mice or rats were orally exposed to 

JP-4. Ten random-bred, male CD-l mice received the compound in their food for 5 consecutive days 

at concentrations of 7.6, 22.8, and 68.4 mg/kg (0.01, 0.03, and 0.09 mL/kg, respectively). Two days 

after the last treatment, each male was caged with two untreated virgin females for 7 days. At the end 

of 1 week, the females were replaced with two new untreated females; this process was repeated for 

7 weeks. The females were killed 14 days after the midweek of mating, and their uteri were examined 

for live, dead, and total implantation. When the negative controls were compared to the treated 

females, no significant differences were noted for dominant lethal effects. This finding suggests that 

JP-4 was not clastogenic in the germinal cells of male mice (Air Force 1978a). However, the results 

cannot be considered conclusive because of the small number of pregnant females used in the study. 

The interpretation of the results is further confounded by the fact that the highest dose used in the 

study was probably too low to cause significant cellular toxicity. 

Ten random-bred male rats were exposed to JP-4 by gavage for 5 consecutive days (Air Force 1978a). 

The concentrations tested were 68.4, 228, and 684 mg/kg (0.09, 0.3, and 0.9 mL/kg, respectively). 

The mating protocol was the same as that used in the mouse dominant lethal experiment. The 

administration of JP-4 did not decrease the average number of implantations per litter except after the 

fourth week of mating, when a transient decrease of 31-50% was noted for the low through high doses 

of JP-4, respectively. Individually significant reductions in the number of implants per litter were 

detected only for the 0.3 mL/kg group at that time. There was no increase in the average number of 

resorptions per litter or in the average number of late fetal deaths. Thus, the effects appeared to be 

confined to the pre-implantation phase. Except for the effects noted for week 4, indices of 

reproductive function were comparable to controls. Since there were no significant dominant lethal 

effects corresponding to the pre-implantation effects, the researchers considered the results to be 

negative (Air Force 1978a). As in the mouse study, the sample size of pregnant female rats per group 

was small, which renders the study inconclusive. 

Other genotoxicity studies are discussed in Section 2.4. 
JET FUELS JP-4 AND JP-7 30 

2.HEALTH EFFECTS 

2.2.2.8 Cancer 

No studies were located regarding cancer in humans or animals after oral exposure to JP-4 or 

JP-7. 

2.2.3 Dermal Exposure 

2.2.3.1 Death 

No studies were located regarding death in humans after dermal exposure to JP-4 or JP-7, or in 

animals after dermal exposure to JP-7. 

Acute (24 hours) dermal application of 2,000 mg/kg shale-derived JP-4 (Clark et al. 1989; Dennis 

1982a) or petroleum-derived JP-4 (Clark et al. 1989) to rabbits did not result in mortality after a 

24-hour or 14-day time period, respectively. No rabbits died after dermal application of 0.5 mL 

undiluted JP-7 to the skin (Air Force 1984a). 

Application of shale-derived JP-4 to the skin of C3H mice on a chronic basis resulted in a greater 

survival rate compared to those treated with petroleum-derived JP-4 (Clark et al. 1988). At week 52 

of a 105-week study in which animals were treated with shale-derived JP-4, the survival rate was 

≈90% compared to ≈72% in animals treated with petroleum-derived JP-4. By the end of the 2-year 

study, both groups had similar survival rates (≈15%). However, petroleum-derived JP-4 appeared to 

have greater toxicity than shale-derived JP-4 by virtue of the higher mortality that occurred in the 

first year of exposure, and both groups had a lower survival rate than controls (≈50%). More 

information regarding the differences between shale- and petroleum-derived jet fuels is provided in the 

introduction to Chapter 4. Both groups appeared to have a higher mortality than did control animals, 

although no statistics were shown. Mortality resulted from inflammatory lesions at the site of the test 

material application and subsequent septicemia. The mortality data from those studies were not 

included in Table 2-2 because of the lack of statistical testing. 
JET FUELS JP-4 AND JP-7 31 

2. HEALTH EFFECTS 

2.2.3.2 Systemic Effects 

No studies were located regarding respiratory, cardiovascular, gastrointestinal, hematological, or 

musculoskeletal effects in humans or animals after dermal exposure to JP-4 or JP-7. The highest 

NOAEL values and all reliable LOAEL values for systemic effects for each study and end point are 

recorded in Table 2-2. 

Hepatic Effects. No studies were located regarding hepatic effects in humans after dermal 

exposure to JP-4 or JP-7 or in animals after dermal exposure to JP-7. 

Application of 2,000 mg/kg shale-derived JP-4 to the skin of rabbits for 24 hours did not result in 

hepatic lesions after a 14-day postexposure period (Dennis 1982a). 

Renal Effects. No studies were located regarding renal effects in humans after dermal exposure to 

JP-4 or JP-7 or in animals after dermal exposure to JP-7. 

Dermal application of 2,000 mg/kg shale-derived JP-4 in five male and five female rabbits for 

24 hours did not result in pathological renal effects related to the test material after a 14-day 

postexposure period (Dennis 1982a). In one animal, a pathological lesion was noted on one kidney 

but was not believed to be related to the test material. 

Dermal Effects. No studies were located regarding dermal effects in humans after dermal exposure 

to JP-4 or JP-7. 

Experiments in rabbits show that acute exposure to JP-4 or JP-7 is irritating to the skin. Application 

of 0.5 mL undiluted JP-4 (both shale- and petroleum-derived) produced severe irritation that was 

characterized by edema and erythema 24 hours post-application (Air Force 1984a; Clark et al. 1989; 

Dennis 1982b; Walter 1982c), whereas the application of the same amount of JP-7 was shown to 

produce slightly greater irritation that persisted for a longer period of time (Air Force 1984a). Chronic 

application of 25 mg undiluted petroleum- or shale-derived (from hydrotreated crude shale) JP-4 to the 

skin of mice resulted in initial dermal irritation that progressed to necrosis and visible separation and 

sloughing of skin (Clark et al. 1988). 



JET FUELS JP-4 AND JP-7 35 

2. HEALTH EFFECTS
 

Ocular Effects. No studies were located regarding ocular effects in humans after dermal exposure 

to JP-4 or JP-7. 

There was no evidence of primary ocular irritation after application of undiluted shale-derived JP-4, 

undiluted petroleum-derived JP-4, or JP-7 to the eyes of rabbits (Air Force 1984a; Clark et al. 1989; 

Dennis 1982c; Walter 1982a). Some studies (Walter 1982a) noted that when shale-derived JP-4 was 

applied and not rinsed from the rabbits’ eyes, minimal irritation (0.3 out of a maximum 2.0 score) 

resulted 24 hours after instillation of test material. The irritation cleared by the 7th day postexposure. 

2.2.3.3 Immunological and Lymphoreticular Effects 

No information is available on the immunological effects of JP-4 or JP-7 in humans or animals 

following dermal exposure. 

JP-4 (shale-derived or petroleum-derived) did not cause dermal sensitization in guinea pigs when 

applied to the skin in a 50% dilution in mineral oil (Clark et al. 1989; Walter 1982c). However, JP-7 

and shale-derived JP-4 have sensitization potential (Air Force 1984a). Data regarding the 

immunological effects of JP-4 are limited to the dermal sensitization tests conducted in guinea pigs 

(Air Force 1984a; Clark et al. 1989; Walter 1982c). In these studies petroleum-derived JP-4 was not 

found to be a dermal sensitizer. However, JP-7 and shale-derived JP-4 have weak-to-mild and mildtomoderate sensitization potential, respectively (Air Force 1984a). 

No studies were located regarding the following health effects in humans or animals after dermal 

exposure to JP-4 or JP-7: 

2.2.3.4 Neurological Effects 

2.2.3.5 Reproductive Effects 

2.2.3.6 Developmental Effects 
JET FUELS JP-4 AND JP-7 36 

2. HEALTH EFFECTS 

2.2.3.7 Genotoxic Effects 

Genotoxicity studies are discussed in Section 2.4. 

2.2.3.8 Cancer 

No studies were located regarding carcinogenic effects after dermal exposure to JP-4 or JP-7 in 

humans, or in animals after dermal exposure to JP-7. 

The effects of intermittent (3 times/week) dermal administration of 25 mg of shale- or petroleumderived JP-4 to 

the skin of mice for 105 weeks on the incidence of neoplasms was studied (Clark et al. 1988). Squamous cell 

carcinoma and fibrosarcoma formation was increased in the mice exposed to shale-derived (50% 

incidence) and petroleum-derived JP-4 (26% incidence) compared to the appropriate control groups 

(2% and 0%, respectively). In general, shale-derived JP-4 (derived from hydrotreated crude shale oil) 

had greater irritant and carcinogenic potency than did petroleum-derived JP-4. The positive control 

substances, crude shale-derived and petroleum-derived oils (not hydrotreated), had skin cancer 

incidences of 54% and 84%, respectively. Other histopathological diagnoses were judged by the 

authors to be secondary to the long-term irritation at the test site. The most noteworthy of these 

diagnoses was reactive hyperplasia of the spleen and bone marrow that probably resulted from 

septicemia that developed from the attendant inflammation, necrosis, and infection at the application 

site. The incidence of these findings was not reported. 

2.3 TOXICOKINETICS 

2.3.1 Absorption 

2.3.1.1 Inhalation Exposure 

No studies were located that examined the absorption of JP-4 or JP-7 in humans or animals after 

inhalation exposure. However, indirect evidence from the case report of a pilot exposed to a JP-4 fuel 

leak indicates that JP-4 can be absorbed following inhalation exposure in humans (Davies 1964). 

Animals exposed to JP-4 on an acute, intermediate, or chronic basis, or exposed chronically to JP-7, 
JET FUELS JP-4 AND JP-7 37 

2. HEALTH EFFECTS
 

also exhibited effects that provide evidence for inhalation absorption in animals (Air Force 1974, 

1976, 1980, 1983, 1984b, 1985b, 1991; Bruner et al. 1993). 

2.3.1.2 Oral Exposure 

There is no quantitative information on the absorption of JP-4 or JP-7 following oral exposure in 

humans or animals. 

2.3.1.3 Dermal Exposure 

There is no quantitative information on the absorption of JP-4 or JP-7 following dermal exposure in 

humans or animals. Animal studies have shown that both JP-4 and JP-7 are irritating to the skin (Air 

Force 1984b; Clark et al. 1988, 1989; Dennis 1982b; Walter 1982a, 1982c), and long-term studies 

have demonstrated the carcinogenic potential of JP-4 at the site of application (Clark et al. 1988). 

However, no effects have been reported in these studies in organs or tissues distant from the site of 

application of the test material. 

2.3.2 Distribution 

There is no quantitative information on the distribution of JP-4 or JP-7 following inhalation, oral, or 

dermal exposure in humans or animals. However, liver effects after treatment of mice with JP-4 

suggest distribution to that organ (Air Force 1984b; Bruner et al. 1991). 

2.3.3 Metabolism 

There is no quantitative information on the metabolism of JP-4 or JP-7 following inhalation, oral, or 

dermal exposure in humans or animals. 

2.3.4 Excretion 

There is no quantitative information on the excretion of JP-4 or JP-7 following inhalation, oral, or 

dermal exposure in humans or animals. 
JET FUELS JP-4 AND JP-7 38 

2. HEALTH EFFECTS 

2.3.5 Mechanisms of Action 

It is apparent from animal studies described in the earlier sections that exposure to JP-4 or JP-7 causes 

toxicity, but data have been descriptive (e.g., decreased liver weight) instead of mechanistic (e.g., 

slows nerve conduction). Additionally, the absorption and distribution of the jet fuels is not 

understood. Thus, insufficient data exist for postulating a mechanism of action. Moreover, since both 

fuels are complex mixtures, it seems likely that elucidating a mechanism of action would be difficult. 

2.4 RELEVANCE TO PUBLIC HEALTH 

Exposure to JP-4 and JP-7 may occur via the inhalation, oral, or dermal routes, but exposure by 

inhalation is most likely because of the high volatility of many of the jet fuel components. Military 

personnel and those involved in the manufacture of the jet fuels are at the greatest risk for exposure 

because the fuels are produced only for military use. Thus, apart from those individuals involved in 

the manufacturing process, persons living or working near or on a military base would constitute the 

greatest population at risk for JP-4 and JP-7 exposure. Additionally, military personnel stationed on 

aircraft carriers or submarines would also be at increased risk. 

JP-4 and JP-7 are also found in waste sites, so exposure of the general public to the fuels in those 

areas is possible, but not likely. Moreover, because the jet fuels are complex mixtures of components 

with differing volatilities, solubilities, and biodegradation potentials, it is probable that people will be 

exposed to only a subset of the components from the original mixture. However, because of the large 

number of components in JP-4 and JP-7, it is impractical, if not impossible, to predict what 

components of the original mixture will be present at a waste site. Therefore, the inhalation exposure 

MRLs described below are based on the concentration of the original complex mixture. Additionally, 

the concentrations of JP-4 or JP-7 reported in the studies used to derive the MRLs are based on the 

concentration of total hydrocarbons present in the vapors after the original mixture was heated 

to 50 °C. 
JET FUELS JP-4 AND JP-7 39 

2. HEALTH EFFECTS 

Minimal Risk Levels for Jet Fuels JP-4 and JP-7. 

Inhalation MRLs. 

Only one controlled acute-duration inhalation exposure study for JP-4 was found (Clark et al. 1989), 

and it was limited by a low number of animals per group. No acute-duration exposure studies were 

located for JP-7. Thus, no acute inhalation MRLs’“were calculated for JP-4 and JP-7. However, 

sufficient information exists for the calculation of intermediate and chronic exposure MRLs for JP-4 

and JP-7, respectively. The MRLs are based on hepatic toxicity because the liver appears to be a 

target organ for JP-4- and JP-7-related toxicity (Air Force 1974, 1984b, 1984c, 1991; Bruner et al. 

1993). 

•	 An MRL of 9 mg/m3

 has been derived for intermediate-duration inhalation exposure 

(15-364 days) to JP-4. 

The intermediate inhalation exposure MRL of 9 mg/m3

 was based on an increase in hepatic toxicity 

observed in mice at 500 mg/m3

 (Air Force 1984b). In that study, female C57BL/6 mice (150/group) 

were exposed to 0, 500, or 1,000 mg/m3

 of petroleum-derived JP-4 continuously for 90 days. The 

variation in the day-to-day concentration of JP-4 was reported to be less that 1%. Hepatocellular fatty 

changes were seen in both dose groups. The changes were described as multiple, discrete vacuoles of 

varying sizes within the cytoplasm of hepatocytes, especially in the centrilobular region of the liver. 

The incidence of the hepatic fatty degenerative changes was 6%, 15%, and 25% in the control, 

500 mg/m3

, and 1,000 mg/m3 groups, respectively. Renal tubular dilatation was also increased at 

500 mg/m3

, but not at 1,000 mg/m3. This was thought to be an incidental finding resulting from mild 

glomerulonephritis, common in aging mice. Inflammation and lymphocytic inflammatory infiltrate 

was found in females exposed to 500 mg/m3

 and was frequently accompanied by hyaline degeneration. 

These findings are common in older C57BW6 mice, and because the effects were not dose-dependent, 

they were not considered to be treatment-related. Based on the increased incidence of hepatic toxicity 

at 500 mg/m3

 JP-4 and an uncertainty factor of 300 (10 for the use of a LOAEL, 3 for interspecies 

extrapolation, and 10 for human variability) and a human equivalent dose conversion factor of 5.7, an 

MRL of 9 mg/m3

 was calculated. However, this MRL may be overly conservative for intermittent 

exposure and should probably used for screening purposes. 
JET FUELS JP-4 AND JP-7 40 

2. HEALTH EFFECTS 

•	 An MRL of 0.3 mg/m3 has been derived for chronic-duration inhalation exposure (365 

days or more) to JP-7. 

The chronic inhalation exposure MRL of 0.3 mg/m3

 was based on an increase in hepatic toxicity 

observed in rats at 150 mg/m3

 (Air Force 1991). The average variability of chamber JP-7 

concentrations during the experiment was 5%. In that study, the tumorigenic effect of JP-7 was 

studied in a year-long exposure (6 hours/day, 5 days/week) of Fischer 344 rats (100/sex/group) to 

0 (air), 150, or 750 mg/m3

 JP-7. Following the exposure period, 10 animals/sex/group were killed and 

examined while the remaining animals were killed after a l-year postexposure period. Liver, kidney, 

and spleen weights were determined at sacrifice, and portal blood samples were taken for clinical 

chemistry and hematologic determinations. Additionally, gross and microscopic histopathological 

examination of the collected tissues was performed. One year after the end of the exposure period, 

hepatic inflammation was discovered in females from both the 150 and 750 mg/m3

 groups. Hepatic 

inflammation was not observed in the exposed males. A LOAEL of 150 mg/m3

 was identified for 

hepatic inflammation in female mice. Exposure to JP-7 did not result in any change in mortality when 

exposed rats were compared to controls. Based on the increased incidence of hepatic toxicity at 

150 mg/m3

 JP-7, an uncertainty factor of 300 (10 for the use of a LOAEL, 3 for interspecies 

extrapolation, and 10 for human variability), a human equivalency dose factor of 3.3 (0.36 

m3/day/0.38 kg x 70 kg/20 m3

/day), and a continuous exposure adjustment of 0.18 (6 hours/24 hours x 

5 days/7 days), an MRL of 0.3 mg/m3

 was calculated. 

Oral MRLs. 

No MRLs for acute-, intermediate-, or chronic-duration exposure to JP-4 or JP-7 were calculated 

because insufficient toxicological data exist for those fuels. The data on the potential toxicity of orally 

administered JP-4 were limited to acute exposure studies (Air Force 1974; Clark et al. 1989). No 

studies designed to determine the toxic effects of oral exposure to JP-7 were found. 

No acute-, intermediate-, or chronic-duration dermal MRLs were derived for JP-4 or JP-7 because of 

the lack of an appropriate methodology for the development of dermal MRLs. 
JET FUELS JP-4 AND JP-7 41 

2. HEALTH EFFECTS
 

Death. No studies were located that reported human deaths resulting from JP-4 or JP-7 exposure by 

any route. The LD50 has not been determined in laboratory animals. However, data indicate that the 

lethal inhalation concentration for JP-4 in monkeys, dogs, rats, and mice exceeds 5,000 mg/m3

 (Air 

Force 1974, 1976, 1980, 1984b, 1985b; Clark et al. 1989; Newton et al. 1991). Inhalation exposure of 

rats or mice to up to 750 mg/m3

 JP-7 did not result in any deaths (Air Force 1982f, 1991). Oral 

administration of up to 8,000 mg/kg JP-4 in rats was not lethal. Some mortality was found in mice 

given 500 or 1,000 mg/kg JP-4 (Air Force 1974), but the small number of animals used in the study 

makes interpretation of the results difficult. No studies were located that reported death from oral 

JP-7 exposure. Death did not occur after acute dermal application of up to 2,000 mg (Dennis 1982a) 

or chronic application of 25 mg of JP-4 to the skin of animals (Clark et al 1988). In rabbits, the 

acute-duration dermal exposure to 0.5 mL JP-7 did not result in any deaths (Air Force 1984a). 

Although environmental data are limited, based on the high doses of JP-4 and JP-7 that are necessary 

to cause death, it is unlikely that JP-4 or JP-7 levels near hazardous waste sites are sufficient to cause 

death in exposed populations. 

Systemic Effects. 

Respiratory Effects. It is uncertain whether exposure to JP-4 causes respiratory effects in humans. In 

fact, there are no reports of chronic human occupational exposure to JP-4. No respiratory effects were 

reported after an acute accidental inhalation exposure to high levels of JP-4 (Davies 1964). In animal 

studies, inhalation exposure to up to 5,000 mg/m3

 JP-4 (Air Force 1974, 1976, 1984b; Bruner et al. 

1993) or up to 750 mg/m3

 JP-7 (Air Force 1982g, 1983e) did not result in any reported alterations in 

respiratory clinical signs. Pulmonary mechanics and function did not change after intermediateduration inhalation exposure to 1,000 mg/m3

 JP-4 (Air Force 1985c; Newton et al. 1991). The data 

regarding respiratory effects of JP-4 and JP-7 are insufficient to draw conclusions about the effects 

that may be seen in the workplace or near waste disposal sites. 

Hematological Effects. No information is available on the hematological effects of JP-4 or JP-7 

exposure in humans. In animals, routine hematological testing revealed occasional differences in 

various hematological tests; however, the values were within the normal range of biological variation 

(Air Force 1974, 1980, 1982f, 1984b, 1985b, 1991; Bruner et al. 1993). Additionally, the 

hematological effects were not dose-dependent or found in both sexes. Thus, they were not regarded 

as physiologically significant. 
JET FUELS JP-4 AND JP-7 42 

2. HEALTH EFFECTS
 

Hepatic Effects The effect of JP-4 or JP-7 on the human liver is unknown. Female mice exposed to 

500 mg/m3

 JP-4 continuously for 90 days had degenerative fatty changes in liver cells (Air Force 

1984b) that were likely reversible (Bruner et al. 1993). The fatty changes were not seen in a 

12-month intermittent (6 hours/day, 5 days/week) exposure. Inflammation of the liver occurred in 

female mice exposed intermittently for 12 months to 150 mg/m3

 JP-7. In general, there were no 

changes in blood chemistry that would indicate abnormal liver function in animals exposed by 

inhalation. It is unknown if liver effects would occur in humans exposed to JP-4 or JP-7 at hazardous 

waste sites. There are no data regarding liver effects after oral or dermal administration of JP-4 or 

JP-7 in animals. 

Renal Effects. There are no data regarding the effect of JP-4 or JP-7 on renal function in humans. In 

animal experiments, male rat nephropathy is a common finding after inhalation exposure to either JP-4 

or JP-7 (Air Force 1976, 1984b, 1991; Bruner et al. 1993). However, the evidence is overwhelming 

that the male rat nephropathy is unique to male rats, and is related to the binding of xenobiotic 

compounds to α2μ-globulin, a low molecular weight serum protein synthesized in the liver of male 

rats. Subsequent accumulation of this complex is thought to trigger pathological responses within the 

kidney (Bruner et al. 1993). This syndrome is characterized by the following progression of lesions 

(Alden 1986; Bruner 1984; Bruner et al. 1993; EPA 1991; Short et al. 1987): 

•	 Excessive accumulation of hyaline droplets in the P2 segment of the proximal tubule 

region of the kidney. This accumulation is evident after 1 or 2 days of exposure and is 

reversible within 3 days to 2 weeks after termination of exposure. The hyaline droplets 

are associated with the protein α2μ-globulin. 

•	 .Evidence of single cell necrosis in the P2 segment epithelium and exfoliation of these 

degenerated cells and cell fragments filled with crystalloid phagolysosomes into the tubule 

lumen after 5 days of continuous exposure. This can also be seen with longer exposure. 

•	 Sustained regenerative tubule cell proliferation with continued exposure. After the initial 

cytotoxic injury, evidence of regeneration of the tubular epithelium can be seen as an 

increase in cell proliferation within the P2 segment in response to cell damage and loss. 

The cell proliferation can be seen following 3 weeks of continuous exposure and is also 
 

 

JET FUELS JP-4 AND JP-7 43 

2. HEALTH EFFECTS 

obvious after 48 weeks of exposure. Tubular dilation and tubular epithelial necrosis are

 often associated with the regenerative changes. 

•	 Accumulation of granular casts, formed from the cellular debris and subsequent tubule 

dilation, is seen at the junction of the P3 segment and the thin loop of Henle. This can be 

seen as early as 2-3 weeks after exposure begins. These casts are not always seen in male 

rat nephropathy and may reflect a more severe response. 

•	 Linear mineralization of the renal papillar tubules with hyperplasia of the renal pelvic 

urothelium. These lesions are thought to be the result of mineralized remnants of debris 

from disintegrating granular casts that lodge in the prebend segments of Henle’s loop. 

Several mechanisms have been proposed to account for this unique sequence of events in male rats 

following exposure to certain hydrocarbons, including the jet fuels. Currently, the most likely 

mechanism is that a metabolite of jet fuel or one of its constituents (especially isoparaffinic 

hydrocarbons) binds to α2μglobulin. The complex is then reabsorbed in the proximal tubule and 

phagocytized by lysosomes within the tubule cells. This protein complex is difficult to catabolize and 

accumulates in the lysosomes. Eventually, the lysosomes burst, and digestive enzymes contained 

within the lysosomes induce cytotoxicity and cell death, which in turn leads to the accumulation of 

casts and the hyperplastic events described above (Swenberg et al. 1989). 

The available data indicate that the nephrotoxic syndrome is induced by hydrocarbons such as jet fuels 

and is unique to male rats. The hepatic synthesis of α2μ-globulin protein is under androgenic control 

and is found at concentrations 100-300 times higher in male rat urine than in female rat urine (Shapiro 

and Sachchidananda 1982; Van Doren et al. 1983). Human urine contains only 1% of the total 

concentration of this protein present in mature male rat urine (Olson et al. 1990). α2μ-Globulin and 

associated hyaline droplet accumulation and the associated constellation of nephrotoxic effects that are 

observed in male rats have not been observed in female rats, or in mice or monkeys of either sex (Air 

Force 1976, 1980, 1984b, 1991; Brnner et al. 1993). In addition, this syndrome could not be induced 

in male NCI-Black-Reiter rats, an inbred strain of rats that does not synthesize α2μ-globulin (Dietrich 

and Swenberg 1991). In light of this evidence, EPA’s Risk Assessment Forum in its document 

entitled Alpha-2μp-Globulin: Association with Chemically-Induced Renal Toxicity and Neoplasia in 

the Male Rat (EPA 1991), made the following conclusions: 
JET FUELS JP-4 AND JP-7 44 

2. HEALTH EFFECTS

 “If a compound induces α2μg accumulation in hyaline droplets, the associated 

nephropathy in male rats is not used as an endpoint to determine noncancer 

(systemic) effects potentially occurring in humans. Likewise, quantitative estimates of 

noncancer risk (e.g., reference doses and margin-of-exposure determinations) are based 

on other endpoints wherever possible.” 

“...If the sequence of lesions characteristic-of the α2μg syndrome are present, the 

associated nephropathy in the male rat does not contribute to determinations of 

noncarcinogenic hazard of risk.” 

Thus, it does not appear that the nephrotoxicity observed in male rats after exposure to JP-4 or JP-7 is 

relevant to humans exposed to JP-4 or JP-7 in the workplace or at hazardous waste sites. 

Dermal Effects. There is no information regarding the dermal effects of JP-4 or JP-7 in humans after 

acute, intermediate, or chronic exposure to JP-4 or JP-7. Experiments in rabbits show that acute 

application of JP-4 or JP-7 is irritating to the skin. Application of 0.5 mL undiluted JP-4 (both 

shaleand petroleum-derived) produced severe irritation that was characterized by edema and erythema 

24 hours post-application (Air Force 1984a; Clark et al. 1989; Dennis 1982b; Walter 1982c), whereas 

the application of the same amount of JP-7 was shown to produce slightly greater irritation that 

persisted for a longer period of time (Air Force 1984a). Skin sensitization assays in guinea pigs have 

shown that petroleum-derived JP-4 is not a dermal sensitizer (Clark et al. 1989; Walter 1982c). 

However, JP-7 and shale-derived JP-4 appear to have weak-to-mild and mild-to-moderate sensitization 

potential, respectively (Air Force 1984a). 

Ocular Effects. There is no information regarding the ocular effects of JP-4 or JP-7 in humans after 

acute, intermediate, or chronic exposure to JP-4 or JP-7. Petroleum-derived JP-4, shale-derived JP-4, 

and JP-7 caused no irritation when applied to the eyes of rabbits (Air Force 1984a; Clark et al. 1989; 

Dennis 1982c; Walter 1982a). 

Body Weight Effects. Decreases in body weight were observed in some, but not all, rats exposed to 

JP-4 in intermediate- or chronic-duration experiments (Air Force 1980, 1981i, 1985b; Bruner et al. 

1993). The decrease in weight gain was found to occur primarily in male rats and may be related to 

altered protein metabolism in male rats, which was related to the synthesis, excretion, and 

conservation 
JET FUELS JP-4 AND JP-7 45 

2. HEALTH EFFECTS
 

of α2μ,-globulin by the kidney (Bruner et al. 1993). The significance of body weight depression for 

humans cannot be determined from these findings. 

Immunological and Lymphoreticular Effects. Data regarding the immunological effects of 

JP-4 are limited to the dermal sensitization tests conducted in guinea pigs (Air Force 1984a; Clark et 

al. 1989; Walter 1982c). In these studies petroleum-derived JP-4 was not found to be a dermal 

sensitizer. However, JP-7 and shale-derived JP-4 have weak-to-mild and mild-to-moderate 

sensitization potential, respectively (Air Force 1984a). No studies were located regarding the 

immunological effects in humans after inhalation, oral, or dermal exposure to JP-7. It is not possible 

to determine the likelihood of immunological effects occurring in humans because of the paucity of 

data. 

Neurological Effects. The only information found regarding human exposure to JP-4 is a case 

study in which a pilot was accidentally exposed to a very high level of the jet fuel from a fuel leak 

(Davies 1964). The exposure concentration was estimated to be approximately 3,000-7,000 ppm. In 

this case report, the overwhelming finding was neurological impairment, specifically described as 

“intoxication.” Other cardiovascular and respiratory functions appeared normal on physical exam. 

Therefore, it is likely that under very high exposure conditions, the nervous system is the target organ 

for JP-4 toxicity. Supportive evidence is found in an acute exposure of rats (number unspecified) to a 

very high concentration of JP-4 (38,000 mg/m3

) that resulted in poor coordination and convulsions 

(Air Force 1974). Those studies are both flawed by poor characterization of exposure concentrations. 

No studies were located regarding neurological effects in animals or humans after oral or dermal 

exposure to JP-4. There is no information regarding the neurological effect of JP-7 exposure in 

humans or animals after inhalation, oral, or dermal exposure. 

Reproductive Effects. No studies were located regarding reproductive effects in humans or 

animals after inhalation, oral, or dermal exposure to JP-4 or JP-7. Since no information is available, 

the likelihood of reproductive effects occurring in humans cannot be determined. 

Developmental Effects. No studies were located regarding developmental effects in humans or 

animals after inhalation, oral, or dermal exposure to JP-4 or JP-7. Since no information is available, 

the likelihood of developmental effects occurring in humans cannot be determined. 
JET FUELS JP-4 AND JP-7 46 

2. HEALTH EFFECTS
 

Genotoxic Effects. No studies involving human exposure to jet fuels were located, and only two 

animal in viva studies were found. Male mice and rats were exposed to JP-4 and then allowed to mate 

with unexposed females in dominant lethal experiments. Statistically significant dominant lethal 

effects were not observed for either mice or rats (Air Force 1978a). However, because of the small 

sample size of pregnant females, the results cannot be considered conclusive. Refer to Table 2-3 for a 

further summary of these results. 

Most of the genotoxicity data concerning jet fuels comes from in vitro studies. Human diploid WI-38 

cells (cells derived from embryonic lung) were treated with JP-4 and examined for unscheduled 

deoxyribonucleic acid (DNA) synthesis (Air Force 1978a). Unscheduled DNA synthesis (UDS) is a 

repair process that occurs when DNA has been damaged. Therefore, UDS activity is an indirect 

measurement of DNA damage. The cells were treated with 0.1, 0.5, 1.0, and 5.0 μL/mL (in water) in 

both activation and nonactivation systems. A dose-dependent increase in UDS activity was observed, 

indicating that JP-4 can produce repairable damage in the DNA of human WI-38 cells. The cells that 

were cultured in the presence of metabolic activators exhibited greater UDS activity suggesting that 

toxic metabolites may be involved. The remaining in vitro investigations were negative for 

chromosome aberrations in Chinese hamster ovary cells (EPA 1982a, 1982b; Galloway 1982a, 

1982b), gene mutations in mouse L5178Y lymphoma cells (Air Force 1978a; Cifone 1982a, 1982b; 

EPA 1982a, 1982b), and gene mutations in Saccharomyces cerevisiae (Air Force 1978a) and 

Salmonella typhimurium (Air Force 1978a; EPA 1982a, 1982b; Jagannath 1982; Rabenold 1982). 

Refer to Table 2-4 for a further summary of these results. One of the series of studies compared the 

effects of two types of JP-4: shale-derived JP-4 (Cifone 1982b; EPA 1982b; Galloway 1982b; 

Rabenold 1982) and petroleum-derived JP-4 (Cifone 1982a; EPA 1982a; Galloway 1982a; Jagannath 

1982). The difference in origin did not produce a difference in effect; the results were negative in all 

tests for both types of JP-4. 

The only positive response to JP-4 was observed in human WI-38 cells tested for UDS; but the nature 

of the DNA damage was not necessarily mutagenic (Air Force 1978a). The negative data for gene 

mutations and chromosome aberrations suggest that JP-4 is not a mutagenic or clastogenic mixture. 

The negative results observed in the dominant lethal experiments and the micronuclei study may not 

be reliable because of low sample size and poor experimental protocol. Results from Ames testing 

indicated that JP-4 was not mutagenic. Additionally, the solubility and volatility of hydrocarbon 

mixtures such as JP-4 or JP-7 is a confounding factor in experiments involving exposure of cultured 


JET FUELS JP-4 AND JP-7 49 

2. HEALTH EFFECTS
 

cells to mixtures of such hydrocarbons. Negative data may, therefore, be misinterpreted in such a 

system. No genotoxicity data were obtained for JP-7. 

Cancer. No studies were located regarding cancer in humans after inhalation, oral, or dermal 

exposure to JP-4 or JP-7. In inhalation animal studies, there does not appear to be any carcinogenic 

potential of chronic JP-7 exposure (Air Force 1991). A l-year JP-4 exposure in rats and mice resulted 

in increased alveolar/bronchiolar tumors in female rats and mice (Bruner et al. 1993). Renal tumor 

increases that were seen in male rats were attributable to α2μ-globulin nephropathy syndrome (see the 

discussion of renal effects above) and are not likely to be relevant to other animals or to humans. 

Finally, an increased hepatocellular tumor incidence occurred in treated female mice (9/80) versus 

controls (2/83). In males, this trend was reversed (l/38 treated versus 14/71 controls). There are 

currently widely divergent views regarding the validity of mouse liver tumors as an indication of 

human carcinogenicity for a compound (EPA 1986b). Squamous cell carcinoma and fibrosarcoma 

formation was increased in the mice exposed to shale-derived (50% incidence) and petroleum-derived 

JP-4 (26% incidence) compared to the appropriate control groups (2% and 0%, respectively) (Clark et 

al. 1988). The current animal data regarding the carcinogenicity of JP-4 are equivocal, and the 

evidence is insufficient to draw conclusions regarding the carcinogenic potential of JP-4 or JP-7 in 

humans exposed at hazardous waste sites. 

2.5 BIOMARKERS OF EXPOSURE AND EFFECT 

Biomarkers are broadly defined as indicators signaling events in biologic systems or samples. They 

have been classified as markers of exposure, markers of effect, and markers of susceptibility 

(NAS/NRC 1989). 

A biomarker of exposure is a xenobiotic substance or its metabolite(s) or the product of an interaction 

between a xenobiotic agent and some target molecule(s) or cell(s) that is measured within a 

compartment of an organism (NAS/NRC 1989). The preferred biomarkers of exposure are generally 

the substance itself or substance-specific metabolites in readily obtainable body fluid(s) or excreta. 

However, several factors can confound the use and interpretation of biomarkers of exposure. The 

body burden of a substance may be the result of exposures from more than one source. The substance 

being measured may be a metabolite of another xenobiotic substance (e.g., high urinary levels of 

phenol can result from exposure to several different aromatic compounds). Depending on the 
JET FUELS JP-4 AND JP-7 50 

2. HEALTH EFFECTS
 

properties of the substance (e.g., biologic half-life) and environmental conditions (e.g., duration and 

route of exposure), the substance and all of its metabolites may have left the body by the time biologic 

samples can be taken. It may be difficult to identify individuals exposed to hazardous substances that 

are commonly found in body tissues and fluids (e.g., essential mineral nutrients such as copper, zinc, 

and selenium). Biomarkers of exposure to JP-4 and JP-7 are discussed in Section 2.5.1. 

Biomarkers of effect are defined as any measurable biochemical, physiologic, or other alteration 

within an organism that, depending on magnitude, can be recognized as an established or potential 

health impairment or disease (NAS/NRC 1989). This definition encompasses biochemical or cellular 

signals of tissue dysfunction (e.g., increased liver enzyme activity or pathologic changes in female 

genital epithelial cells), as well as physiologic signs of dysfunction such as increased blood pressure or 

decreased lung capacity. Note that these markers are often not substance specific. They also may not 

be directly adverse, but can indicate potential health impairment (e.g., DNA adducts). Biomarkers of 

effects caused by JP-4 and JP-7 are discussed in Section 2.5.2. 

A biomarker of susceptibility is an indicator of an inherent or acquired limitation of an organism’s 

ability to respond to the challenge of exposure to a specific xenobiotic substance. It can be an 

intrinsic genetic or other characteristic or a preexisting disease that results in an increase in absorbed 

dose, biologically effective dose, or target tissue response. If biomarkers of susceptibility exist, they 

are discussed in Section 2.7, Populations That Are Unusually Susceptible. 

2.5.1 Biomarkers Used to Identify or Quantify Exposure to Jet Fuels JP-4 and JP-7 

No biomarkers of exposure were identified for JP-4 or JP-7. No standard procedures exist for 

identifying or quantifying exposure to JP-4 or JP-7. For information on biomarkers of exposure for 

the individual components in JP-4 and JP-7, the ATSDR profiles on benzene (ATSDR 1991a), toluene 

(ATSDR 1990), total xylenes (ATSDR 1991c) and polycyclic aromatic hydrocarbons (ATSDR 1991b) 

can be consulted. However, the biomarkers of exposure for these chemicals are not specific for JP-4 

or JP-7 exposure. 
JET FUELS JP-4 AND JP-7 51 

2. HEALTH EFFECTS 

2.5.2 Biomarkers Used to Characterize Effects Caused by Jet Fuels JP-4 and JP-7 

No biomarkers of effect were found for JP-7. Potential biomarkers for neurological effects of JP-4 are 

mild muscular weakness, staggering gait, and decreased sensitivity to painful stimuli (Davies 1964). 

Those effects are not specific enough to be useful as biomarkers for JP-4 exposure since they are a 

component of the clinical signs associated with the exposure to most volatile organic compounds. 

For more information on biomarkers for renal and hepatic effects of chemicals see ATSDR/CDC 

Subcommittee Report on Biological Indicators of Organ Damage (1990) and for information on 

biomarkers for neurological effects see OTA (1990). 

2.6 INTERACTIONS WITH OTHER CHEMICALS 

When benzene was added to a JP-4 inhalation mixture, experimental animals did not demonstrate any 

difference in hematological, blood chemistry, or histopathological results when compared to 

airexposed controls (Air Force 1974, 1976). No other information was located regarding the influence 

of other chemicals on the toxicity of JP-4 or JP-7. 

2.7 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE 

A susceptible population will exhibit a different or enhanced response to JP-4 and JP-7 than will most 

persons exposed to the same level of JP-4 and JP-7 in the environment. Reasons include genetic 

make-up, developmental stage, health and nutritional status, and chemical exposure history. These 

parameters result in decreased function of the detoxification and excretory processes (mainly hepatic 

and renal) or the pre-existing compromised function of target organs. For these reasons we expect the 

elderly with declining organ function and the youngest of the population with immature and 

developing organs will generally be more vulnerable to toxic substances than healthy adults. 

Populations who are at greater risk due to their unusually high exposure are discussed in Section 5.6, 

Populations With Potentially High Exposure. 

Review of the literature regarding the effects of exposure to JP-4 or JP-7 does not indicate 

susceptibility of specific populations to these chemicals. There are very limited data on exposure of 

humans to JP-4 or JP-7; however, the results from animal studies do not indicate sensitivity in specific 

groups to the toxicity of these mixtures. 
JET FUELS JP-4 AND JP-7 52 

2. HEALTH EFFECTS 

2.8 METHODS FOR REDUCING TOXIC EFFECTS 

This section will describe clinical practice and research concerning methods for reducing toxic effects 

of exposure to JP-4 or JP-7. However, because some of the treatments discussed may be experimental 

and unproven, this section should not be used as a guide for treatment of exposures to JP-4 or JP-7. 

When specific exposures have occurred, poison control centers and medical toxicologists should be 

consulted for medical advice. 

2.8.1 Reducing Peak Absorption Following Exposure 

Following dermal contact with JP-4 or JP-7, the skin should be wiped off and washed with soap and 

warm water. After washing, hand cream may be applied to the exposed skin to restore lost oils. If 

the eyes have been exposed, it is recommended that they be flushed with copious amounts of cool, 

clean water for at least 15 minutes. Common treatments of the eyes include application of antibiotic 

creams to prevent secondary infection and a soothing or anesthetic agent. Following ingestion, it is 

recommended that the victim drink water or milk. Vomiting should not be induced because of the risk 

of aspiration of jet fuel hydrocarbons. Following inhalation of jet fuel vapors, it has been suggested 

that the victim be administered oxygen (Tupper 1989; Weiss 1986). 

2.8.2 Reducing Body Burden 

There is no specific method for enhancing the elimination of JP-4 or JP-7 because the metabolic 

pathways and excretion pathways for these jet fuels is essentially unknown. Interventions designed to 

increase elimination may be of limited effectiveness because many of the components of JP-4 and JP7 are lipophilic. However, it may be possible to increase the elimination of the highly volatile 

components of the fuels by increasing the respiratory frequency, 

2.8.3 Interfering with the Mechanism of Action for Toxic Effects 

No information on interfering with the mechanism of action for toxic effects of either JP-4 or JP-7 is 

provided because the metabolic pathways and excretion pathways for these jet fuels is essentially 

unknown. 
JET FUELS JP-4 AND JP-7 53 

2. HEALTH EFFECTS 

2.9 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with 

the Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of JP-4 and JP-7 is available. Where adequate information 

is not available, ATSDR, in conjunction with the National Toxicology Program (NTP), is required to 

assure the initiation of a program of research designed to determine the health effects (and techniques 

for developing methods to determine such health effects) of JP-4 and JP-7. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that, if met, 

would reduce or eliminate the uncertainties of human health assessment. This definition should not be 

interpreted to mean that all data needs discussed in this section must be filled. In the future, the 

identified data needs will be evaluated and prioritized, and a substance-specific research agenda may 

be proposed. 

2.9.1 EXISTING INFORMATION ON HEALTH EFFECTS OF JET FUELS JP-4 AND JP-7 

The existing data on health effects of inhalation, oral, and dermal exposure of humans and animals to 

JP-4 and JP-7 are summarized in Figures 2-2 and 2-3. The purpose of the figures is to illustrate the 

existing information concerning the health’effects of JP-4 and JP-7. Each dot in the figures indicates 

that one or more studies provide information associated with that particular effect. The dot does not 

imply anything about the quality of the study or studies. Gaps in the figures should not be interpreted 

as “data needs” information (i.e., data gaps that must necessarily be filled). 

One case study was located detailing the acute neurological effects of accidental JP-4 exposure 

(Davies 1964). No other data were found on the health effects of inhalation exposure to JP-4 or JP-7 in 

humans. Animal data exist for death and for intermediate and chronic neurological, and cancer effects 

following inhalation exposure to JP-4; for death and genotoxic effects following oral exposure to JP-4; 

and for death and acute and chronic cancer effects following dermal exposure to JP-4. Therefore, as 

can be seen in Figure 2-2, the majority of the available information for JP-4 is on the health effects of 

inhalation and dermal exposure in animals. Very limited information exists on the effects of oral 

exposure in animals. No data were found on the health effects of oral and dermal exposure in 


JET FUELS JP-4 AND JP-7 56 

2. HEALTH EFFECTS
 

humans. The only available information for JP-7 was on death and intermediate, chronic, and cancer 

effects following inhalation exposure in animals. As can be seen in Figure 2-3, limited data were 

found on the health effects of inhalation exposure in animals to JP-7. Data on dermal exposure to 

JP-7 exist for death and acute effects. No other health effects data were found for either humans or 

animals. 

2.9.2 Identification of Data Needs 

Acute-Duration Exposure. The central nervous system appears to be the target of JP-4 toxicity 

following acute-duration inhalation exposure in humans. Acute inhalation exposure to JP-4 is 

characterized by a groggy, weak, intoxicated state including staggering gait, mild muscular weakness, 

and decreased sensitivity to painful stimuli (Davies 1964). Accidental inhalation exposure of a pilot to 

a high concentration of JP-4 from a fuel leak did not result in any abnormalities in hematological or 

clinical chemistry tests (Davies 1964). No information was available on acute-duration oral or dermal 

exposure of humans to JP-4 or JP-7, or on acute-duration inhalation, oral, or dermal exposure of 

humans to JP-7. Animals acutely exposed by inhalation to very high concentrations of JP-4 

(38,000 mg/m3

) exhibited neurotoxic effects including poor coordination and convulsions (Air Force 

1974). Acute dermal exposures to JP-4 and JP-7 indicate that both substances are skin irritants (Air 

Force 1984a; Clark et al. 1989; Dennis 1982a, 1982b; Walter 1982c). No pharmacokinetic data were 

available for either substance to support the identification of target organs across routes of exposure 

for animals or humans. No evidence was seen of primary ocular irritation following acute exposure to 

JP-4 or JP-7 (Air Force 1984a; Clark et al. 1989; Dennis 1982c; Walter 1982a). Petroleum-derived 

JP-4 was not a dermal sensitizer in guinea pigs (Clark et al. 1989; Walter 1982c). However, JP-7 and 

shale-derived JP-4 have sensitizing potential (Air Force 1984a). Acute exposure to high levels of JP-4, 

by all three routes, did not result in any mortality (Clark et al. 1989; Dennis 1982a). No quantitative 

information was available on acute-duration inhalation or oral exposure of animals to JP-7. No acute 

MRLs have been developed because of the absence of quantitative information regarding 

acuteduration inhalation or oral exposure to JP-4 or JP-7. More quantitative information on the levels 

of exposure that elicit various acute-duration oral, inhalation, or dermal exposure effects in humans 

and animals would be helpful, as would information on what the thresholds are for these effects. 
JET FUELS JP-4 AND JP-7 57 

2. HEALTH EFFECTS
 

Intermediate-Duration Exposure. No information is available on the effects of intermediate-duration 

exposure to JP-4 or JP-7 in humans. No pharmacokinetic data were available to support the 

identification of target organs across routes of exposure for either humans or animals. 

Intermediateduration inhalation exposure to JP-4 or JP-7 did not result in any dose-dependent 

pathophysiological responses in routine hematological tests in monkeys, dogs, or rats (Air Force 1974, 

1980, 1984b, 1984c) with the exception of a decrease in white blood cell count after intermediate- or 

chronicduration exposure in rats (Air Force 1980). Increased blood urea nitrogen was measured in rats 

exposed continuously by inhalation for 90 days to 500 or 1,000 mg/m3

 JP-4 (Air Force 1980, 1984c). 

That effect was not repeated in later studies using intermittent exposure to 5,000 mg/m3

 JP-4 (Air 

Force 1981i). In that study, blood urea nitrogen was found to be decreased after exposure. Kidney 

weight was increased in male rats exposed by inhalation to JP-4 for an intermediate duration (Air 

Force 1976, 1980). Histopathological changes related to α2μ-globulin nephropathy were seen in these 

male rats. The results of dominant lethal studies in rats and mice orally exposed to JP-4 were negative 

(Air Force 1978a). More information is needed on the effects of intermediate-duration inhalation, oral, 

and dermal exposures to JP-4 and JP-7 in humans and animals in order to adequately identify target 

organs. This is especially true for neurological effects, one of the most sensitive end points for JP-4 

(Air Force 1974; Davies 1964) and, most likely, JP-7 exposures. Sufficient inhalation data exist to 

calculate an intermediate-duration inhalation exposure MRL of 9 mg/m3

. 

Chronic-Duration Exposure and Cancer. No chronic-duration exposure studies were found in 

humans for exposure to JP-4 or JP-7 following inhalation exposure. No chronic-duration exposure 

studies in humans were found for exposure to JP-4 or JP-7 by the oral or dermal routes. 

No chronic-duration exposure studies were found that identified the central nervous system as the 

target of JP-4 or JP-7 toxicity in animals. Chronic-duration inhalation exposure studies using JP-4 or 

JP-7 in rats and mice showed no increase in mortality during the exposure period or 12 months 

postexposure (Air Force 1981i, 1982f, 1982g, 1983e, 1991; Bruner et al. 1993). Chronic inhalation of 

JP-4 did not result in statistically significant respiratory tract irritation or pulmonary lesions in rats or 

mice (Bruner et al. 1993). Chronic inhalation exposure to JP-4 resulted in decreased white blood cell 

count in rats (Bruner et al. 1993). Hepatic inflammation of female mice was seen after inhalation 

exposure to JP-7 (Air Force 1991). 
JET FUELS JP-4 AND JP-7 58 

2. HEALTH EFFECTS
 

No information is available on the carcinogenicity of JP-4 or JP-7 in humans following chronic 

inhalation, oral, or dermal exposure. Chronic inhalation exposure to JP-4 or JP-7 did not result in an 

increased incidence of cancer in animals except for an increase in hepatocellular adenomas in female 

mice exposed high doses of JP-4 (Bruner et al. 1993). The incidence of this cancer is of unknown 

significance in mice (EPA 1986b). There was equivocal evidence for alveolar/bronchiolar tumors after 

inhalation exposure of rats (Bruner et al. 1993). JP-7 inhalation exposure did not result in significant 

increases in the incidence of cancer in rats (Air Force 1991). However, there were slight increases in 

the incidence of C-cell adenomas and kidney adenomas in the groups of male rats exposed to 

750 mg/m3

 of JP-7 (Air Force 1991). Dermal application of undiluted JP-4 to the skin on a chronic 

basis resulted in increased incidence of squamous cell carcinoma and fibrosarcoma formation in mice 

at the site of application. There were no oncogenic effects in other organs (Clark et al. 1988). No 

information is available on the carcinogenicity of JP-4 or JP-7 in animals following chronic oral 

exposure. Further chronic inhalation or oral studies are recommended to help elucidate the 

carcinogenic potential of JP-4 and JP-7. Sufficient inhalation data exist to calculate a chronic 

exposure MRL of 0.3 mg/m3

. 

Genotoxicity. JP-4 does not appear to be highly genotoxic in in vitro studies; however, there are 

no human data to indicate whether this substance acts by a genotoxic mechanism. Consistently 

negative results were gathered for gene mutations in both microbial species (Air Force 1978a; EPA 

1982a, 1982b; Jagannath 1982; Rabenold 1982) and mammals (Air Force 1978a, 1979b; Cifone 

1982a, 1982b; EPA 1982b; Galloway 1982a, 1982b). In addition, JP-4 was not clastogenic in Chinese 

hamster ovary cells (Jagannath 1982; Rabenold 1982). Although significant UDS was observed in 

human WI-38 cells (Air Force 1978a), more research is needed in order to determine the nature of the 

DNA damage. The only two in vivo (oral) studies obtained were inconclusive for JP-4’s effects on the 

germinal cells of rats and mice due to small sample size of test animals (Air Force 1978a). Testing 

for sister chromatid exchange chromosome aberrations, UDS, and gene mutations in animals exposed 

to JP-4 in vivo would be helpful in determining whether or not this jet fuel poses a genotoxic threat to 

humans. Epidemiology studies of exposed workers, pilots, military personnel, or Air Force personnel 

would help even further in evaluating JP-4 as a potential human genotoxin. No studies were found in 

which JP-7 was used as a test chemical in genotoxicity experiments. Therefore, research is needed in 

order to evaluate the toxicity of this particular jet fuel. 
JET FUELS JP-4 AND JP-7 59 

2.HEALTH EFFECTS
 

Reproductive Toxicity. No information is available on the reproductive effects of-JP-4 or JP-7 in 

humans or animals following inhalation, oral, or dermal exposure. No pharmacokinetic data were 

located to support the potential of JP-4 or JP-7 to affect reproduction across routes of exposure. 

Reproductive organ toxicity data from studies of acute, intermediate (90-day), and chronic duration are 

needed for all three routes of exposure in order to establish whether JP-4 or JP-7 has the potential to 

induce reproductive effects. 

Developmental Toxicity. No information is available on the developmental effects of JP-4 or 

JP-7 in humans or animals following inhalation, oral, or dermal exposure. No pharmacokinetic data 

were located to support the potential of JP-4 or JP-7 to affect development across routes of exposure. 

Developmental toxicity data are needed for all three routes of exposure in order to establish whether 

JP-4 or JP-7 has the potential to induce developmental effects in humans. 

lmmunotoxicity and Lymphoreticular Effects. Data regarding the immunological effects of 

JP-4 are limited to the dermal sensitization tests conducted in guinea pigs (Air Force 1984a; Clark et 

al. 1989; Walter 1982c). In these studies petroleum-derived JP-4 was not found to be a dermal 

sensitizer. However, JP-7 and shale-derived JP-4 have weak-to-mild and mild-to-moderate 

sensitization potential, respectively (Air Force 1984a). No studies were located regarding the 

immunological effects in humans after inhalation, oral, or dermal exposure to JP-7. It is not possible 

to determine the likelihood of immunological effects occurring in humans because of the paucity of 

data. These results suggest that JP-4 may affect immune function. Thus, assessing the effects of oral 

or inhaled JP-4 on immune function in laboratory animals would be helpful. 

Neurotoxicity. No information is available on the neurotoxic effects of JP-4 or JP-7 following oral 

or dermal exposure in humans and animals, or of JP-7 following inhalation exposure in humans. The 

central nervous system appears to be the target of JP-4 toxicity following acute inhalation exposure in 

humans. Acute exposure to a very high concentration of JP-4 produced a groggy, weak, intoxicated 

state in a pilot exposed to a fuel leak (Davies 1964). The pilot had a staggering gait, mild muscular 

weakness, and decreased sensitivity to pain; these effects were no longer evident by 36 hours 

postexposure (Davies 1964). No information was found on neurotoxic effects of JP-4 or JP-7 in 

humans following intermediate-duration or chronic-duration exposure. Long-term exposure of 

experimental animals to JP-7 does not result in overt signs of neurotoxicity or any gross pathological 
JET FUELS JP-4 AND JP-7 60 

2.HEALTH EFFECTS
 

responses (Air Force 1991). Acute exposure of rats to very high concentrations of JP-4 by inhalation 

produced poor coordination and convulsions (Air Force 1974). 

Additional studies in humans and animals using all modes of exposure that examine sensitive 

neuropathological end points specifically for JP-4 or JP-7 would be useful to definitely determine the 

symptoms associated with both fuels. 

Epidemiological and Human Dosimetry Studies. Limited epidemiological information exists 

from an early study regarding acute-duration exposure to JP-4 (Davies 1964). Exposure levels in this 

study were only grossly approximated. No chronic-duration epidemiological studies were located 

regarding exposure to JP-4 or JP-7. Exposure to JP-4 or JP-7 is thought to occur primarily in a small 

segment of the population, namely Air Force personnel. Thus, collecting sufficient numbers of 

exposed persons for meaningful epidemiological studies is difficult. However, because the population 

most likely to be exposed consists mainly of Air Force personnel, follow-up studies may be more 

easily performed. Thus, studies examining chronic-duration neurological, immunological, 

developmental, and systemic effects would be valuable if a sufficient number of exposed persons are 

identified. In the absence of studies on persons exposed to JP-4 or JP-7, epidemiological studies on 

persons exposed to the individual components of JP-4 or JP-7 are not a priority because the results of 

the genetic toxicology tests with JP-4 were negative. 

Biomarkers of Exposure and Effect. 

Exposure. No biomarkers of exposure were identified for JP-4 or JP-7. No standard procedures exist 

for identifying or quantifying exposure to JP-4 or JP-7. Studies delineating the metabolism and 

excretion of JP-4 or JP-7 are needed in order to identify potential biomarkers of exposure following 

acute, intermediate, and chronic exposures to these chemicals. 

Effect. No biomarkers of effect were found for JP-7. Potential biomarkers for neurological effects of 

JP-4 are mild muscular weakness, staggering gait, and decreased sensitivity to painful stimuli (Davies 

1964). Studies of acute, intermediate, and chronic exposures are needed in order to identify 

biomarkers of effects for specific target organs following exposure to JP-4 or JP-7. 
JET FUELS JP-4 AND JP-7 61 

2. HEALTH EFFECTS 

Absorption, Distribution, Metabolism, and Excretion. No quantitative data were located 

regarding the absorption, distribution, metabolism, or excretion of JP-4 or JP-7 following inhalation, 

oral, or dermal exposure in humans or animals. Therefore, acute, intermediate, and chronic data are 

needed in order to assess the relative rates and extent of absorption, distribution, metabolism, and 

excretion with respect to all three routes of exposure, as well as with respect to time or dose. 

Comparative Toxicokinetics. No studies were located regarding comparative toxicokinetics of 

JP-4 or JP-7. Human and animal data are needed in order to examine toxicokinetics across species 

(i.e., in humans and animals and in multiple species). This information is needed in order to identify 

similar target organs and to adequately assess which animals can serve as the best models for humans. 

Mitigation of Effects. All of the treatment methods currently available for use in jet fuel exposure 

are supportive in nature (Tupper 1989; Weiss 1986). Since the mechanism(s) of jet fuel toxicity are 

not known, there are currently no methods specifically tailored to mitigating the effects of jet fuels by 

interfering with the mode of action. Additional information on the ultimate mechanism of jet fuel 

toxicity is needed before insights can be gained regarding treatment of exposure victims. 

2.9.3 Ongoing Studies 

No ongoing studies evaluating either the health effects or toxicokinetics of JP-4 or JP-7 were located. 

JET FUELS JP-4 AND JP-7 63 

3. CHEMICAL AND PHYSICAL INFORMATION 

3.1 CHEMICAL IDENTITY 

The composition of aviation fuels has been established by the U.S. Air Force (Air Force 1977, 1981g, 

1982d, 1988a, 1989c, 1990) using specifications that are based primarily on the characteristics that 

give the maximum performance of the aircraft for which the fuel is used (CRC 1984). JP-4 and JP-7 

were developed for use by the U.S. Air Force. JP-4 is called a wide-cut fuel because it is produced 

from a broad distillation temperature range and contains a wide array of carbon chain-lengths, from 

4 to 16 carbons long. It was initially developed for broad availability in times of need. The 

composition of JP-4 is approximately 13% (v/v) aromatic hydrocarbons, 1.0% olefin hydrocarbons, 

and 86% saturated hydrocarbons (ITC 1985). It has a distillation temperature range of 60 to 270 °C 

(MacNaughton and Uddin 1984). JP-7 was developed for use in advanced supersonic aircraft because 

of its thermal stability and high flashpoint (CRC 1984; Dukek 1978). It has a distillation temperature 

range of 182 to 288 °C and contains a maximum of 5% (by volume) aromatic compounds (see 

Table 3-7). 

Aviation fuels consist primarily of hydrocarbon compounds (paraffins, cycloparaffins or naphthenes, 

aromatics, and olefins) and contains additives that are determined by the specific uses of the fuel 

(CRC 1984; Dukek 1978; IARC 1989). Paraffins and cycloparaffins are the major components. 

Paraffins have a high hydrogen-to-carbon ratio, with a high heat release per unit of weight and a 

cleaner burn than other hydrocarbons. Cycloparaffins have a lower hydrogen-to-carbon ratio, which 

results in less heat released per unit of weight but increases the fuel’s density. These components 

reduce the freezing point of the fuel. Aromatic hydrocarbons are a good energy source but produce 

smoke when burned; therefore, the maximum levels are restricted (20-25% by volume in JP-4, 5% by 

volume in JP-7). Finally, olefins are similar to the paraffins but are unsaturated with lower 

hydrogento- carbon ratios. They are the most reactive of the hydrocarbons and are permitted at only 

5% by volume in JP-4 (CRC 1984). Benzene, present in wide-cut fuels such as JP-4, is an ineffectual 

contaminant usually present below 0.5% (CONCAWE 1985; IARC 1989). Nonhydrocarbon 

compounds such as sulfur and sulfur compounds are also found. Additives such as antioxidants, metal 

deactivators, fuel system icing inhibitors, corrosion inhibitors, and static dissipator additives are all 

present in limited quantities in jet fuels in order to improve performance (CRC 1984). 
JET FUELS JP-4 AND JP-7 64 

3. CHEMICAL AND PHYSICAL INFORMATION
 

Information regarding the chemical identity of JP-4 and JP-7 is located in Tables 3-l and 3-2, 

respectively. 

3.2 PHYSICAL AND CHEMICAL PROPERTIES 

Information regarding the physical and chemical properties of JP-4 and JP-7 is located in Tables 3-3 

and 3-4, respectively. Information regarding the major components of JP-4 derived from petroleum 

and shale oil is presented in Table 3-5. Depending on the origin of the crude and the production 

method, there could be considerable compositional variability between fuel oils of the same grade (Air 

Force 1988b). This variation is reflected in the allowed military specifications (mil spec) for JP-4 and 

JP-7 fuel oils as shown in Tables 3-6 and 3-7, respectively, and in the compositional variability of 

JP-4 fuels as shown in Tables 3-5 and 3-8. 










JET FUELS JP-4 AND JP-7 75 

4. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

4.1 PRODUCTION 

Jet fuels are primarily derived from crude oil, the common name for liquid petroleum. These jet fuels 

can be referred to as petroleum-derived jet fuels. Jet fuels can also originate from an organic material 

found in shale, called kerogen or petroleum solids: that can be converted by heat to shale oil. Jet fuels 

from this source are called shale-derived jet fuels (Hoffman 1983). Jet fuels are typically made by 

blending and refining various crude oil petroleum distillation products such as naphtha, gasoline, or 

kerosene in order to meet specific military or commercial specifications (Air Force 1989b). Since 

there is great variability in the concentrations of major components of crude oil, there is also a great 

variation in the final jet fuel product (Air Force 1989b). Therefore, there are many types of each jet 

fuel, and each jet fuel is not specified by chemical composition (Air Force 1989b; CRC 1984). JP-4 is 

a naphtha-type fuel made by blending straight-run kerosene streams with lower boiling distillates to fit 

the specifications given in Table 3-6 (Air Force 1989b; IARC 1989). JP-4 is known as a wide-cut 

fuel; it is made from the distillation products obtained over a wide range of temperatures and has a 

broad spectrum of hydrocarbon chain lengths varying from C4 to C16 (Air Force 1989b; CONCAWE 

1985). JP-4 is also made by blending and refining shale oil distillate streams (Stallard and Krautter 

1984). JP-7 is made by blending kerosene distillates in order to achieve a product containing a 

maximum of 5% aromatics by volume and a maximum total weight of 0.1% sulfur (CRC 1984; IARC 

1989). Once jet fuels are made, they are often transported through pipelines to terminals where 

additional substances such as metal deactivators, electrical conductivity additives, and fuel system 

icing inhibitors are added to the mixture (IARC 1989). 

In 1970, total U.S. production of military and commercial jet fuels was approximately 38 million 

metric tons (IARC 1989). Production in the United States steadily increased over the next 15 years to 

about 57 million metric tons in 1985. Data on amounts of JP-4 and JP-7 produced during this 15-year 

period, as well as data on current production volumes of JP-4 and JP-7, are not available. 

Data on specific manufacturers of JP-4 and JP-7 are not available. In 1978, the Standard Oil 

Company (SOHIO, Cleveland, Ohio) refined 87,000 barrels of crude shale oil to produce different fuel 

oils including jet fuels (Stallard and Krautter 1984). However, no report was located in the literature 
JET FUELS JP-4 AND JP-7 76 

4. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL
 

that would indicate shale has been mined or retorted on a commercial scale for the production of jet 

fuels in recent years. 

Since JP-4 and JP-7 are not required to be reported under SARA Section 313, there are no data for 

JP-4 and JP-7 in the Toxics Release Inventory (TRI 1993). 

4.2 IMPORT/EXPORT 

Import volumes of naphtha-type jet fuels such as JP-4 decreased considerably between 1981 and 1983 

(ITC 1985). Total amounts of naphtha-type jet fuels imported into the United States were ≈2.7 million 

barrels in 1981, ≈1.9 million barrels in 1982, and 322,000 barrels in 1983. Current import data for 

JP-4 and JP-7 are not available. No export data were located for JP-4 or JP-7. 

4.3 USE 

Aviation turbine fuels such as JP-4 and JP-7 were not used until the 1930s when the first turbojet 

engine was developed (IARC 1989). Jet-powered aircraft had only limited use in World War II, but 

further military and commercial developments brought jet engines to the forefront as power sources 

for aircraft in the 1960s. The Air Force has used turbine-powered aircraft, which require the use of 

aviation turbine fuels such as JP-4 and JP-7, for over 25 years (Gleason and Martone 1979). 

Both JP-4 and JP-7 are used exclusively as military aviation fuels by the U.S. military, especially the 

U.S. Air Force (Air Force 1989b; IARC 1989). However, there are indications that JP-4 has been 

used and stored at one U.S. Coast Guard Facility (Grand Traverse County, Michigan) (Twenter et al. 

1985). JP-4 is a wide-cut fuel that meets operational requirements and offers a broad availability in 

the event of a war (CRC 1984; Dukek 1978). JP-4 is used in military aircraft such as the F-4 (Air 

Force 1981h). JP-7 is a kerosene fuel used by the Air Force for specific applications that require high 

thermal stability. Since JP-7 has a high flashpoint, it is used in supersonic Air Force aircraft (CRC 

1984; Dukek 1978). 

At one time, the U.S. Department of Defense consumed approximately 2.7% of the total petroleum 

products made in the United States (Gleason and Martone 1979). Approximately 50%, or 250,000 
JET FUELS JP-4 AND JP-7 77 

4.PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL
 

barrels per day, has been used as JP-4. JP-4 has constituted 85% of the turbine fuels used by the 

Department of Defense (Air Force 1989b). 

4.4 DISPOSAL 

Since JP-4 and JP-7 have been widely used by the U.S. Air Force, disposal information for JP-4 and 

JP-7 involves mostly the disposal of JP-4 released into the air, water, or soil in the case of accidental 

spills and normal aircraft operations. 

Vapors generated in tank truck loading of JP-4 can be disposed of by the installation of a vapor 

recovery system (NIOSH 1989). Runoff of jet fuels from loading and unloading aircraft operations 

can be separated by an on-site oil/water separation system. 

Several methods have been investigated for the disposal of JP-4 spilled onto soil from normal aircraft 

operations or from accidental spills. One method, in situ soil venting, involves using vacuum blowers 

to pull large amounts of air through soil contaminated with JP-4 (Elliot and DePaoli 1990). The air 

pulls out the soil gas, and the JP-4 contaminants volatilize as a result of disrupted equilibrium. 

Freeproduct extraction of JP-4 from soil and subsequent off-site cement kiln incineration have also 

been investigated as a means of disposal of JP-4 spills in soil and groundwater (EPA 1990b). Another 

process called in-situ bioventing, whereby oxygen is delivered by forced air movement through the 

contaminated unsaturated soils to stimulate in-situ biodegradation in an otherwise oxygen-limited 

zone, has been successfully applied to a contaminated test site (Air Force 1992). Thermophilic 

cornposting in the presence of horse manure and chicken manure has shown considerable promise for 

treating JP-4 contaminated soil (McMullen and Regan 1992). Excavation of soil contaminated with 

JP-4 and subsequent incineration at an approved EPA hazardous waste incineration site is another 

means of disposal that has been investigated for JP-4 (EPA 1990b). Additional information on the 

EPA hazardous waste regulations that apply to JP-4, JP-7 and incineration practices is available in 

Chapter 7. 

Biodegradation of JP-4 in groundwater has also been investigated as a means to treat contaminated 

groundwater (EPA 1990b). This process involves the extraction of JP-4 from contaminated 

groundwater, addition of nutrients for subsequent reinjection, and in situ biodegradation of the volatile 

organic compounds found in JP-4. Carbon adsorption is another suggested method of treatment of 
JET FUELS JP-4 AND JP-7 78 

4. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

JP-4 in which activated carbon is injected into JP-4 contaminated groundwater. The activated carbon 

is later removed along with the JP-4. 
JET FUELS JP-4 AND JP-7 79 

5. POTENTIAL FOR HUMAN EXPOSURE 

5.1 OVERVIEW 

JP-4 and JP-7 are complex mixtures of hydrocarbons whose environmental fate depends primarily on 

the specific chemical and physical properties of their individual components. The individual 

components can be categorized into basic groups (paraffins, cycloparaffins, aromatics, and olefins), 

and these groups are common to both jet fuels. No information on the environmental fate of JP-7 was 

located. However, since the hydrocarbon groups making up the two compounds are similar, JP-7 can 

be expected to behave similarly to JP-4. 

Jet fuel may be released to the environment by in-flight jettisoning of fuel and from spills or leaks to 

soil or water. Jet fuel jettisoned from planes can be transported by the wind. Some of it is 

transformed photochemically to ozone and other components of smog. It has been shown to form 

aerosols as a result of reactions with atmospheric chemicals, but the specific composition of the 

particulate material is not known. Most of the jet fuel released to water evaporates to the air. The 

components with the lowest boiling points volatilize most rapidly (e.g., short-chain alkanes, 

aromatics). Those with higher boiling points (e.g., branched alkanes, long-chain alkanes) persist 

longer in the water. Some of the hydrocarbons making up jet fuel are soluble in water (e.g., the 

aromaticsbenzene, toluene, and xylene). Under turbulent water conditions, the more soluble 

hydrocarbons remain dissolved longer and may partition to sediment or be biodegraded. The primary 

degradative fate process for jet fuel components in soil is biodegradation. While volatilization is 

expected to be the dominant fate process for these fuels from soil surfaces, biodegradation will 

become increasingly dominant as the soil depth increases. Some components of these fuels also 

migrate through the soil to groundwater. 

Hydrocarbons associated with JP-4 and JP-7 have been detected in air in closed buildings where the 

fuels were being used or burned. Organic compounds found in JP-4 have been detected in 

groundwater following JP-4 leaks and spills. Hydrocarbons associated with JP-4 have also been found 

in soil surrounding fuel spill and leak sites. No data were located on the contamination of food, fish, 

shellfish, or terrestrial plants or animals. 
JET FUELS JP-4 AND JP-7 80 

5. POTENTIAL FOR HUMAN EXPOSURE
 

The National Occupational Exposure Survey conducted by NIOSH between 1980 and 1983 estimated 

that 4,866 employees had the potential to be exposed to JP-4 in the workplace (NOES 1990). 

Populations most likely to be exposed to JP-4 and JP-7 include those involved in jet fuel 

manufacturing or refueling operations, populations working or living on Air Force bases where the 

fuels are used and stored (and where leaks or spills are likely to occur), and those living or working 

near waste sites where the fuels are dumped. 

JP-4 has been found in at least 4 of the 1,397 NPL hazardous waste sites that have been proposed for 

inclusion on the EPA National Priorities List (NPL) (HazDat 1994). JP-7 has not been found in any 

NPL site. However, the number of NPL sites evaluated for JP-4 and JP-7 is not known. The 

frequency of these sites within the United States can be seen in Figure 5-1. 

5.2 RELEASES TO THE ENVIRONMENT 

JP-4 and JP-7 are fuel mixtures used by the U.S. military as aviation fuels. As a result of normal 

aircraft operations and fuel storage, JP-4 and JP-7 can be released into the environment. Under some 

conditions, it is common practice for aircraft to jettison excess fuel, releasing it into the environment 

(IARC 1989). 

Since JP-4 and JP-7 releases are not required to be reported under SARA Section 313, there are no 

data for JP-4 and JP-7 in the Toxics Release Inventory (TRI 1993). 

5.2.1 Air 

JP-4 may be released into the atmosphere as vapors in loading and unloading operations in closed 

aircraft shelters (Air Force 1981h; NIOSH 1989). Releases into the air may also occur as a result of 

evaporation of JP-4 from contaminated soils or other spill sites (Air Force 1984b). 

5.2.2 Water 

JP-4 and JP-7 may be released into groundwaters as a result of seepage from contaminated soils during 

storage, aircraft maintenance, and fuel storage and dispensing operations (Twenter et al. 1985). A fuel 

layer of approximately 2 feet was identified in groundwater from shallow wells at Robins Air Force 

JET FUELS JP-4 AND JP-7 82 

5. POTENTIAL FOR HUMAN EXPOSURE
 

Base (Georgia) on a site where an undetermined amount of JP-4 was released into the soil from an 

underground fuel supply line in the 1960s (Air Force 1985a). 

Groundwater intrusions of JP-4 were reported to have occurred as a result of cracks in the gunnite 

lining of the diked area surrounding three aboveground storage. tanks at the Niagara Falls Air Force 

Reserve Facility in New York (Air Force 1983a). Additional JP-4 was found in storm water drainings 

at the facility from underground inlet pipe, and in&t and outlet pipe leaks discovered in 1979 and 

1982, respectively. Hydrocarbon groundwater contamination from leaking pipes in a JP-4 fuel farm 

occurred in a residential area surrounding the U.S. Navy air station in Traverse City, Michigan 

(Sammons and Armstrong 1986). 

5.2.3 Soil 

JP-4 and JP-7 may be released into soil as a result of leaks in underground or aboveground storage 

tank systems. In October 1975, approximately 83,000 gallons of JP-4 were lost from the bottom of a 

newly cleaned, aboveground storage tank at the Defense Fuel Supply Center in Charleston, South 

Carolina (Talts et al. 1977). Investigation of the soil revealed that JP-4 had moved through porous 

soil to a depth of approximately 7-14 feet. In 1972, approximately 42,000 gallons of JP-4 were 

released into the soil as a result of an external pipe leak at O’Hare Air Reserve Forces Facility, Illinois 

(Air Force 1983b). The dike had accumulated excess water as a result of heavy rains, and a drop in 

temperature caused the water to freeze and crush external piping to the tank. An undetermined 

amount of JP-4 was released into the soil from a leak in a 4-inch diameter pipe in 1965 at Robins Air 

Force Base (Air Force 1985a). Approximately 27,000 gallons of JP-4 were released into the soil in 

January 1985 as a result of an automatic filling system malfunction which caused underground storage 

tanks to overfill at Hill Air Force Base in Utah (Elliot and DePaoli 1990). 

5.3 ENVIRONMENTAL FATE 

5.3.1. Transport and Partitioning 

Since JP-4 and JP-7 are mixtures of hydrocarbons, their movement in the environment is actually a 

function of the chemical and physical properties of the component hydrocarbons. Following release of 

jet fuel to air, water, or soil, the component hydrocarbons partition relatively independently of each 
JET FUELS JP-4 AND JP-7 83 

5. POTENTIAL FOR HUMAN EXPOSURE
 

other based on their respective vapor pressures, solubilities, and Henry’s law and sorption constants. 

For JP-4 and JP-7 mixtures, these values are ranges based on the component hydrocarbons. 

Information on the specific physical and chemical properties of several of the component 

hydrocarbons (e.g., benzene, toluene, xylene, naphthalene, etc.) can be found in the ATSDR 

toxicological profiles for these chemicals. The hundreds of hydrocarbons making up JP-4 and JP-7 

fuel mixtures can be divided into a few groups of hydrocarbon classes with similar properties (Air 

Force 1989b; CRC 1984). These include paraffins (saturated straight-chain hydrocarbons), 

cycloparaffins (saturated cyclic hydrocarbons), aromatics (fully unsaturated six-carbon ring 

compounds), and olefins (unsaturated straight-chain and cyclic hydrocarbons). Paraffins and 

cycloparaffins are the major components and comprise about 90% of JP-4 by volume (79% by weight) 

(Air Force 1989b). Aromatics make up about 10-25% by volume of JP-4 but only about 5% of JP-7 

(Air Force 1989b; IARC 1989); however, the specific composition of these fuels varies among 

manufacturers and probably between batches (Cooper et al. 1982). Jet fuel may also contain low and 

variable levels of nonhydrocarbon contaminants and additives such as sulfur compounds, gums, 

alcohols, naphthenic acids, antioxidants, metal deactivators, and icing and corrosion inhibitors (CRC 

1984; IARC 1989). The variability in the composition contributes to the difficulty in making general 

conclusions about the fate and transport processes of these fuels in the environment. 

Most of the principal JP-4 component hydrocarbons rapidly evaporate from water following a spill. 

Tests with both petroleum- and shale-derived JP-4 under various environmental conditions all showed 

volatilization of JP-4 component hydrocarbons to be the dominant fate process (Air Force 1987b, 

1988b; EPA 1985). Complete evaporation of benzene, toluene, and p-xylene occurred within 24 hours 

in shake-flask experiments using water from three natural sources (EPA 1985). Ninety percent of the 

JP-4 evaporated within 6 days under the laboratory conditions used (Air Force 1988b). As expected, 

the hydrocarbons with the lowest boiling points evaporated most rapidly. Simulated spills of JP-4 to 

water suggested that most JP-4 component hydrocarbons evaporated within l-2 weeks following 

release (Air Force 1981f). In a model petroleum-derived JP-4 fuel spill into a natural freshwater 

sample, initial concentrations of total dissolved hydrocarbons were about 1 mg/L. At 1 and 2 weeks 

following the simulated spill, concentrations did not exceed 0.005 mg/L for any of the measured fuel 

components. This was attributed to the high volatility of the fuel. Shake-flask experiments have 

shown that increased dissolved organic carbon decreases the rate of hydrocarbon evaporation (Air 

Force 1988b). Laboratory experiments have shown that the evaporation rate of jet fuel and its 

components increases with wind velocity and, to a lesser extent, with temperature and fuel-layer 
JET FUELS JP-4 AND JP-7 84 

5. POTENTIAL FOR HUMAN EXPOSURE 

thickness (Air Force 1988d). Comparisons of dissolution and evaporation rates under several 

windspeed and mixing conditions showed that evaporation was the dominant fate process for jet fuel 

components in water. 

JP-4 also evaporates from soil, although evaporation is not as important a fate process in soil as it is in 

water. A model soil core ecosystem was treated with JP-4 to simulate a spill (Air Force 1981e, 

1982c). Headspace above the soil core revealed hydrocarbons from the JP-4 indicating that 

evaporation of component hydrocarbons had occurred. In model soil core ecosystems, volatilization 

accounted for 7% of the hydrocarbon loss compared to 93% for biodegradation (Coho 1990). 

Some downward migration of JP-4 component hydrocarbons occurred in model soil core ecosystems 

treated with JP-4 to mimic a spill and watered to simulate rainfall (Air Force 1982c). Of nine 

hydrocarbons monitored for vertical migration through the core, only n-pentadecane and n-heptane 

migrated the 50 cm to the bottom of the core. They were first found at this depth 197 days following 

initiation of the experiment. These two compounds also persisted in the soil longer than the other 

hydrocarbons monitored. n-Decane, n-undecane, dodecane, n-tridecane, and n-tetradecane were found 

only at 10 cm below the surface. They were observed for 50-134 days following onset of the 

experiment and were not detected again. Additional data obtained by leachate collection indicated that 

the migration of hydrocarbons was best explained by channeling effects caused by biota and/or 

physical stresses since there was no direct correlation between leachate collection and hydrocarbon 

transport. Additional evidence for vertical migration of jet fuel hydrocarbons through soil comes from 

their detection in groundwater following leaks and spills to surface soil (EPA 1990b; Talts et al. 

1977). Horizontal and vertical migration through soil has been confirmed by detection of JP-4 

hydrocarbons in soil several meters from the spill site (EPA 1988a, 1990b). 

The difficulties of determining the fate of JP-4 and its components are epitomized by the problems in 

determining the composition of its water-soluble fraction. Various results are likely to be obtained by 

different investigators even when the fuel tested and the methods used appear to be similar. Seventeen 

hydrocarbons were detected in an analysis of the water-soluble fractions of shale-derived and 

petroleum-derived JP-4, with the most abundant hydrocarbons being benzene, methylbenzene, and 

3-methylhexane (Air Force 1988b). In contrast, only benzene, toluene, and p-xylene were found in 

significant concentrations in the water-soluble fraction of JP-4 (origin not specified) in laboratory 

simulations of field conditions, although other hydrocarbons could be detected (EPA 1985). The 
JET FUELS JP-4 AND JP-7 85 

5. POTENTIAL FOR HUMAN EXPOSURE 

aqueous concentration of JP-4 components under spill conditions was found to depend on the 

solubility of the individual components, the mixing of the mixture due to wind speed, the thickness of 

the fuel layer, the ionic strength of the aqueous solution, and the rate of evaporation of components 

(Air Force 198%). Laboratory experiments simulating a JP-4 spill to water measured both evaporation 

and dissolution of components under slow and fast wind speeds and under conditions that enhanced 

complete mixing. Under both conditions, only the component aromatics (benzene, toluene, 

ethylbenzene, and xylene) were soluble enough to-be detected in the aqueous phase before evaporative 

processes reduced their concentrations below detectable limits. Concentration measurements of these 

components in both the fuel and water suggested that, in general, the concentration of the lighter 

aromatics decreased in the fuel layer and increased in the water phase until evaporation began to 

substantially affect their concentration in the aqueous phase. Heavier aromatics initially decreased in 

the fuel but then increased as the lighter aromatics decreased. Aqueous concentrations increased over 

time and generally reached higher levels, and their evaporation was not as rapid. Increased wind 

speed increased both dissolution and evaporation of JP-4 components, but evaporation was increased 

substantially more than dissolution (a 5fold increase for evaporation compared to a 2-3-fold increase 

for dissolution). At both wind speeds, evaporation was dominant with rates on the order of mg/minute 

compared to dissolution rates in the pg/minute range. When sea water was used as the test medium, 

results were similar; however, the concentrations of the hydrocarbons dissolved in sea water were 

considerably less than when distilled water was used. This was attributed to the effect of high ionic 

strength on the solubility of the hydrocarbons. Increased thickness of the fuel layer increased the 

concentration of the dissolved hydrocarbons because evaporation was reduced. This increased the 

contact time between fuel components and the water. Solubility has also been found to increase with 

increasing concentrations of dissolved organic carbon (Air Force 1988b). 

Movement of JP-4 on and in water was found to affect the important processes of evaporation and 

dissolution of JP-4 components. Variations in wind speed, the force responsible for mixing of fuel, 

created eddies in the aqueous medium that caused non-uniform variations in concentration of fuel 

components with water depth and increased evaporation. Experiments that examined spreading rate of 

a fuel film on water indicated that spreading was very rapid (Air Force 1988d). Tests showed that 

spreading was initially uniform, but as evaporative effects became noticeable, spreading became less 

uniform and the film eventually disintegrated. Rapid spreading reduced dissolution of the fuel by 

increasing evaporation and decreasing contact time. 
JET FUELS JP-4 AND JP-7 86 

5. POTENTIAL FOR HUMAN EXPOSURE
 

The data on the role of sediments in the fate of JP-4 and its components are contradictory. However, 

partitioning of jet fuel hydrocarbons to sediment does not seem to be an important fate process (Air 

Force 1981f; EPA 1985). Some data suggest that, under certain conditions, JP-4 hydrocarbons may 

adsorb to sediment and reduce volatilization (Air Force 1988b; EPA 1985). Quiescent bottle tests 

using natural water from a salt water marsh, a brackish polluted bay, and a freshwater river showed 

that volatility was reduced in sterile controls containing water and sediment compared to sterile 

controls containing only water (Air Force 1988b). “In contrast, when undisturbed or shaken gently, 

flasks containing water and sediment, or water only, and sterile control flasks containing water from 

the same sources exhibited no difference in the rate of disappearance of components (EPA 1985). 

When the flasks were shaken vigorously to imitate turbulent water conditions, volatilization of some 

components was reduced in the flasks with sediment and water compared to the flasks containing 

water only. Field and laboratory data on sediment that was dosed with JP-4 and then either returned 

to the pond or introduced to model laboratory systems indicate that sediment interaction of JP-4 

components occurs and affects the volatility of JP-4. Sediment interactions increased persistence of 

JP-4 components to as much as 20 days in the field tests. Differences between laboratory and field 

data indicated that laboratory data were not good predictors of what would occur in the field. 

Evidence acquired using simulated petroleum- and shale-derived jet fuels indicates that neither the 

major representative components nor the JP-4 mixture have strong adsorption to standard clays or to 

sediments from natural fresh, brackish, or salt water sources (Air Force 1981f). The data also 

indicated that the magnitude of the adsorption constant on a particular sediment was dependent on the 

size and complexity of the dissolved hydrocarbon, the nature of the sediment, and the salinity of the 

water and inversely correlated with the water solubility of the dissolved hydrocarbon. Temperature 

and pH did not appear to have an effect on adsorption. 

There are no bioconcentration data on JP-4 or JP-7; however, JP-8 was found to accumulate in flagfish 

exposed to concentrations ranging from 1.0 to 6.8 mg/L in the surrounding water from the egg stage to 

128 days after hatching (Klein and Jenkins 1983). Similar results would be expected for JP-4 because 

of the similarity in composition and chemical and physical properties of these two fuels. The mean 

concentration of JP-8 in the whole-body tissue samples increased with increasing concentration of the 

water-soluble fraction (WSF) of the fuel. The bioconcentration factor (BCF), expressed as the ratio of 

the concentration in fish tissue to the concentration of the WSF of JP-8 in the aqueous environment, 

was found to be 159 (log value = 2.2). An additional experiment in adult flagfish exposed to 

2.54 mg/L for a 14-day period yielded a BCF of 130 (log value = 2.1). The concentrations in liver, 
 

JET FUELS JP-4 AND JP-7 87 

5. POTENTIAL FOR HUMAN EXPOSURE
 

muscle, and whole-body tissue following the 14-day exposure were 448, 165, and 329 mglkg wet 

weight of tissue. Placement of the fish in uncontaminated water showed a depuration rate similar to 

the accumulation rate. In 14 days, whole-body tissue levels of JP-8 were reduced by about 10%. 

Similar experiments in rainbow trout did not show a relationship between concentrations of JP-8 in the 

surrounding water and the whole-body concentration in the fish. The calculated BCF for trout was 

only 63-112 (log value of 1.8-2.1) indicating that the WSF of JP-8 does not concentrate as readily in 

this species. 

5.3.2 Transformation and Degradation 

5.3.2.1 Air 

JP-4 has been found to react photochemically in air in the presence of nitrogen oxide compounds to 

form ozone (Air Force 1981b, 1982e; Carter et al. 1984). The formation of ozone decreased with 

increasing altitude, decreasing temperature, and decreasing ultraviolet light intensity. Initial 

experiments suggested that the nitrous oxide oxidation rates decreased with increasing pressure and 

decreasing temperature. However, further tests indicated that the temperature effect may have been an 

artifact of the radical source used in the simulation and that the nitrous oxide oxidation rate caused by 

JP-4 may actually increase with altitude. Therefore, the effect of temperature on the nitrous oxide 

oxidation rate is uncertain. Reactions of JP-4 in the air resulted in the formation of large amounts of 

aerosol material (Air Force 1981b). 

5.3.2.2 Water 

Data on the biodegradation of JP-4 components are mixed. Evidence from experiments using the WSF 

of JP-4 and water from three different natural sources (a pristine salt water marsh, a polluted brackish 

bay, and a pristine freshwater river) did not show any biodegradation (Air Force 1983f; EPA 1985). 

The authors of these studies attributed this to the rapid evaporation of the components from the water. 

In quiescent tests on the WSF of JP-4, biodegradation was observed in several flasks, but different 

results were obtained with water and/or sediment from different sources. In most tests, ethylbenzene, 

trimethylbenzene, and 1,4-dimethylethylbenzene were degraded. Benzene, cyclohexane, and toluene 

seemed to be more resistant to biodegradation. When the sample flasks were vigorously shaken to 

enhance hydrocarbon-sediment interactions, evidence of biodegradation of some of the component 
JET FUELS JP-4 AND JP-7 88 

5. POTENTIAL FOR HUMAN EXPOSURE
 

hydrocarbons was observed. In general, the more substituted benzenes (e.g., p-xylene, ethylbenzene, 

methylethylbenzene, trimethylbenzene) and less volatile hydrocarbons seemed to be biodegraded. 

Some components were also biodegraded in similarly shaken, water-only flasks. There were some 

differences in biodegradation among the three water samples used, and biodegradation could not be 

detected in the polluted bay water. The variable results obtained with the three water sources, varying 

conditions, and inclusion or exclusion of sediment make it difficult to assess the relative importance of 

biodegradation of jet fuel in water. It is apparent, ‘however, that biodegradation of at least some of the 

JP-4 hydrocarbons does occur. Sediment appeared to decrease biodegradation. Similar experiments 

using water from the same three sources supported evidence that biodegradation of JP-4 component 

hydrocarbons did occur (Air Force 1988b). Disappearance of hydrocarbons from the experimental 

flasks was compared to sterile flasks containing the same type of water or water/sediment. 

Measurement of biodegradation rates was difficult to determine because evaporation rates were so 

rapid. However, some differences between experimental and control flasks were observed and 

inclusion of selected radiolabeled hydrocarbons supported the assertion that biodegradation did occur 

and could play a role in removal of JP-4 hydrocarbons from aquatic systems, particularly under 

conditions that reduce volatility. 

A comparison of field and laboratory data obtained from experiments on natural sediment dosed with 

JP-4 suggested that biodegradation did not occur in the field (Air Force 1987b). This was in contrast 

to laboratory data with the same sediment in which biodegradation was observed. The study authors 

determined that the conflicting results indicated that laboratory tests (quiescent bottles and plexiglass 

trays) were not good predictors of field behavior of JP-4 and its components. Studies of shallow water 

aquifers contaminated with JP-4 indicate that the mixture does not inhibit microbial activity and that 

selective aerobic biodegradation of component hydrocarbons may occur (Aelion and Bradley 1991). 

Results indicated that biodegradation might be limited by the available nitrogen in the ecosystem. 

Samples from a contaminated aquifer have also been shown to degrade aromatic JP-4 components 

under denitrifying (anaerobic) conditions, although at a very low rate (Hutchins et al. 1991). 

5.3.2.3 Sediment and Soil 

Considerable evidence exists to indicate that jet fuel is biodegraded in the soil. This is not unexpected 

since several components of jet fuel are known to be degraded by soil microorganisms. Application of 

shale-derived JP-4 to model soil core ecosystems resulted in increased production of carbon dioxide in 
JET FUELS JP-4 AND JP-7 89 

5. POTENTIAL FOR HUMAN EXPOSURE
 

the system (Air Force 1981e, 1982c). Increased activity following addition of JP-4 to soil has been 

associated with increased microbial growth and decreased hydrocarbon residues (Song and Bartha 

1990; Wang and Bartha 1990). The likely reason for this increase was increased activity of 

microorganisms that use the JP-4 component hydrocarbons. Laboratory comparisons of soil 

contaminated with JP-4 and uncontaminated soil showed that both degraded JP-4 hydrocarbons under 

aerobic conditions when nitrogen, phosphorus, and trace minerals were added (Yong and Mourato 

1987). The uncontaminated soil had a lag time before biodegradation was initiated, whereas the 

contaminated soil showed immediate initiation of biodegradation. These data indicate the importance 

of microbial adaptation to biological breakdown of jet fuel in soil. Additional experiments in 

nonaerated soils showed that biodegradation of JP-4 hydrocarbons occurred under these conditions but 

was considerably reduced compared to degradation in aerated soils. Other studies have supported the 

evidence that most JP-4 degradation is aerobic (Song and Bartha 1990). In these experiments, 

decreased biodegradation in subsurface soils was associated with decreased oxygen. Model soil core 

ecosystems composed of contaminated soil taken from the site of a JP-4 spill were tested for 

biodegradation under a range of soil and water content conditions (Coho 1990). Two columns were 

vented with a mix of oxygen and nitrogen, and a control column was vented with nitrogen only. The 

venting rates were kept low to reduce losses through volatilization. An average of 44% of the original 

mass of JP-4 present in the soil (3,560 mg/kg moist soil; 4,590 mg/kg dry soil) was removed over the 

Sl-89-day experimental period. Biodegradation accounted for 93% of the total removed and 

volatilization accounted for 7%. The maximum rate of biodegradation, 14.3 mg/kg moist soil/day, 

occurred at a soil/water content of 72% saturation. The average rate of degradation due to microbial 

activity was about 10.6 mg/kg moist soil/day. Biodegradation of JP-4 has also been shown to be 

affected by soil type, temperature, and jet fuel concentration (Song et al. 1990). Biodegradation was 

greater in clay soil than sand or loam. The optimum temperature was 27 °C, with decreased 

degradation at higher and lower temperatures. The half-life of JP-4 in clay at 27 oC was 3.5 weeks. 

Bioremediation treatment to increase the oxygen and mineral content of the soil decreased the half-life 

to 1.7 weeks. Some products of JP-4 metabolism appeared to be inhibitory to the microbiota, resulting 

in slightly decreased biodegradation rates at higher fuel concentrations (Song and Bartha 1990). At a 

concentration of 50 mg/g dry soil, 85% of the JP-4 had disappeared in 4 weeks, and with a 

concentration of 135 mg/g dry soil, 75% was degraded in 4 weeks. The components of JP-4 fuel 

found to be biodegradable in soil were tridecane, tetradecane and pentadecane, but undecane, 

dodecane and hexadecane were resistant to aerobic biodegradation (Dean-Ross 1993). Although 

anaerobic biodegradation of components in JP-4 fuel is slower than aerobic biodegradation, anaerobic 
JET FUELS JP-4 AND JP-7 90 

5. POTENTIAL FOR HUMAN EXPOSURE
 

biodegradation of JP-4 fuel was observed in sediments. The carbon mineralization rate was most 

favorable at an added nitrate concentration of approximately 1 mmol and a pH of 6-7 (Bradley et al. 

1992). 

5.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT 

JP-4 and JP-7 consist of various hydrocarbon components such as benzene, toluene, and xylene. 

These components can be measured in high concentrations in air, water, and soil. 

5.4.1 Air 

JP-4 and JP-7 enter the atmosphere through various mechanisms such as evaporation of spills, 

vaporization in loading and unloading operations, and burning in engines. JP-4 was detected in 

samples in a closed aircraft shelter that housed F-4 aircraft (Air Force 1981h). The JP-4 

concentrations in the air ranged from 533 mg/m3

 (in the area of the shelter) to 1,160 mg/m3 (in the 

vicinity of the refueler technician). 

5.4.2 Water 

Between 1986 and 1988, a hydrocarbon plume of JP-4 was discovered floating on the water table at 

the Federal Aviation Administration (FAA) Technical Center (Atlantic County, New Jersey) after JP-4 

fuel contamination was discovered (EPA 1990b). The organic contaminants benzene, toluene, and 

naphthalene (identical to the components in jet fuel) were detected in groundwater samples at 

concentrations of 4,000, 3,100, and 1,000 ppb, respectively. The total volume of jet fuel-contaminated 

groundwater at the site was estimated to be 13.3 million gallons. In October of 1975, JP-4 was 

detected in water samples taken from the Defense Fuel Supply Center (Charleston, South Carolina) at 

a depth of 15 feet and at distances of 2.5 feet, 40 feet, and 50 feet from an 83,000-gallon fuel spill 

(Talts et al. 1977). From a distance of 25 feet, pure fuel was measured, while a concentration of 

33 μg/mL was measured at 40 feet, and 22 μg/mL was measured at 50 feet. 

Groundwater contamination was reported in East Bay Township, Michigan, in the vicinity of a U.S. 

Coast Guard Air Station (Twenter et al. 1985). The amount of toluene detected in groundwater 

samples was 74 μg/L. This concentration may possibly be attributed to JP-4 contamination, although 
JET FUELS JP-4 AND JP-7 91 

5. POTENTIAL FOR HUMAN EXPOSURE
 

there were many other organics used on the base that could be sources of major groundwater 

contamination. 

5.4.3 Soil 

JP-4 as determined by total hydrocarbons in soil samples was detected at Robins Air Force Base 

(Georgia) at a depth of 1 meter in the soil around the site of a 20-year-old JP-4 spill; concentrations 

ranged from <0.1 μg/L at an approximate distance of 90 meters from the spill site to 180,000 μg/L 

within the vicinity of the fuel spill (EPA 1988a). Soil gas samples taken at 2 meters revealed a 

concentration ranging from <0.05 μg/L at an approximate distance of 50 meters from the fuel spill to a 

concentration of 310,000 μg/L in the vicinity of the fuel spill. Soil contamination of JP-4 

hydrocarbons was also measured at the FAA Technical Center (Atlantic County, New Jersey); the 

maximum petroleum hydrocarbon concentration detected in surface soils was 284 ppm and the 

maximum concentration in subsurface soils was 18,500 ppm (EPA 1990b). 

5.4.4 Other Environmental Media 

No data were located that discussed concentrations of JP-4 or JP-7 in other environmental media such 

as food, fish and shellfish, or terrestrial plants and animals. 

5.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE 

The National Occupational Exposure Survey, conducted by NIOSH between 1981 and 1983, estimated 

that 4,866 employees were exposed to JP-4 in the workplace (NOES 1990). No workplace exposure 

data were available for JP-7. 

General population exposure to JP-4 and JP-7 is likely. However, exposure would be limited to 

populations living on or near Air Force bases where JP-4 and JP-7 are used in aircraft. These 

populations could be exposed to JP-4 and JP-7 from hydrocarbon release into air from aircraft or 

groundwater contaminated with spilled JP-4 or JP-7. 
JET FUELS JP-4 AND JP-7 92 

5. POTENTIAL FOR HUMAN EXPOSURE 

5.6 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES 

Air Force base workers engaged in fuel cell maintenance operations such as defueling and fueling 

aircraft and cleaning jet fuel spills are exposed to higher levels of JP-4 and JP-7 than those to which 

the general population is exposed (Bishop 1982). Other workers that are exposed to higher levels of 

JP-4 and JP-7 than the general population are component testers, engine testers, and mechanics (Knave 

et al. 1978). Maintenance workers who monitor fuel storage tanks may be exposed to jet fuels by 

inhalation or dermal exposure to draining water (due to condensation) from the fuel tanks (NIOSH 

1989). Potentially high exposure through inhalation and dermal route may also occur for workers in 

petroleum plants that manufacture JP-4 and JP-7. Populations living on or very near Air Force bases, 

populations living near hazardous waste disposal sites for JP-4 and JP-7, and populations exposed as a 

result of spills and leaks that may occur during storage, transfer, and use of the these jet fuels are 

potentially exposed to higher levels of JP-4 and JP-7 than those to which the general population is 

exposed. However, data correlating the levels of these fuels or their biomarkers in body tissues and 

fluids (e.g., blood) with levels of exposure among these groups of population were not located. 

Military pilots have a potentially higher risk of exposure to JP-4 and JP-7 than the general population. 

The concentration of JP-4 vapors sampled from the cockpit of an F-4 was 1,110 mg/m3 (Air Force 

1981h). 

5.7 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with 

the Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of JP-4 and JP-7 is available. Where adequate information 

is not available, ATSDR, in conjunction with NTP, is required to assure the initiation of a program of 

research designed to determine the health effects (and techniques for developing methods to determine 

such health effects) of JP-4 and JP-7. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that, if met, 

would reduce or eliminate the uncertainties of human health assessment. This definition should not be 

interpreted to mean that all data needs discussed in this section must be filled. In the future, the 
JET FUELS JP-4 AND JP-7 93 

5. POTENTIAL FOR HUMAN EXPOSURE
 

identified data needs will be evaluated and prioritized, and a substance-specific research agenda may 

be proposed. 

5.7.1 Identification of Data Needs 

Physical and Chemical Properties. The values for many of the physicochemical parameters 

(e.g., Kow Koc and Henry’s law constants) needed to model the fate and transport processes of JP-4 and 

JP-7 in the environment have not been determined. However, since these fuels are complex mixtures 

of hydrocarbons with small amounts of non-hydrocarbon additives, their behavior in the environment 

is determined by both the characteristics of the mixture and the characteristics of the individual 

components, making modeling based on physical and chemical properties difficult. 

Production, Import/Export, Use, and Release and Disposal. Current production and 

import/export data are lacking and would aid in determining how pervasive the risk of exposure to 

JP-4 and JP-7 is to the general population. The uses of JP-4 and JP-7 are restricted to military aircraft 

(Air Force 1989b; IARC 1989). The primary releases to the environment come from in-flight 

jettisoning of fuel and from leaks and spills during storage, transfer, and use (IARC 1989; Talts et al. 

1977; Twenter et al. 1985). Several disposal methods have been proposed, tested, and/or used (Elliot 

and DePaoli 1990; EPA 1990b; NIOSH 1989). However, data are needed on the risk posed by past 

disposal methods and improper disposal of the fuels. 

According to the Emergency Planning and Community Right-to-Know Act of 1986, 42 U.S.C. Section 

11023, industries are required to submit chemical release and off-site transfer information to the EPA. 

The Toxics Release Inventory (TRI), which contains this information for 1992, became available in 

May of 1994. This database will be updated yearly and should provide a list of industrial production 

facilities and emissions. However, since JP-4 and JP-7 are not reported under SARA Section 313, 

there are no data in the TRI. 

Environmental Fate. The environmental fate of JP-4 has been studied extensively by the Air 

Force, EPA, and independent researchers. No data were located on the environmental fate of JP-7, 

although it can be assumed to behave in a manner similar to JP-4. Most JP-4 jettisoned in the 

atmosphere probably reacts photochemically to form ozone and particulates (Air Force 1981b, 1981e). 

Some of the fuel components or reactant products are probably transported by wind currents. The 
JET FUELS JP-4 AND JP-7 94 

5. POTENTIAL FOR HUMAN EXPOSURE
 

primary fate process for JP-4 in water is volatilization, although some biodegradation and partitioning
 

to sediment may occur (Air Force 1983f, 1988b; EPA 1985). The primary fate process for JP-4
 

spilled to soil is biodegradation (Air Force 1982c; Coho 1990; Song and Bartha 1990). A small
 

fraction is likely to volatilize and some components may bind to soil particles. JP-4 that spills or
 

leaks to soil migrates both horizontally and vertically, but that migration does not seem to be due
 

primarily to leaching. Information on the degradation products of some of the components of JP-4 and
 

JP-7 may be found in ATSDR profiles on benzene (ATSDR 1991a), toluene (ATSDR 1990), total
 

xylenes (ATSDR 1991c), and polycyclic aromatic hydrocarbons (ATSDR 1991b). Components of jet
 

fuel that migrate through the soil may contaminate groundwater (EPA 1990b; Talts et al. 1977). More
 

information on chemical and light-mediated reactions of jet fuel components would help in assessing
 

the persistence of jet fuel hydrocarbons in water and soil. In addition, more studies on the
 

environmental fate of jet fuel under various water and soil conditions might provide insight into the
 

variations in the fate of components that have been found under varying environmental conditions.
 

Specifically, data pertaining to the interaction of JP-4 or JP-7 with various types of soils, including
 

clays, sands, and mixtures would be useful, in order to determine horizontal and vertical migration
 

patterns for assessing groundwater contamination in the vicinity of Air Force bases and hazardous
 

waste sites. This information could also help in determining which jet fuel components persist in the
 

environment and under what conditions.
 

Bioavailability from Environmental Media. There are no data on the absorption of JP-4 or
 

JP-7 by the inhalation, oral, or dermal routes. However, several of the components of these fuels are
 

known to be absorbed. For more information on absorption of individual components (e.g., benzene,
 

xylene, toluene), see the ATSDR toxicological profiles on these compounds.
 

Food Chain Bioaccumulation. There are no data on the bioaccumulation or biomagnification of
 

JP-4 or JP-7 in plants, aquatic organisms, or animals. Studies on the bioaccumulation of JP-4 and
 

JP-7 are needed for plants, animals, and aquatic organisms, especially shellfish which, historically,
 

have exhibited sensitivity to hydrocarbons. Data on a similar jet fuel, JP-8, suggest that
 

bioaccumulation and biomagnification are low (Klein and Jenkins 1983). The mixtures are expected to
 

separate into the individual components in the environment and these components are expected behave
 

independently and differently in terms of their ability to accumulate in the food chain. For
 

information on the bioaccumulation of the different components of JP-4 and JP-7 (e.g., benzene,
 

xylene, toluene, ethylbenzene), see the ATSDR toxicological profiles for these compounds.
 
JET FUELS JP-4 AND JP-7 95 

5. POTENTIAL FOR HUMAN EXPOSURE
 

Exposure Levels in Environmental Media. Some information exists on the levels of JP-4 and 

JP-7 in the air in closed buildings where the fuel is used (Air Force 1981h). Limited information was 

also located on levels in water and soil following spills or leaks (EPA 1988a, 1990b; Talts et al. 

1977). No data were located on levels of jet fuels or component hydrocarbons in food, fish and 

shellfish, or terrestrial animals and plants. More data on levels in all environmental media are needed 

to fully assess the extent of exposure for populations with a high probability of exposure to jet fuels or 

their component hydrocarbons. 

Exposure Levels in Humans. Certain populations are known to have a higher risk of exposure 

to JP-4, JP-7, and/or their component hydrocarbons. These are workers who manufacture or use the 

fuel; people living or working on Air Force bases where the fuel is stored and used; and populations 

living or working in the vicinity of a spill, leak, or dump site (Air Force 1981h; Bishop 1982; NIOSH 

1989). More data are needed to assess the approximate levels of intermediate and chronic exposure 

for these populations. 

Exposure Registries. No exposure registries for JP-4 and JP-7 were located. Components of 

JP-4 and JP-7 will be considered for inclusion in the National Exposure Registry in the future. The 

information that is amassed in the National Exposure Registry facilitates the epidemiological research 

needed to assess adverse health outcomes that may be related to exposure to these compounds. 

5.7.2 Ongoing Studies 

Investigations into the bioremediation of sites contaminated with jet fuels are providing information 

on the biodegradation of these compounds. Bioremediation studies are being conducted by the 

Department of the Interior, U.S. Geological Survey at a spill site in Charleston, South Carolina 

(FEDRIP 1994). 

As part of the Third National Health and Nutrition Evaluation Survey (NHANES III), the 

Environmental Health Laboratory Sciences Division of the Center for Environmental Health and 

Injury Control, Centers for Disease Control and Prevention, will be analyzing human blood samples 

for certain components of JP-4 and JP-7 and other volatile organic compounds. These data will give an 

indication of the frequency of occurrence and background levels of these compounds in the general 

population. 

JET FUELS JP-4 AND JP-7 97 

6. ANALYTICAL METHODS
 

The purpose of this chapter is to describe the analytical methods that are available for detecting and/or 

measuring and monitoring JP-4 and JP-7 in environmental media and in biological samples. The 

intent is not to provide an exhaustive list of analytical methods that could be used to detect and 

quantify JP-4 and JP-7. Rather, the intention is to identify well-established methods that are used as 

a the standard methods of analysis. Many of the analytical methods used to detect JP-4 and JP-7 in 

environmental samples are the methods approved by federal organizations such as EPA and the 

National Institute for Occupational Safety and Health (NIOSH). Other methods presented in this 

chapter are those that are approved by groups such as the Association of Official Analytical Chemists 

(AOAC) and the American Public Health Association (APHA). Additionally, analytical methods are 

included that refine previously used methods to obtain lower detection limits, and/or to improve 

accuracy and precision. 

6.1 BIOLOGICAL SAMPLES 

No analytical methods were located for detecting either JP-4 or JP-7 in biological samples. For 

analytical methods information on some hydrocarbon components of jet fuels, see the ATSDR 

toxicological profiles for benzene (ATSDR 1991a), toluene (ATSDR 1990), xylenes (ATSDR 1991c), 

and polycyclic aromatic hydrocarbons (ATSDR 1991b). 

6.2 ENVIRONMENTAL SAMPLES 

Since JP-4 and JP-7 are composed of a complex mixture of hydrocarbons, there are few methods for 

the analysis of all of these components in environmental samples, but methods are reported for the 

analysis of some of the individual components or the amount of total hydrocarbon in the mixture 

(IARC 1989). The analysis of individual components usually involves separation of the components 

by column chromatography (i.e., packed or capillary column) followed by a suitable quantification 

method. These methods included gas chromatography (GC) and high-resolution gas chromatography 

(HRGC) combined with flame ionization detector (FID), or infrared (IR) spectroscopy. GC combined 

with mass spectrometry (MS) has been used to identify the principal hydrocarbon components present 

in jet fuels. Nuclear magnetic resonance (NMR), supercritical fluid chromatography (SFC)/FID, and 

laser raman spectroscopy can be used specifically to characterize the aromatic hydrocarbon makeup 

for 
JET FUELS JP-4 AND JP-7 98 

6. ANALYTICAL METHODS
 

JP-4 and JP-7 (Clarke et al. 1991; Di Sanzo and Yoder 1991; DOE 1981). Although no methods were 

located specifically for analyzing JP-7 in environmental samples, the methods used to measure the 

hydrocarbon components of JP-4 can be used for measuring the hydrocarbon components of JP-7. The 

few analytical methods that have been used are summarized in Table 6-l. Several of the jet fuel 

components have been discussed in detail in their individual ATSDR toxicological profiles (e.g., 

benzene and polycyclic aromatic hydrocarbons), which should be consulted for more information on 

analytical methods (ATSDR 1991a, 1991b). 

Analytical methods for detecting JP-4 and jet fuel (petroleum naphtha and kerosene vapors) in air 

include IR spectroscopy and GC/FID (IARC 1989; NIOSH 1984; Thomas and Richardson 1981). The 

total hydrocarbon content of JP-4 in air can be determined by IR spectroscopy. The IR technique is 

best adapted to pure hydrocarbon exposures, such as exposure to JP-4. For both methods, samples are 

collected with either charcoal tubes or vapor monitor badges. Poor recovery (<75%) was obtained 

with the IR method using only Freon®113 as a desorbent. Recovery was improved (86-88%) using a 

mixture of Freon®1 13 and perchloroethylene. For the IR method, precision was excellent, ranging 

from 0.006% to 0.020% coefficient of variation (CV). Recoveries with the GCLFID method were 

excellent (97-101%) (NIOSH 1984; Thomas and Richardson 1981). For the GC/FID method, 

precision was also excellent (0.052% relative standard deviation [RSD]) (NIOSH 1984). Sensitivity 

for both methods is in the ppm range (IARC 1989; NIOSH 1984; Thomas and Richardson 1981). 

GC/FID, HRGCLFID, and IR spectroscopy have been used to measure JP-4 in water (Puyear et al. 

1981; Roberts and Thomas 1986). GCLFID was used to measure the major water-soluble 

hydrocarbons, the aliphatics and alkylbenzenes, of JP-4 (Puyear et al. 1981). The average recovery of 

all hydrocarbons tested (aliphatics and alkylbenzenes) was 43-72%; however, the recovery of the 

aliphatics only was 90-94% (Puyear et al. 1981). Overall recovery was improved from 43% to 72% 

with the use of ethyl acetate as an extraction solvent for JP-4. Under the chromatographic conditions 

used, the individual aliphatics were not well resolved. However, the alkylbenzenes were well 

separated and quantitation of each component was possible (Puyear et al. 1981). Sensitivity and 

precision were not reported (Puyear et al. 1981). The total hydrocarbon content of JP-4 in water can 

also be determined by IR spectroscopy (EPA 1978; Roberts and Thomas 1986) and fluorescence 

spectroscopy (ASTM 1982). Since JP-4 has a distinctive gas chromatographic profile, it is possible to 

distinguish JP-4 from other fuels present in environmental samples by examining selected peak areas 

or peak ratios for certain hydrocarbons (Roberts and Thomas 1986). 

JET FUELS JP-4 AND JP-7 100 

6. ANALYTICAL METHODS
 

GC/FID has been used to quantify JP-4 in soil samples, while GC/MS has been used to identify the 

principal components in JP-4 (Vandegrift and Kampbell 1988). Sample preparation for GC/FID 

included extracting the fuel from soil with methylene chloride in an ultrasonic bath. Recovery was 

good (83.9%). Precision was adequate (12.6% CV). Sensitivity was in the low-ppm range 

(Vandegrift and Kampbell 1988). 

Other methods reported for the analysis of the aromatic components in aircraft fuels, including JP-4, 

include HRGC combined with an ultraviolet detector (UVD), photoionization detector (PID), and GC 

combined with a nitrogen specific alkali-flame detector (AFD) (Air Force 1982a). Sample preparation 

includes fractionation of the fuel into an aromatic fraction and a nonaromatic fraction. The 

fractionation is accomplished by using adsorption column chromatography with silica gel, alumina, or 

Florisil. The aromatic fraction is then eluted using moderately polar solvents such as methylene 

chloride, benzene, or ethyl ether. The UV detector is specific for aromatic compounds. The estimated 

detection limits for benzenes and naphthalenes were 10 μg/mL and 2 μg rnL, respectively. Precision 

ranged from 5% to 10%. The photoionization detector is about 10 times as sensitive as a UVD or FID 

for the detection of aromatic hydrocarbons, although it does not provide the selectivity obtainable with 

the UVD. Nitrogen-containing compounds in fuels are detected using a nitrogen-specific AFD. A gas 

chromatographic method involving the simultaneous use of a UVD, FID, and AFD was recommended 

as a rapid, inexpensive, and selective method for the analysis of aircraft fuels (Air Force 1982a). 

6.3 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with 

the Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of JP-4 and JP-7 is available. Where adequate information 

is not available, ATSDR, in conjunction with NTP, is required to assure the initiation of a program of 

research designed to determine the health effects (and techniques for developing methods to determine 

such health effects) of JP-4 and JP-7. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that, if met, 

would reduce or eliminate the uncertainties of human health assessment. This definition should not be 
JET FUELS JP-4 AND JP-7 101 

6. ANALYTICAL METHODS
 

interpreted to mean that all data needs discussed in this section must be filled. In the future, the 

identified data needs will be evaluated and prioritized, and a substance-specific research agenda may 

be proposed. 

6.3.1 Identification of Data Needs 

Methods for Determining Biomarkers of Exposure and Effect. No biomarkers of exposure 

were identified for JP-4 or JP-7. No standard procedures exist for identifying or quantifying exposure 

to JP-4 or JP-7 in biological media. Therefore, it is not possible to state whether existing methods are 

sensitive to measure background levels in the population or levels at which health effects occur. 

Biomonitoring studies are needed to adequately assess exposure to JP-4 and JP-7. 

No biomarkers of effect were found for JP-7. Potential biomarkers for neurological effects of JP-4 are 

mild muscular weakness, staggering gait, and decreased sensitivity to painful stimuli (Davies 1964). 

No standard procedures exist for identifying and quantifying these biomarkers of effect for JP-4. 

Methods for Determining Parent Compounds and Degradation Products in 

Environmental Media. Methods exist for measuring the hydrocarbon components of jet fuels, 

specifically JP-4, in air, water, and soil (IARC 1989; NIOSH 1984; Puyear et al. 1981; Roberts and 

Thomas 1986; Thomas and Richardson 1981; Vandegrift and Kampbell 1988). Although no methods 

were located specifically for analyzing JP-7 in environmental samples, the methods used to measure 

the hydrocarbon components of JP-4 can be used for measuring the hydrocarbon components of JP-7. 

These methods are relatively sensitive, selective, and reliable and can be used to detect the levels of jet 

fuel components found in the environment and levels at which health effects occur. Sensitivity and 

precision data are needed for measuring the components in water. These data will aid in comparison 

of sensitivity and precision between methods and indicate where improvements in sensitivity are 

needed. This information will be useful in monitoring contamination in the environment, 

6.3.2 Ongoing Studies 

The Environmental Health Laboratory Sciences Division of the Center for Environmental Health and 

Injury Control, Centers for Disease Control and Prevention, is developing methods for the analysis of 

certain components of JP-4 and JP-7 and other volatile organic compounds in blood. These methods 
JET FUELS JP-4 AND JP-7 102 

6. ANALYTICAL METHODS 

use purge and trap methodology and magnetic sector mass spectrometry which gives detection limits
 

in the low parts per trillion range.
 

No other ongoing studies were located for JP-4 or JP-7.
 
JET FUELS JP-4 AND JP-7 103 

7. REGULATIONS AND ADVISORIES
 

The international, national, and state regulations and guidelines regarding JP-4 and JP-7 in air, water, 

and other media are summarized in Table 7- 1. There are only a few regulations that are specific to 

JP-4 and JP-7, but there are more regulations on the major components of JP-4 and JP-7. 

ATSDR has derived an intermediate-duration inhalation MRL of 9 mg/m3

 for JP-4, based on an 

increase in hepatic toxicity observed in mice at 500 mg/m3

 (Air Force 1984b). 

ATSDR has derived a chronic-duration inhalation MRL of 0.3 mg/m3

 for JP-7, based on an increase in 

hepatic toxicity observed in rats at 150 mg/m3

 (Air Force 1991). 

Under the Hazardous Materials Transportation Act, aviation fuel is designated as a hazardous 

substance subject to special requirements for packaging, labeling, and transportation (DOT 1989). 

EPA has established guidelines to control air pollution from aircraft and aircraft engines (EPA 1982e, 

1982f) and underground storage tank regulations for petroleum products (EPA 1988e). 

______________________ 

JET FUELS JP-4 AND JP-7 105 

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*DOE. 198 1. Hydrocarbon type analysis of jet fuels by 1H and 13-C NMR. Laramie, WY: Laramie 

Energy Technology Center, U.S. Department of Energy. Document no. DOE/LETC/RI-81-1. 
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*EPA. 1982a. Overview summary compound L13-B. Washington, DC: U.S. Environmental 

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*EPA. 1985. Biodegradation of jet fuel by aquatic microbial communities. Report no. 

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*EPA. 1986b. Guidelines for carcinogen risk assessment. U.S. Environmental Protection Agency. 

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*EPA 1988b. General pretreatment regulations. U.S. Environmental Protection Agency. Code of 

Federal Regulations. 40 CFR 403.2 Appendix B. 
JET FUELS JP-4 AND JP-7 113 

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*EPA 1988c. Conventional pollutants. U.S. Environmental Protection Agency. Code of Federal 

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EPA. 1990a. Interim methods for development of inhalation reference doses. Washington, DC: U.S. 

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Fajen JM, McCammon CS. 1988. Exposure characterization study of workers exposed to hydrazines. 

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chromosome aberration frequencies in Chinese hamster ovary (CHO) cells. Washington DC: U.S. 

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*Galloway SM. 1982b. Mutagenicity evaluation of L14-B in an in vitro cytogenetic assay measuring 

chromosome aberration frequencies in Chinese hamster ovary (CHO) cells. Washington DC: U.S. 

Environmental Protection Agency, Office of Toxic Substances. Document no. 88-8100388. 

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*Hoffman HL. 1983. Petroleum and its products. Chapter 14 In: Kent JA, ed. Riegel’s handbook 

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Holm S, Norbaeck D, Frenning B, et al. 1987. Hydrocarbon exposure from handling jet fuel at some 

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*Hutchins SR, Sewell GW, Kovacs DA, et al. 1991. Biodegradation of aromatic hydrocarbons by 

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*Jagannath DR. 1982. Mutagenicity evaluation of L13-B in the Ames salmonella/microsome plate 

test. Washington DC: U.S. Environmental Protection Agency, Office of Toxic Substances. 

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*Kinkead ER, DiPasquale LC, Vernot EH, et al. 1974. Chronic toxicity of JP-4 jet fuel. Proceedings 

of the Annual Conference of Environmental Toxicology 5: 145-154. 

*Klein SA, Jenkins D. 1983. The toxicity of jet fuels to fish: II. The toxicity of JP-8 to flagfish 

(Jordanella floridae) and rainbow trout (Salmo gairdneri) and golden shiners (Noternigonus 

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*Knave B, Olson BA, Elofsson S, et al. 1978. Long-term exposure to jet fuel: II. A cross-sectional 

epidemiologic investigation on occupationally exposed industrial workers with special references to 

the nervous system. Stand J Work Environ Health 4:19-45. 

*MacNaughton MG, Uddin DE. 1984. Toxicology of mixed distillate and high-energy synthetic 

fuels: Renal effects of petroleum hydrocarbons. Adv Mod Environ Toxicol 7:121-132. 

*Martel CR. 1992. Written communication (June 4) to Diane Mandell, Clement Associates Inc., 

regarding physical characteristics of JP-4 and JP-7. Retired, U.S. Air Force, Aero Propulsion and 

Power Directorate, Wright Laboratory, Wright-Patterson Air Force Base, OH. 

Martone JA. 1986. USAF toxicology research on petroleum and shale-derived aviation gas turbine 

fuels. Journal of Engineering for Gas Turbines and Power 198:387-390. 

*McMullen PT, Regan RW. 1992. Thermophilic composting of a synthetic JP-4 fuel mixture. In: 

46th Purdue Industrial Waste Conference Proceedings. Chelsea, MI: Lewis Publishers, Inc. 

Moler JL, Steward EM. 1989. Thermal-decomposition studies of jet fuel components: Dodecane, 

octane, 2-methylundecane, and bicyclohexyl. Abstracts of Papers of the American Chemical Society 

198:P18-PETR. 

*NAS/NRC. 1989. Biologic markers in reproductive toxicology. National Academy of Sciences/ 

National Research Council. Washington, DC: National Academy Press, 15-35. 

NASA. 1980. Analysis of NASA JP-4 fire tests data and development of a simple fire model. 

Hampton, VA: National Aeronautics and Space Association, Langley Research Center. Issue 

NASA-CR-159209, 58. 
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*Newton PE, Becker SV, Hixon CJ. 1991. Pulmonary function and particle deposition and clearance 

in rats after a 90-day exposure to shale-oil-derived jet fuel JP-4. Inhalation Toxicol 3:195-210. 

*NFPA. 1986. Jet fuels. In: Fire protection guide on hazardous materials. 9th edition. 

325M:623-624. Quincy, MA: National Fire Protection Association. 

*NIOSH. 1984. NIOSH manual of analytical methods. 3rd edition. Washington, DC: U.S. 

Government Printing Office, National Institute for Occupational Safety and Health, 2: 1550-l-5. 

Publication no. 84-100. 

*NIOSH. 1989. Industrial hygiene survey report of defense fuel support point. Cincinnati, OH: 

Centers for Disease Control, National Institute of Occupational Safety and Health, Division of 

Surveillance, Hazard Evaluations, and Field Studies. 

*NOES. 1990. National Occupational Exposure Survey (1981-1983). Cincinnati, OH: U.S. 

Department of Health and Human Services, National Institute for Occupational Safety and Health. 

Odkvist LM, Arlinger SD, Edling C, et al. 1987. Audiological and vestibulo-oculomotor findings in 

workers exposed to solvents and jet fuel. Scandinavian Audiology 16:75-81. 

*OHM/TADS. 1985. JP-4. Oil and Hazardous Material/Technical Assistance Data System. 

Chemical Information Systems, Inc., Baltimore, MD. December, 1985. 

*Olson MJ, Johnson JT, Reidy CA. 1990. A comparison of male rat and human urinary proteins: 

Implications for human resistance to hyaline droplet nephropathy. Toxicol Appl Pharmacol 

102:524-536. 

*OSHA. 1989. Air contaminants. Occupational Safety and Health Administration. Code of Federal 

Regulations. 29 CFR part 1910.1000. 

*OTA. 1990. Neurotoxicity: Identifying and controlling poisons of the nervous system. Office of 

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*Puyear RL, Fleckenstein KJ, Montz WE Jr, et al. 1981. Use of reverse phase C-18 minicolumns for 

concentrating water-soluble hydrocarbons. Bull Environ Contam Toxicol 27:790-797. 

*Rabenold C. 1982. Mutagenicity evaluation of L14-B in the Ames salmonella/microsome plate test. 

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88-8100388. 

Rifai HS, Bedient PB, Wilson JT, et al. 1988. Biodegradation modeling at aviation fuel spill site. 

Journal of Environmental Engineering 114(5): 1007-1029. 

*Roberts AJ, Thomas TC. 1986. Characterization and evaluation of JP-4, jet A and mixtures of these 

fuels in environmental water samples. Environ Toxicol Chem 5:3-l 1. 

*RTECS. 1994a. JP-4. Registry of Toxic Effects of Chemical Substances. U.S. Department of 

Health and Human Services, National Institute for Occupational Safety and Health, Washington, DC. 
JET FUELS JP-4 AND JP-7 116 

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*RTECS. 1994b. JP-7. Registry of Toxic Effects of Chemical Substances. U.S. Department of 

Health and Human Services, National Institute for Occupational Safety and Health, Washington, DC. 

*Sammons JH, Armstrong JM. 1986. Aviation fuel contamination of groundwater: A case history of 

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York, NY: Van Nostrand Reinhold, 3:2075. 

Sewell G, Smith G, Gibson S. 1989. Biodegradation of jet fuel under anaerobic conditions. In: 89th 

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glucocorticoid: The responses of hepatic alpha-2p-globulin and pituitary growth hormone differ in 

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*Short BG, Burnett VL, Cox MG, et al. 1987. Site-specific renal cytotoxicity and cell proliferation in 

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*Song H-G, Wang X, Bartha R. 1990. Bioremediation potential of terrestrial fuel spills. Appl 

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*Talts A, Bauer J, Martin C, et al. 1977. Discovery, containment and recovery of a jet fuel storage 

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Washington, DC: American Petroleum Institute, 259-263. 
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*Thomas TC, Richardson AI. 1981. An infrared analysis method for the determination of 

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*Tupper CR. 1989. Chemical hazards in aeromedical aircraft. Aviat Space Environ Med 60:73-75. 

*Twenter FK, Cummings TR, Grannemann NG. 1985. Groundwater contamination in East Bay 

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Investigations. 

*Van Doren G, Mertens B, Heyns W, et al. 1983. Different forms of alpha-2p-globulin in male and 

female rat urine. Eur J Biochem 134:175-181. 

*Vandegrift SA, Kampbell DH. 1988. Gas chromatographic determination of aviation gasoline and 

JP-4 jet fuel in subsurface core samples. J Chromatogr Sci 26:566-569. 

*Walter MK. 1982a. Primary eye irritation study E-l, E-3, E-5, and E-13B. Washington, DC: U.S. 

Environmental Protection Agency, Office of Toxic Substances. Document no. 88-8200416. 

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Protection Agency, Office of Toxic Substances. Document no. 88-8200416. 

*Walter MK. 1982c. Skin sensitization study E-l, E-3, E-5, and E-13B. Washington, DC: U.S. 

Environmental Protection Agency, Office of Toxic Substances. Document no. 88-8200416. 

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*Yong RN, Mourato D. 1987. Stimulation of microbial biodegradation in a jet fuel contaminated 

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Management. Cincinnati, OH: U.S. Environmental Protection Agency, 131-147. 

JET FUELS JP-4 AND JP-7 119 

9. GLOSSARY
 

Acute Exposure -- Exposure to a chemical for a duration of 14 days or less, as specified in the 

Toxicological Profiles. 

Adsorption Coefficient (Koc) -- The ratio of the amount of a chemical adsorbed per unit weight of 

organic carbon in the soil or sediment to the concentration of the chemical in solution at equilibrium. 

Adsorption Ratio (Kd) -- The amount of a chemi”Ea1 adsorbed by a sediment or soil (i.e., the solid 

phase) divided by the amount of chemical in the solution phase, which is in equilibrium with the solid 

phase, at a fixed solid/solution ratio. It is generally expressed in micrograms of chemical sorbed per 

gram of soil or sediment. 

Bioconcentration Factor (BCF) -- The quotient of the concentration of a chemical in aquatic 

organisms at a specific time or during a discrete time period of exposure divided by the concentration 

in the surrounding water at the same time or during the same period. 

Cancer Effect Level (CEL) -- The lowest dose of chemical in a study, or group of studies, that 

produces significant increases in the incidence of cancer (or tumors) between the exposed population 

and its appropriate control. 

Carcinogen -- A chemical capable of inducing cancer. 

Ceiling Value -- A concentration of a substance that should not be exceeded, even instantaneously. 

Chronic Exposure -- Exposure to a chemical for 365 days or more, as specified in the Toxicological 

Profiles. 

Developmental Toxicity -- The occurrence of adverse effects on the developing organism that may 

result from exposure to a chemical prior to conception (either parent), during prenatal development, or 

postnatally to the time of sexual maturation. Adverse developmental effects may be detected at any 

point in the life span of the organism. 

Embryotoxicity and Fetotoxicity -- Any toxic effect on the conceptus as a result of prenatal exposure 

to a chemical; the distinguishing feature between the two terms is the stage of development during 

which the insult occurred. The terms, as used here, include malformations and variations, altered 

growth, and in utero death. 

EPA Health Advisory -- An estimate of acceptable drinking water levels for a chemical substance 

based on health effects information. A health advisory is not a legally enforceable federal standard, 

bnt serves as technical guidance to assist federal, state, and local officials. 

Immediately Dangerous to Life or Health (IDLH) -- The maximum environmental concentration of 

a contaminant from which one could escape within 30 min without any escape-impairing symptoms or 

irreversible health effects. 

Intermediate Exposure -- Exposure to a chemical for a duration of 15-364 days, as specified in the 

Toxicological Profiles. 
JET FUELS JP-4 AND JP-7 120 

9. GLOSSARY
 

Immunologic Toxicity -- The occurrence of adverse effects on the immune system that may result 

from exposure to environmental agents such as chemicals. 

In Vitro -- Isolated from the living organism and artificially maintained, as in a test tube. 

In Vivo -- Occurring within the living organism. 

Lethal Concentratiorq(LO) (LC50) -- The lowest concentration of a chemical in air which has been 

reported to have caused death in humans or animals. 

Lethal Concentratioq(LO) (LC50) -- A calculated concentration of a chemical in air to which exposure 

for a specific length of time is expected to cause death in 50% of a defined experimental animal 

population. 

Lethal Dose(LO) ( LD50) -- The lowest dose of a chemical introduced by a route other than inhalation 

that is expected to have caused death in humans or animals. 

Lethal Dose(LO) (LD50) -- The dose of a chemical which has been calculated to cause death in 50% of 

a defined experimental animal population. 

Lethal Time(LO) ( LT50) -- A calculated period of time within which a specific concentration of a 

chemical is expected to cause death in 50% of a defined experimental animal population. 

Lowest-Observed-Adverse-Effect Level (LOAEL) -- The lowest dose of chemical in a study, or 

group of studies, that produces statistically or biologically significant increases in frequency or 

severity 

of adverse effects between the exposed population and its appropriate control. 

Malformations -- Permanent structural changes that may adversely affect survival, development, or 

function. 

Minimal Risk Level -- An estimate of daily human exposure to a dose of a chemical that is likely to 

be without an appreciable risk of adverse noncancerous effects over a specified duration of exposure. 

Mutagen -- A substance that causes mutations. A mutation is a change in the genetic material in a 

body cell. Mutations can lead to birth defects, miscarriages, or cancer. 

Neurotoxicity -- The occurrence of adverse effects on the nervous system following exposure to 

chemical. 

No-Observed-Adverse-Effect Level (NOAEL) -- The dose of chemical at which there were no 

statistically or biologically significant increases in frequency or severity of adverse effects seen 

between the exposed population and its appropriate control. Effects may be produced at this dose, but 

they are not considered to be adverse. 

Octanol-Water Partition Coefficient (Kow) -- The equilibrium ratio of the concentrations of a 

chemical in n-octanol and water, in dilute solution. 

Permissible Exposure Limit (PEL) -- An allowable exposure level in workplace air averaged over an 

8-hour shift. 
JET FUELS JP-4 AND JP-7 121 

9. GLOSSARY
 

q1 * -- The upper-bound estimate of the low-dose slope of the dose-response curve as determined by 

the multistage procedure. The q1* can be used to calculate an estimate of carcinogenic potency, the 

incremental excess cancer risk per unit of exposure (usually μg/L for water, mg/kg/day for food, and 

μg/m3

 for air). 

Reference Dose (RfD) -- An estimate (with uncertainty spanning perhaps an order of magnitude) of 

the daily exposure of the human population to a potential hazard that is likely to be without risk of 

deleterious effects during a lifetime. The RfD is operationally derived from the NOAEL (from animal 

and human studies) by a consistent application of uncertainty factors that reflect various types of data 

used to estimate RfDs and an additional modifying factor, which is based on a professional judgment 

of the entire database on the chemical. The RfDs are not applicable to nonthreshold effects such as 

cancer. 

Reportable Quantity (RQ) -- The quantity of a hazardous substance that is considered reportable 

under CERCLA. Reportable quantities are (1) 1 pound or greater or (2) for selected substances, an 

amount established by regulation either under CERCLA or under Sect. 3 11 of the Clean Water Act. 

Quantities are measured over a 24-hour period. 

Reproductive Toxicity -- The occurrence of adverse effects on the reproductive system that may 

result from exposure to a chemical. The toxicity may be directed to the reproductive organs and/or the 

related endocrine system. The manifestation of such toxicity may be noted as alterations in sexual 

behavior, fertility, pregnancy outcomes, or modifications in other functions that are dependent on the 

integrity of this system. 

Short-Term Exposure Limit (STEL) -- The maximum concentration to which workers can be 

exposed for up to 15 min continually. No more than four excursions are allowed per day, and there 

must be at least 60 min between exposure periods. The daily TLV-TWA may not be exceeded. 

Target Organ Toxicity -- This term covers a broad range of adverse effects on target organs or 

physiological systems (e.g., renal, cardiovascular) extending from those arising through a single 

limited 

exposure to those assumed over a lifetime of exposure to a chemical. 

Teratogen -- A chemical that causes structural defects that affect the development of an organism. 

Threshold Limit Value (TLV) -- A concentration of a substance to which most workers can be 

exposed without adverse effect. The TLV may be expressed as a TWA, as a STEL, or as a CL. 

Time-Weighted Average (TWA) -- An allowable exposure concentration averaged over a normal 

Shour 

workday or 40-hour workweek. 

Toxic Dose (TD50) -- A calculated dose of a chemical, introduced by a route other than inhalation, 

which is expected to cause a specific toxic effect in 50% of a defined experimental animal population. 

Uncertainty Factor (UF) -- A factor used in operationally deriving the RfD from experimental data. 

UFs are intended to account for (1) the variation in sensitivity among the members of the human 

population, (2) the uncertainty in extrapolating animal data to the case of human, (3) the uncertainty in 

extrapolating from data obtained in a study that is of less than lifetime exposure, and (4) the 

uncertainty in using LOAEL data rather than NOAEL data. Usually each of these factors is set equal 

to 10. 
JET FUELS JP-4 AND JP-7 A-l 

APPENDIX A 

USER’S GUIDE 

Chapter 1 

Public Health Statement 

This chapter of the profile is a health effects summary written in non-technical language. Its intended 

audience is the general public especially people living in the vicinity of a hazardous waste site or 

chemical release. If the Public Health Statement were removed from the rest of the document, it would 

still communicate to the lay public essential information about the chemical. 

The major headings in the Public Health Statement are useful to find specific topics of concern. The 

topics are written in a question and answer format. The answer to each question includes a sentence 

that will direct the reader to chapters in the profile that will provide more information on the given 

topic. 

The descriptive sentences (bullets) at the end of section 1.4 can be used to link significant health 

effects seen in humans and animals to chemical concentration and duration of exposure. These bullets 

give the reader a capsule understanding of the essential exposure-duration-effect relationships that 

have been developed in greater details throughout the rest of the profile. Significant effects at low and 

high doses are presented wherever the data permit. 

Chapter 2 

Tables and Figures for Levels of Significant Exposure (LSE) 

Tables (2-1, 2-2, and 2-3) and figures (2-l and 2-2) are used to summarize health effects and illustrate 

graphically levels of exposure associated with those effects. These levels cover health effects observed 

at increasing dose concentrations and durations, differences in response by species, minimal risk levels 

(MRLs) to humans for noncancer endpoints, and EPA’s estimated range associated with an upperbound individual lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. Use the LSE tables and figures 

for a quick review of the health effects and to locate data for a specific exposure scenario. The LSE 

tables and figures should always be used in conjunction with the text. All entries in these tables and 

figures represent studies that provide reliable, quantitative estimates of No-Observed-Adverse-Effect 

Levels (NOAELs), Lowest-Observed-Adverse-Effect Levels (LOAELs), or Cancer Effect Levels 

(CELs). The legends presented below demonstrate the application of these tables and figures. 

Representative examples of LSE Table 2-l and Figure 2-l are shown. The numbers in the left column 

of the legends correspond to the numbers in the example table and figure. 

LEGEND 

See LSE Table 2-l 

(1) Route of Exposure One of the first considerations when reviewing the toxicity of a substance 

using these tables and figures should be the relevant and appropriate route of exposure. When 

sufficient data exists, three LSE tables and two LSE figures are presented in the document. 

The three LSE tables present data on the three principal routes of exposure, i.e., inhalation, 

oral, and dermal (LSE Table 2-1, 2-2, and 2-3, respectively). LSE figures are limited to the 

inhalation (LSE 
JET FUELS JP-4 AND JP-7 A-2 

APPENDIX A 

Figure 2-l) and oral (LSE Figure 2-2) routes. Not all substances will have data on each route 

of exposure and will not therefore have all five of the tables and figures. 

(2)	 Exposure Period Three exposure periods - acute (less than 15 days), intermediate (15 to 

364 days), and chronic (365 days or more) are presented within each relevant route of 

exposure. In 

this example, an inhalation study of intermediate exposure duration is reported. For quick 

reference to health effects occurring from a known length of exposure, locate the applicable 

exposure period within the LSE table and figure. 

(3)	 Health Effect the major categories of health effects included in LSE tables and figures are 

death, systemic, immunological, neurological, developmental, reproductive, and cancer. 

NOAELs and LOAELs can be reported in the tables and figures for all effects but cancer. 

Systemic effects are further defined in the “System” column of the LSE table (see key number 

18). 

(4)	 Key to Figure Each key number in the LSE table links study information to one or more data 

points using the same key number in the corresponding LSE figure. In this example, the study 

represented by key number 18 has been used to derive a NOAEL and a Less Serious LOAEL 

(also see the 2 ” 18r” data points in Figure 2-l). 

(5)	 Species The test species, whether animal or human, are identified in this column. Section 2.4, 

“Relevance to Public Health,” covers the relevance of animal data to human toxicity and 

Section 2.3, “Toxicokinetics,” contains any available information on comparative 

toxicokinetics. Although NOAELs and LOAELs are species specific, the levels are 

extrapolated to equivalent human doses to derive an MRL. 

(6)	 Exposure Frequency/Duration The duration of the study and the weekly and daily exposure 

regimen are provided in this column. This permits comparison of NOAELs and LOAELs from 

different studies. In this case (key number 18), rats were exposed to JP-4 and JP-7 via 

inhalation for 6 hours per day, 5 days per week, for 3 weeks. For a more complete review of 

the dosing regimen refer to the appropriate sections of the text or the original reference paper, 

i.e., Nitschke et al. 1981. 

(7)	 System This column further defines the systemic effects. These systems include: respiratory, 

cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, and 

dermal/ocular. “Other” refers to any systemic effect (e.g., a decrease in body weight) not 

covered in these systems. In the example of key number 18, 1 systemic effect (respiratory) 

was investigated. 

(8)	 NOAEL A No-Observed-Adverse-Effect Level (NOAEL) is the highest exposure level at 

which no harmful effects were seen in the organ system studied. Key number 18 reports a 

NOAEL of 3 ppm for the respiratory system which was used to derive an intermediate 

exposure, inhalation MRL of 0.005 ppm (see footnote “b”). 

(9)	 LOAEL A Lowest-Observed-Adverse-Effect Level (LOAEL) is the lowest dose used in the 

study that caused a harmful health effect. LOAELs have been classified into “Less Serious” 

and “Serious” effects. These distinctions help readers identify the levels of exposure at which 

adverse health effects first appear and the gradation of effects with increasing dose. A brief 

description of the specific endpoint used to quantify the adverse effect accompanies the 

LOAEL. The respiratory effect reported in key number 18 (hyperplasia) is a Less serious 

LOAEL of 10 ppm. MRLs are not derived from Serious LOAELs. 
JET FUELS JP-4 AND JP-7 A-3 

APPENDIX A 

(10)	 Reference The complete reference citation is given in chapter 8 of the profile. 

(11) CEL A Cancer Effect Level (CEL) is the lowest exposure level associated with the onset of 

carcinogenesis in experimental or epidemiologic studies. CELs are always considered serious 

effects. The LSE tables and figures do not contain NOAELs for cancer, but the text may report 

doses not causing measurable cancer increases. 

(12) Footnotes Explanations of abbreviations or reference notes for data in the LSE tables are 

found in the footnotes. Footnote “b” indicates the NOAEL of 3 ppm in key number 18 was 

used to derive an MRL of 0.005 ppm. 

LEGEND 

See Figure 2-1 

LSE figures graphically illustrate the data presented in the corresponding LSE tables. Figures help the 

reader quickly compare health effects according to exposure concentrations for particular exposure 

periods. 

(13) Exposure Period The same exposure periods appear as in the LSE table. In this example, 

health effects observed within the intermediate and chronic exposure periods are illustrated. 

(14) Health Effect these are the categories of health effects for which reliable quantitative data 

exists. The same health effects appear in the LSE table. 

(15) Levels of Exposure Exposure concentrations or doses for each health effect in the LSE tables 

are graphically displayed in the LSE figures. Exposure concentration or dose is measured on 

the log scale “y” axis. Inhalation exposure is reported in mg/m3 or ppm and oral exposure is 

reported in mg/kg/day. 

(16) NOAEL In this example, 18r NOAEL is the critical endpoint for which an intermediate 

inhalation exposure MRL is based. As you can see from the LSE figure key, the open-circle 

symbol indicates to a NOAEL for the test species-rat. The key number 18 corresponds to the 

entry in the LSE table. The dashed descending arrow indicates the extrapolation from the 

exposure level of 3 ppm (see entry 18 in the Table) to the MRL of 0.005 ppm (see footnote 

“b” in the LSE table). 

(17) CEL Key number 38r is 1 of 3 studies for which Cancer Effect Levels were derived. The 

diamond symbol refers to a Cancer Effect Level for the test species-mouse. The number 38 

corresponds to the entry in the LSE table. 

(18) Estimated Upper-Bound Human Cancer Risk Levels This is the range associated with the 

upper-bound for lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. These risk levels are 

derived from the EPA’s Human Health Assessment Group’s upper-bound estimates of the 

slope of the cancer dose response curve at low dose levels (q1*). 

(19) Key to LSE Figure The Key explains the abbreviations and symbols used in the figure. 


JET FUELS JP-4 AND JP-7 A-6 

APPENDIX A 

Chapter 2 (Section 2.4) 

Relevance to Public Health 

The Relevance to Public Health section provides a health effects summary based on evaluations of 

existing toxicologic, epidemiologic, and toxicokinetic information. This summary is designed to 

present interpretive, weight-of-evidence discussions for human health endpoints by addressing the 

following questions. 

1. What effects are known to occur in humans? 

2. What effects observed in animals are likely to be of concern to humans? 

3. What exposure conditions are likely to be of concern to humans, especially around 

hazardous waste sites? 

The section covers endpoints in the same order they appear within the Discussion of Health Effects by 

Route of Exposure section, by route (inhalation, oral, dermal) and within route by effect. Human data 

are presented first, then animal data. Both are organized by duration (acute, intermediate, chronic). In 

vitro data and data from parenteral routes (intramuscular, intravenous, subcutaneous, etc.) are also 

considered in this section. If data are located in the scientific literature, a table of genotoxicity 

information is included. 

The carcinogenic potential of the profiled substance is qualitatively evaluated, when appropriate, using 

existing toxicokinetic, genotoxic, and carcinogenic data. ATSDR does not currently assess cancer 

potency or perform cancer risk assessments. Minimal risk levels (MRLs) for noncancer endpoints (if 

derived) and the endpoints from which they were derived are indicated and discussed. 

Limitations to existing scientific literature that prevent a satisfactory evaluation of the relevance to 

public health are identified in the Data Needs section. 

Interpretation of Minimal Risk Levels 

Where sufficient toxicologic information is available, we have derived minimal risk levels (MRLs) for 

inhalation and oral routes of entry at each duration of exposure (acute, intermediate, and chronic). 

These MRLs are not meant to support regulatory action; but to acquaint health professionals with 

exposure levels at which adverse health effects are not expected to occur in humans. They should help 

physicians and public health officials determine the safety of a community living near a chemical 

emission, given the concentration of a contaminant in air or the estimated daily dose in water. MRLs 

are based largely on toxicological studies in animals and on reports of human occupational exposure. 

MRL users should be familiar with the toxicologic information on which the number is based. Chapter 

2.4, “Relevance to Public Health,” contains basic information known about the substance. Other 

sections such as 2.7, “Interactions with Other Chemicals”, and 2.8, “Populations that are Unusually 

Susceptible” provide important supplemental information. 
JET FUELS JP-4 AND JP-7 A-7 

APPENDIX A
 

To derive an MRL, ATSDR generally selects the most sensitive endpoint which, in its best judgement, 

represents the most sensitive human health effect for a given exposure route and duration. ATSDR 

cannot make this judgement or derive an MRL unless information (quantitative or qualitative) is 

available for all potential systemic, neurological, and developmental effects. If this information and 

reliable quantitative data on the chosen endpoint are available, ATSDR derives an MRL using the 

most sensitive species (when information from multiple species is available) with the highest NOAEL 

that does not exceed any adverse effect levels. When a NOAEL is not available, a lowest-observedadverse-effect level (LOAEL) can be used to derive an MRL, and an uncertainty factor (UF) of 10 

must be employed. Additional uncertainty factors of 10 must be used both for human variability to 

protect sensitive subpopulations (people who are most susceptible to the health effects caused by the 

substance) and for interspecies variability (extrapolation from animals to humans). In deriving an 

MRL, these individual uncertainty factors are multiplied together. The product is then divided into the 

inhalation concentration or oral dosage selected from the study. Uncertainty factors used in developing 

a substance-specific MRL are provided in the footnotes of the LSE Tables.