MOBILE VIEW  | 

JET FUELS

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) JET FUEL 4 (JP-4; jet propellant 4): General-purpose military aircraft fuel, developed and used by the US Air Force, in limited use. Petroleum - or shale - derived hydrocarbon mixture with performance additives (corrosion inhibitor and de-icing additives). JP-4 has a higher flammability than JP-8. Civilian designation Jet B (without performance additives). JP-4 has been superceded by JP-8 for US Air Force aircraft.
    B) JET FUEL 5 (JP-5; jet propellant 5): High flash point jet fuel. Mixture of wide cut kerosene (blend of gasoline and kerosene). Rarely used except in cold climates.
    C) JET FUEL 7 (JP-7; jet propellant 7): US Air Force military aircraft fuel, for use in specialized supersonic aircraft. Kerosene blend.
    D) JET FUEL 8 (JP-8; jet propellant 8): Main US Air Force jet fuel in use. JP-8 is a kerosene grade fuel. It is the equivalent of civilian Jet A-1 with the addition of corrosion and anti-icing additives. JP-8 is the standard US Air Force aircraft fuel. JP-8 is also used for other military vehicles.
    E) JET A: Kerosene type fuel similar to JET A-1. Same flash point as Jet A-1: 38 degrees C (100 degrees F) with higher freeze point: maximum (-40 degrees C).
    F) JET A-1: Civilian equivalent of JP-8 without additives. Flash point: 38 degrees C (100 degrees F); freeze point maximum of -47 degrees C.
    G) JET B: Fuel distillate covering both naptha and kerosene fractions. With higher flammability than Jet A-1, it is more difficult to handle. May be used in very cold climates.

Specific Substances

    A) JP-4
    1) MIL-T-5624-L-Amd.1 wide cut
    2) JP-4 military (gasoline-type)
    3) References: US Air Force, 1989; IARC, 1989;
    4) Dickson & Woodward, 1987; Dukek, 1978
    JP-5
    1) MIL -T-5624N Grade JP-5, high flash point kerosene,
    2) low volatility
    3) References: US Air Force 1989
    JP-7
    1) MIL-T-38219A-Amd.2, kerosene, low volatility
    2) References: IARC, 1989
    JP-8
    1) MIL-T-83133D, kerosene, low volatility
    2) References: IARC, 1989
    UNSPECIFIED JET FUEL
    1) Usually a kerosene-like petroleum blend, with
    2) performance additives
    3) JET FUEL, MILITARY
    4) AVIATION KEROSENE
    5) JET A
    6) JET FUEL A
    7) TURBO FUEL A
    8) JET A-1
    9) TURBO FUEL A-1
    10) JET KEROSENE
    11) MILITARY JET FUEL
    12) WIDE-CUT JET FUEL

Available Forms Sources

    A) FORMS
    1) COMPOSITION OF J-P4
    a) Complex mixture; petroleum or shale oil wide-cut naphtha type hydrocarbons, mainly in the C-4 to C-16 range (Stallard & Krautter, 1984; CONCAWE, 1985). Actual composition may vary with required performance specifications (CRC & Inc, 1984).
    b) Typical composition of JP-4 is shown in the following table (US Air Force, 1989; IARC, 1989):
    c) Hydrocarbons (C-4 to C-16), consisting of:
    TYPICAL COMPOSITION OF JP-4
    Hydrocarbons (C4 to C-16Paraffins 32% n-alkanes 31% branched alkanes 31% Cycloparaffins (Naphthenes) 16% Benzenes, alkylbenzenes 3% Naphthalenes 5% Olefins <0.5% Benzene (contaminant)
    Sulfur, sulfur compoundsĀ 
    Additivescorrosion and/or icing inhibitors (2-methoxyethanol), metal deactivators, antioxidants, static dissipators (Piacitelli et al,1989)

    d) COMPOSITION OF JP-5
    1) Mixture of parrafinic, aromatic and olefinic hydrocarbons. Actual composition may vary with required performance specifications.
    2) Typical composition of JP-5 is shown in the following table (US Air Force, 1989; (Anon, 2001)):
    1) Parafinic hydrocarbons various 83%
    2) Aromatic hydrocarbons various 15%
    3) Olefinic hydrocarbons various 2%
    e) COMPOSITION OF JP-7
    1) Petroleum hydrocarbons, produced by blending kerosenes (CRC & Inc, 1984; IARC, 1989)
    2) Typical composition of JP-7 is shown in the following table (US Air Force, 1989; IARC, 1989; CRC & Inc, 1984; Piacitelli et al, 1989):
    1) Hydrocarbons
    2) Paraffins
    3) Cycloparaffins
    4) 5% Maximum Aromatics
    5) Olefins
    6) 0.1% Maximum Sulfur, sulfur compounds
    7) Additives: corrosion and/or icing inhibitors (2-methoxyethanol), metal deactivators, antioxidants, static dissipator additives
    f) COMPOSITION OF JP-8
    1) Complex mixture of aliphatic and aromatic hydrocarbons, mainly in the C-6 to C-18 range with 28% in the C9 to C14 n-alkane range (Pliel et al 2000). Actual composition may vary with required performance specifications.
    2) Typical composition of JP-8 is shown in the following table (Pleil et al 2001):
    1) Hydrocarbons (C-6 to C-18):
    2)
    a) 85.5% structural aliphatic isomers C6-C18
    b) 14.5% aromatics
    c) Additives: corrosion and/or icing inhibitors (2-methoxyethanol), metal deactivators, antioxidants, static dissipators (Piacitelli et al, 1989).
    B) SOURCES
    1) Exposure to jet fuel can occur from both occupational and environmental sources. Jet fuel is not used in consumer products. In 1991, JP-4 represented approximately 50% of the total US military consumption of petroleum products (ATSDR, 1991). JP-8 is the most common chemical exposure in the US Air Force for flight crews, ground crews performing preflight duties and maintenance personnel (Pleil et al, 2000).
    2) Sources of OCCUPATIONAL EXPOSURE include:
    a) Transfer operations to storage tanks, tanker trucks or railroad cars, or fueling of aircraft (IARC, 1989);
    b) Inside buildings where aircraft maintenance operations are taking place (US Air Force, 1981);
    c) Operations involving refining, blending, or final formulation of the fuels with additives;
    d) Filling, draining, and maintenance of fuel tanks, maintenance of distribution tanks and pipelines, engine maintenance, and laboratory sampling and analysis (Lombardi & Lurie, 1957; IARC, 1989; Pleil et al, 2000);
    e) Manufacture and/or testing of jet aircraft engines (Struwe et al, 1983; IARC, 1989);
    f) Jet aircraft pilots.
    g) NIOSH has estimated that 9,730 employees were occupationally exposed to JP-4 between 1980 and 1983 (NIOSH, 1990).
    3) ENVIRONMENTAL SOURCES of jet fuels include:
    a) Evaporation or leakage from fuel storage tanks; aircraft fueling operations; in industrial waste streams; or in pipeline, trucking, or railroad leaks or accidents;
    b) Jettison maneuvers from aircraft, or spills on the ground or into surface water in aircraft crashes (IARC, 1989);
    c) Household activities such as bathing, laundering, and cooking with contaminated water, or other activities using contaminated hot water.

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) WITH POISONING/EXPOSURE
    1) Acute exposure to jet fuel can cause CNS depression, headache, dizziness, anxiety, respiratory irritation, and palpitations. Inhalation of liquid hydrocarbons may also induce euphoria, cardiac dysrhythmias, and respiratory arrest. Ingestion may cause potentially fatal aspiration pneumonitis. Human exposure primarily occurs as a result of inhalation or dermal contact.
    a) Effects secondary to aspiration may include hypoxia, infection, pneumatocele formation, and chronic lung dysfunction.
    b) Chronic exposure has been linked with neuropsychiatric disorders.
    c) Chronic exposure to jet fuels has been linked with kidney cancer in humans in one study. Jet fuel is not classified as a confirmed human carcinogen. Potential human reproductive hazards, if any, have not yet been defined.
    d) Similar effects have been seen with petroleum- and shale oil-derived jet fuel in experimental animals.
    e) This review is based on information from JP-4, JP-5, JP-7, JP-8, unspecified jet fuel, and liquid hydrocarbons such as kerosene.
    0.2.4) HEENT
    A) WITH POISONING/EXPOSURE
    1) Jet fuel is slightly irritating to the eyes and nose. Ear loss has been associated with persistent jet fuel exposure.
    0.2.5) CARDIOVASCULAR
    A) WITH POISONING/EXPOSURE
    1) Palpitations have been reported from exposure to jet fuel. Dysrhythmias may occur following inhalation of some hydrocarbons.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Jet fuel vapors are irritating to the respiratory tract.
    2) Ingestion with subsequent pulmonary aspiration may produce pulmonary edema and possibly fatal chemical pneumonitis; this is one of the most serious hazards.
    3) Coughing, choking, tachypnea, dyspnea, cyanosis, rales, hemoptysis, and pulmonary edema may occur following ingestion with pulmonary aspiration of liquid hydrocarbons.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) Transient CNS excitation followed by depression may occur, especially after inhalation of liquid hydrocarbons.
    2) Peripheral sensory neuropathies and motor deficits have been reported from exposure to jet fuel.
    3) Neuropsychiatric abnormalities have been seen. These may include anxiety, memory loss, and irritability.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Liquid Jet fuel is irritating to the stomach.
    0.2.9) HEPATIC
    A) WITH POISONING/EXPOSURE
    1) Liver injury, as manifested by elevated transaminases, may occur following ingestion of liquid hydrocarbons.
    2) Antipyrene clearance has been altered in humans exposed to jet fuel, but clinical liver function was not altered. Experimental animal studies have shown degenerative fatty changes in the liver.
    0.2.10) GENITOURINARY
    A) WITH POISONING/EXPOSURE
    1) Acute renal tubular necrosis, proteinuria, or hematuria occur infrequently following acute hydrocarbon exposure.
    2) Renal effects seen in male rats exposed to jet fuel may not be relevant to humans.
    0.2.13) HEMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Hemolysis may occur with aspiration pneumonitis. Hematologic depression has been seen in experimental animals, but not in humans.
    0.2.14) DERMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Jet fuel is a strong skin irritant and can cause a defatting dermatitis.
    2) Shale-derived jet fuels were dermal sensitizers in guinea pigs. Jet fuels can induce inflammatory responses from dermal application to experimental animals.
    0.2.17) METABOLISM
    A) WITH POISONING/EXPOSURE
    1) Increased antipyrene clearance has been seen in humans.
    0.2.18) PSYCHIATRIC
    A) WITH POISONING/EXPOSURE
    1) Neuropsychiatric disorders including anxiety and depression, fatigue, personality changes, neurasthenic syndrome, memory deficits, mood changes, attention deficits, psychosomatic symptoms, attention deficits, sleep disturbances, anxiety, irritability, and impairment of memory have been reported.
    0.2.19) IMMUNOLOGIC
    A) WITH POISONING/EXPOSURE
    1) One case of Goodpasture's syndrome has been reported.
    0.2.20) REPRODUCTIVE
    A) Jet fuel A was not embryotoxic or teratogenic in rats.
    0.2.21) CARCINOGENICITY
    A) An association between exposure to jet fuel and kidney cancer has been reported in one study; however, jet fuel is not currently considered to be a human carcinogen. Kidney cancers have also been linked with exposure to other hydrocarbons in humans and experimental animals.

Laboratory Monitoring

    A) No common analytical methods are available for jet fuel, since it is a complex mixture.
    B) Obtain arterial blood gases, serum electrolytes, liver and renal function tests, and urinalysis in symptomatic patients.
    1) Standard clinical laboratory tests have usually been normal in all but the most severe exposures.
    C) Neuropsychiatric tests are controversial without self-referent baseline values.
    D) Monitor arterial blood gases and/or pulse oximetry, pulmonary function tests, and chest x-ray in patients with significant exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Gastric emptying may be indicated after very large ingestions, because of the potential for renal, liver, or CNS toxicity and because of the potential presence of additives in jet fuel.
    B) Consider insertion of a small nasogastric tube for gastric aspiration after large ingestions.
    C) Activated charcoal adsorbs kerosene, turpentine, and benzene in vitro and in animal models, and may absorb jet fuel. Activated charcoal may cause vomiting, which may increase the risk of aspiration. Activated charcoal may be indicated in patients who have coingested an adsorbable toxic substance.
    1) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    D) IN SYMPTOMATIC PATIENTS - (coughing, choking, tachypnea, etc) monitor blood gases to assure adequate ventilation. Admit the patient for observation.
    E) Observe patient for 6 hours. If vital signs become abnormal or symptoms develop, admit the patient to the hospital and obtain a chest X-ray. Asymptomatic patients can be discharged.
    F) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    G) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    H) ANTIBIOTICS - Are indicated only if bacterial superinfection of the lungs occurs.
    I) CORTICOSTEROIDS - have not been shown to be of benefit for hydrocarbon pneumonitis.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) CNS effects, palpitations, and respiratory irritation occur at approximately 500 ppm.
    B) Less than 1 mL of some liquid hydrocarbons has produced severe pneumonitis when directly aspirated into the lungs in animals.

Summary Of Exposure

    A) WITH POISONING/EXPOSURE
    1) Acute exposure to jet fuel can cause CNS depression, headache, dizziness, anxiety, respiratory irritation, and palpitations. Inhalation of liquid hydrocarbons may also induce euphoria, cardiac dysrhythmias, and respiratory arrest. Ingestion may cause potentially fatal aspiration pneumonitis. Human exposure primarily occurs as a result of inhalation or dermal contact.
    a) Effects secondary to aspiration may include hypoxia, infection, pneumatocele formation, and chronic lung dysfunction.
    b) Chronic exposure has been linked with neuropsychiatric disorders.
    c) Chronic exposure to jet fuels has been linked with kidney cancer in humans in one study. Jet fuel is not classified as a confirmed human carcinogen. Potential human reproductive hazards, if any, have not yet been defined.
    d) Similar effects have been seen with petroleum- and shale oil-derived jet fuel in experimental animals.
    e) This review is based on information from JP-4, JP-5, JP-7, JP-8, unspecified jet fuel, and liquid hydrocarbons such as kerosene.

Heent

    3.4.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Jet fuel is slightly irritating to the eyes and nose. Ear loss has been associated with persistent jet fuel exposure.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Neither JP-4 nor JP-7 was irritating to the eye in rabbits (US Air Force, 1984)(Clark, 1989) (EPA, 1982a).
    3.4.4) EARS
    A) WITH POISONING/EXPOSURE
    1) CHRONIC EXPOSURE - In a case-control study of current noised-exposed workers with and without jet fuel (JP-4) exposure at a military instillation, workers with 3 years of exposure had a 70% increase in adjusted odds of hearing loss (OR = 1.7; 95% CI = 1.14-2.53). Odds increased to 2.41 (95% CI = 1.04-5.57) for 12 years of noise and jet fuel exposure. The duration of exposure was associated with an increased risk of persistent hearing loss even though exposure was below normal limits for organic solvents. Overall, fuel oil exposure was less than 34% of the OSHA Threshold Limit Values (TLV). In the persistent hearing loss model, regular consumption of alcohol was the most significant factor, with a 3-fold increase in risk (OR = 3.03; 95% CI = 1.42-6.45); jet fuel exposure was also significant (OR = 1.23; 95% CI = 1.05-1.44) (Kaufman et al, 2005).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) JP-4 vapor is slightly irritating to the nose (CHRIS , 1993).

Cardiovascular

    3.5.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Palpitations have been reported from exposure to jet fuel. Dysrhythmias may occur following inhalation of some hydrocarbons.
    3.5.2) CLINICAL EFFECTS
    A) PALPITATIONS
    1) WITH POISONING/EXPOSURE
    a) PALPITATIONS have been reported from acute exposure to jet fuel (Struwe et al, 1983).
    B) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) INGESTION - Cardiac dysrhythmias, including ventricular fibrillation, have been reported rarely following ingestion of liquid hydrocarbons and are most likely due to indirect effects of hypoxia or acidosis, rather than to the hydrocarbon itself (Kulig & Rumack, 1981).
    b) INHALATION - Inhalation of liquid hydrocarbons may cause various dysrhythmias and ventricular fibrillation, which, in a few cases, have been linked with sudden death (Kulig & Rumack, 1981; Bass, 1978; Anderson et al, 1985; Anderson et al, 1986; Nierenberg et al, 1991).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Jet fuel vapors are irritating to the respiratory tract.
    2) Ingestion with subsequent pulmonary aspiration may produce pulmonary edema and possibly fatal chemical pneumonitis; this is one of the most serious hazards.
    3) Coughing, choking, tachypnea, dyspnea, cyanosis, rales, hemoptysis, and pulmonary edema may occur following ingestion with pulmonary aspiration of liquid hydrocarbons.
    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) WITH POISONING/EXPOSURE
    a) COUGHING
    1) COUGH may occur with acute exposure to jet fuel (Struwe et al, 1983). Jet fuel is a respiratory irritant (CHRIS , 1993).
    b) PNEUMONITIS
    1) No reports of ingestion of jet fuel have been found for humans. However, chemical pneumonitis may be a hazard of pulmonary aspiration, as with other liquid hydrocarbons (Tupper, 1989).
    2) Aspiration is indicated by coughing, choking, or gagging during swallowing, followed by persistent coughing. Aspiration pneumonitis can cause fever and leukocytosis, tachypnea, dyspnea, cyanosis, rhonchi, rales, and decreased breath sounds (AH Hall , 1993).
    a) Signs and symptoms of chemical pneumonitis include coughing, dyspnea, tachypnea, and rapidly developing pulmonary edema with respiratory arrest (CHRIS , 1993; AH Hall , 1993).
    3) Refer to the HYDROCARBONS medical management for more information.
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CHANGES IN PULMONARY FUNCTION - Increases in dynamic compliance, pulmonary resistance, and alveolar clearance of [Tc-99m]-diethylenetriamine pentaacetate, and decreased concentrations of substance P in bronchoalveolar lavage fluid, were seen in Fischer 344 rats exposed to JP-8 jet fuel by inhalation under conditions simulating military flightline exposure (Pfaff et al, 1995).
    2) Significant (p < 0.05) cytosolic and whole lung protein expression alterations were seen in a study of 30 male Swiss-Webster mice (n = 15 exposure; n = 15 controls) exposed to aerosolized JP-8 vapors. Total exposure time was 1 hour per day for 7 days, an equivalent of 250, 1000 and 2300 mg/m(3). At the highest level, a total of 165 proteins were altered in the lung cytol tissue. Seven proteins were identified and found to be significant markers of JP-8-induced stress on lung epithelial cells. One protein, alpha1-anti-trypsin (AAT), has potential implications for the development of chronic obstructive pulmonary disorder (COPD) and pulmonary emphysema (Drake et al, 2003).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Transient CNS excitation followed by depression may occur, especially after inhalation of liquid hydrocarbons.
    2) Peripheral sensory neuropathies and motor deficits have been reported from exposure to jet fuel.
    3) Neuropsychiatric abnormalities have been seen. These may include anxiety, memory loss, and irritability.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) CNS DEPRESSION
    1) Occurs during or immediately after acute exposure to jet fuel (Struwe et al, 1983). Other physical and laboratory findings may be normal (Lombardi & Lurie, 1957).
    2) Headache, dizziness, and nausea have been seen in persons exposed to MC77, a type of jet fuel (Knave et al, 1979; Knave et al, 1978; Knave et al, 1976).
    3) Profound CNS depression probably represents hypoxia secondary to hydrocarbon pneumonitis (Eade et al, 1974).
    4) Since jet fuels may be contaminated with agents or additives (aniline, heavy metals, camphor, or pesticides) which commonly produce CNS toxicity, the presence of these agents must be ruled out in a patient demonstrating severe CNS depression or excitation following exposure.
    b) EEG ABNORMAL
    1) EEG changes have been seen in persons chronically exposed to jet fuel (Knave et al, 1978).
    c) CHRONIC TOXICITY
    1) Persons chronically exposed to an average concentration of 250 mg/m(3) of jet fuel for 4 to 32 years had a higher incidence of neuropsychiatric symptoms than unexposed persons (Struwe et al, 1983).
    2) Symptoms may include anxiety and depression, fatigue, personality changes, neurasthenic syndrome, attention and memory deficits, mood changes, and psychosomatic symptoms (Knave et al, 1979; Knave et al, 1978; Struwe et al, 1983).
    3) Sleep disturbances, anxiety, irritability, and impairment of memory were reported in persons chronically exposed to MC77, a type of jet fuel (Knave et al, 1979; Knave et al, 1978; Knave et al, 1976).
    B) SECONDARY PERIPHERAL NEUROPATHY
    1) WITH POISONING/EXPOSURE
    a) SENSORY NEUROPATHY has been reported from chronic exposure to jet fuel (Knave et al, 1976). One of the components of jet fuel, n-hexane, is known to cause peripheral neuropathy (Krasavage et al, 1980; Ruff et al, 1981).
    1) Changes in nerve conduction velocity have been seen (Knave et al, 1978).
    2) Elevations in sensory vibratory thresholds in the extremities have been seen in persons chronically exposed to jet fuel in an aircraft factory (Knave et al, 1976).
    b) MOTOR DEFICITS - Movement disorders were reported in eight persons with chronic exposure to unspecified jet fuel (Odkvist et al, 1987; Bergholtz & Odkvist, 1984).
    c) No quantitative dose-response information on peripheral neurological effects was available at the time of this review.
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SEIZURES
    a) EFFECTS IN EXPERIMENTAL ANIMALS - Convulsions and poor coordination were seen in rats exposed to 38,000 mg/m(3) of JP-4 (US Air Force, 1974).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Liquid Jet fuel is irritating to the stomach.
    3.8.2) CLINICAL EFFECTS
    A) DRUG-INDUCED GASTROINTESTINAL DISTURBANCE
    1) WITH POISONING/EXPOSURE
    a) IRRITATION - Liquid JP-4 is irritating to the stomach (CHRIS , 1993). Nausea, vomiting, diarrhea, and abdominal pain may occur following ingestion of liquid hydrocarbons (AH Hall , 1993).

Hepatic

    3.9.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Liver injury, as manifested by elevated transaminases, may occur following ingestion of liquid hydrocarbons.
    2) Antipyrene clearance has been altered in humans exposed to jet fuel, but clinical liver function was not altered. Experimental animal studies have shown degenerative fatty changes in the liver.
    3.9.2) CLINICAL EFFECTS
    A) ABNORMAL LIVER FUNCTION
    1) WITH POISONING/EXPOSURE
    a) HEPATOTOXICITY - Hepatic damage may rarely follow hydrocarbon vapor inhalation (Gosselin et al, 1976). Liver injury may occur following acute ingestion, but is uncommon (Shirkey, 1971; Janssen et al, 1988).
    b) ANTIPYRENE CLEARANCE was reported to be enhanced in jet fuel filling attendants, but other laboratory tests of liver function were normal (Dossing et al, 1985). This result indicates induction of hepatic microsomal enzymes by one or more components in jet fuel.
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) LIVER FATTY
    a) EXPERIMENTAL STUDIES - Degenerative fatty changes were seen in livers of experimental animals exposed to 500 mg/m(3) JP-4 continuously for 90 days (US Air Force, 1984)(Clark et al, 1989).
    1) Signs of inflammation were seen in the livers of female mice intermittently exposed to 150 mg/m(3) JP-4 for 12 months.

Genitourinary

    3.10.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Acute renal tubular necrosis, proteinuria, or hematuria occur infrequently following acute hydrocarbon exposure.
    2) Renal effects seen in male rats exposed to jet fuel may not be relevant to humans.
    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) WITH POISONING/EXPOSURE
    a) ACUTE TOXICITY
    1) GOODPASTURE'S SYNDROME - One case of Goodpasture's syndrome (antiglomerular basement membrane antibody-mediated glomerulonephritis) has been reported after a high-dose acute exposure to unspecified jet fuel, however (Beirne & Brennan, 1972).
    2) RENAL EFFECTS - Acute renal tubular necrosis, proteinuria, or hematuria occur infrequently following acute hydrocarbon exposure. The following effects have been associated with exposure to liquid hydrocarbons:
    3) ACUTE TUBULAR NECROSIS (Crisp et al, 1979; Barrientos et al, 1977), sometimes with proteinuria and hematuria (Goldfrank et al, 1979; Janssen et al, 1988; Roy et al, 1991).
    b) CHRONIC TOXICITY
    1) GLOMERULONEPHRITIS and resultant nephrotic syndrome following long-term inhalation or dermal exposure (Zimmerman et al, 1975; Cagnoli et al, 1980; Beirne & Brennan, 1972; Ehrenreich, 1977)(Raunskov, 1979) (Roy et al, 1991).
    2) PROGRESSIVE TUBULOINTERSTITIAL NEPHRITIS following inhalation and dermal occupational exposure (Narvarte et al, 1989).
    3) Problems with SEXUAL FUNCTIONING were reported in a single occupational study on persons chronically exposed to jet fuel (Struwe et al, 1983; Knave et al, 1978; Knave et al, 1979; Knave et al, 1976).
    a) These sexual problems are possibly neurologic in origin and related to effects of chronic exposure on the CNS; they are NOT due to direct toxicity to the reproductive organs.
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) TOXIC NEPHROPATHY
    a) Male rats exposed to jet fuel developed nephropathy (US Air Force, 1984; Bruner et al, 1991; US Air Force, 1991; US Air Force, 1976)(Clark et al, 1989).
    b) Accumulation of hyaline droplets occurred in the proximal tubule region, necrosis and exfoliation of epithelial cells in the P2 segment, tubule cell proliferation with prolonged exposure, appearance of granular casts at the junction of the thin loop of Henle and P3 segment, and mineralization of the renal papillar tubules (Bruner, 1984).
    c) These renal effects are similar to those produced in male rats from exposure to other petroleum products containing branched-chain paraffins (Alden, 1986).
    d) Hyaline droplets, necrosis, and mineralization of kidneys seen in animal studies are thought not to be relevant to humans, and the US Environmental Protection Agency has stated that these renal effects should not be used in human risk assessment (EPA, 1991).

Hematologic

    3.13.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Hemolysis may occur with aspiration pneumonitis. Hematologic depression has been seen in experimental animals, but not in humans.
    3.13.2) CLINICAL EFFECTS
    A) HEMOLYSIS
    1) WITH POISONING/EXPOSURE
    a) HEMOLYSIS has occurred in some cases of hydrocarbon aspiration pneumonia (Banner & Walson, 1983; Janssen et al, 1988; Algren & Rodgers, 1992).
    B) LACK OF EFFECT
    1) WITH POISONING/EXPOSURE
    a) No reports of changes in hematologic parameters were found for humans exposed to jet fuel.
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) BLOOD DYSCRASIA
    a) EXPERIMENTAL ANIMAL DATA - Mild hematologic depression has occurred in experimental animals (Clark et al, 1989). Leukopenia has been noted (US Air Force, 1980; Bruner et al, 1991; Kjaergaard & Molhave, 1987).
    b) Occasional changes in hematologic parameters have been seen in experimental animals, which were not related to dose or within the limits of normal variation (US Air Force, 1984; US Air Force, 1974; US Air Force, 1980; Bruner et al, 1991)(US Air Force, 1982) (US Air Force, 1985; US Air Force, 1991).
    c) These results are consistent with those expected from low levels of benzene in jet fuel.
    d) Refer to the benzene management for more information.

Dermatologic

    3.14.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Jet fuel is a strong skin irritant and can cause a defatting dermatitis.
    2) Shale-derived jet fuels were dermal sensitizers in guinea pigs. Jet fuels can induce inflammatory responses from dermal application to experimental animals.
    3.14.2) CLINICAL EFFECTS
    A) CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) IRRITATION - Jet fuel is a strong skin irritant, and can cause a defatting dermatitis upon exposure of the skin to contaminated clothing (Lombardi & Lurie, 1957). Direct contact with JP-4 or exposure to contaminated clothing can cause a burning sensation (CHRIS , 1993).
    B) POISONING
    1) WITH POISONING/EXPOSURE
    a) Although JP-8 is less volatile than JP-4, skin or clothing contact may present a prolonged exposure hazard both to the worker as well as others. Pleil et al (2000) analyzed breath samples from several groups of US Air Force personnel. JP-8 exposure was found in all subjects. Values ranged from slight elevations to greater than 100 times cohort controls. Because of the potential inhalation risk, the investigators concluded that further study was needed in this area (Pleil et al, 2000).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) JP-4 and JP-7 were severe skin irritants in rabbits (US Air Force, 1984)(Clark et al, 1989)(EPA, 1982).
    1) Jet Fuel A was a mild skin irritant in rabbits (RTECS, 2004).
    b) SENSITIZATION - Shale-derived JP-4 and JP-7 were mild skin sensitizers in guinea pigs, but petroleum-derived JP-4 was not (US Air Force, 1984)(Clark et al, 1989) (EPA, 1982).
    c) INFLAMMATION - Unspecified jet fuel caused severe inflammatory and proliferative changes in mouse skin after two to three weeks of application (Freeman et al, 1990).

Immunologic

    3.19.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) One case of Goodpasture's syndrome has been reported.
    3.19.2) CLINICAL EFFECTS
    A) DISORDER OF IMMUNE FUNCTION
    1) WITH POISONING/EXPOSURE
    a) GOODPASTURE'S SYNDROME - One case of Goodpasture's syndrome (antiglomerular basement membrane antibody-mediated glomerulonephritis) has been reported after a high-dose acute exposure to unspecified jet fuel (Beirne & Brennan, 1972).

Reproductive

    3.20.1) SUMMARY
    A) Jet fuel A was not embryotoxic or teratogenic in rats.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) HUMANS - No reproductive studies were found for military jet fuel in either humans or animals.
    2) Some of the components of jet fuel, such as BENZENE and TOLUENE, are suspect human reproductive hazards.
    3) HYDROCARBONS/GENERAL - Paternal exposure to hydrocarbons has been suggested as a causative factor in Prader-Willi syndrome (Strakowski & Butler, 1987). Approximately half of patients' fathers had occupational exposure to hydrocarbons at or around the time of conception in one study (Cassidy et al, 1989).
    4) Refer to individual TOMES(R) MEDITEXT(TM) Medical Managements on these substances for more information.
    B) ANIMAL STUDIES
    1) EXPERIMENTAL ANIMAL DATA - Jet fuel A, a related commercial jet fuel, did not cause birth defects in rats (Beliles & Mecler, 1982; Schreiner, 1983). Jet fuel was not embryotoxic or teratogenic in rats exposed to 100 or 400 ppm (Beliles & Mecler, 1983).
    3.20.3) EFFECTS IN PREGNANCY
    A) ABORTION
    1) An association between SPONTANEOUS ABORTION and exposure to aliphatic hydrocarbons during pregnancy has been reported (Lindbohm et al, 1990).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) No information was found on the possible effects of exposure to jet fuel during lactation or breast feeding.

Carcinogenicity

    3.21.2) SUMMARY/HUMAN
    A) An association between exposure to jet fuel and kidney cancer has been reported in one study; however, jet fuel is not currently considered to be a human carcinogen. Kidney cancers have also been linked with exposure to other hydrocarbons in humans and experimental animals.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) HUMANS - No studies were found on the possible carcinogenic activity of JP-4 or JP-7 in humans.
    2) IARC/INADEQUATE EVIDENCE - IARC has concluded that there is inadequate evidence for assessing the carcinogenicity of jet fuel in humans or animals (IARC, 1989).
    B) RENAL CARCINOMA
    1) An association between exposure to unspecified jet fuel and kidney cancer was reported in male cancer patients in Montreal, Canada (Odds Ratio = 2.5, statistically significant) (Siemiatycki et al, 1987).
    a) A dose-response pattern was seen, with "substantial" exposure more likely to be associated with kidney cancer than "nonsubstantial" exposure (Siemiatycki et al, 1987).
    b) Renal cancers have also been associated with exposure to other liquid hydrocarbons in humans and animals (Nelson et al, 1990).
    C) GASTRIC CARCINOMA
    1) COLORECTAL CANCER - A weaker association with colorectal cancers has also been reported for jet fuel (Siemiatycki et al, 1987) Milham, 1976) .
    D) ANIMAL STUDIES
    1) JP-7 was NOT carcinogenic in chronic inhalation studies (US Air Force, 1991).
    2) JP-4 induced alveolar/bronchiolar tumors in female rats (Bruner et al, 1991), and pulmonary adenomas and lymphosarcomas in mice (Kinkead et al, 1974).
    3) Hepatocellular tumors were seen in female mice, and renal tumors in male rats. The renal tumors were similar to those seen in male rats exposed to other petroleum products (Bruner et al, 1991).
    4) Unspecified jet fuel was not carcinogenic in a mouse skin painting study (Freeman et al, 1990).
    5) Both shale- and petroleum-derived JP-4 increased skin tumors in mice exposed for up to 105 weeks (Clark et al, 1988).
    E) LACK OF EFFECT
    1) LACK OF HUMAN CARCINOGENICITY - Jet fuel is not considered a human carcinogen at this time. Further epidemiological studies would need to be done before jet fuel could be considered to cause cancer in humans.

Genotoxicity

    A) Jet fuel was mutagenic in Salmonella and mouse lymphoma cells, and induced chromosome aberrations in rats and mice in vivo.

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No common analytical methods are available for jet fuel, since it is a complex mixture.
    B) Obtain arterial blood gases, serum electrolytes, liver and renal function tests, and urinalysis in symptomatic patients.
    1) Standard clinical laboratory tests have usually been normal in all but the most severe exposures.
    C) Neuropsychiatric tests are controversial without self-referent baseline values.
    D) Monitor arterial blood gases and/or pulse oximetry, pulmonary function tests, and chest x-ray in patients with significant exposure.
    4.1.2) SERUM/BLOOD
    A) ACID/BASE
    1) Obtain arterial blood gases in symptomatic patients with possible pulmonary aspiration.
    B) HEMATOLOGIC
    1) Monitor CBC, including peripheral smear, in patients with aspiration pneumonitis or CNS symptoms.
    C) BLOOD/SERUM CHEMISTRY
    1) Monitor liver and kidney function in patients with CNS symptoms.
    a) Liver function tests should include SGOT (AST), SGPT (ALT), lactic dehydrogenase (LDH), bilirubin, and alkaline phosphatase.
    b) Testing should be repeated after several days to monitor for possible effects. If levels are mildly elevated, tests should be repeated in several weeks to document return to baseline. If levels remain elevated, other causes of hepatic dysfunction should be investigated.
    c) Clinical tests of liver function may remain normal, even with signs of CNS depression; antipyrene clearance may be elevated (Dossing et al, 1985) Lombardi & Lurie, 1957).
    2) Renal function tests including BUN and creatinine.
    a) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    4.1.3) URINE
    1) Urinalysis for protein, albumin, and casts should be obtained and monitored in patients with CNS symptoms.
    4.1.4) OTHER
    A) OTHER
    1) ELECTROPHYSIOLOGICAL TESTING
    a) Changes in nerve conduction velocity and sensory vibratory thresholds have occurred in groups of persons exposed to jet fuel (Knave et al, 1976).
    1) The nerve conduction velocity test is invasive and painful, and should be done only in cases where there is other evidence of peripheral nerve dysfunction.
    2) NEUROPSYCHOLOGICAL TESTING
    a) Other tests which have been recommended for symptomatic persons chronically exposed to jet fuels are cortical response audiometry (using frequency ramps as stimulus) and interrupted speech audiometry (Bergholst & Odkvist, 1984).
    1) Lower performance in associative learning, digit span, and block design were noted in a chronically exposed group when compared to their non-exposed monozygotic twins (Hanninen et al, 1991).
    b) Such tests require previous self-referent values for best interpretation, and would therefore be less useful for patients with symptoms upon initial presentation.
    3) PULMONARY FUNCTION TESTS
    a) Pulmonary function tests may be indicated in symptomatic patients with possible hydrocarbon aspiration pneumonitis.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Chest X-ray may be indicated in cases of aspiration of the liquid. Early chest x-rays were NOT useful in predicting pneumonitis in symptomatic or asymptomatic patients with hydrocarbon ingestion (Wason S & Katona B, 1987).
    B) RADIOGRAPHIC-OTHER
    1) CT scans, MRI scanning, and other diagnostic methods may be necessary to determine if structural damage to the brain has occurred from either acute or chronic exposure in patients with significant CNS symptomatology.

Methods

    A) OTHER
    1) No single method is available for analyzing jet fuel in biological samples, because it is a complex mixture. Individual components can be determined, but such determination would not be specific for exposure to jet fuel.
    a) NMR SPECTROSCOPY has been used to analyze gastric contents for kerosene, which is closely related to jet fuel (Yamaguchi et al, 1992).
    b) GAS CHROMATOGRAPHY - MASS SPECTROMETRY: A non-invasive tape-strip technique coupled with gas chromatography - mass spectrometry analysis has been used experimentally to detect exposure to JP-8. Napthalene was used as a marker of dermal exposure (Chao et al, 2006).

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) If a patient is symptomatic, admission is indicated.
    1) Asymptomatic patients can be observed for 4 to 6 hours and discharged if they remain asymptomatic (Linden, 1990).
    a) In a series of 184 cases of accidental hydrocarbon ingestions, none of the 120 patients with no initial symptoms developed later complications (Machado et al, 1988).
    6.3.1.2) HOME CRITERIA/ORAL
    A) Accidental ingestions of small quantities of hydrocarbons can safely be monitored at home, provided that the patient is asymptomatic, there is access to a follow-up mechanism, and no suspicious indications of child abuse or attempted suicide exist (Machado et al, 1988).

Monitoring

    A) No common analytical methods are available for jet fuel, since it is a complex mixture.
    B) Obtain arterial blood gases, serum electrolytes, liver and renal function tests, and urinalysis in symptomatic patients.
    1) Standard clinical laboratory tests have usually been normal in all but the most severe exposures.
    C) Neuropsychiatric tests are controversial without self-referent baseline values.
    D) Monitor arterial blood gases and/or pulse oximetry, pulmonary function tests, and chest x-ray in patients with significant exposure.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Gastric decontamination may be indicated in cases of ingestion of very large amounts of jet fuel, because of the possible presence of additives with potential for systemic toxicity.
    2) Consider aspiration of gastric contents using a small nasogastric tube after large ingestions. The risk of aspiration pneumonitis must be weighed against the potential benefits.
    3) Activated charcoal adsorbs the related substances kerosene, turpentine, and benzene, and may be indicated in patients who have ingested large amounts of jet fuel.
    4) In a series of 255 patients ingesting hydrocarbons (35 to 37% ingested turpentine) pulmonary complications were less frequent in those given syrup of ipecac than in those receiving gastric lavage without a cuffed endotracheal tube. Pneumonitis occurred in 28% treated with ipecac and 56% treated with lavage (Ng et al, 1974).
    B) ACTIVATED CHARCOAL
    1) Activated charcoal adsorbs kerosene, turpentine, and benzene in vitro and in animal models (Chin et al, 1969; Laass, 1974; Laass, 1980) Raush, 1935; (Decker et al, 1981). Its efficacy for other hydrocarbons is not documented.
    a) PRECAUTION - Activated charcoal may cause vomiting, which may be hazardous to patients who have ingested hydrocarbons.
    2) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    3) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) If the patient is symptomatic upon arrival at the medical facility, pulmonary aspiration may have already occurred. Monitor arterial blood gases in cases of severe aspiration pneumonitis to ensure adequate ventilation. Administer supplemental oxygen as indicated.
    B) MONITORING OF PATIENT
    1) CHEST X-RAY - Obtain a baseline chest X-ray in all patients with respiratory symptoms.
    a) If respiratory symptoms develop, obtain chest X-ray. Observe patient for 6 hours. Discharge if asymptomatic after 6 hours of observation.
    C) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    D) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    E) CONTRAINDICATED TREATMENT
    1) Catecholamines should be used with caution due to a possible decreased myocardial threshold for development of arrhythmias.
    F) CORTICOSTEROID
    1) Have not been shown to be of benefit in treating hydrocarbon pneumonitis.
    G) INTRAVENOUS INJECTION
    1) Parenteral Exposure - Close medical follow-up for potential pneumonitis or local reaction is imperative. Aggressive management of local abscess with incision and drainage, as well as appropriate antibiotic usage, is indicated.
    H) EXTRACORPOREAL MEMBRANE OXYGENATION
    1) Extracorporeal membrane oxygenation (ECMO) has been reported to be successful in pediatric aspiration involving hydrocarbons.
    a) Such children received standard therapy for hydrocarbon aspiration without success prior to the institution of extracorporeal membrane oxygenation (Jaeger RW, Scalzo AS & Thompson MW, 1987; Hart et al, 1991).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) CLOTHING
    1) Remove all contaminated clothing as soon as possible, without endangerment of medical personnel.
    B) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Dermal irritation should be treated with standard therapy, including cortisone creams for persistent redness or swelling. Lubricating creams may be helpful for replacing skin oils lost to defatting action.
    B) OBSERVATION REGIMES
    1) The patient should be observed under controlled conditions for 4 to 6 hours for possible development of systemic effects.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Summary

    A) CNS effects, palpitations, and respiratory irritation occur at approximately 500 ppm.
    B) Less than 1 mL of some liquid hydrocarbons has produced severe pneumonitis when directly aspirated into the lungs in animals.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal exposure to jet fuel is not known. No reports of fatal overexposures were found for either JP-4 or JP-7.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.
    B) OCCUPATIONAL
    1) About half of persons occupationally exposed to unspecified jet fuel at a concentration of 500 ppm self-reported signs of central nervous system depression, including headache, nausea, and dizziness.
    a) Other symptoms self-reported in this group included palpitations, a feeling of pressure in the chest, and respiratory irritation (Struwe et al, 1983).
    2) Very high-dose acute exposure to JP-4, estimated in the range of 3000 to 7000 ppm, caused "intoxication" in a pilot (Davies, 1964).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (ORAL)RAT:
    1) 25 g/kg

Toxicologic Mechanism

    A) Aspiration toxicity of hydrocarbons is related to viscosity; the lower viscosity products are the greater aspiration hazard.

Physical Characteristics

    A) JP-4: Colorless to light brown, flammable liquid with an odor like that of fuel oil or kerosene. Although JP-4 is a liquid at room temperature, it evaporates easily (CRC & Inc, 1984; ATSDR , 2001).
    B) JP-5: Colorless, flammable liquid with an odor like kerosene. Although JP-5 is a liquid at room temperature, it can evaporate (ATSDR , 2001).
    C) JP-7: Colorless to straw-colored, flammable liquid with an odor like that of kerosene. Although JP-7 is a liquid at room temperature, it evaporates easily (ATSDR , 2001).
    D) JP-8: Colorless, flammable liquid with an odor like kerosene. Although JP-8 is a liquid at room temperature, it can evaporate (ASTDR 2001). JP-8 is less volatile than JP-4 (Pleil et al, 2000).

Molecular Weight

    A) JP-4: Variable composition based on performance specifications (CRC & Inc, 1984)
    B) JP-5: Variable
    C) JP-7: Variable
    D) JP-8: Variable
    E) Jet fuel: Variable

General Bibliography

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