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HEXANE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) n-Hexane is a hydrocarbon used as a solvent or thinning agent in paints, lacquers, and glues.

Specific Substances

    1) Esani (Italian)
    2) Gettysolve B
    3) Heksan (Polish)
    4) Hexanen (Dutch)
    5) Hexyl hydride
    6) n-Hexane
    7) N-hexane
    8) Skellysolve B
    9) CAS 110-54-3
    10) Molecular Formula: C6-H14
    11) NCI-c 60571
    12) STCC 4908183
    13) UPDT 8212
    14) NORMAL-HESANE
    1.2.1) MOLECULAR FORMULA
    1) C6H14
    2) CH3[CH2]4CH3

Available Forms Sources

    A) FORMS
    1) The technical grades of hexane may contain a mixture of approximately 50% n-hexane and 50% isohexane and cyclohexane (Verschueren, 2000). Small amounts of cyclopentane, pentane and heptane isomers may also be present (OSHA, 2003)
    2) A mixture of commercial grade hexane may contain from 20% to 80% normal hexane (ACGIH, 2001).
    3) Hexane is a colorless, volatile liquid with a gasoline-like odor (HSDB, 2003).
    B) SOURCES
    1) Hexane, a six-carbon alkane, is distilled from petroleum (Lewis, 1998).
    C) USES
    1) Hexane is used as a solvent (in adhesives, coatings, paints and paint thinner, as well as in vegetable oils), paraffin processing desorbent, and chemical reaction medium. It is also used in determining the refractive index of minerals and, when dyed red or blue, as a filling for low-temperature thermometers (instead of mercury) (AAR, 2000; ACGIH, 2001; Ashford, 2001; Budavari, 2000).
    2) Hexane is used as a solvent to extract oils from seeds such as cotton and sunflower. It is also used in the separation of fatty acids, as a denaturant for alcohol, a laboratory reagent, and a cleaning agent for the textile, furniture, and leather industries. Approximately 30% of all hexane is used for soybean extraction(HSDB, 2003; Lewis, 1998).
    3) Hexane is a component of many products that are associated with the gasoline and petroleum industries (HSDB, 2003).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Industrial solvent used as a component of glues, silicones, spray paints, specialized cements, and break cleaners.
    B) TOXICOLOGY: Hexanes, especially, n-hexane, are metabolized to a 2,5-hexanedione intermediate that decreases the phosphorylation of neurofilament proteins and there disrupts the axonal cytoskeleton.
    C) EPIDEMIOLOGY: Toxicology and poisoning from exposure to hexanes is uncommon.
    D) WITH POISONING/EXPOSURE
    1) DERMAL: Hexane is irritating to skin, and can cause redness, pain and blister formation. Chronic exposure can cause defatting dermatitis.
    2) INGESTION: Not well described. Can cause gastrointestinal irritation, aspiration pneumonitis, and likely CNS depression.
    3) OCULAR: Hexane is an eye irritant. Splash contact might cause corneal injury.
    4) INHALATION: Is the most common route of exposure. Low concentrations cause eye and respiratory irritation, dizziness, headache, nausea, and vomiting. High concentrations can also cause CNS depression. At very high concentrations, hexane can cause death from asphyxiation as it displaces oxygen. Chronic inhalation can cause a peripheral neuropathy characterized by pain, weakness, loss of sensation, impaired gait, myalgias, muscle atrophy, hyporeflexia, and sometimes visual disturbances.
    0.2.20) REPRODUCTIVE
    A) Hexane is reported to affect female and male reproductive capacity. Other than decreased weight gain in the offspring, negative results were obtained for teratogenicity. Fetotoxicity was found in rats and mice. An increase in fertility index and a decrease in resorptions was noted in mice, but mating, fertility, litter size, and postnatal survival were not affected in rats.
    0.2.21) CARCINOGENICITY
    A) Hexane is considered neoplastic by RTECS criteria.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor pulse oximetry and arterial blood gases and obtain a chest radiograph in any patient with cough, respiratory distress, or irritation.
    C) Obtain serum electrolytes, renal function, and liver enzymes in patients with more than mild symptoms.
    D) Obtain electromyogram and nerve conduction studies in patients with evidence of peripheral neuropathy.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. Administer oxygen for respiratory irritation.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Administer inhaled beta2-agonists (eg, albuterol) for wheezing, severe cough or respiratory irritation. Treat vomiting with antiemetics and IV fluids. Monitor mental status.
    C) DECONTAMINATION
    1) ORAL EXPOSURE: In general, gastrointestinal decontamination is not indicated because of the risk of aspiration.
    2) INHALATION EXPOSURE: 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 inhaled beta2-agonist and oral or parenteral corticosteroids.
    3) EYE EXPOSURE: Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist, perform a slit lamp exam.
    4) DERMAL EXPOSURE: Remove contaminated clothing and wash exposed area thoroughly with soap and water.
    D) AIRWAY MANAGEMENT
    1) Airway management may be necessary for rare patients with CNS depression or severe respiratory irritation or aspiration.
    E) ANTIDOTE
    1) None.
    F) ACUTE LUNG INJURY
    1) Maintain ventilation and oxygenation and evaluate with frequent arterial blood gas or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. Call you local poison control center for recommendations about surfactant as therapy.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Most unintentional exposures in patients who are asymptomatic may be watched at home.
    2) OBSERVATION CRITERIA: Any patient with a history suggesting aspiration (eg, cough, wheezing) should be evaluated in a healthcare setting.
    3) ADMISSION CRITERIA: Patients who remain symptomatic despite adequate supportive care should be admitted.
    4) CONSULT CRITERIA: Please consult a medical toxicologist or your local poison control center for any patients displaying anything other mild symptoms. An industrial hygienist and/or occupational medicine specialist may be useful to evaluate occupational exposures.
    H) PITFALLS
    1) Failure to decontaminate the patient appropriately, failure to monitor patients with respiratory symptoms.
    I) DIFFERENTIAL DIAGNOSIS
    1) Demyelinating neurologic disease, heavy metal-induced neuropathy, metabolic-induced neuropathy, such as diabetes mellitus, proximal and distal myopathies, spinal cord pathology.
    0.4.3) INHALATION EXPOSURE
    A) 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 inhaled beta2-agonist and oral or parenteral corticosteroids.
    0.4.4) EYE EXPOSURE
    A) Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist, perform a slit lamp exam.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Remove contaminated clothing and wash exposed area thoroughly with soap and water.

Range Of Toxicity

    A) TOXICITY: OSHA permissible exposure limit (PEL): 500 ppm (1800 mg/m(3)) as an 8-hour TWA. NIOSH recommended exposure limit (REL): 50 ppm (180 mg/m(3)) as a TWA for up to a 10-hour workday and a 40-hour workweek. ACGIH threshold limit value (TLV): 50 ppm (176 mg/m(3)) as a TWA for a normal 8-hour workday and a 40-hour workweek. IDLH: 1100 ppm is considered immediately dangerous to life and health. INJECTION: A man developed gas-producing cellulitis after injecting his left antecubital fossa with about 5 mL of spot remover containing more than 95% n-hexane. He recovered following an extensive incision and debridement of the limb.

Clinical Effects

Summary Of Exposure

    A) USES: Industrial solvent used as a component of glues, silicones, spray paints, specialized cements, and break cleaners.
    B) TOXICOLOGY: Hexanes, especially, n-hexane, are metabolized to a 2,5-hexanedione intermediate that decreases the phosphorylation of neurofilament proteins and there disrupts the axonal cytoskeleton.
    C) EPIDEMIOLOGY: Toxicology and poisoning from exposure to hexanes is uncommon.
    D) WITH POISONING/EXPOSURE
    1) DERMAL: Hexane is irritating to skin, and can cause redness, pain and blister formation. Chronic exposure can cause defatting dermatitis.
    2) INGESTION: Not well described. Can cause gastrointestinal irritation, aspiration pneumonitis, and likely CNS depression.
    3) OCULAR: Hexane is an eye irritant. Splash contact might cause corneal injury.
    4) INHALATION: Is the most common route of exposure. Low concentrations cause eye and respiratory irritation, dizziness, headache, nausea, and vomiting. High concentrations can also cause CNS depression. At very high concentrations, hexane can cause death from asphyxiation as it displaces oxygen. Chronic inhalation can cause a peripheral neuropathy characterized by pain, weakness, loss of sensation, impaired gait, myalgias, muscle atrophy, hyporeflexia, and sometimes visual disturbances.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Eye irritation may occur at a concentration of about 1400 to 1500 ppm (Proctor et al, 1988; ACGIH, 2001; Hathaway et al, 1996), with redness and pain (ILO, 1998). A visual function deficit may occur with serious intoxication, due to degeneration of the visual nuclei (ILO, 1998).
    2) BLURRED VISION has been reported with hexane-induced peripheral neuropathy (Pohanish, 2002). Other visual findings have included constriction of the visual field, optic nerve atrophy, retrobulbar neuritis, color vision changes, and abnormal visual evoked potentials in industrial workers (Grant & Schuman, 1993a; Chang, 1987; Seppalainen et al, 1979).
    3) Hexane caused eye lesions in the macula of 11 of 15 workers working in an adhesive bandage factory who were exposed for 5 to 21 years (Bingham et al, 2001a).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) Hexane exposure irritates the nose (Budavari, 1996).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) Throat irritation may occur at a concentration of about 1300 to 1500 ppm (Proctor et al, 1988; ACGIH, 2001; Hathaway et al, 1996; Pohanish, 2002).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) TOXIC EFFECT OF GAS, FUMES AND/OR VAPORS
    1) WITH POISONING/EXPOSURE
    a) Inhalation is the main route of hexane exposure (Harbison, 1998).
    B) INJURY DUE TO ASPHYXIATION
    1) WITH POISONING/EXPOSURE
    a) Hexane is a simple asphyxiant that works by displacing oxygen in the air. When the oxygen concentration drops to 10% or less of ambient air levels, hypoxia results; death occurs swiftly at this level of oxygen deprivation (Clayton & Clayton, 1994).
    C) PNEUMONIA
    1) WITH POISONING/EXPOSURE
    a) Chemical pneumonia is a symptom of overexposure (Budavari, 1996), and can also occur with aspiration of the liquid (ILO, 1998; NIOSH , 2000); hexane presents an acute aspiration hazard (Clayton & Clayton, 1994).
    D) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Inhalation exposure produces mild upper respiratory irritation (Proctor et al, 1988) Hathaway, 1996; (Lewis, 2000a) and labored breathing (ILO, 1998).
    b) Irritation of the bronchi can also result (ITI, 1995).
    E) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Hexane may produce pulmonary edema (Harada et al, 1999). Chemical pneumonitis and aspiration pneumonia may result from ingestion of hydrocarbons or kerosene (Bonte & Reynolds, 1958; Reynolds & Bonte, 1960; Brunner et al, 1964; Baldachin & Melmed, 1964).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) NEUROTOXICITY
    1) WITH POISONING/EXPOSURE
    a) Hexane is considered moderately neurotoxic (Bingham et al, 2001a; Lewis, 1998). It is narcotic at high concentrations (Lewis, 2000a).
    B) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) General initial symptoms include lightheadedness, giddiness, headache, hallucinations, numb extremities and muscle weakness (Budavari, 1996; Harbison, 1998; Lewis, 2000a).
    C) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Central nervous system depression, with dizziness and confusion (Hathaway et al, 1996; ILO, 1998), may occur with an inhalation exposure of 5000 ppm for 10 minutes (Graham et al, 1987). Mild CNS depression has been reported from industrial exposures exceeding 1000 ppm, but not below 500 ppm (Proctor et al, 1988).
    D) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache has been reported from exposures to 1400 to 1500 ppm (Proctor et al, 1988; ACGIH, 2001; Hathaway et al, 1996).
    E) SECONDARY PERIPHERAL NEUROPATHY
    1) WITH POISONING/EXPOSURE
    a) Sensorimotor peripheral polyneuropathy has been associated with chronic and low-grade exposure to n-hexane (Proctor et al, 1988; Barregard et al, 1991; Hathaway et al, 1996; Baselt, 1997), with muscle weakness, loss of sensation and impaired gait or difficulty walking (Baselt, 1997; ITI, 1995).
    b) Numbness may occur in a glove-and-stocking distribution, followed by hand and foot weakness without ataxia or spasticity (Grant & Schuman, 1993a).
    c) Huang et al (1991) found that the severity of polyneuropathy was directly related to the index of hexane exposure, whereas Chang (1993) discussed that individual susceptibility may be more important (Huang et al, 1991; Chang et al, 1993).
    d) Recovery may be biphasic; progression of neuropathy may continue for several months when exposure is stopped, followed by a slow recovery (Huang et al, 1989). Recovery can take up to 1 to 2 years but is generally complete (ILO, 1998).
    e) CASE SERIES: Three workers of a shoe factory with chronic exposure to n-hexane via glue inhalation presented with extremity weakness and difficulty walking. All three patients received rehabilitation and stopped working in the shoe factory, resulting in some improvements of their clinical status within 3 months. However, although the workers had symptomatic relief at the 3 month follow-up, electroneuromyographic findings still indicated residual neuropathy. The authors concluded that motor recovery may not necessarily correlate with electrophysiological changes in hexane-induced neuropathies (Sendur et al, 2009).
    f) Return of motor and sensory function may be significant; however, residual spinal cord damage has been noted in the most severely injured patients (Graham et al, 1987; Oryshkevich et al, 1986).
    g) It has been noted that the reported polyneuritis attributed to hexane may result from a mixture of solvents of which hexane is only a minor component (ACGIH, 2001).
    h) A study of eight patients exposed to 578 ppm reported polyneuropathy with amyotrophy in all eight patients (Harbison, 1998). Quadriplegia without full recovery has been reported after intense intentional solvent abuse (Harbison, 1998).
    i) Weakness in the lower extremities, absent or decreased Achilles tendon reflex, and absent or decreased patellar reflex were peripheral nervous system manifestations noted in 22 of 22 patients studied (Chang, 1987). Abnormalities of evoked potentials were noted in both polyneuropathy and subclinical groups compared with normal controls (Chang, 1987).
    j) Degeneration and paranodal swelling was seen on a sural nerve biopsy in a patient with occupational hexane poisoning. The distribution of conduction velocities of sensory fibers on nerve conduction testing accompanied these findings (Yokoyama et al, 1990).
    1) Chang (1991) found that after patients regained full motor capability, motor nerve conduction velocities were still significantly slowed.
    2) Chang (1993) has found changes that indicate primary axonal degeneration with secondary demyelination (Chang et al, 1993).
    k) All six employees in one factory developed polyneuropathy with air concentrations of n-hexane measured at 190 ppm. Twelve of thirteen (92%) workers who slept regularly in the factory had polyneuropathy, whereas only 3/46 (7%) who did not sleep in the factory had polyneuropathy (Wang, 1986).
    l) The neurotoxicity of n-hexane does not seem to be associated with the other hexane isomers (Sax & Lewis, 1989).
    m) The neurotoxic properties of hexane are potentiated by exposure to methyl ethyl ketone. Because other compounds may also have this effect, human exposure to mixed solvents containing any neurotoxic hexacarbon compound should be minimized (Proctor et al, 1988).
    n) CASE REPORT: One study found that automotive technicians have also been found to have peripheral neuropathy associated with occupational exposure to hexane. A 24-year-old male automotive technician who had worked in the industry for almost 2 years reported numbness and tingling in his hands and feet which spread to his forearms and waist. On physical exam, diminished reflexes were found and nerve conduction velocity studies revealed a subacute progressive mixed motor-sensory neuropathy with distal nerve involvement. The worker reported using one to nine cans of brake cleaner containing 50% to 60% hexane per day during the 22 months of his employment. Symptoms improved upon discontinuation of the exposure, although he continued to have paresthesias in the hands and feet (MMWR, 2001).
    F) PARALYSIS
    1) WITH POISONING/EXPOSURE
    a) Paralysis may occur from exposure to high vapor concentrations (ITI, 1995).
    G) EXTRAPYRAMIDAL DISEASE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORTS: Pezzoli et al have reported two cases of parkinsonism in patients occupationally exposed to n-hexane for 30 years. In the first, a mixture of solvents was involved, so hexane could not be identified as the sole causative agent (Pezzoli et al, 1989). In the second, the parkinsonism progressively worsened despite a reduction in exposure levels after diagnosis (Pezzoli et al, 1995).
    H) ELECTROENCEPHALOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Electroencephalogram (EEG) results are generally normal (ILO, 1998).
    b) CASE SERIES: A study of 97 children who had chronic inhalant abuse of glues (volatile solvents containing hexane), but who had ostensibly suspended inhalation, showed they had both clinical and normative evidence of continuing brain disturbance, by EEG. The authors concluded that glue sniffing may have long-term electrocerebral sequelae (Griesel et al, 1990).
    I) ALTERED MENTAL STATUS
    1) WITH POISONING/EXPOSURE
    a) Memory deficits may occur with serious intoxication, due to degeneration of the hypothalamic tracts (ILO, 1998).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CNS EFFECTS
    a) Synergism of n-hexane-induced neurotoxicity with concomitant methyl isobutyl ketone exposure has been seen in laboratory animals. It was theorized that induction of cytochrome P-450 by the ketone may have been responsible for increased production of neurotoxic metabolites (Abou-Donia et al, 1985).
    2) LACK OF EFFECT
    a) Other hydrocarbons such as n-pentane and n-heptane have not shown the neuropathic neurotoxicity seen with n-hexane in laboratory animals (Takeuchi et al, 1980).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTROINTESTINAL IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Ingestion of hexane produces general intestinal irritation (Clayton & Clayton, 1994).
    B) NAUSEA
    1) WITH POISONING/EXPOSURE
    a) Nausea has been reported from inhalation exposure of hexane in concentrations of 1400 to 1500 ppm (Proctor et al, 1988; Hathaway et al, 1996; ACGIH, 2001; Pohanish, 2002).
    C) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Abdominal cramps may occur at concentrations above 500 ppm (Pohanish, 2002).
    D) TASTE SENSE ALTERED
    1) WITH POISONING/EXPOSURE
    a) A persistent taste of gasoline may occur (Finkel, 1983).
    E) LOSS OF APPETITE
    1) WITH POISONING/EXPOSURE
    a) Anorexia and weight loss may occur (Iida, 1982).
    b) A loss of appetite occurs at concentrations of 1000 to 2500 ppm for 12 hours, with anorexia occurring at 500 to 2500 ppm (Lewis, 2000a).

Hepatic

    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) RODENTS: Hepatic lipid accumulation was reported by Bohlen et al (1973) in a rat study suggesting n-hexane may cause liver damage. No hepatotoxic effects have been reported in humans (Bohlen et al, 1973).

Hematologic

    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) LEUKOPENIA
    a) RODENTS: n-Hexane and its metabolite, 2,5-hexanediol, produced a decrease in white blood cell and lymphocyte counts, and an increase in percent neutrophils, hemoglobin, and hematocrit in exposed animals (Goel et al, 1987).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Irritation with redness and increased blood flow, swelling, pain, itching and painful burning, followed by blister formation, occur after contact with hexane (Hathaway et al, 1996; Pohanish, 2002). The skin irritation reported after prolonged exposure to n-hexane is due to its defatting property (Proctor et al, 1988).
    B) CELLULITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 21-year-old man presented with redness of the left forearm after injecting his left antecubital fossa with about 5 mL of spot remover containing more than 95% n-hexane. Although he was discharged after receiving tetanus prophylaxis, he returned about 14 hours later with pain, edema, erythema, and swelling around the injection site extending to the axilla. Both a radiograph and a CT scan revealed a significant volume of air in the soft tissue of the affected extremity. He recovered following an extensive incision and debridement of the limb. Tissue necrosis was not noted intraoperatively and cultures were negative (Omori et al, 2013).
    C) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) A symptom of overexposure is dermatitis (Budavari, 1996a).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE WEAKNESS
    1) WITH POISONING/EXPOSURE
    a) Initial symptoms include muscle weakness with muscle atrophy, and decreased muscle strength with chronic exposure (Hathaway et al, 1996).
    B) MUSCLE PAIN
    1) WITH POISONING/EXPOSURE
    a) Myalgia has been reported as a presenting symptom of peripheral neuropathy from chronic hexane exposure (Proctor et al, 1988). Muscle pain may persist long after other symptoms of polyneuropathy have subsided (Chang, 1990).
    C) HYPOREFLEXIA
    1) WITH POISONING/EXPOSURE
    a) Weakness of distal legs and hyporeflexia of ankles and knees have been reported from chronic exposure (Proctor et al, 1988).

Immunologic

    3.19.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) WBC ABNORMAL
    a) RODENTS: n-Hexane and its metabolite, 2,5-hexanediol, produced a decrease in white blood cell and lymphocyte counts, and an increase in percent neutrophils, hemoglobin, and hematocrit in exposed animals (Goel et al, 1987).

Reproductive

    3.20.1) SUMMARY
    A) Hexane is reported to affect female and male reproductive capacity. Other than decreased weight gain in the offspring, negative results were obtained for teratogenicity. Fetotoxicity was found in rats and mice. An increase in fertility index and a decrease in resorptions was noted in mice, but mating, fertility, litter size, and postnatal survival were not affected in rats.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) Hexane at a concentration of 1,000 ppm for 6 hours, inhaled by rats on days 8 to 16 of pregnancy, produced decreased weight gain in the offspring (RTECS, 2003). Postnatal growth was somewhat affected in rats exposed to n-hexane prenatally, but the effects were not permanent (Bus, 1979).
    2) An inhalation teratology study in rats using 100 and 400 ppm n-hexane reported negative results (Christian et al, 1983).
    3) n-Hexane was not found to be teratogenic in rats or in mice, even at high doses toxic to the dams (Bus, 1979; Marks, 1980). An inhalation teratology study in rats using 100 and 400 ppm n-hexane reported negative results (Christian et al, 1983). However, behavioral effects were seen in the offspring of rats treated with airborne levels of 10,000 ppm of n-hexane before and during pregnancy (RTECS, 2003).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) FETOTOXICITY
    a) Hexane produced fetotoxicity in rats when inhaled for 20 hours at a concentration of 5000 ppm on days 6 to 19 of pregnancy (RTECS, 2003).
    b) In mice, an oral dose of 238 g/kg on days 6 to 15 of pregnancy produced fetotoxicity (RTECS, 2003).
    3.20.5) FERTILITY
    A) ANIMAL STUDIES
    1) A dominant lethal test in mice showed an increase in fertility index and a decrease in resorptions in females mated to males receiving 400 ppm hexane 6 hours a day, 5 days a week, for 8 weeks (HSDB, 2003).
    2) In a 2-generation reproductive study in rats exposed to airborne concentrations of up to 9,000 ppm for 6 hours per day, 5 or 7 days per week, mating, fertility, litter size, and postnatal survival were not significantly affected, although reduced weight gains were seen in the highest dose group (Daughtrey et al, 1994).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS110-54-3 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) Hexane is considered neoplastic by RTECS criteria.
    3.21.3) HUMAN STUDIES
    A) PULMONARY CARCINOMA
    1) There has been one report of an increased incidence of respiratory cancer among white male rubber workers exposed to n-hexane and other solvents (Wilcosky, 1984).
    CARCINOMA
    2) One study found that workers in the shoe manufacture and repair industry may be at an increased risk for nasal carcinoma and leukemia. The results suggested that occupational exposure to organic solvents, including n-hexane may cause cytogenic damage to buccal cells (Burgaz et al, 2002)

    3.21.4) ANIMAL STUDIES
    A) HEPATIC CARCINOMA
    1) Hexane produced liver tumors in mice when inhaled intermittently at a concentration of 9018 ppm for 6 hours for 2 years (RTECS, 2003). However, n-hexane was not found to be a tumor promoter in mice (Sice, 1966).

Genotoxicity

    A) Hexane did not induce chromosome aberrations in Chinese hamster ovary cells or in rat lymphocytes, but did induce them in rat bone marrow. It was negative for mutagenicity in Salmonella/microsome preparations and for inducing specific locus mutations in cultured mouse lymphoma cells. Hexane induced sister chromatid exchanges in Chinese hamster ovary cells. Hexane also produced sex chromosome loss/nondisjunction in S. cerevisia.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Monitor pulse oximetry and arterial blood gases and obtain a chest radiograph in any patient with cough, respiratory distress, or irritation.
    C) Obtain serum electrolytes, renal function, and liver enzymes in patients with more than mild symptoms.
    D) Obtain electromyogram and nerve conduction studies in patients with evidence of peripheral neuropathy.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) The usual hematological tests fail to show characteristic changes (ILO, 1998). However, measuring hexane itself in blood has been suggested as a useful biological indicator of exposure. Hexane concentrations in blood averaged 0.6 mcg/L in the blood of unexposed adults(Baselt, 1997).
    2) Liver function tests might be useful in evaluating hepatotoxic potential in humans (Couri & Milks, 1982).
    4.1.3) URINE
    A) Measurement of the metabolite 2,5-hexanedione in urine correlates well with the concentration and duration of exposure (Harbison, 1998), thus this has been suggested as a useful biological indicator (Baselt, 1997).
    B) Urinary 2,5-hexanedione is recommended as a better tool than air-monitoring in the early detection of n-hexane neurotoxicity (Mayan et al, 2002).
    C) A study of subjects exposed to n-hexane between 1991 and 1998 showed that overall urinary 2,5-hexanedione levels have dropped over the 7 year time span of the study by 31.9 percent. The yearly decrease over the entire period was 5.4 percent. The greatest decreases were in individuals with high initial urinary levels. The data suggests that these patients were monitored more frequently, but reductions may have been related to better industrial hygiene and the awareness of the need for biological monitoring of exposed subjects (Baldasseroni et al, 2003).
    4.1.4) OTHER
    A) OTHER
    1) EMG
    a) ELECTROMYOGRAM may be useful for differential diagnosis. Nerve conduction time may be prolonged and there may be signs of denervation in muscle (Proctor et al, 1988).
    b) Early signs of hexane-induced neuropathy were decreases in the amplitude of sensory nerve action potentials (SNAP) in the sural, median and ulnar nerves, compared with those of healthy age-matched adults. Decreases were related to duration of exposure and were detectable when other neurological signs were still normal (Pastore et al, 1994).
    c) The authors concluded this might serve as a sensitive method of early detection of n-hexane-induced neurologicval changes in asymptomatic individuals (Pastore et al, 1994).
    d) Electroencephalogram (EEG) results are generally normal (ILO, 1998).

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Chest x-ray may be of value in evaluating aspiration pneumonia or pulmonary edema.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients who remain symptomatic despite adequate supportive care should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Most unintentional exposures in patients who are asymptomatic may be watched at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Please consult a medical toxicologist or your local poison control center for any patients displaying anything other mild symptoms. An industrial hygienist and/or occupational medicine specialist may be useful to evaluate occupational exposures.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Any patient with a history suggesting aspiration (eg, cough, wheezing) should be evaluated in a healthcare setting.

Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor pulse oximetry and arterial blood gases and obtain a chest radiograph in any patient with cough, respiratory distress, or irritation.
    C) Obtain serum electrolytes, renal function, and liver enzymes in patients with more than mild symptoms.
    D) Obtain electromyogram and nerve conduction studies in patients with evidence of peripheral neuropathy.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ORAL EXPOSURE: In general, gastrointestinal decontamination is not indicated because of the risk of aspiration.
    B) INHALATION EXPOSURE: 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 inhaled beta2-agonist and oral or parenteral corticosteroids.
    C) EYE EXPOSURE: Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist, perform a slit lamp exam.
    D) DERMAL EXPOSURE: Remove contaminated clothing and wash exposed area thoroughly with soap and water.
    6.5.2) PREVENTION OF ABSORPTION
    A) In general, gastrointestinal decontamination is not indicated because of the risk of aspiration.
    B) GASTRIC LAVAGE
    1) In very select cases after a large ingestion (more than 30 mL) that has occurred recently, removal by lavage or suction may be beneficial.
    2) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    3) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    4) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    5) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    6) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Monitor vital signs and mental status.
    2) Monitor pulse oximetry and arterial blood gases and obtain a chest radiograph in any patient with cough, respiratory distress, or irritation.
    3) Obtain serum electrolytes, renal function, and liver enzymes in patients with more than mild symptoms.
    4) Obtain electromyogram and nerve conduction studies in patients with evidence of peripheral neuropathy.
    B) PULMONARY ASPIRATION
    1) If the patient is coughing upon arrival at the medical facility, aspiration has probably already occurred. Monitor respiratory status and room air arterial blood gases in cases of severe aspiration pneumonitis to ensure adequate ventilation.
    C) CONTRAINDICATED TREATMENT
    1) Catecholamines should be used with caution due to possible increased sensitivity of the myocardium secondary to the hydrocarbon. Ventricular arrhythmias may occur in this setting.
    D) CORTICOSTEROID
    1) These have not been shown to be of benefit except anecdotally. Immunocompetence may be compromised with their use, and risk/benefits must be weighed.
    E) ACUTE LUNG INJURY
    1) Aspiration pneumonia, chemical pneumonitis, and pulmonary edema have been reported to result from aspiration or ingestion of hydrocarbons or kerosene (Bonte & Reynolds, 1958; Reynolds & Bonte, 1960; Baldachin & Melmed, 1964; Brunner et al, 1964).
    a) Aspiration may occur. Baseline chest x-ray may be useful in detecting aspiration pneumonia. The aspirate may vaporize, resulting in a rapid decrease in oxygen in the lungs leading to asphyxia, brain damage, or cardiac arrest.
    2) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    3) 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)
    4) 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).
    5) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    6) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    7) 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).
    8) 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).

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.
    6.7.2) TREATMENT
    A) AIRWAY MANAGEMENT
    1) Airway management may be necessary for rare patients with CNS depression or severe respiratory irritation or aspiration.
    B) NEUROPATHY
    1) Analgesics may be necessary for pain management. Following cessation of pain, formal physical therapy may be beneficial.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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) 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).

Abstracts

Case Reports

    A) ADULT
    1) CHRONIC EFFECTS
    a) A 60-year-old man with a 5-year history of progressive lower extremity weakness and sensory loss worked as a janitor for an adhesive tape manufacturer. He had discovered in 1971 that n-hexane worked well as a solvent for the removal of glue on a laboratory table. He wore gloves while using n-hexane. The room in which he worked was centrally ventilated. The cleaning procedure took 2 hours/day to complete. The average exposure level was reported to be 325 ppm for 10 hours/week based on random spot checks of the room once the plant safety manager became aware of it. He continued to allow the employee to use n-hexane based on the criteria that the concentration did not exceed the TLV. The authors contend that this case demonstrates the current TLV for n-hexane of 500 ppm is probably too high (Ruff et al, 1981).
    b) Polyneuropathy with severe involvement of the legs was associated with occupational exposure to glue fumes in a cabinet-making factory. Despite intensive medical treatment and physical rehabilitation in this 63-year-old man, no improvement in EMG was noted over a 16-year follow-up period (Oryshkevich et al, 1986).

Range Of Toxicity

Summary

    A) TOXICITY: OSHA permissible exposure limit (PEL): 500 ppm (1800 mg/m(3)) as an 8-hour TWA. NIOSH recommended exposure limit (REL): 50 ppm (180 mg/m(3)) as a TWA for up to a 10-hour workday and a 40-hour workweek. ACGIH threshold limit value (TLV): 50 ppm (176 mg/m(3)) as a TWA for a normal 8-hour workday and a 40-hour workweek. IDLH: 1100 ppm is considered immediately dangerous to life and health. INJECTION: A man developed gas-producing cellulitis after injecting his left antecubital fossa with about 5 mL of spot remover containing more than 95% n-hexane. He recovered following an extensive incision and debridement of the limb.

Minimum Lethal Exposure

    A) Hexane may be one of the most highly toxic members of the alkane family. Ingestion of approximately 50 grams of hexane may be fatal to humans (Bingham et al, 2001).

Maximum Tolerated Exposure

    A) OSHA permissible exposure limit (PEL): 500 ppm (1800 mg/m(3)) as an 8-hour TWA. NIOSH recommended exposure limit (REL): 50 ppm (180 mg/m(3)) as a TWA for up to a 10-hour workday and a 40-hour workweek. ACGIH threshold limit value (TLV): 50 ppm (176 mg/m(3)) as a TWA for a normal 8-hour workday and a 40-hour workweek. IDLH: 1100 ppm is considered immediately dangerous to life and health (U.S. Occupational Safety and Health Administration, 2010; American Conference of Governmental Industrial Hygienists, 2010; National Institute for Occupational Safety and Health, 2007; ACGIH, 2001).
    B) Workers exposed to 1000 to 25,500 ppm of hexane for 30 to 60 minutes experienced drowsiness (Bingham et al, 2001).
    C) Humans exposed to 2000 ppm for 10 minutes suffered no effects, but exposure to 5000 ppm caused dizziness and giddiness (ACGIH, 2001).
    D) Exposure to 1500 ppm caused slight nausea, headache, and irritation of the eyes and throat (Hathaway et al, 1996).
    E) In an industrial setting, exposure to 1000 ppm of solvents containing hexane produced mild symptoms, such as dizziness. No symptoms were observed for exposure to less than 500 ppm (Hathaway et al, 1996).

Workplace Standards

    A) ACGIH TLV Values for CAS110-54-3 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) n-Hexane
    a) TLV:
    1) TLV-TWA: 50 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: BEI, Skin
    3) Definitions:
    a) BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.
    b) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): CNS impair; peripheral neuropathy; eye irr
    d) Molecular Weight: 86.18
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS110-54-3 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: n-Hexane
    2) REL:
    a) TWA: 50 ppm (180 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 1100 ppm
    b) Note(s): [10%LEL]
    1) [10%LEL]: The 10%LEL designation is provided where the IDLH was based on 10% of the lower explosive limit. This is used for safety purposes in some cases even though toxicity is not indicative of irreversible health effects or impairment of escape exists only at higher concentrations.

    C) Carcinogenicity Ratings for CAS110-54-3 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: n-Hexane
    2) EPA (U.S. Environmental Protection Agency, 2011): Inadequate information to assess carcinogenic potential. ; Listed as: n-Hexane
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: n-Hexane
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS110-54-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: n-Hexane
    2) Table Z-1 for n-Hexane:
    a) 8-hour TWA:
    1) ppm: 500
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 1800
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Bingham et al, 2001; Budavari, 2000; HSDB, 2003; ITI, 1995; Lewis, 2000; RTECS, 2003 Note: Values are from RTECS unless otherwise noted.
    1) LD50- (ORAL)RAT:
    a) 25 g/kg
    b) Juvenile, 24 ml/kg (HSDB, 2003)
    c) Adult, 45 ml/kg (HSDB, 2003)
    d) Young Adult, 49.0 ml/kg (Budavari, 2000)
    e) 28.7 mg/kg (Bingham et al, 2001a)
    f) 28,710 mg/kg (Lewis, 2000a)
    g) 750 mg/kg (Lewis, 2000a)
    2) TCLo- (INHALATION)HUMAN:
    a) 190 ppm for 8W -- nerve or sheath changes
    b) 1400 ppm -- CNS effects (ITI, 1995)
    3) TCLo- (INHALATION)MOUSE:
    a) 9018 ppm for 6H/2Y- intermittent -- neoplastic, tumors
    b) 10,000 ppm for 6H/13W- intermittent -- changes in sense organs, motor activity, and cell count
    4) TCLo- (INHALATION)RAT:
    a) Female, 5000 ppm for 20H at 6-19D of pregnancy -- fetotoxicity (except death)
    b) Female, 1000 ppm for 6H at 8-16D of pregnancy -- reduced weight gain in newborns
    c) Female, 10,000 ppm for 7H at 15D prior to mating and 1-18D of pregnancy -- behavioral changes in newborns
    d) 1000 ppm for 4H/59W- intermittent -- carcinogenic, testicular tumors
    e) 1200 ppm for 12H/16W- intermittent -- peripheral nerve changes, weight loss or decreased weight gain, biochemical changes
    f) 1 pph for 6H/13W-intermittent -- changes in brain weight, weight loss or decreased weight gain
    g) 2000 ppm for 12H/24W- intermittent -- spinal cord, peripheral nerve and biochemical changes
    h) 500 ppm for 24H/9W-continuous -- spastic paralysis, weight loss or decreased weight gain
    i) 1000 ppm for 24H/11W-continuous -- brain and coverings changes, muscle weakness, weight loss or decreased weight gain
    j) 476 ppm for 6H/4W-intermittent -- respiratory and biochemical changes
    k) 3000 ppm for 6H/2Y-intermittent -- weight loss or decreased weight gain

Pharmacology Toxicology

Toxicologic Mechanism

    A) The main n-hexane metabolite in humans is 2,5-hexanedione (Governa et al, 1987). This metabolite has been identified as the main molecular cause of the n-hexane-induced neurotoxic effects, through its reaction with the lysyl amino groups of proteins (Graham et al, 1987; Harbison, 1998a).
    B) Other n-hexane metabolites, such as 2-hexanone (methyl n-butyl ketone) and 2-hexanol, are associated with neurotoxicity (Couri & Milks, 1982; Perbellini et al, 1978). However, it is not clear whether these compounds themselves are responsible for neurotoxicity, as they are further metabolized to 2,5-hexanedione (Couri & Milks, 1982).
    C) In experimental animals, 2,5-hexanedione has produced neuropathy undistinguishable from that of n-hexane when administered by subcutaneous injection, oral gavage, or in the drinking water (Couri & Milks, 1982). Hexanol-1 and hexanol-2 (hexane metabolites) were reported to cause neurotoxicity in rats given these compounds for up to 8 months (Perbellini et al, 1978).

Physicochemical

Physical Characteristics

    A) Hexane exists as a colorless liquid with a gasoline-like odor (HSDB, 2003).

Molecular Weight

    A) 86.18

Other

    A) ODOR THRESHOLD
    1) 130 ppm (ACGIH, 2001)
    2) 875 mg/m(3) (Verschueren, 2000)
    3) 230 mg/m(3) (Verschueren, 2000)
    4) Water-odor threshold is 0.0064 mg/l (Pohanish, 2002).
    5) Air-odor threshold is 230 to 875 mg/m(3) (Pohanish, 2002).
    6) Hexane odors are irritating at 1800 mg/m(3) (Bingham et al, 2001)

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