Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

TRICHLOROETHANE

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Trichloroethane is a halogenated aliphatic hydrocarbon containing chlorine. It is almost exclusively used as a solvent, with a small percent used as an intermediate. By inhalation, this is probably the least toxic of the chlorinated solvents, but its high volatility and careless use and abuse have resulted in fatalities from gross exposure in confined spaces or deliberate inhalation. Routes of toxic exposures are via inhalation, ingestion, and skin and/or eye contact; however, cutaneous absorption is probably too slow to produce significant toxicity.

Specific Substances

    A) 1,1,1-TRICHLOROETHANE
    1) 1,1,1-TCE
    2) alpha-Trichloroethane
    3) Chloroform, methyl-
    4) Chlorothene
    5) Methyl chloroform
    6) Methyltrichloromethane
    7) Trichloromethylmethane
    8) Molecular formula: C-H3-CCl3
    9) CAS 71-55-6
    1,1,2-TRICHLOROETHANE
    1) TCA
    2) Ethane trichloride
    3) Vinyl trichloride
    4) Molecular formula: C2-H3-Cl3
    5) CAS 79-00-5
    GENERAL TERMS
    1) 1,1,1-TRICHLOROETHANE
    2) TCE (Tetrachloroethane)
    3) TCA (Trichloroethane)
    4) TETRACHLOROETHANE (1,1,1,2)
    5) CHLORETHANE
    6) TCE (Trichloroethane)
    7) MC (Methyl Chloroform)

    1.2.1) MOLECULAR FORMULA
    1) C2H3Cl3
    2) CH3CCl3

Available Forms Sources

    A) FORMS
    1) 1,1,1-trichlorethane is available in the following grades: cold cleaning; industrial inhibited; inhibited; uninhibited; white room (CHRIS, 2003).
    2) In the United States, 1,1,1-trichloroethane is commercially available as technical or solvent grades. They differ in the amount of stabilizer (such as alcohols, esters, ketones, or nitrogen compounds) that has been added to prevent corrosion of metal (Harbison, 1998; HSDB, 2003).
    B) SOURCES
    1) 1,1,1-trichloroethane can be produced by the chlorination of 1,1-dichloroethane, ethane, or vinyl chloride, the catalytic addition of hydrochloric acid to 1,1-dichloroethylene (vinylidene chloride), or by refluxing carbon monoxide with chloroethane and carbon tetrachloride (Ashford, 2001; Budavari, 1996; HSDB, 2003).
    C) USES
    1) 1,1,1-trichloroethane is encountered both in industrial and domestic uses. It is used as a degreaser, pesticide, a solvent in paints, glues, and aerosol products, as a dry cleaning agent, and in household products for the removal of stains (Baselt, 2000a; Lewis, 2001a; Verschueren, 2001).
    2) "Because of its ozone-depleting properties, methyl chloroform is scheduled to be phased out of use by the year 2005 as part of the Montreal Protocol" (Harbison, 1998).
    a) After the phase-out, the only allowed use of methyl chloroform will be as a chemical intermediate feedstock ((HSIA, 1994)).
    3) Cases of intentional abuse of 1,1,1-trichloroethane in substances such as typewriter correction fluid for euphoric symptoms have been documented (Troutman, 1988).

Overview

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) 1,1,1-Trichloroethane is a central nervous system and respiratory depressant, as well as a skin, eye, mucous membrane and respiratory tract irritant. It is harmful by inhalation, ingestion and dermal exposure, and is absorbed mainly through the lungs and skin, with low oral toxicity. 1,1,1-Trichloroethane is one of the least toxic chlorinated hydrocarbon solvents.
    2) Exposure produces a burning sensation of the eyes and skin. Repeated dermal exposure can defat the skin, causing erythema, rash, and dry, scaly, fissured dermatitis. Lengthy contact with the skin can result in pain and irritation. Eye exposure produces irritation, lacrimation, conjunctivitis and transient, superficial eye injury. Corneal burns are possible.
    3) Systemic effects include headache, lightheadedness, dizziness, fainting, drowsiness, helplessness, hallucinations or distorted perceptions, impaired judgement, motor activity changes, ataxia, decreased reaction time, decreased manual dexterity, loss of proprioception, irritability, aggression, hypermotility, diarrhea, nausea or vomiting, abdominal cramps and other gastrointestinal changes, hypotension, cardiac fibrillation, lassitude and coma.
    4) Central nervous system effects may be most pronounced at higher exposures and include loss of coordination and equilibrium, central nervous system impairment and central anesthetic effects (possibly fatal). CNS depressant effects are seen with high concentrations.
    5) Cardiac sensitization to epinephrine, which can result from exposure to high concentrations, can produce fatal cardiac dysrhythmias and cardiac arrest. In patients who abuse halogenated hydrocarbons, this is referred to as "sudden sniffing death".
    6) Asphyxiation may result from inhalational exposure. Chemical pneumonitis (particularly after aspiration of gastric contents) and acute lung injury with hemorrhage are also possible consequences of exposure.
    7) Intentional exposure to high concentrations in recreational abuse for euphoria may produce unconsciousness, seizures, respiratory arrest, dysrhythmias and sudden death.
    0.2.4) HEENT
    A) Contact with eyes will result in superficial and transient conjunctival irritation and hyperemia.
    0.2.5) CARDIOVASCULAR
    A) WITH POISONING/EXPOSURE
    1) Following an acute exposure, hypotension and cardiac dysrhythmias due to myocardial sensitization have led to ventricular fibrillation and death. Myocardial ischemia has been reported.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Respiratory depression and acute lung injury may be noted following acute exposure.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) Trichloroethane has a rapid anesthetic action. Acute overdoses may cause dizziness, unconsciousness, coma and seizures. Cerebral hypoxia and cerebral edema have been reported. Lethargy has been reported with chronic exposure.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, diarrhea, and burns of the esophagus have been noted after large ingestions.
    0.2.9) HEPATIC
    A) WITH POISONING/EXPOSURE
    1) Toxic exposures may cause transient increases in liver enzymes. Fatty liver disease has also been reported.
    0.2.10) GENITOURINARY
    A) WITH POISONING/EXPOSURE
    1) Toxic exposures may cause transient renal impairment.
    0.2.14) DERMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Cutaneous vesiculations and erythema may occur after prolonged contact. Allergic contact dermatitis has been reported.
    0.2.20) REPRODUCTIVE
    A) Teratogenic effects have not been reported in humans or experimental animals.
    0.2.21) CARCINOGENICITY
    A) The US EPA classifies 1,1,1-trichloroethane in Group D (not classifiable as to human carcinogenicity); however, evidence is inadequate.

Laboratory Monitoring

    A) Trichloroethane can be found in expired air, blood, and urine. Its metabolites can be detected in the urine.
    B) Monitor ECG, vital signs and mental status following acute exposures.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Significant esophageal or gastrointestinal tract irritation or burns may occur following ingestion. The possible benefit of early removal of some ingested material by cautious gastric lavage must be weighed against potential complications of bleeding or perforation.
    B) 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.
    C) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    D) There is no specific treatment for trichloroethane poisoning. Supportive measures should be instituted to treat the effects of CNS and respiratory depression.
    E) Keep patient calm to minimize effects of endogenous catecholamines on the myocardium. Avoid administration of adrenergic agonist drugs whenever possible.
    F) Obtain baseline hepatic and kidney function tests, as dysfunction may occur transiently after recovery from CNS depression.
    G) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    H) 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.
    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.
    B) 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.
    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, the patient should be seen in a health care facility by an ophthalmologist.
    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) The acute lethal dose in humans is 500 to 5000 mg/kg. Inhalation of 20,000 ppm for 60 minutes will result in surgical anesthesia and possibly death.
    B) Based on effects caused in monkeys and rats, the following effects are expected in humans: 20,000 ppm for 60 minutes, coma and possibly death; 10,000 ppm for 30 minutes, marked incoordination; 2000 ppm for 5 minutes, disturbance of equilibrium.

Clinical Effects

Summary Of Exposure

    A) WITH POISONING/EXPOSURE
    1) 1,1,1-Trichloroethane is a central nervous system and respiratory depressant, as well as a skin, eye, mucous membrane and respiratory tract irritant. It is harmful by inhalation, ingestion and dermal exposure, and is absorbed mainly through the lungs and skin, with low oral toxicity. 1,1,1-Trichloroethane is one of the least toxic chlorinated hydrocarbon solvents.
    2) Exposure produces a burning sensation of the eyes and skin. Repeated dermal exposure can defat the skin, causing erythema, rash, and dry, scaly, fissured dermatitis. Lengthy contact with the skin can result in pain and irritation. Eye exposure produces irritation, lacrimation, conjunctivitis and transient, superficial eye injury. Corneal burns are possible.
    3) Systemic effects include headache, lightheadedness, dizziness, fainting, drowsiness, helplessness, hallucinations or distorted perceptions, impaired judgement, motor activity changes, ataxia, decreased reaction time, decreased manual dexterity, loss of proprioception, irritability, aggression, hypermotility, diarrhea, nausea or vomiting, abdominal cramps and other gastrointestinal changes, hypotension, cardiac fibrillation, lassitude and coma.
    4) Central nervous system effects may be most pronounced at higher exposures and include loss of coordination and equilibrium, central nervous system impairment and central anesthetic effects (possibly fatal). CNS depressant effects are seen with high concentrations.
    5) Cardiac sensitization to epinephrine, which can result from exposure to high concentrations, can produce fatal cardiac dysrhythmias and cardiac arrest. In patients who abuse halogenated hydrocarbons, this is referred to as "sudden sniffing death".
    6) Asphyxiation may result from inhalational exposure. Chemical pneumonitis (particularly after aspiration of gastric contents) and acute lung injury with hemorrhage are also possible consequences of exposure.
    7) Intentional exposure to high concentrations in recreational abuse for euphoria may produce unconsciousness, seizures, respiratory arrest, dysrhythmias and sudden death.

Heent

    3.4.1) SUMMARY
    A) Contact with eyes will result in superficial and transient conjunctival irritation and hyperemia.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) CHEMOSIS - Superficial and transient conjunctival irritation and hyperemia can occur (Torkelson, 1994). When tested by drop application in rabbit eyes, slight conjunctival irritation and no corneal damage was seen (Grant & Schuman, 1993).
    2) DIPLOPIA - May be noted following acute exposure (D'Costa & Gunasekera, 1990).

Cardiovascular

    3.5.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Following an acute exposure, hypotension and cardiac dysrhythmias due to myocardial sensitization have led to ventricular fibrillation and death. Myocardial ischemia has been reported.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Following acute exposure, hypotension may be noted(HSDB, 2003).
    B) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Cardiovascular collapse has been reported following single, large exposures (Stewart, 1971).
    C) VENTRICULAR ARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) Cardiac dysrhythmias may result from a lowering of the myocardial threshold to the arrhythmogenic effects of catecholamines. Premature ventricular contractions, depressed S-T segments, and one case of cardiac arrest were seen at anesthetic concentrations (Donaldson HM, Levy BS & Plotnick HB et al, 1976).
    1) CASE REPORT - Ventricular dysrhythmias and cardiopulmonary arrest were reported in a 15-year-old male who inhaled typewriter correction fluid (Wodka & Jeong, 1991). Serial electrocardiograms and subsequent stress echocardiogram findings were consistent with recent antero-apical subendocardial infarction. The patient was discharged 4 days after admission.
    D) MYOCARDIAL INFARCTION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - A 37-year-old female with no past cardiac history developed a silent myocardial infarction (positive ECG and CPK-MB) following inhalation of a product containing 30% trichloroethane. Total occlusion of the proximal right coronary artery was angiographically demonstrated (Bailey et al, 1997).
    E) DEAD - SUDDEN DEATH
    1) WITH POISONING/EXPOSURE
    a) Sudden death ("sudden sniffing death") has been reported. It is believed to be related to the onset of cardiac dysrhythmias from exposure to 1,1,1 trichloroethane (King et al, 1985; Banathy & Chan, 1983; Ranson & Berry, 1986).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEART DISORDER
    a) Chronic respiratory exposure in animals has been reported to result in cardiovascular insufficiency.
    b) Aoki et al (1997) reported decreases in peripheral vascular resistance, transient disturbances of pulmonary blood flow, and right ventricle overload in anesthetized dogs delivered trichloroethane via inhalation.
    c) Intravenous injections of epinephrine given to dogs in conjunction with inhaled trichloroethane at 2500, 5000 or 10,000 ppm showed no cardiac effects at 2500 ppm conditions. Three of the 18 dogs were affected at 5000 ppm; however, at 10,000 ppm all of the dogs showed cardiac effects(ACGIH, 2001).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Respiratory depression and acute lung injury may be noted following acute exposure.
    3.6.2) CLINICAL EFFECTS
    A) ACUTE RESPIRATORY INSUFFICIENCY
    1) WITH POISONING/EXPOSURE
    a) Respiratory depression may occur following acute exposure (Stewart, 1971). Fatalities following inhalation may be a result of respiratory distress with subsequent asphyxiation (Winek et al, 1997; Fosseus, 1991).
    b) Increased incidence of sleep apnea may result from chronic occupational exposure to trichloroethane (Monstad et al, 1987).
    B) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Acute lung injury may occur following acute exposure (D'Costa & Gunasekera, 1990).
    b) CASE REPORT - Postmortem findings of congestion and edema of the lung tissue were observed in a 13-year-old boy following an intentional inhalation. Death was due to respiratory distress with subsequent asphyxiation (Winek et al, 1997).
    c) CASE REPORT - Acute lung injury and hypoxemia (PaO2 = 59 mm Hg) were seen in a 34-year-old woman soon after spraying a water-proofing chemical containing 1,1,1-trichloroethane on a ski suit while smoking a cigarette. CT scan showed ground-glass opacities in both lung fields which returned to normal without any treatment. The water-proofing spray also contained fluoride resin which may have also contributed to the symptoms (Jinn et al, 1998).
    C) PNEUMONIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - A case of acute eosinophilic pneumonia accompanied by respiratory failure was reported in a 15-year-old male following repetitive intentional inhalation of Scotchguard. The patient recovered following assisted ventilation and corticosteroid therapy (Kelly & Ruffing, 1993).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HYPERVENTILATION
    a) DOGS - Dose dependent rapid and shallow breathing was observed in dogs during inhalational studies with trichloroethane concentrations greater than 0.9% in inspired air. Vagotomy appeared to inhibit the rapid and shallow breathing following inhalation of higher concentrations of trichloroethane. The authors suggested that an enhancement of the Hering Breuer reflex elicited decreased inspiration and that trichloroethane had a stimulating effect on the lung stretch receptor (Kobayashi et al, 1986).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Trichloroethane has a rapid anesthetic action. Acute overdoses may cause dizziness, unconsciousness, coma and seizures. Cerebral hypoxia and cerebral edema have been reported. Lethargy has been reported with chronic exposure.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Trichloroethane has a rapid general anesthetic action, with resultant coma (del Amo et al, 1996). A 17-year-old patient sustained damage to the basal ganglia and occipital sulci and remained in a coma for 6 months following the intentional inhalation of typewriter correction fluid containing trichloroethane(del Amo et al, 1996).
    B) HYPOXEMIA
    1) WITH POISONING/EXPOSURE
    a) CEREBRAL HYPOXIA - Report of a post-mortem evaluation revealed a pattern of cerebral hypoxia similar to but not identical to carbon monoxide poisoning -- selective to lentricular nuclei and calcarine cortex with loss of Purkinje cells in cerebellum (Gresham & Treip, 1983).
    b) del Amo et al (1996) reported CT and MR findings of basal ganglia and cortex lesions similar to those observed in methanol and carbon monoxide poisonings in a patient with acute trichloroethane intoxication due to inhalation of typewriter correction fluid.
    C) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) The symptoms of acute overdosage include dizziness, fainting, unconsciousness, and coma. CNS depression and disturbances in equilibrium have been reported (Stewart, 1971).
    D) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Tonic-clonic seizures have been reported following a suicide attempt with inhalation of trichloroethane in a 17-year-old. An EEG showed epileptiform activity. Seizure activity responded to phenobarbital (Winek et al, 1997).
    E) PSYCHOMOTOR AGITATION
    1) WITH POISONING/EXPOSURE
    a) gitation may occur as a result of acute intoxications (King et al, 1985; Lewis, 2000).
    F) HALLUCINATIONS
    1) WITH POISONING/EXPOSURE
    a) Hallucinations may be noted following acute exposure (Lewis, 2000; D'Costa & Gunasekera, 1990).
    G) CEREBRAL EDEMA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - A 15-year-old boy suffered cerebral edema with tonsillar herniation following acute exposure (suspected abuse) to trichloroethane in typewriter correction fluid and subsequently died (D'Costa & Gunasekera, 1990).
    H) COGNITIVE FUNCTION FINDING
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES - Exposure of volunteers to 2 different concentrations of trichloroethane for 3.5 hours demonstrated a pattern of performance deficits which followed the time course of blood solvent concentrations (MacKay et al, 1987).
    b) Workers exposed to long-term repetitive moderate to high exposures have experienced toxic encephalopathy, with memory loss, disequilibrium, personality changes, decreased ability to concentrate, and deficits in vestibular, somatosensory, and ocular components of balance (Kelafant et al, 1994). A definite causal relationship has not been established however.
    I) NEUROPATHY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORTS - Two workers who immersed their hands into trichloroethane-containing solvent for several hours at a time presented to their physicians with symptoms of preponderantly distal sensory peripheral neuropathy. Four years after stopping the exposures, one patient was shown to have chronic ongoing neuropathy (axonopathy and myelinopathy) as seen on sural nerve biopsies. A absolute causal link to trichloroethane was not established (Liss, 1988).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CNS DEPRESSION
    a) MICE - Locomotor activity in mice was reduced with the highest concentrations of inhaled 1,1,1-trichloroethane. Following 30 minute inhalations of 10,000 ppm, motor activity was reduced to 26% of baseline values (Bowen & Balster, 1996).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, diarrhea, and burns of the esophagus have been noted after large ingestions.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting have been noted within 30 minutes following ingestion of 1,1,1-trichloroethane (Lewis, 2000; Gerace, 1981).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea has been reported 30 to 60 minutes following 1,1,1 trichloroethane oral ingestion (Lewis, 2000; Gerace, 1981).
    C) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) Burns of the esophagus have been noted after large ingestions (Gerace, 1981).

Hepatic

    3.9.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Toxic exposures may cause transient increases in liver enzymes. Fatty liver disease has also been reported.
    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Toxic exposures may cause transient increases in liver enzymes (Gerace, 1981).
    b) CASE REPORT - Fibrotic liver changes were reported in a 26-year-old male as a result of a chronic (4 years) occupational exposure to trichloroethane while spraying an adhesive with no respirator. Several months after cessation of exposure, his liver function tests showed improvement (Cohen & Frank, 1994).
    B) STEATOSIS OF LIVER
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES - Hodgson et al (1989) reported 4 cases of fatty liver disease in workers with substantial exposure to 1,1,1-trichloroethane. No cause and effect relationship could be established.
    C) LARGE LIVER
    1) WITH POISONING/EXPOSURE
    a) Hepatic edema may be noted following acute exposure (D'Costa & Gunasekera, 1990).
    b) LACK OF ADVERSE EFFECT
    1) CASE SERIES - There was no indication of liver or kidney damage in subjects exposed to 7 hours/day for 5 days to 440 to 4560 ppm (Stewart et al, 1969).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) Hepatic lesions have been seen in animals after chronic, continuous exposure to 1000 ppm trichloroethane (McNutt et al, 1975).

Genitourinary

    3.10.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Toxic exposures may cause transient renal impairment.
    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) WITH POISONING/EXPOSURE
    a) Toxic exposures may cause transient renal impairment (Stewart et al, 1961).
    B) ABNORMAL URINE
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES - Positive urinary urobilinogen occurred 7 hours after 2 subjects were exposed to 0 to 2650 ppm over a 15-minute period (Stewart et al, 1961).
    b) LACK OF ADVERSE EFFECT
    1) CASE SERIES - There was no indication of liver or kidney damage in subjects exposed 7 hours/day for 5 days to 440 to 4560 ppm (Stewart et al, 1969).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) LACK OF EFFECT
    a) Animal LD50 studies have shown that trichloroethane has minimal capacity to produce organ injury, including the kidney, from either single or repeated exposures. However, at very high concentrations it can sensitize the heart to epinephrine (Torkelson, 1994).

Dermatologic

    3.14.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Cutaneous vesiculations and erythema may occur after prolonged contact. Allergic contact dermatitis has been reported.
    3.14.2) CLINICAL EFFECTS
    A) BULLOUS ERUPTION
    1) WITH POISONING/EXPOSURE
    a) Cutaneous vesiculations may occur with prolonged contact (Jones & Winter, 1983).
    B) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) An erythematous reaction may occur from prolonged contact (Stewart & Dodd, 1964).
    C) CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Allergic contact dermatitis presenting as severe eczema has been reported following exposure to 1,1,1-trichloroethane (Ingber, 1991).
    D) DRY SKIN
    1) WITH POISONING/EXPOSURE
    a) Like many solvents, 1,1,1-trichloroethane will defat the skin, causing redness and scaliness. Absorption through the skin can occur, but is not a significant route of toxic exposure (ACGIH, 2001).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RASH
    a) A single topical application of 1 ml or repeated contact over 3 days caused edema, erythema, inflammation and cellular degeneration in guinea pig skin (ACGIH, 2001).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) EOSINOPHIL COUNT RAISED
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Eosinophilic pneumonia, responding to corticosteroid therapy, has been reported following repetitive inhalational abuse of a trichloroethane product in a 15-year-old male (Kelly & Ruffing, 1993).
    B) SYSTEMIC SCLEROSIS
    1) WITH POISONING/EXPOSURE
    a) Cases of scleroderma, with positive ANA's, have been reported following chronic occupational dermal exposures to trichloroethane when used as a solvent. Definite causal relationships have not been established (Flindt-Hansen & Isager, 1987).

Reproductive

    3.20.1) SUMMARY
    A) Teratogenic effects have not been reported in humans or experimental animals.
    3.20.2) TERATOGENICITY
    A) ENVIRONMENTAL EXPOSURE
    1) Two cases of multiple malformations were reported in infants whose mothers were exposed to 1,1,1-trichloroethane together with other chemicals (Schardein, 1993).
    2) In an epidemiological study, pregnant women exposed to trichloroethane in contaminated drinking water appeared to have an excess of spontaneous abortions and infants with birth defects, including cardiac anomalies, when compared to controls not exposed to the water (Deane et al, 1989; Epstein et al, 1991; Swan et al, 1989). A direct causal relationship was not established.
    3) Studies have been done of a population whose drinking water was contaminated with 1,1,1-trichloroethane from a leaking underground storage tank (Schardein, 1993). Although there were 22 spontaneous abortions, 7 infants who died of congenital cardiac defects, and 18 infants with other cardiac conditions in this population, studies could not make a causal association between these reproductive effects and 1,1,1-trichloroethane exposure (Schardein, 1993).
    B) ANIMAL STUDIES
    1) LACK OF EFFECT
    a) In a 2-generation study, trichloroethane given orally to mice at 0.58 to 5.83 mg/mL in the drinking water (corresponding to 100 to 1000 mg/kg/day) had no effects on fertility and was not teratogenic (Lane, 1982). Rats given 2100 ppm trichloroethane by inhalation had offspring with lower fetal weights and delayed development of bones and kidneys, findings not regarded as teratogenic by the authors (York et al, 1982). This study was interpreted by the authors as showing embryotoxic effects of trichloroethane.
    b) In another inhalation study in rats and mice, trichloroethane at 875 ppm given from day 6 to 15 of pregnancy was not teratogenic (Schwetz, 1975). In an unconfirmed and unpublished study, trichloroethane was reported to cause persistent ductus arteriosus in rats (Hutcheon et al, 1985). Trichloroethane was teratogenic when injected into the air space of chicken eggs (Elovaara, 1979), but the latter study has questionable pertinence to occupational exposures.
    c) When trichloroethane was administered via drinking water (at 3, 10, and 30 ppm) to female rats, no significant morphological developmental effects were seen in the offspring (George et al, 1989).
    d) Offspring of pregnant CD-1 mice exposed by inhalation to airborne concentrations of 2,000 ppm of 1,1,1-trichloroethane for 17 hours on days 12 through 17 of gestation or to 8,000 ppm for 60 minutes on the same days had poorer weight gain and delays in developmental and kinesthesic landmarks (Jones et al, 1996).
    2) FETOTOXICITY
    a) Fetotoxicity was seen in rats when the dams were exposed to 2100 ppm of 1,1,1-trichloroethane 6 hours/day on days 1 through 20 of gestation (RTECS, 2003). Specific abnormalities of the cardiovascular system were seen in the offspring when the dams were given oral doses of 43 mg/kg of 1,1,1-trichloroethane daily on days 1 through 22 of pregnancy and for 21 days after delivery(RTECS, 2003) .
    3) SKELETAL MALFORMATION
    a) One report showed an increased incidence of skeletal and soft tissue abnormalities in fetal rats when their mothers were exposed to higher than TLV levels of trichloroethane prior to and during gestation.
    1) These abnormalities appeared to resemble developmental delays rather than true teratogenicity (York et al, 1982).
    b) In a 2-generation study, 1,1,1-trichloroethane given orally to mice at 0.58 to 5.83 mg/mL in the drinking water (corresponding to 100 to 1000 mg/kg/day) had no effects on fertility and was not teratogenic (Lane, 1982). Rats exposed to airborne concentration of 2100 ppm of 1,1,1-trichloroethane had offspring with lower fetal weights and delayed development of bones and kidneys, findings not regarded as teratogenic (York et al, 1982).
    3.20.3) EFFECTS IN PREGNANCY
    A) SPONTANEOUS ABORTION
    1) A study of spontaneous abortion rates in women exposed to drinking water contaminated with 1,1,1-trichloroethane showed no statistical significance between rates in exposed and non-exposed women (Epstein et al, 1991).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS71-55-6 (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) IARC Classification
    a) Listed as: 1,1,1-Trichloroethane
    b) Carcinogen Rating: 3
    1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    3.21.2) SUMMARY/HUMAN
    A) The US EPA classifies 1,1,1-trichloroethane in Group D (not classifiable as to human carcinogenicity); however, evidence is inadequate.
    3.21.3) HUMAN STUDIES
    A) PANCREATIC DISORDER
    1) Three men less than 45 years of age developed biliary-pancreatic cancer after heavy exposure to 1,1,1-trichloroethane. While other risk factors were involved such as exposure to other solvents and a family history of cancer, this report supports a possible association between chronic 1,1,1-trichloroethane exposure and biliary-pancreatic cancer (Zarchy, 1996).
    B) CARCINOMA
    1) The US EPA classifies 1,1,1-trichloroethane in Group D (not classifiable as to human carcinogenicity) (HSDB, 2003). The ACGIH lists it in category A4 (not classifiable as a human carcinogen) (ACGIH, 2001).
    2) A case-control study conducted in Montreal, Canada of occupational exposures to any of 6 chlorinated solvents (carbon tetrachloride, methylene chloride, 1,1,1-trichloroethane, chloroform, trichloroethylene, and tetrachloroethylene) and association with cancer found an increased risk of prostate cancer with tetrachloroethylene exposure and an increased risk of melanoma with trichloroethylene exposure. The analysis that included 3730 cancer cases (occurring from 1979 to 1985) and 533 population controls focused on the following 11 cancer types: esophagus, stomach, colon, rectum, liver, pancreas, prostate, bladder, kidney, melanoma, and non-Hodgkin lymphoma. An association was observed between tetrachloroethylene exposure and risk of prostate cancer (odds ratio [OR], 2.2; 95% CI, 0.8 to 5.7 for any exposure and OR, 4.3; 95% CI, 1.4 to 13 for substantial exposure), as well as between trichloroethylene exposure and melanoma risk (OR, 3; 95% CI, 1.2 to 7.2 for any exposure and OR, 3.2; 95% CI, 1 to 9.9 for substantial exposure). There was also an association between substantial exposure to chlorinated alkenes (ie, trichloroethylene and tetrachloroethylene) in general and melanoma risk (OR, 2.6; 95% CI, 1 to 7.1). Substantial exposure was defined as a degree of confidence that the exposure actually occurred of probable or definite, a medium or high solvent concentration and frequency of exposure, and a duration of exposure that was greater than 5 years. While an association between substantial exposure to chloroform and risk of pancreatic cancer exists (OR, 10.6; 95% CI, 1.2 to 93), this was based on only 2 exposed workers. The majority of ORs were close to null or like the chloroform and pancreatic association, were based on very small numbers, thereby providing limited power to detect real risk (Christensen et al, 2013).
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) A lifetime inhalation bioassay for chronic toxicity and possible carcinogenicity of trichloroethane in rats and mice given concentrations up to 1500 ppm for 6 hours/day, 5 days/week for 24 months found no statistically significant oncologic effects. Survival rates were also unaffected (ACGIH, 2001).

Genotoxicity

    A) 1,1,1-Trichloroethane has induced DNA repair in E. coli, mutations in mouse lymphocytes and S. typhimurium, was positive for cytogenetic analysis in hamster ovary cells, and caused morphological transformation in rat, mouse, and hamster embryo cells and hamster kidney cells.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Trichloroethane can be found in expired air, blood, and urine. Its metabolites can be detected in the urine.
    B) Monitor ECG, vital signs and mental status following acute exposures.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) Trichloroethane can be measured in expired air, blood and urine. Its metabolites can be detected in urine. These tests are not readily available at most institutions and cannot be used to guide therapy.
    B) BLOOD/SERUM CHEMISTRY
    1) Obtain baseline hepatic and kidney function tests; dysfunction may occur transiently after recovery from CNS depression and hypotension (Stewart, 1971).
    4.1.4) OTHER
    A) OTHER
    1) ECG
    a) Monitor ECG in all symptomatic patients.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Monitor chest x-ray in all symptomatic patients.
    B) RADIOGRAPHIC-OTHER
    1) Trichloroethane was shown to be radio-opaque in rats (Dally et al, 1987).

Methods

    A) SAMPLING
    1) SAMPLE - Trichloroethane can be found in expired air, blood and urine. Its metabolites, trichloroacetic acid and trichloroethanol, can be detected in the urine (Baselt, 2000).
    B) CHROMATOGRAPHY
    1) Trichloroethane quantification in blood and tissues has been made using a gas chromatography/flame ionization detector (Winek et al, 1997).
    C) OTHER
    1) BREATH ANALYSIS - Of air collected in a plastic bag and analysis by IR or GC is becoming more widely used (Stewart et al, 1969). Serial breath analyses may allow for an estimation of the amount absorbed.
    2) LIVER STRESS - Excessive single exposures to trichloroethane produce liver stress. The most sensitive test of liver stress has been reported as urinary urobilinogen (Gerace, 1981).
    3) TITANIUM - Typewriter correction fluid contains titanium dioxide and the finding of white particulate matter in nose and/or on hands may be a clue to diagnosis.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Any patient suspected of a toxic oral or inhalational exposure to trichloroethane should be monitored in a controlled setting until all signs and symptoms of toxicity have subsided.

Monitoring

    A) Trichloroethane can be found in expired air, blood, and urine. Its metabolites can be detected in the urine.
    B) Monitor ECG, vital signs and mental status following acute exposures.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) 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).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) 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.
    2) 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) There is no specific antidote for toxic exposures to trichloroethane. Treatment is symptomatic and supportive. Monitor for CNS depression and treat symptomatically. Monitor respiratory function; airway management and ventilation may be necessary. Monitor ECG in patients with significant exposure. Avoid administration of adrenergic agonist medications whenever possible.
    2) Although trichloroethane is eliminated via the lung, there is no evidence that administration of an oxygen carbon dioxide mix, to stimulate respiration, has any effect (Stewart, 1971).
    3) Keeping the patient calm may reduce the possibility of endogenous catecholamines enhancing cardiac irritability.
    B) MONITORING OF PATIENT
    1) CARDIAC MONITORING
    a) Monitor ECG and cardiac function closely.
    b) Kobayashi et al (1987), working with dogs, suggested the sympathetic nervous system may play a major role in intoxication. They found favorable effects on the heart rate by using propranolol.
    2) HEPATIC/RENAL FUNCTION
    a) Obtain baseline hepatic and kidney function tests, a dysfunction may occur transiently after recovery from CNS depression, and hypotension (Stewart, 1971).
    C) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    D) 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).

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) 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 persists after 15 minutes of irrigation, an ophthalmologic examination should be performed.

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).

Enhanced Elimination

    A) HEMODIALYSIS
    1) Hemodialysis is of no benefit to eliminate trichloroethane after exposure.

Abstracts

Case Reports

    A) CHRONIC EFFECTS - McLeod (1987) reported two patients with repeated exposure to 1,1,1-trichloroethane who experienced cardiac deterioration with halothane (a related compound) anesthesia. They propose the possibility of chronic cardiac toxicity induced by repeated exposure to TCE followed by a toxic interaction with halothane.
    B) ADULT
    1) Troutman (1988) reported 3 deaths from the intentional inhalation abuse of a typewriter correction fluid containing both 1,1,1-trichloroethane and trichloroethylene. One patient was found collapsed in a field with a bottle of this material in his hand, one was found locked in a bathroom with a bag containing the material over his head, and the third collapsed during an altercation after abusing the material throughout the day.
    a) None of the three patients could be resuscitated. Although mustard oil has been added to this product to discourage abuse, it did not deter these three victims (Troutman, 1988).
    C) PEDIATRIC
    1) A 15-year-old boy suspected of intentionally inhaling trichloroethane contained in Tipp-Ex(R), a typewriter correction fluid, developed double vision and hallucinations. He was transported to the ER where he subsequently died. Postmortem examination revealed a grossly edematous brain with marked tonsillar herniation; edema was also found in the lungs, liver, and gut. The blood trichloroethane concentration was 1.7 mg/L (D'Costa & Gunasekera, 1990).

Range Of Toxicity

Summary

    A) The acute lethal dose in humans is 500 to 5000 mg/kg. Inhalation of 20,000 ppm for 60 minutes will result in surgical anesthesia and possibly death.
    B) Based on effects caused in monkeys and rats, the following effects are expected in humans: 20,000 ppm for 60 minutes, coma and possibly death; 10,000 ppm for 30 minutes, marked incoordination; 2000 ppm for 5 minutes, disturbance of equilibrium.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The acute lethal dose in humans has been estimated as 500 to 5000 mg/kg (Fasset & Irish, 1973).
    2) Torkelson (1994) reports that inhalation of 20,000 ppm for 60 minutes will result in a surgical anesthesia and possible death in humans (Torkelson, 1994).
    3) Inhalation of 1,1,1-trichloroethane at concentrations greater than 14,000 to 15,000 is capable of causing death (ACGIH, 2001; Bingham et al, 2001).
    4) Death occurred after a few minutes of exposure to 70,000 ppm of 1,1,1- trichloroethane. In another case, a concentration of greater than 5000 ppm caused death to occur within 10 minutes (IPCS (International Programme on Chemical Safety), 1992).
    5) Based on effects caused in monkeys and rats, the following effects are expected in humans: 20,000 ppm for 60 minutes, coma and possibly death; 10,000 ppm for 30 minutes, marked incoordination; 2000 ppm for 5 minutes, disturbance of equilibrium (Proctor et al, 1988).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The highest concentration of unintentional exposure to 1,1,1-trichloroethane for five minutes or less that would not cause irreversible damage or incapacitation which would prevent escape is 2500 ppm (OHM/TADS, 2003).
    2) The lowest published toxic dose (TDLo) in humans is reported to be 670 mg/kg, with resultant nausea, vomiting and diarrhea (RTECS, 2003). The lowest published inhalational toxic concentration (TCLo) in man is reported to be 200 ppm for 4 hours, with resultant behavioral changes (RTECS, 2003).
    3) "The anesthetic effects of trichloroethane, such as lightheadedness and loss of coordination, are displayed by persons exposed to vapor concentrations exceeding 1000 ppm" (Baselt, 1997; Baselt, 2000a).
    4) CARCINOGENICITY RATINGS
    a) The American Conference of Governmental Industrial Hygienists (ACGIH) has states that 1,1,1-trichloroethane is not classifiable as a human carcinogen; this corresponds to a carcinogenicity rating of A4 (HSDB, 2003).
    b) The International Agency for Research of Cancer (IARC) defines 1,1,1-trichloroethane as a Group 3 carcinogen, not classifiable as to its carcinogenicity in humans. Evidence of carcinogenicity was inadequate in both humans and experimental animals ((IARC, 1999)).
    B) CASE REPORTS
    1) An epidemiological study of 151 men and women exposed to 1,1,1-trichloroethane (exposure periods ranged from several months to six years) at exposure levels sometimes exceeding 200 ppm found no adverse effects related to exposure in workers as compared to control subjects (Hathaway et al, 1996; ACGIH, 2001).
    2) When exposed to 900 to 1000 ppm for 20 minutes, human subjects experienced light-headedness, incoordination, and impaired equilibrium; at similar concentrations, transient eye irritation has also been reported. Impairments in psychomotor task performance have been demonstrated at levels around 350 ppm (Hathaway et al, 1996).
    3) A 37-year-old female with no cardiac history inhaled a product containing 30% trichloroethane for 20 minutes in a closed bathroom and experienced a silent myocardial infarction (Bailey et al, 1997).
    C) ANIMAL DATA
    1) Trichloroethane at concentrations above 14,000 to 15,000 ppm is fatal to experimental animals (Torkelson, 1994).
    2) When doses of 0.5 g/kg were applied repeatedly for 90 days to rabbits, no effects were caused except for slight reversible irritation of the skin at the site of application (ACGIH, 2001).
    3) Exposure to the vapor at 500 ppm for seven hours a day, five days per week for six months did not cause any toxic changes of significance in rats, guinea pigs, rabbits, or monkeys (ACGIH, 2001).
    4) Animal studies confirm the low hepatotoxicity of 1,1,1-trichloroethane but indicate that a lowered myocardial threshold to the dysrhythmogenic effects of epinephrine can occur if exposures are excessive (ACGIH, 2001).
    5) Based on effects caused in monkeys and rats, the following effects are predicted to occur in humans: 20,000 ppm for 60 minutes, coma and possibly death; 10,000 ppm for 30 minutes, marked incoordination; 2000 ppm for 5 minutes, disturbance of equilibrium (Hathaway et al, 1996).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CASE REPORTS
    a) In three fatal cases of apparent 1,1,1-trichloroethane inhalation, blood concentrations of 1,1,1-trichloroethane were 0.003, 0.2, and 7.4 micrograms/gram of blood (Macdougall et al, 1987).
    b) In other reported fatalities, blood concentrations of trichloroethane have ranged from 2 to 42 milligrams/liter (Jones & Winter, 1983; King et al, 1985).
    c) In one reported fatality involving a 15-year-old boy, the blood trichloroethane concentration was 1.7 milligrams/liter (D'Costa & Gunasekera, 1990).

Workplace Standards

    A) ACGIH TLV Values for CAS71-55-6 (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) Methyl chloroform
    a) TLV:
    1) TLV-TWA: 350 ppm
    2) TLV-STEL: 450 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: BEI
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) 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.
    c) TLV Basis - Critical Effect(s): CNS impair; liver dam
    d) Molecular Weight: 133.42
    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 CAS71-55-6 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Methyl chloroform
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling: 350 ppm (1900 mg/m(3)) [15-minute]
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix C (Chloroethanes)
    3) IDLH:
    a) IDLH: 700 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS71-55-6 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Methyl chloroform
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) EPA (U.S. Environmental Protection Agency, 2011): Inadequate information to assess carcinogenic potential ; Listed as: 1,1,1-Trichloroethane
    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): 3 ; Listed as: 1,1,1-Trichloroethane
    a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Methyl chloroform
    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 CAS71-55-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Methyl chloroform (1,1,1-Trichloroethane)
    2) Table Z-1 for Methyl chloroform (1,1,1-Trichloroethane):
    a) 8-hour TWA:
    1) ppm: 350
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 1900
    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) LD50- (INTRAPERITONEAL)MOUSE:
    1) 5083 mg/kg (Hayes & Laws, 1991)
    2) Female, 3700 mg/kg (IPCS (International Programme on Chemical Safety), 1992)
    3) Male, 5080 mg/kg(HSDB, 2003; IPCS (International Programme on Chemical Safety), 1992)
    4) 2568 mg/kg(RTECS, 2003)
    5) 3636 mg/kg (Lewis, 2000)
    B) LD50- (ORAL)MOUSE:
    1) Female, 11.24 g/kg(HSDB, 2003; Lewis, 2000)
    2) Female, 9700 mg/kg (IPCS (International Programme on Chemical Safety), 1992)
    3) 6 g/mg - weight loss/decreased weight gain; change in pulse rate(RTECS, 2003)
    C) LD50- (SUBCUTANEOUS)MOUSE:
    1) 16 g/kg - changes in sleep; ataxia(RTECS, 2003)
    D) LD50- (INTRAPERITONEAL)RAT:
    1) 3593 mg/kg(RTECS, 2003)
    2) 3.9 g/kg (Bingham et al, 2001a)
    E) LD50- (ORAL)RAT:
    1) Female, 11,000 ppm (IPCS (International Programme on Chemical Safety), 1992)
    2) Female, 10,300 ppm (ATSDR, 1995)
    3) Sprague-Dawley, Female, 12,996 ppm (ATSDR, 1995)
    4) Sprague-Dawley, Male, 17,148 ppm (ATSDR, 1995)
    5) Male, 12,300 mg/kg (ATSDR, 1995)
    6) Male, 14,300 mg/kg (IPCS (International Programme on Chemical Safety), 1992)
    7) 9600 mg/kg - change in pulse rate; weight loss/decreased weight gain(RTECS, 2003)
    F) TCLo- (INHALATION)HUMAN:
    1) 350 ppm - behavioral changes(RTECS, 2003)
    2) 350 ppm -- central nervous system effects (Lewis, 2000)
    3) 200 ppm for 4H - changes in sense organs(RTECS, 2003)
    4) 200 ppm for 4H - motor activity changes; irritability(RTECS, 2003)
    5) 920 ppm for 70M - behavioral changes; conjunctive irritation(RTECS, 2003)
    G) TCLo- (INHALATION)MOUSE:
    1) 1000 ppm for 2H/3W-intermittent - motor activity changes; liver changes; red blood cell count changes(RTECS, 2003)
    H) TCLo- (INHALATION)RAT:
    1) female, 2100 ppm for 6H at 1-20D of pregnancy - fetotoxicity (except death)(RTECS, 2003)
    2) female, 7000 ppm for 3H at 13-19D of pregnancy - maternal effects; effects on live birth index; behavioral effects on newborns(RTECS, 2003)
    3) 10,000 ppm for 1H/13W-intermittent - changes to liver(RTECS, 2003)
    4) 2100 ppm for 24H/14D/1-20D preg -- teratogenic effects (Lewis, 2000)

Pharmacology Toxicology

Toxicologic Mechanism

    A) Trichloroethane has a rapid anesthetic action and was used for this purpose medically but was abandoned with the advent of safer agents. Vasospasm or myocardial sensitization to endogenous catecholamines, caused by trichloroethane toxicity, may precipitate dysrhythmias or ischemia secondary to increased oxygen demand (Bailey et al, 1997).

Physicochemical

Physical Characteristics

    A) Trichloroethane is a colorless, watery, nonflammable liquid with an odor that has been described as ethereal, chloroform-like, sweetish and pleasant (ATSDR, 1995; Budavari, 1996; CHRIS, 2003; Lewis, 2000; Pohanish, 2002). At 1500-2000 ppm, the odor has been described as unpleasant and strong (Bingham et al, 2001).
    B) It has no flash point or fire point by ASTM procedures for Tag closed cup and Cleveland open cup tests. Even though trichloroethane has no flash point, it will burn as a vapor, although not as a liquid (de Nevers, 1986). A considerable amount of energy is necessary for ignition, and it will not sustain combustion (Torkelson, 1994).

Molecular Weight

    A) 133.40

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.
    5) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    6) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    7) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    9) 66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.
    10) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
    11) 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
    12) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
    13) AAR: Emergency Handling of Hazardous Materials in Surface Transportation, Bureau of Explosives, Association of American Railroads, Washington, DC, 2000.
    14) ACGIH: Documentation of the Threshold Limit Value and Biological Exposure Indices, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991a.
    15) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices (Supplement), 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1996.
    16) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991.
    17) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, 7th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 2001.
    18) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    19) AMA Department of DrugsAMA Department of Drugs: AMA Evaluations Subscription, American Medical Association, Chicago, IL, 1992.
    20) ATSDR: Toxicological Profile for 1,1,1-Trichloroethane. US Dept, Agency for Toxic Substances and Disease Registry, US Dept of Health and Human Services, Atlanta, GA, 1995.
    21) Ahlert RC & Enzminger JD: Anaerobic processes for the dechlorination of 1,1,1-trichloroethane. J Environ Sci Health 1992; 7(Part A):1675-1699.
    22) Alaspaa AO, Kuisma MJ, Hoppu K, et al: Out-of-hospital administration of activated charcoal by emergency medical services. Ann Emerg Med 2005; 45:207-12.
    23) American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.
    24) Ansell-Edmont: SpecWare Chemical Application and Recommendation Guide. Ansell-Edmont. Coshocton, OH. 2001. Available from URL: http://www.ansellpro.com/specware. As accessed 10/31/2001.
    25) Ashford R: Ashford's Dictionary of Industrial Chemicals, 2nd ed, Wavelength Publications Ltd, London, England, 2001.
    26) Ashford R: Ashford's Dictionary of Industrial Chemicals, Wavelength Publications Ltd, London, England, 1994.
    27) Bailey B, Loebstein R, & Lai C: Chlorinated hydrocarbon-associated myocardial ischemia: report of two cases (abstract). J Tox - Clin Tox 1997; 35(5):515.
    28) Banathy LJ & Chan LT: Fatality caused by inhalation of "liquid paper" correction fluid. Med J Aust 1983; 2:606.
    29) Baselt RC: Biological Monitoring Methods for Industrial Chemicals, 3rd ed, Chemical Toxicology Institute, Foster City, CA, 1997.
    30) Baselt RC: Disposition of Toxic Drugs and Chemical in Man, 5th ed, Chemical Toxicology Institute, Foster City, CA, 2000.
    31) Baselt RC: Disposition of Toxic Drugs and Chemicals in Man, 5th ed, Chemical Toxicology Institute, Foster City, CA, 2000a.
    32) Bata Shoe Company: Industrial Footwear Catalog, Bata Shoe Company, Belcamp, MD, 1995.
    33) Best Manufacturing: ChemRest Chemical Resistance Guide. Best Manufacturing. Menlo, GA. 2002. Available from URL: http://www.chemrest.com. As accessed 10/8/2002.
    34) Best Manufacturing: Degradation and Permeation Data. Best Manufacturing. Menlo, GA. 2004. Available from URL: http://www.chemrest.com/DomesticPrep2/. As accessed 04/09/2004.
    35) Bingham E, Cohrssen B, & Powell CH: Patty's Toxicology 5th ed, John Wiley & Sons, Inc, New York, NY, 2001a.
    36) Bingham E, Cohrssen B, & Powell CH: Patty's Toxicology, Vol 5, 5th ed, John Wiley & Sons, New York, NY, 2001.
    37) Boss Manufacturing Company: Work Gloves, Boss Manufacturing Company, Kewanee, IL, 1998.
    38) Bowen SE & Balster RL: Effects of inhaled 1,1,1-trichloroethane on locomotor activity in mice. Neurotoxicol Teratol 1996; 18:77-81.
    39) Brophy GM, Bell R, Claassen J, et al: Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 2012; 17(1):3-23.
    40) Budavari S: The Merck Index, 12th ed, Merck & Co, Inc, Whitehouse Station, NJ, 1996, pp 1642-1643.
    41) Budavari S: The Merck Index, 12th edition, Merck & Co, Inc, Whitehouse Station, NJ, 1996a.
    42) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    43) CHRIS : CHRIS Hazardous Chemical Data. US Department of Transportation, US Coast Guard. Washington, DC (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    44) CHRIS: CHRIS Hazardous Chemical Data. U.S. Department of Transportation, U.S. Coast Guard. Washington, DC, USA (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    45) CHRIS: CHRIS Hazardous Chemical Data. US Department of Transportation, US Coast Guard. Washington, DC (Internet Version). Edition expires 2003; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    46) Caperos JR: Internat Arch Occupat Environ Health 1982; 49:293-303.
    47) Chamberlain JM, Altieri MA, & Futterman C: A prospective, randomized study comparing intramuscular midazolam with intravenous diazepam for the treatment of seizures in children. Ped Emerg Care 1997; 13:92-94.
    48) ChemFab Corporation: Chemical Permeation Guide Challenge Protective Clothing Fabrics, ChemFab Corporation, Merrimack, NH, 1993.
    49) Chin RF , Neville BG , Peckham C , et al: Treatment of community-onset, childhood convulsive status epilepticus: a prospective, population-based study. Lancet Neurol 2008; 7(8):696-703.
    50) Choonara IA & Rane A: Therapeutic drug monitoring of anticonvulsants state of the art. Clin Pharmacokinet 1990; 18:318-328.
    51) Christensen KY, Vizcaya D, Richardson H, et al: Risk of selected cancers due to occupational exposure to chlorinated solvents in a case-control study in Montreal. J Occup Environ Med 2013; 55(2):198-208.
    52) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    53) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Volume 2A, Toxicology, 4th ed, John Wiley & Sons, New York, NY, 1993, pp 752-763.
    54) Cohen C & Frank AL: Liver disease following occupational exposure to 1,1,1-trichloroethane: a case report. Amer J Ind Med 1994; 26:237-241.
    55) Comasec Safety, Inc.: Chemical Resistance to Permeation Chart. Comasec Safety, Inc.. Enfield, CT. 2003. Available from URL: http://www.comasec.com/webcomasec/english/catalogue/mtabgb.html. As accessed 4/28/2003.
    56) Comasec Safety, Inc.: Product Literature, Comasec Safety, Inc., Enfield, CT, 2003a.
    57) D'Costa DF & Gunasekera NPR: Fatal cerebral edema following trichloroethane abuse. J Royal Soc Med 1990; 83:533-534.
    58) DFG: List of MAK and BAT Values 2002, Report No. 38, Deutsche Forschungsgemeinschaft, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Wiley-VCH, Weinheim, Federal Republic of Germany, 2002.
    59) Dagnone D, Matsui D, & Rieder MJ: Assessment of the palatability of vehicles for activated charcoal in pediatric volunteers. Pediatr Emerg Care 2002; 18:19-21.
    60) Dally S, Garnier R, & Bismuth C: Diagnosis of chlorinated hydrocarbon poisoning by x ray examination. Br J Ind Med 1987; 44:424-425.
    61) Deane M, Swan SH, & Harris JA: Adverse pregnancy outcomes in relation to water contamination, Santa Clara County, California, 1980-1981. Amer J Epidemiol 1989; 129:894-904.
    62) Donaldson HM, Levy BS & Plotnick HB et al: Occupational exposure to 1,1,1-trichloroethane (methyl chloroform), DHEW [NIOSH] No 76-184. Government Printing Office, 1976.
    63) Droz PO: in, Colling AJ & Luxon SG (Eds), Safe Use of Solvents, Academic Press, London, UK, 1982, pp 153-159.
    64) DuPont: DuPont Suit Smart: Interactive Tool for the Selection of Protective Apparel. DuPont. Wilmington, DE. 2002. Available from URL: http://personalprotection.dupont.com/protectiveapparel/suitsmart/smartsuit2/na_english.asp. As accessed 10/31/2002.
    65) DuPont: Permeation Guide for DuPont Tychem Protective Fabrics. DuPont. Wilmington, DE. 2003. Available from URL: http://personalprotection.dupont.com/en/pdf/tyvektychem/pgcomplete20030128.pdf. As accessed 4/26/2004.
    66) DuPont: Permeation Test Results. DuPont. Wilmington, DE. 2002a. Available from URL: http://www.tyvekprotectiveapprl.com/databases/default.htm. As accessed 7/31/2002.
    67) EPA: Search results for Toxic Substances Control Act (TSCA) Inventory Chemicals. US Environmental Protection Agency, Substance Registry System, U.S. EPA's Office of Pollution Prevention and Toxics. Washington, DC. 2005. Available from URL: http://www.epa.gov/srs/.
    68) ERG: Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident, U.S. Department of Transportation, Research and Special Programs Administration, Washington, DC, 2004.
    69) Eben A & Kimmerle G: Archiv Fuer Toxikologie 1974; 31:233-242.
    70) Ehrenfeld JR, Ong J, & Farino W: Controlling Volatile Emissions at Hazardous Waste Sites, Noyes Publications, Park Ridge, NJ, 1986, pp 393-401.
    71) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    72) Elovaara E: Toxicol 1979; 12:111-120.
    73) Epstein D, Neutra R, & Wrensch M: No apparent excess of spontaneous abortions in subsequent pregnancies following closure of a drinking water well contaminated with trichloroethane. Arch Environ Health 1991; 46:184.
    74) Evans EB & Balster RL: Inhaled 1,1,1-trichloroethane-produced physical dependence in mice: effects of drugs and vapors on withdrawal. J Pharmacol Exp Ther 1993; 264:726-733.
    75) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    76) Fasset DW & Irish DD: Industrial Hygiene and Toxicology, 2nd revised ed, Vol 2, Wiley-Interscience, New York, NY, 1973.
    77) Flindt-Hansen H & Isager H: Scleroderma after occupational exposure to trichloethylene and trichlorethane. Acta Derm Venereol 1987; 67:263-264.
    78) Fosseus CG: Danger of inhaling trichloro-ethane (letter). SAMJ 1991; 80:629-630.
    79) Freeman HM: Standard Handbook of Hazardous Waste Treatment and Disposal, McGraw-Hill Book Company, New York, NY, 1989.
    80) Gallagher JS & Kurt TL: Neonatal exposure to methyl chloroform in tape remover. Vet Human Toxicol 1990; 32:43-45.
    81) George JD, Price CJ, & Marr MC: Developmental toxicity of 1,1,1-trichloroethane in CD rats. Fund Appl Toxicol 1989; 13:641-651.
    82) Gerace RV: Near fatal intoxication by 1,1,1-trichloroethane. Ann Emerg Med 1981; 10:533-534.
    83) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    84) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    85) Grant WM & Schuman JS: Toxicology of the Eye, 4th ed, Charles C Thomas, Springfield, IL, 1993.
    86) Gresham GA & Treip CS: Fatal poisoning by 1,1,1-trichloroethane after prolonged survival. Forens Sci Internat 1983; 23:249-253.
    87) Guardian Manufacturing Group: Guardian Gloves Test Results. Guardian Manufacturing Group. Willard, OH. 2001. Available from URL: http://www.guardian-mfg.com/guardianmfg.html. As accessed 12/11/2001.
    88) Guenther Skokan E, Junkins EP, & Corneli HM: Taste test: children rate flavoring agents used with activated charcoal. Arch Pediatr Adolesc Med 2001; 155:683-686.
    89) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 1998; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    90) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2003a; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    91) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires October/31/2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    92) HSDB: Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    93) HSDB: Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires May/31/2003; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    94) HSIA: White Paper on Methyl Chloroform (1,1,1-Trichloroethane). Halogenated Solvents Industry Alliance, Inc.. Washington, D.C.. 1994. Available from URL: http://www.hsia.org/white_papers/111tri.html. As accessed 17 April 2003.
    95) Hake CL, Waggoner TB, & Robertson DN: The metabolism of 1,1,1-trichloroethane by the rat. Arch Environ Health 1960; 1:101-105.
    96) Harbison RD: Hamilton & Hardy's Industrial Toxicology, 5th ed, Mosby-Year Books, St. Louis, MO, 1998.
    97) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    98) Hathaway GJ, Proctor NH, & Hughes JP: Proctor and Hughes' Chemical Hazards of the Workplace, 4th ed, Van Nostrand Reinhold, Co, New York, NY, 1996, pp 615-616.
    99) Hayes WJ Jr & Laws ER Jr: Handbook of Pesticide Toxicology, vol I, Academic Press, Inc, San Diego, CA, 1991, pp 687-690.
    100) Hegenbarth MA & American Academy of Pediatrics Committee on Drugs: Preparing for pediatric emergencies: drugs to consider. Pediatrics 2008; 121(2):433-443.
    101) Hodgson MJ, Heyl AE, & Van Thiel DH: Liver disease associated with exposure to 1,1,1-trichloroethane. Arch Intern Med 1989; 149:1793-1798.
    102) House RA, Liss GM, & Wills MC: Paresthesias and sensory neuropathy due to 1,1,1-trichloroethane. J Occup Environ Med 1996; 38:123-124.
    103) House RA, Liss GM, & Wills MC: Peripheral sensory neuropathy associated with 1,1,1-trichloroethane. Arch Environ Health 1994; 49:196-199.
    104) Howard PH, Boethling RS, & Jarvis WF: Handbook of Environmental Degradation Rates, Lewis Publishers, Chelsea, MI, 1991.
    105) Howard PH: Handbook of Environmental Fate & Exposure Data for Organic Chemicals, Vol 2, Lewis Publishers, Chelsea, MI, 1990a.
    106) Howard PH: Handbook of Environmental Fate and Exposure Data for Organic Chemicals. Volume I: Large Production and Priority Pollutants, Lewis Publishers, Chelsea, MI, 1990.
    107) Hughes JB & Parkin GF: The effect of mixtures of xenobiotics and primary electron donors on the anaerobic biotransformation of high concentrations of chlorinated aliphatics. Water Sci Technol 1992; 26:117-126.
    108) Hvidberg EF & Dam M: Clinical pharmacokinetics of anticonvulsants. Clin Pharmacokinet 1976; 1:161.
    109) IARC : Monographs on the Evaluation of the Carcinogenicity of Chemicals to Humans. Trichloroethylene [79-01-6]. 71. International Agency for Research on Cancer, World Health Organization. Geneva, Switzerland. 1999a. Available from URL: http://www.iarc.fr.
    110) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: 1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide), 97, International Agency for Research on Cancer, Lyon, France, 2008.
    111) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol, 88, International Agency for Research on Cancer, Lyon, France, 2006.
    112) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Household Use of Solid Fuels and High-temperature Frying, 95, International Agency for Research on Cancer, Lyon, France, 2010a.
    113) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Smokeless Tobacco and Some Tobacco-specific N-Nitrosamines, 89, International Agency for Research on Cancer, Lyon, France, 2007.
    114) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Some Non-heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures, 92, International Agency for Research on Cancer, Lyon, France, 2010.
    115) IARC: List of all agents, mixtures and exposures evaluated to date - IARC Monographs: Overall Evaluations of Carcinogenicity to Humans, Volumes 1-88, 1972-PRESENT. World Health Organization, International Agency for Research on Cancer. Lyon, FranceAvailable from URL: http://monographs.iarc.fr/monoeval/crthall.html. As accessed Oct 07, 2004.
    116) IARC: Monographs on the Evaluation of the Carcinogenicity of Chemicals to Humans. 1,1,1-Trichloroethane [71-55-6].. 71. International Agency for Research on Cancer. Lyon, France. 1999. Available from URL: http://www.iarc.fr. As accessed 17 April 03.
    117) ICAO: Technical Instructions for the Safe Transport of Dangerous Goods by Air, 2003-2004. International Civil Aviation Organization, Montreal, Quebec, Canada, 2002.
    118) ILC Dover, Inc.: Ready 1 The Chemturion Limited Use Chemical Protective Suit, ILC Dover, Inc., Frederica, DE, 1998.
    119) IPCS (International Programme on Chemical Safety): Environmental Health Criteria 136 - 1,1,1-trichloroethane, World Health Organization, Geneva, Switzerland, 1992.
    120) ITI: Toxic and Hazardous Industrial Chemicals Safety Manual, The International Technical Information Institute, Tokyo, Japan, 1995.
    121) Ingber A: Occupational allergic contact dermatitis from methyl chloroform (1,1,1-trichloroethane). Contact Dermatitis 1991; 25:193.
    122) International Agency for Research on Cancer (IARC): IARC monographs on the evaluation of carcinogenic risks to humans: list of classifications, volumes 1-116. International Agency for Research on Cancer (IARC). Lyon, France. 2016. Available from URL: http://monographs.iarc.fr/ENG/Classification/latest_classif.php. As accessed 2016-08-24.
    123) International Agency for Research on Cancer: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. World Health Organization. Geneva, Switzerland. 2015. Available from URL: http://monographs.iarc.fr/ENG/Classification/. As accessed 2015-08-06.
    124) Jinn Y, Akizuki N, Ohkouchi M, et al: Acute lung injury after inhalation of water-proofing spray while smoking a cigarette.. Respiration 1998; 65:486-488.
    125) Jones HE, Kunko PM, & Robinson SE: Developmental consequences of intermittent and continuous prenatal exposure to 1,1,1-trichloroethane in mice. Pharmacol Biochem Behav 1996; 55:635-646.
    126) Jones RD & Winter DP: Two case reports of death on industrial premises attributed to 1,1,1-trichloroethane. Arch Environ Health 1983; 38:59-61.
    127) Kappler, Inc.: Suit Smart. Kappler, Inc.. Guntersville, AL. 2001. Available from URL: http://www.kappler.com/suitsmart/smartsuit2/na_english.asp?select=1. As accessed 7/10/2001.
    128) Kelafant GA, Berg RA, & Schleenbaker R: Toxic encephalopathy due to 1,1,1-trichloroethane exposure. Am J Ind Med 1994; 25:439-446.
    129) Kelly KJ & Ruffing R: Acute eosinophilic pneumonia following intentional inhalation of Scotchguard. Ann Allergy 1993; 71:358-361.
    130) Kimberly-Clark, Inc.: Chemical Test Results. Kimberly-Clark, Inc.. Atlanta, GA. 2002. Available from URL: http://www.kc-safety.com/tech_cres.html. As accessed 10/4/2002.
    131) King GS, Smialek JE, & Troutman WG: Sudden death in adolescents resulting from the inhalation of typewriter correction fluid. JAMA 1985; 253:1604-1606.
    132) Kobayashi H, Hobara T, & Satoh T: Respiratory disorders following 1,1,1-trichloroethane inhalation: a role of reflex mechanism arising from lungs. Arch Environ Health 1986; 41:149-154.
    133) Kramer CG et al: Report from the Dow Chemical Company to NIOSH. Dow Chemical Co (May 10), 1976.
    134) LaCrosse-Rainfair: Safety Products, LaCrosse-Rainfair, Racine, WI, 1997.
    135) Laine A, Seppalainen AM, & Savolainen K: Acute effects of 1,1,1-trichloroethane inhalation on the human central nervous system. Internat Arch Occup Environ Health 1996; 69:53-61.
    136) Lane RW: Toxicol Appl Pharmacol 1982; 63:409-421.
    137) Lapare S, Tardif R, & Brodeur J: Effect of various exposure scenarios on the biological monitoring of organic solvents in alveolar air. II. 1,1,1-trichloroethane and trichloroethylene. Internat Arch Occup Environ Health 1995; 67:375-394.
    138) Larsen T, Kjeldsen P, & Christensen TH: Correlation of benzene, 1,1,1-trichloroethane, and naphthalene distribution coefficients to the characteristics of aquifer materials with low organic carbon content. Chemosphere 1992; 24:979-991.
    139) Lewis RJ: Hawley's Condensed Chemical Dictionary, 13th ed, John Wiley & Sons, Inc, New York, NY, 1997.
    140) Lewis RJ: Hawley's Condensed Chemical Dictionary, 13th ed, John Wiley & Sons, Inc, New York, NY, 2001a.
    141) Lewis RJ: Hawley's Condensed Chemical Dictionary, 14th ed, John Wiley & Sons, Inc, New York, NY, 2001.
    142) Lewis RJ: Sax's Dangerous Properties of Industrial Materials, 10th ed, John Wiley & Sons, New York, NY, 2000a.
    143) Lewis RJ: Sax's Dangerous Properties of Industrial Materials, 10th ed, Van Nostrand Reinhold Company, New York, NY, 2000.
    144) Lewis RJ: Sax's Dangerous Properties of Industrial Materials, 10th ed, Van Nostrand Reinhold, a Division of International Thomson Publishing Inc, New York, NY, 2000b.
    145) Liss GM: Peripheral neuropathy in two workers exposed to 1,1,1-trichloroethane (letter). J Amer Med Assc 1988; 260:2217.
    146) Loddenkemper T & Goodkin HP: Treatment of Pediatric Status Epilepticus. Curr Treat Options Neurol 2011; Epub:Epub.
    147) MAPA Professional: Chemical Resistance Guide. MAPA North America. Columbia, TN. 2003. Available from URL: http://www.mapaglove.com/pro/ChemicalSearch.asp. As accessed 4/21/2003.
    148) MAPA Professional: Chemical Resistance Guide. MAPA North America. Columbia, TN. 2004. Available from URL: http://www.mapaglove.com/ProductSearch.cfm?id=1. As accessed 6/10/2004.
    149) MacKay CJ, Campbell L, & Samuel AM: Behavioral changes during exposure to 1,1,1 Trichloroethane: Time-course and relationship to blood solvent levels. Am J Ind Med 1987; 11:223-239.
    150) Macdougall IC, Isles C, & Oliver JS: Fatal outcome following inhalation of Tipp-Ex. Scot Med J 1987; 32:55.
    151) Manno EM: New management strategies in the treatment of status epilepticus. Mayo Clin Proc 2003; 78(4):508-518.
    152) Mar-Mac Manufacturing, Inc: Product Literature, Protective Apparel, Mar-Mac Manufacturing, Inc., McBee, SC, 1995.
    153) Marigold Industrial: US Chemical Resistance Chart, on-line version. Marigold Industrial. Norcross, GA. 2003. Available from URL: www.marigoldindustrial.com/charts/uschart/uschart.html. As accessed 4/14/2003.
    154) Marjot R & McLeod AA: Chronic non-neurological toxicity from volatile substance abuse. Human Toxicol 1989; 8:301-306.
    155) Maroni M: Scand J Work Environ Health 1977; 3:16-22.
    156) Mattsson JL, Albee RR, & Lomax LG: Neurotoxicologic examination of rats exposed to 1,1,1-trichloroethane vapor for 13 weeks. Neurotoxicol Teratol 1993; 15:313-326.
    157) McNutt NS, Amster RL, & McConnell EE: Hepatic lesions in mice after continuous inhalation exposure to 1,1,1-trichloroethane. Lab Invest 1975; 32:642-654.
    158) Memphis Glove Company: Permeation Guide. Memphis Glove Company. Memphis, TN. 2001. Available from URL: http://www.memphisglove.com/permeation.html. As accessed 7/2/2001.
    159) Monstad P, Nissen T, & Sulg IA: Sleep apnoea and organic solvent exposure. J Neurol 1987; 234:152-154.
    160) Montgomery Safety Products: Montgomery Safety Products Chemical Resistant Glove Guide, Montgomery Safety Products, Canton, OH, 1995.
    161) NFPA: Fire Protection Guide to Hazardous Materials, 12th ed, National Fire Protection Association, Quincy, MA, 1997.
    162) NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
    163) NIOSH : Pocket Guide to Chemical Hazards. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    164) NIOSH: Pocket Guide to Chemical Hazards. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    165) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 1, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2001.
    166) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 2, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2002.
    167) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 3, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2003.
    168) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 4, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2004.
    169) Nat-Wear: Protective Clothing, Hazards Chart. Nat-Wear. Miora, NY. 2001. Available from URL: http://www.natwear.com/hazchart1.htm. As accessed 7/12/2001.
    170) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,3-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    171) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,4-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    172) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Butylene Oxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648083cdbb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    173) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Dibromoethane (Proposed). United States Environmental Protection Agency. Washington, DC. 2007g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802796db&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    174) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,3,5-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    175) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 2-Ethylhexyl Chloroformate (Proposed). United States Environmental Protection Agency. Washington, DC. 2007b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037904e&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    176) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Acrylonitrile (Proposed). United States Environmental Protection Agency. Washington, DC. 2007c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648028e6a3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    177) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Adamsite (Proposed). United States Environmental Protection Agency. Washington, DC. 2007h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    178) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Agent BZ (3-quinuclidinyl benzilate) (Proposed). United States Environmental Protection Agency. Washington, DC. 2007f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ad507&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    179) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Allyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039d9ee&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    180) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    181) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Arsenic Trioxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480220305&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    182) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Automotive Gasoline Unleaded (Proposed). United States Environmental Protection Agency. Washington, DC. 2009a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cc17&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    183) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Biphenyl (Proposed). United States Environmental Protection Agency. Washington, DC. 2005j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1b7&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    184) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bis-Chloromethyl Ether (BCME) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648022db11&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    185) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Boron Tribromide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae1d3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    186) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    187) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    188) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    189) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    190) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    191) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    192) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    193) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Dimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbf3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    194) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    195) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091884e&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    196) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Phosphorodichloridate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480920347&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    197) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809203e7&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    198) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    199) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    200) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    201) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    202) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    203) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    204) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Malathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2009k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809639df&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    205) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    206) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Isothiocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a03&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    207) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a57&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    208) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl tertiary-butyl ether (Proposed). United States Environmental Protection Agency. Washington, DC. 2007a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802a4985&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    209) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methylchlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5f4&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    210) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    211) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c646&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    212) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN1 CAS Reg. No. 538-07-8) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    213) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN2 CAS Reg. No. 51-75-2) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    214) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN3 CAS Reg. No. 555-77-1) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    215) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Tetroxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091855b&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    216) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Trifluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e0c&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    217) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008o. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e32&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    218) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perchloryl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e268&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    219) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perfluoroisobutylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2009d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26a&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    220) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008p. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dd58&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    221) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2006d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020cc0c&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    222) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    223) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phorate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008q. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dcc8&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    224) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene (Draft-Revised). United States Environmental Protection Agency. Washington, DC. 2009e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a08a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    225) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene Oxime (Proposed). United States Environmental Protection Agency. Washington, DC. 2009f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26d&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    226) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    227) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    228) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Propargyl Alcohol (Proposed). United States Environmental Protection Agency. Washington, DC. 2006e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec91&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    229) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Selenium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec55&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    230) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Silane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d523&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    231) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    232) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    233) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Strontium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    234) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sulfuryl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec7a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    235) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tear Gas (Proposed). United States Environmental Protection Agency. Washington, DC. 2008s. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e551&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    236) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tellurium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e2a1&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    237) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tert-Octyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2008r. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5c7&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    238) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tetramethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-17.
    239) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    240) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7d608&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    241) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethylacetyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008t. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5cc&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    242) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Zinc Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    243) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for n-Butyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064808f9591&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    244) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    245) National Institute for Occupational Safety and Health: NIOSH Pocket Guide to Chemical Hazards, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Cincinnati, OH, 2007.
    246) National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
    247) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
    248) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
    249) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
    250) Neese Industries, Inc.: Fabric Properties Rating Chart. Neese Industries, Inc.. Gonzales, LA. 2003. Available from URL: http://www.neeseind.com/new/TechGroup.asp?Group=Fabric+Properties&Family=Technical. As accessed 4/15/2003.
    251) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    252) North: Chemical Resistance Comparison Chart - Protective Footwear . North Safety. Cranston, RI. 2002. Available from URL: http://www.linkpath.com/index2gisufrm.php?t=N-USA1. As accessed April 30, 2004.
    253) North: eZ Guide Interactive Software. North Safety. Cranston, RI. 2002a. Available from URL: http://www.northsafety.com/feature1.htm. As accessed 8/31/2002.
    254) OHM/TADS : Oil and Hazardous Materials/Technical Assistance Data System. US Environmental Protection Agency. Washington, DC (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    255) OHM/TADS: Oil and Hazardous Materials Technical Assistance Data System. US Environmental Protection Agency. Washington, D.C. (Internet Version). Edition expires 2003; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    256) OHM/TADS: Oil and Hazardous Materials/Technical Assistance Data System. US Environmental Protection Agency. Washington, DC (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    257) Playtex: Fits Tough Jobs Like a Glove, Playtex, Westport, CT, 1995.
    258) Pohanish RP & Greene SA: Rapid Guide to Chemical Incompatibilities, Van Nostrand Reinhold Company, New York, NY, 1997.
    259) Pohanish RP: Sittig's Handbook of Toxic and Hazardous Chemicals and Carcinogens, 4th ed, Noyes Publications/William Andrew Publishing, Norwich, NY, 2002.
    260) Pointer J: Typewriter correction fluid inhalation: a new substance of abuse. J Toxicol - Clin Toxicol 1982; 19:493-499.
    261) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    262) Proctor NH, Hughes JP, & Fischman ML: Chemical Hazards of the Workplace, 2nd ed, JB Lippincott Co, Philadelphia, PA, 1988, pp 357.
    263) Product Information: diazepam IM, IV injection, diazepam IM, IV injection. Hospira, Inc (per Manufacturer), Lake Forest, IL, 2008.
    264) Product Information: dopamine hcl, 5% dextrose IV injection, dopamine hcl, 5% dextrose IV injection. Hospira,Inc, Lake Forest, IL, 2004.
    265) Product Information: lorazepam IM, IV injection, lorazepam IM, IV injection. Akorn, Inc, Lake Forest, IL, 2008.
    266) Psychem : 1,1,1-TRICHLOROETHANE. . 1997. Available from URL: http://www.psychem.ox.ac.uk. As accessed URL non-functional -- can't find pub or location info - bas.
    267) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    268) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 5/31/1998; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    269) RTECS: Registry of Toxic Effects of Chemical Substances.. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2003; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    270) Ranson DL & Berry PJ: Death associated with the abuse of typewriter correction fluid. 1986; 26:308-310.
    271) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    272) Reinhardt CF, Mullin LS, & Maxfield ME: Epinephrine-induced cardiac arrhythmia potential of some common industrial solvents. J Occup Med 1973; 15:953-955.
    273) River City: Protective Wear Product Literature, River City, Memphis, TN, 1995.
    274) Safety 4: North Safety Products: Chemical Protection Guide. North Safety. Cranston, RI. 2002. Available from URL: http://www.safety4.com/guide/set_guide.htm. As accessed 8/14/2002.
    275) Schardein JC: Chemically Induced Birth Defects, 2nd ed, Marcel Dekker, Inc, New York, NY, 1993, pp 752-763.
    276) Schwetz BA: Toxicol Appl Pharmacol 1975; 32:84-96.
    277) Scott R, Besag FMC, & Neville BGR: Buccal midazolam and rectal diazepam for treatment of prolonged seizures in childhood and adolescence: a randomized trial. Lancet 1999; 353:623-626.
    278) Servus: Norcross Safety Products, Servus Rubber, Servus, Rock Island, IL, 1995.
    279) Sittig M: Handbook of Toxic and Hazardous Chemicals and Carcinogens, 3rd ed, Noyes Publications, Park Ridge, NJ, 1991.
    280) Spiller HA & Rogers GC: Evaluation of administration of activated charcoal in the home. Pediatrics 2002; 108:E100.
    281) Sreenath TG, Gupta P, Sharma KK, et al: Lorazepam versus diazepam-phenytoin combination in the treatment of convulsive status epilepticus in children: A randomized controlled trial. Eur J Paediatr Neurol 2009; Epub:Epub.
    282) Standard Safety Equipment: Product Literature, Standard Safety Equipment, McHenry, IL, 1995.
    283) Stewart RD & Dodd HC: Absorption of 1,1,1 trichloroethane through the skin. Am Ind Hyg Assoc J 1964; 25:439-446.
    284) Stewart RD, Gay HH, & Erley DS: Human exposure to 1,1,1-trichloroethane vapor - relationship of expired air and blood concentration to exposure and toxicity. Am Ind Hyg Assoc J 1961; 22:252-262.
    285) Stewart RD, Gay HH, & Schaffer AW: Experimental human exposure to methylchloroform vapor. Arch Environ Health 1969; 19:467-472.
    286) Stewart RD: Methyl chloroform intoxication: diagnosis and treatment. JAMA 1971; 215:1789-1790.
    287) Stewart RD: The toxicology of methyl chloroform. J Occup Med 1963; 5:259-262.
    288) Swan SH, Shaw G, & Harris JA: Congenital cardiac anomalies in relation to water contamination, Santa Clara County, California, 1981-1983. Amer J Epidemiol 1989; 129:885-893.
    289) Talukdar RK, Mellouki A, & Schmoltner AM: Kinetics of the OH reaction with methyl chloroform and its atmospheric implications. Science 1992; 257:227-230.
    290) Thakore S & Murphy N: The potential role of prehospital administration of activated charcoal. Emerg Med J 2002; 19:63-65.
    291) Tingley: Chemical Degradation for Footwear and Clothing. Tingley. South Plainfield, NJ. 2002. Available from URL: http://www.tingleyrubber.com/tingley/Guide_ChemDeg.pdf. As accessed 10/16/2002.
    292) Topudurti K: A UV oxidation technology demonstration to treat groundwater contaminated with VOCs. Water Sci Technol 1992; 25:347-354.
    293) Torkelson TR: Halogenated aliphatic hydrocarbons containing chlorine, bromine, and iodine. In: Clayton GD & Clayton FE (Eds): Patty's Industrial Hygiene and Toxicology, Volume 2E, Toxicology, 4th ed, John Wiley & Sons, New York, NY, 1994, pp 4117-4128.
    294) Trelleborg-Viking, Inc.: Chemical and Biological Tests (database). Trelleborg-Viking, Inc.. Portsmouth, NH. 2002. Available from URL: http://www.trelleborg.com/protective/. As accessed 10/18/2002.
    295) Trelleborg-Viking, Inc.: Trellchem Chemical Protective Suits, Interactive manual & Chemical Database. Trelleborg-Viking, Inc.. Portsmouth, NH. 2001.
    296) Trochimowicz HJ: J Occup Med 1976; 18:26-30.
    297) Troutman WG: Additional deaths associated with the intentional inhalation of typewriter correction fluid. Vet Hum Toxicol 1988; 30:130-132.
    298) U.S. Department of Energy, Office of Emergency Management: Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: Rev. 26 for chemicals of concern. U.S. Department of Energy, Office of Emergency Management. Washington, DC. 2010. Available from URL: http://www.hss.doe.gov/HealthSafety/WSHP/Chem_Safety/teel.html. As accessed 2011-06-27.
    299) U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project : 11th Report on Carcinogens. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Washington, DC. 2005. Available from URL: http://ntp.niehs.nih.gov/INDEXA5E1.HTM?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932. As accessed 2011-06-27.
    300) U.S. Environmental Protection Agency: Discarded commercial chemical products, off-specification species, container residues, and spill residues thereof. Environmental Protection Agency's (EPA) Resource Conservation and Recovery Act (RCRA); List of hazardous substances and reportable quantities 2010b; 40CFR(261.33, e-f):77-.
    301) U.S. Environmental Protection Agency: Integrated Risk Information System (IRIS). U.S. Environmental Protection Agency. Washington, DC. 2011. Available from URL: http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showSubstanceList&list_type=date. As accessed 2011-06-21.
    302) U.S. Environmental Protection Agency: List of Radionuclides. U.S. Environmental Protection Agency. Washington, DC. 2010a. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    303) U.S. Environmental Protection Agency: List of hazardous substances and reportable quantities. U.S. Environmental Protection Agency. Washington, DC. 2010. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    304) U.S. Environmental Protection Agency: The list of extremely hazardous substances and their threshold planning quantities (CAS Number Order). U.S. Environmental Protection Agency. Washington, DC. 2010c. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-part355.pdf. As accessed 2011-06-17.
    305) U.S. Occupational Safety and Health Administration: Part 1910 - Occupational safety and health standards (continued) Occupational Safety, and Health Administration's (OSHA) list of highly hazardous chemicals, toxics and reactives. Subpart Z - toxic and hazardous substances. CFR 2010 2010; Vol6(SEC1910):7-.
    306) U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
    307) United States Environmental Protection Agency Office of Pollution Prevention and Toxics: Acute Exposure Guideline Levels (AEGLs) for Vinyl Acetate (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6af&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    308) Urben PG: Bretherick's Reactive Chemical Hazards Database, Version 2.0, Butterworth-Heinemann Ltd, Oxford, UK, 2000.
    309) Verschueren K: Handbook of Environmental Data on Organic Chemicals. 4th ed. CD-ROM version. Wiley-Interscience. Hoboken, NJ. 2001.
    310) Wells Lamont Industrial: Chemical Resistant Glove Application Chart. Wells Lamont Industrial. Morton Grove, IL. 2002. Available from URL: http://www.wellslamontindustry.com. As accessed 10/31/2002.
    311) Winek CL, Wahba WW, & Huston R: Fatal inhalation of 1,1,1-trichloroethane. Forensic Sci Intn 1997; 87:161-165.
    312) Wodka RM & Jeong EWS: Myocardial injury following the intentional inhalation of typewriter correction fluid. Milit Med 1991; 156:204-205.
    313) Wooverton WL & Balster RL: Toxicol Appl Pharmacol 1981; 59:1-7.
    314) Workrite: Chemical Splash Protection Garments, Technical Data and Application Guide, W.L. Gore Material Chemical Resistance Guide, Workrite, Oxnard, CA, 1997.
    315) York RG, Sowry BM, & Hastings L: Evaluation of teratogenicity and neurotoxicity maternal inhalation exposure to methylchloroform. J Toxicol Environ Health 1982; 9:251-266.
    316) Zarchy TM: Chlorinated hydrocarbon solvents and biliary-pancreatic cancer -- report of three cases. Am J Ind Med 1996; 30:341-342.
    317) de Nevers N: A fatal fire with "nonflammable" methyl chloroform. Arch Environ Health 1986; 41:279-281.
    318) del Amo M, Berenguer J, & Pujol T: MR in trichloroethane poisoning. Amer J Neuroradiol 1996; 17:1180-1182.