TRICHLOROETHYLENE
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
 -IDENTIFICATION
SYNONYMS
TRICHLOROETHYLENE ACETYLENE TRICHLORIDE ALGYLEN ANAMENTH BENZINOL BLACOSOLV BLANCOSOLV CECOLENE CHLORILEN 1-CHLORO-2,2-DICHLOROETHYLENE CHLORYLEA CHLORYLEN CHORYLEN CIRCOSOLV CRAWHASPOL DENSINFLUAT 1,1-DICHLORO-2-CHLOROETHYLENE DOW-TRI DUKERON DUKERSON ETHENE, TRICHLORO- ETHINYL TRICHLORIDE ETHYLENE, TRICHLORO- ETHYLENE TRICHLORIDE FLECK-FLIP FLOCK FLIP FLUATE GEMALGENE GERMALGENE LANADIN LETHURIN NARCOGEN NARKOGEN NARKOSOID NIALK PERM-A-CHLOR PER-A-CLOR PETZINOL PHILEX TCE THRETHYLEN THRETHYLENE TRETHYLENE TRI TRIAD TRIAL TRIASOL TRIC TRICHLOORETHEEN (Dutch) TRICHLOORETHYLEEN (Dutch) TRICHLOORETHYLEEN, TRI (Dutch) TRICHLORAETHEN (German) TRICHLORAETHYLEN (German) TRICHLORAETHYLEN, TRI (German) TRICHLOR TRICHLORAN TRICHLOREN TRICHLORETHENE (French) TRICHLORETHYLENE TRICHLORETHYLENE (French) TRICHLORETHYLENE, TRI (French) TRICHLOROETHENE 1,1,2-TRICHLOROETHYLENE 1,2,2-TRICHLOROETHYLENE TRICHLORAN TRICHLOREN TRI-CLENE TRICLENE TRICLORETENE (Italian) TRICLOROETILENE (Italian) TRIELENE TRIELIN TRIELINA (Italian) TRIELINE TRIKLONE TRILEN TRILENE TRILENE TE-141 TRILINE TRIMAR TRIOL TRI-PLUS TRI-PLUS M VESTROL VITRAN WESTROSOL TRICHLOROETILENE (ITALIAN)
IDENTIFIERS
BEILSTEIN HANDBOOK REFERENCE:4-01-00-00712 EPA PESTICIDE CHEMICAL CODE:081202 IMO CLASSIFICATION:6.1 - Trichloroethylene NSC NUMBER:389 STANDARD INDUSTRIAL TRADE CLASSIFICATION NUMBER:51132
SYNONYM REFERENCE
- (Ashford, 1994; Hathaway et al, 1996; Hayes & Laws, 1991; HSDB , 2001)(IARC, 1995;(Lewis, 2000; OHM/TADS , 2001; RTECS , 2001)
USES/FORMS/SOURCES
Trichloroethylene is used as an industrial degreaser, extraction medium and household cleaning solvent (Ashford, 1994; Ellenhorn & Barceloux, 1988; ILO , 1998; Sittig, 1991). It is used in the preparation of insecticidal fumigants and in both extraction and degreasing processes (Hayes & Laws, 1991). It is used for olive oil extraction, to remove basting threads in textile industry and as swelling agent for dyeing polyester (ILO , 1998). It is used as a solvent for fats, waxes, resins, oils, rubber, paints and varnishes, as well as cellulose esters and ethers; for solvent extraction in many industries; in degreasing; in dry cleaning; and in organic chemicals, pharmaceuticals, and chloroacetic acid manufacturing (Budavari, 2000; Sittig, 1991). It is also used in solvent dyeing; as a refrigerant and heat-exchange liquid; as a fumigant; for cleaning and drying electronic parts; as a diluent in paints and adhesives; in textile processing; and in aerospace operations (flushing liquid oxygen) (Lewis, 1997). Trichloroethylene has been used as a surgical inhalation anesthetic and analgesic (ACGIH, 1996a; Hathaway et al, 1996). It is a potent analgesic with poor muscle-relaxant properties (ACGIH, 1996a; JEF Reynolds , 2000). The use of trichloroethylene as an extractant in food processing was discontinued in 1975. The National Cancer Institute issued an alert warning that trichloroethylene may be a carcinogen on the basis of liver tumors in mice (ACGIH, 1996a). Prior to trichloroethylene's removal in 1977, it was an ingredient in grain fumigants, disinfectants and pet food, and was an extractant of caffeine in coffee (Barceloux & Rosenberg, 1990). However, the FDA has prohibited the use of this compound in foods, drugs and cosmetics (Lewis, 1997). In caffeine extraction from coffee, most trichloroethylene has been replaced with methylene chloride (Lewis, 1998). Consumer products containing trichloroethylene include typewriter correction fluids, paint removers and strippers, cosmetics, adhesives, rug-cleaning fluids and spot removers (Barceloux & Rosenberg, 1990). Trichloroethylene is used in gas purification, as a solvent for sulfur and phosphorus (HSDB , 2001). It is also used as chain-transfer agent in polyvinyl chloride production and as heat-transfer fluid (Ashford, 1994). Other uses include: solvent in characterization tests for asphalt and in metal phosphatizing systems; entrainer for recovery of formic acid; extractant for spice olefins (HSDB , 2001).
Trichloroethylene is a stable, photoreactive liquid with a low boiling point. It is colorless or dyed blue, and has a sweet, chloroform-like odor (Lewis, 1997; Harbison, 1998). It is available in the following grades: USP, technical, high-purity, electronic, metal-degreasing and extraction (Lewis, 1997). Trichloroethylene may contain thymol as preservative (medicinal form) or stabilizers such as triethylamine (industrial grade) (Budavari, 2000).
Trichloroethylene is prepared from sym-tetrachloroethane. This is done by eliminating hydrogen chloride (by boiling with lime) (Budavari, 2000). It also can be produced using the following methods (Ashford, 1994): Ethylene dichloride + chlorine (chlorination; coproduced with perchlorethylene) Ethylene dichloride + chlorine + oxygen (oxychlorination/dehydrochlorination; coproduced with perchlorethylene) Acetylene + chlorine (addition/dehydrochlorination)
It can be manufactured by treating tetrachloroethane with alkali or lime in the presence of water; or via thermal decomposition and subsequent steam distillation (Lewis, 1997). It can be manufactured through chlorination or oxychlorination of C2-chlorinated halocarbons such as 1,2-dichloroethane. Prior to 1978, it was mainly generated through chlorination of acetylene with subsequent dechlorination (HSDB , 2001).
SYNONYM EXPLANATION
- Trichloroethylene industrial solvent TRADE NAMES include: Benzinol(R), Circosolve(R), Flock Flip(R), Narcogen(R), Perm-A-Chlor(R), Tri-clene(R) and Vestrol(R) (Barceloux & Rosenberg, 1990).
- Other registered tradenames are: Algylen (R), Blacosolv (R), Dukerson (R), Gemalgene (R), Germalgene (R), Trethylene (R), Trichloran (R), Trichloren (R), Trilene (R), Triline (R) and Trimar (R) (Hayes & Laws, 1991).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- GENERAL - Trichloroethylene (TCE) is toxic by ingestion, inhalation or dermal exposure. Inhalation of TCE can cause euphoria, hallucinations and distorted perceptions; inhalational abuse, with addiction, has been reported. TCE vapor may be irritating to the nose and throat.
- INHALATION - Narcosis and anesthesia occur after inhalation. Adverse effects from inhalation exposure include bronchial irritation, dyspnea, pulmonary edema, respiratory depression, euphoria, dizziness, restlessness, irritability, incoordination, central nervous system depression, impaired concentration, confusion, drowsiness, loss of consciousness, seizures, renal and hepatic damage, as well as fatal cardiac dysrhythmias.
- INGESTION - Effects from ingestion include nausea, vomiting, diarrhea, abdominal pain, dysphagia, jaundice, somnolence, headache, dizziness, incoordination, elevated creatine kinase, hallucinations or distorted perceptions, paresthesia, partial paralysis, dysrhythmias and circulatory collapse. The main systemic response is CNS depression.
- OCULAR - Direct contact with the eye may result in pain and injury to the corneal epithelium; recovery usually occurs within a few days. Double vision, blurred vision, optic neuritis and blindness can occur after exposure.
- DERMAL - TCE is a skin irritant and may cause defatting dermatitis of the skin. Scleroderma has been linked with TCE exposure. Dermal absorption is not likely to be significant if dermatitis is prevented. Vasodilation and malaise ('degreasers flush') recur in workers who drink ethanol after exposure to TCE. Chemical burns have been reported with concentrated exposure to TCE vapors.
- CHRONIC - Long-term occupational exposure may result in hearing loss, memory loss, fatigue, flushing, ECG changes, vomiting, renal and hepatic damage, CNS depression, irritability, encephalopathy, dementia, neuropathy, paresthesias and possibly systemic sclerosis. Visual disturbances, oculomotor paralysis and trigeminal palsies have been reported after occupational exposure.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 160 (ERG, 2004)
Toxic by ingestion. Vapors may cause dizziness or suffocation. Exposure in an enclosed area may be very harmful. Contact may irritate or burn skin and eyes. Fire may produce irritating and/or toxic gases. Runoff from fire control or dilution water may cause pollution.
ACUTE CLINICAL EFFECTS
- Trichloroethylene (TCE) may produce toxic effects after inhalation, ingestion, or contact with the skin or eyes (ACGIH, 1996; (Lewis, 2000). Dermal absorption of TCE vapor is poor, and is not likely to contribute appreciably to systemic toxicity, provided dermatitis is prevented (ACGIH, 1996).
- INGESTION of TCE causes a burning sensation in the throat, inebriation, headache, fatigue, excitement, and other central nervous system (CNS) effects, similar to those seen after inhalation. Gastrointestinal irritation with nausea, vomiting, diarrhea and abdominal pain may also occur (Hayes & Laws, 1991; ILO , 1998; Moritz et al, 2000).
Ingestion of approximately 40 mL TCE has been associated with symptoms of intoxication (ACGIH, 1992). Unconsciousness may be produced by ingestion of 40 to 150 mL (Gosselin et al, 1984). Human consumption of an undetermined amount of TCE has produced severe liver and kidney damage, and death due to ventricular fibrillation (Kleinfeld & Habershaw, 1954). Ingested TCE is considered to be moderately toxic to humans, with a probable oral lethal dose of 3 to 5 mL/kg for a 150-pound person (Gosselin et al, 1984).
- INHALATION of TCE vapors is the main route of occupational exposure (Hathaway et al, 1996). The principal effect of acute exposure involves CNS depression with euphoria at low levels, analgesia at moderate levels and anesthesia at high levels of exposure. CNS depression seems to be due to the unmetabolized substance (Clayton & Clayton, 1994).
Controlled laboratory studies showed no significant effects on visual perception or motor skills in healthy volunteers exposed to airborne concentrations of 100 to 300 ppm over 5 days; a 2-hour exposure to 1,000 ppm did produce significant effects on these parameters (ACGIH, 1996; (Clayton & Clayton, 1994). The Dow Chemical Company reports minimal effects with exposures as long as 3 hours at airborne concentrations equal to or less than 400 ppm (Clayton & Clayton, 1994). Occupational studies have documented a variety of neurological disturbances associated with exposure to airborne concentrations as low as 1.0 ppm (ACGIH, 1996). Headache, dizziness, sleepiness, and irritation of the eyes, nose, and throat have been reported following exposure to estimated concentrations of 10 to 40 ppm TCE (Crandall & Albrecht, 1989). Exposure to concentrations of 100 to 200 ppm has been associated with fatigue, dizziness, headaches, memory deficits, inability to concentrate, tingling, muscle discomfort, paraesthesia and gastrointestinal disturbances (Hathaway et al, 1996). Visual disturbances, inebriation, vomiting, chest pain, breathing difficulties, and eye and throat irritation have also been reported with exposure to concentrations between 200 and 300 ppm (Sinks et al, 1989; Hathaway et al, 1996). Brief exposure to 300 ppm or more results in dizziness, fatigue, headache, nausea, visual disturbances, confusion, loss of coordination and narcosis; coma and death may also occur (Baxter et al, 2000). Exposure to 500 to 1,000 ppm produced dizziness, light-headedness, lethargy and impaired visual-motor response tests in volunteers (Hathaway et al, 1996). Extremely high vapor exposure may cause lung irritation, unconsciousness, convulsions, coma, and death due to respiratory or cardiac failure (ACGIH, 1996). Unconsciousness may occur at concentrations of 3,000 ppm or greater (Gosselin et al, 1984). Levels of 1,000 ppm or greater are considered Immediately Dangerous to Life or Health (Chemsoft(R) , 1996). Concentrations of 5,000 to 20,000 ppm produce anesthesia (Hathaway et al, 1996).
- TCE may produce convulsions in children (Hayes & Laws, 1991).
- Multiple nerve palsies and peripheral neuropathy have been noted after TCE intoxication (NIOSH, 1973; Joron et al, 1955).
Occupational exposure to TCE results in a cranial nerve syndrome, especially trigeminal, with loss of facial sensation and difficulty chewing (Goldfrank, 1998). Palsies of the third, fifth and sixth cranial nerves were seen in a patient with acute intentional exposure to TCE (Szlatenyi & Wang, 1996). Bilateral, symmetrical sixth cranial nerve deafness has been reported with TCE exposure (NIOSH, 1973). Peripheral myelinopathy, sensory and motor, is linked with TCE exposure (Goldfrank, 1998). Some evidence indicates that TCE decomposition products or impurities may be responsible for cranial nerve injuries, producing palsies of the oculomotor and trigeminal nerves and optic neuropathy (Grant & Schuman, 1993) Cavanaugh & Buxton, 1989; (Feldman et al, 1988).
- In some occupational case studies, the disturbances seemed to increase with increasing length of exposure (years), and therefore may reflect the consequences of chronic exposure. Evaluation of these case reports is difficult, as many of the symptoms reported are subjective and commonly occur in unexposed people, the exact circumstances of the exposures were often not known, and there were other variables that were not controlled (ACGIH, 1996).
- Ventricular fibrillation may occur as a result of cardiac sensitization to endogenous catecholamines and is thought to be the cause of death in fatal exposure (Anon, 1974; Lewis, 2000). Atrial fibrillation, beginning within 12 hours of admission to the emergency department and resolving over 2 days, occurred in a 35-year-old male after intentional TCE inhalation (Szlatenyi & Wang, 1994). Hypotension and first-degree heart block have been reported after ingestion of TCE (Wells, 1982; Perbellini et al, 1991).
Some individuals may have a greater likelihood of developing arrhythmias when exposed to extremely high concentrations of TCE, particularly during physical exertion (ATSDR, 1992a). Ventricular arrhythmias are unlikely to occur in most humans unless TCE concentrations sufficient cause anesthesia are present. Concentrations in excess of 15,000 ppm may predispose to development of ventricular arrhythmias (ACGIH, 1996).
- Respiratory depression, cyanosis, bronchial irritation, dyspnea, pulmonary hemorrhages and edema have been reported with exposure to TCE (Anderssen, 1957) Derobert, 1952; (Koch, 1931; McCarthy & Jones, 1983; Patel, 1973). Pulmonary edema and severe dyspnea were reportedly caused by the decomposition products phosgene and dichloroacetyl chloride, created by welding in the presence of TCE (Sjogren et al, 1991; Selden & Sundell, 1991).
- Acute hepatic damage has been reported infrequently and usually only after massive exposure (ACGIH, 1996; (AMA, 1985; Joron et al, 1955; James, 1963). Concentrations of TCE that produce intense CNS effects have been associated with only mild liver dysfunction (Hathaway et al, 1991). Very extreme exposures have produced substantial liver and kidney damage (David et al, 1989; Nakajima et al, 1988; Rempel, 1990). Acute tubular necrosis and renal failure may follow oral or respiratory exposure (Gutch et al, 1965; JEF Reynolds , 2000; David et al, 1989).
- Brief skin contact with TCE causes mild irritation. Prolonged exposure may produce a burning sensation. Blistering of the skin has occurred when unconscious individuals have experienced prolonged exposure to concentrated liquid TCE (ILO , 1998).
Direct dermal contact results in a burning sensation within 3 to 18 minutes; this becomes more severe immediately after removal from exposure, with tingling persisting for as much as 30 minutes. Erythema persists for 2 hours (Hayes & Laws, 1991). Contact with the liquid defats the skin, causing dermatitis. Although it is absorbed through the skin, dermal absorption is not likely to be significant if dermatitis is prevented (ACGIH, 1986). Occupational exposure to TCE is reportedly a possible cause of scleroderma-like disorder (Zenz, 1994). 'Degreaser's flush', a transient face and neck erythema (vasodilation), is accompanied by a feeling of fullness in the chest, with dyspnea and feeling of malaise; although transient, it may recur when alcohol is consumed (Baxter et al, 2000; Waters et al, 1977; Stewart et al, 1974).
- Direct eye contact with TCE vapor can cause inflammation of the conjunctiva. Eye irritation is not likely to occur at vapor concentrations less than 100 to 200 ppm. Direct eye contact with liquid TCE can cause smarting pain, swelling and reddening of the conjunctiva and eyelids, and damage to the cornea (loss of corneal epithelium and clouding), which resolves after exposure has ceased (Grant & Schuman, 1993; Hathaway et al, 1996).
Disturbed vision and facial numbness have also been reported in some workers exposed to TCE (ATSDR, 1992). Dichloroacetylene, a decomposition product and contaminant of TCE, may be the cause of these effects (Grant, 1986).
- TCE is metabolized mainly in the liver, via a cytochrome P450 oxidase, with probable formation of an epoxide intermediate; another principal pathway forms chloral (Fahrig et al, 1995).
TCE is metabolized mainly by cytochrome P450 CYP2E1 in humans. The results of tests on a series of 23 human hepatic microsomal samples indicate there is variation in the ability of humans to metabolize TCE to its more toxic metabolite, chloral hydrate (Lipscomb et al, 1997). In TCE exposure by ingestion as a contaminant in tap water, the TCE was completely metabolized before appearing in the bloodstream, whereas the dose from the inhalation or dermal routes was dispersed throughout the body (Weisel & Jo, 1996).
CHRONIC CLINICAL EFFECTS
- Toxicity may result from inhalation, ingestion or contact with trichloroethylene (TCE) liquid or vapors (ACGIH, 1996; (Lewis, 2000).
- Repeated excessive exposure has been associated with a variety of CNS effects that may persist for weeks or months after exposure ceases (ILO , 1998; Hayes & Laws, 1991). Symptoms include fatigue, headache, memory loss, decreased appetite, irritability, euphoria or depression, and difficulty in walking. In one study, these symptoms were noted more often in workers chronically exposed to higher mean concentrations of TCE (85 ppm), compared with workers who were exposed to low (14 ppm) mean concentrations (ATSDR, 1992a).
- TCE has been a solvent of abuse, producing euphoria and addiction (JEF Reynolds , 2000). People who intentionally inhale high concentrations of TCE suffer persistent neurological defects and degenerative changes (cerebellar degeneration) in the brain (ATSDR, 1992).
- Chronic occupational exposure to TCE has resulted in damage to the cranial nerves (Barret et al, 1987; (Ruijten et al, 1991). TCE has been shown to be ototoxic in occupational exposure of 1 to 23 years (Bingham et al, 2000; (Morata et al, 1994).
- Long-term exposure to concentrations of approximately 35 ppm may produce slight effects involving the trigeminal nerve (Ruijten et al, 1991). The decomposition product and contaminant dichloroacetylene may be responsible (Grant & Schuman, 1993).
- Digestive disturbances, other intestinal disorders and adverse effects on the peripheral nervous system have also been described in individuals chronically exposed to TCE (ATSDR, 1992; Fleming, 1992; Takeuchi et al, 1986).
- Repeated exposure to TCE may result in liver and/or kidney damage (ATSDR, 1992; Brown et al, 1990). Most reports of frank liver and kidney damage have involved individuals who chronically abused TCE (Finkel, 1983). Liver and kidney damage are unlikely to occur in individuals exposed in the workplace or in the community at current permissible exposure limits (ATSDR, 1992a). Persistent changes to the proximal tubules can result from chronic exposure to high doses of TCE (Bruning et al, 1999).
- Liver damage has been produced in animals after intermediate periods (3 to 4 weeks) of daily exposure to TCE (Buben & O'Flaherty, 1985; Merrick et al, 1989). Male mice seem more likely to develop liver damage than female mice or rats (Merrick et al, 1989; ATSDR, 1992). Kidney damage has been produced in chronic exposure studies involving rats and mice (ATSDR, 1992).
- Prolonged or repeated skin contact with TCE can cause dermatitis, with drying, reddening, irritation and cracking. Increased risk of skin infections may result (ILO , 1998). There have been a few reported cases of apparent sensitization to TCE. In one case, a male worker developed an itchy rash with eosinophilia (Bond, 1996).
- TCE is statistically associated with systemic sclerosis, an autoimmune disorder, and has been shown to bind covalently to proteins after metabolic activation in isolated mouse microsomal systems (Halmes et al, 1996).
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 160 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. For minor skin contact, avoid spreading material on unaffected skin. Wash skin with soap and water. Keep victim warm and quiet. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
FIRST AID INHALATION EXPOSURE 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. If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents. ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. 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). Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years). Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
DERMAL EXPOSURE 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). Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
EYE EXPOSURE DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
ORAL EXPOSURE Because of the potential for CNS depression and seizures, DO NOT induce emesis. PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION 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). 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. 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).
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. ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. 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). Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years). Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
Avoid epinephrine and other catecholamines (especially beta agonists). These agents may increase the risk of arrhythmias. DEGREASERS FLUSH - May respond to propranolol (40 to 80 mg PO).
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
The estimated human lethal dose is between 3 and 5 mg/kg (HSDB , 2002). Inhalation of between 5000 and 20,000 ppm of trichloroethylene has produced light anesthesia, followed by death from cardiac arrest in rare cases (Hathaway et al, 1996). After administration of trichloroethylene as an anesthetic, fatal hepatic failure has occurred in patients with conditions such as toxemia, malnutrition or burns (HSDB , 2002). A 24-year-old male died after ingesting 200 to 300 milliliters (3 to 5 milliliters/kilogram) of pure trichloroethylene (Froboese, 1943). A 24-year-old deceased male reportedly had been exposed to TCE concentrations between 7,500 and 10,000 ppm in an industrial accident (Ford et al, 1995). Exposure to 8,000 ppm can lead to death (Sittig, 1991).
The lowest dose that has produced death in cats, dogs and rabbits is reported to be 6,000 to 7,000 mg/kg (ACGIH, 1996a). Animal deaths are mainly due to anesthesia, which results from trichloroethylene exposure. Full anesthesia occurs at airborne concentrations of 4,800 ppm or more (Clayton & Clayton, 1994). Dogs died after exposure to 150 mg/kg, administered intravenously (Hayes & Laws, 1991). Rats died after inhalation exposure to 17,000 ppm for 7 hours (Hayes & Laws, 1991).
MAXIMUM TOLERATED EXPOSURE
ACUTE GENERAL The central nervous system depressant effects of trichloroethylene may be potentiated by ethanol (Barceloux & Rosenberg, 1990; Hayes & Laws, 1991). Exposure to concentrations above 1,500 mg/m(3) may first lead to an excitatory or euphoric stage, which is followed by dizziness, confusion, drowsiness, nausea, vomiting, and possibly loss of consciousness (Baselt, 2000). Volunteers who had placed their thumbs in trichloroethylene for 30 minutes experienced a burning sensation on the dorsum of their thumbs within 3 to 18 minutes. Within 5 minutes after the onset of the sensation, burning became severe in two of the three volunteers. After removal of their thumbs from the solution, pain became more intense and tingling persisted for 30 minutes. Erythema subsided within 2 hours (Hayes & Laws, 1991). Volunteers exposed to 500 to 1,000 ppm showed symptoms of CNS disturbance (dizziness, light-headedness, lethargy, impairment in visual-motor response tests) (Hathaway et al, 1996).
ORAL EXPOSURE Ingestion of a glassful of trichloroethylene (25%) and water produced coma with cardiovascular collapse, renal injury, and blood streaked liquid diarrhea (Calvet et al, 1959). After swallowing 70 mL of trichloroethylene, a 17-year-old male developed prolonged coma and renal tubular damage. He survived with treatment (Baselt, 2000).
INHALATION EXPOSURE An estimated 0.5% to 2% trichloroethylene vapor produces analgesia and light anesthesia within 3 to 5 minutes (JEF Reynolds , 1988). Hepatotoxicity has been reported after exposure to airborne concentrations greater than 15,000 ppm (ACGIH, 1996a). Inhalation exposure of 8 volunteers to concentrations of 100, 200 and 1,000 ppm for two hours showed significantly impaired performance of visual-motor tasks only at the 1,000-ppm level. Tasks were performed within the 2 hour exposure period, and consisted of tests in depth perception, steadiness and manual skills (Hayes & Laws, 1991). Short-term inhalation of 100 ppm caused headache, sleepiness, nausea, vomiting, dizziness and coughing. Long-term exposure to the same concentration caused giddiness, nervous exhaustion and increased sensitivity to alcohol (leading to facial trichloroethylene blush). Addiction to the vapors may also occur at this concentration (Sittig, 1991).
OCCUPATIONAL EXPOSURE Industrial experience and human studies (Clayton & Clayton, 1994) - Pre-narcotic symptoms were seen in workers exposed to 200 to 300 ppm (Hathaway et al, 1996). Workers exposed to 100 to 200 ppm have reported fatigue, vertigo, dizziness, headache, memory loss and impaired ability to concentrate (Hathaway et al, 1996). After a 5-minute exposure to trichloroethylene, a worker developed nausea, lethargy, confusion, blurred vision and numbness of face and mouth within 10 hours. All symptoms except for some hypoalgesia in the face subsided within 18 months (Baselt, 1997). An update to a Swedish study evaluated the effects of low-level occupational exposure (<20 ppm) to trichloroethylene. The results showed that within the parameters of this study, there was no evidence for carcinogenic effects at this level (Hathaway et al, 1996).
Chronic occupational exposure to concentrations between 40 and 270 ppm often results in symptoms of fatigue, headache, irritability, vomiting, flushing of the skin, intolerance to alcohol and electrocardiographic changes (Baselt, 2000).
Rats experienced hepatic injury after a 2-hour exposure to 10,000 ppm of the compound, following pretreatment with phenobarbital, Aroclor 1254, hexachlorobenzene, and 3-methyl cholanthrene or pregneolone-16-alpha- carbonitrile (ACGIH, 1996a). For single exposures survived by all rats, the maximum time-concentrations were the following: 18 min at 20,000 ppm; 1.5 hr at 6400 ppm; 8 hr at 3000 (Clayton & Clayton, 1994). Dogs survived exposure to oral doses of 6000 mg/kg and intravenous doses of 125 mg/kg (Hayes & Laws, 1991). Rats survived inhalation exposure to 3,000 ppm for 7 hours (Hayes & Laws, 1991). Animals tolerated without adverse effects the following inhalation exposures (Hayes & Laws, 1991): Rats - 151 exposures at 200 ppm for 7H/D,5D/W Monkeys - 400 ppm for 6 months Rabbits - 200 ppm for 6 months Guinea Pig - 100 ppm for 6 months
Following intragastric administration of trichloroethylene at the indicated levels five times per week for 78 weeks showed the effects listed below. Trichloroethylene was technical grade but later found to be contaminated with other chemicals (Hathaway et al, 1996): 2.4 g/kg - male B6C3F1 mice: hepatocellular carcinomas in 31 of 48 animals; 1.2 g/kg - male B6C3F1 mice: hepatocellular carcinoma in 26 of 50 animals (control group 5% incidence rat); 1.2 g/kg - female B6C3F1 mice: hepatocellular carcinoma in 11 of 47 animals (control group 1 of 80 animals).
Intragastric administration of epichlorohydrin-free trichloroethylene at 1.0 g/kg for 2 years resulted in increased incidences for hepatocellular adenomas and carcinomas in mice, and an increase in renal adenocarcinomas in rats (Hathaway et al, 1996). Inhalation exposure to 500 ppm of trichloroethylene for 6 hours/day, 5 days/week for 18 months resulted in an increased incidence of malignant lymphomas in female MRI mice. No change in incidence rate for tumor formation was found for rats and hamsters exposed to the same levels (Hathaway et al, 1996). ICR mice, exposed for 107 weeks to trichloroethylene vapor showed the following effects (Hathaway et al, 1996): 150 ppm - 16% incidence for lung carcinoma (control group 2%); 450 ppm - 15% incidence for lung carcinoma (control group 2%); No change in incidence rate was found for rats exposed to the same levels.
- Carcinogenicity Ratings for CAS79-01-6 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A2 ; Listed as: Trichloroethylene A2 :Suspected Human Carcinogen: Human data are accepted as adequate in quality but are conflicting or insufficient to classify the agent as a confirmed human carcinogen; OR, the agent is carcinogenic in experimental animals at dose(s), by route(s) of exposure, at site(s), of histologic type(s), or by mechanism(s) considered relevant to worker exposure. The A2 is used primarily when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals with relevance to humans.
EPA (U.S. Environmental Protection Agency, 2011): Information reviewed but value not estimated. Refer to Full IRIS Summary. ; Listed as: Trichloroethylene 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): 1 ; Listed as: Trichloroethylene 1 : The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.
NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Trichloroethylene MAK (DFG, 2002): Category 1 ; Listed as: Trichloroethylene NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS79-01-6 (U.S. Environmental Protection Agency, 2011):
Oral: Inhalation: Drinking Water:
References: ATSDR, 2001 ATSDR, 1997; Budavari, 2000 Clayton & Clayton, 1994 ITI, 1995 HSDB, 2002 Lewis, 2000 OHM/TADS, 2002 RTECS, 2002 NOEL- (INHALATION)GUINEA_PIG: NOEL- (INHALATION)PRIMATE: NOEL- (INHALATION)RABBIT: 1,200 ppm for 473H (HSDB, 2002) 730 ppm for 6W, 8H/D (HSDB, 2002)
NOEL- (INHALATION)RAT: 100 ppm for 8H (HSDB, 2002) 730 ppm for 6W, 8H/D (HSDB, 2002)
References: ATSDR, 2001 ATSDR, 1997; Budavari, 2000 Clayton & Clayton, 1994 ITI, 1995 HSDB, 2002 Lewis, 2000 OHM/TADS, 2002 RTECS, 2002 LC50- (INHALATION)MOUSE: 49,000 ppm for 30M (HSDB, 2002) 5,500 ppm for 10H (HSDB, 2002) 8450 ppm for 4H (Lewis, 2000)
LC50- (INHALATION)RAT: 25,700 ppm for 1H (Lewis, 2000) 26,000 ppm for 1H (HSDB, 2002) 12,000 ppm for 4H (HSDB, 2002) Male, 12,500 ppm/4H; Sprague-Dawley (ATSDR, 1997)
LCLo- (INHALATION)CAT: LCLo- (INHALATION)GUINEA_PIG: LCLo- (INHALATION)HUMAN: LCLo- (INHALATION)MOUSE: LCLo- (INHALATION)RABBIT: LCLo- (INHALATION)RAT: LD- (ORAL)MOUSE: Female, 5500 mg/kg (HSDB, 2002) Male, 6000 mg/kg (HSDB, 2002)
LD50- (INTRAPERITONEAL)DOG: LD50- (ORAL)DOG: 5680 mg/kg (Clayton & Clayton, 1994; ITI, 1995) 5860 mg/kg (OHM/TADS, 2002)
LD50- (INTRAPERITONEAL)MOUSE: LD50- (INTRAVENOUS)MOUSE: LD50- (ORAL)MOUSE: Male, 2402 mg/kg - change in sleep time; change in righting reflex; ataxia; hair changes 2850 mg/kg (Clayton & Clayton, 1994) Female, 2443 mg/kg (Clayton & Clayton, 1994; Hayes & Laws, 1991)
LD50- (SUBCUTANEOUS)MOUSE: LD50- (SKIN)RABBIT: 29 g/kg (HSDB, 2002) > 20 g/kg > 29,200 mg/kg for 14D (OHM/TADS, 2002) 20 mL/kg (HSDB, 2002) (OHM/TADS, 2002)
LD50- (INTRAPERITONEAL)RAT: LD50- (ORAL)RAT: 5650 mg/kg (Lewis, 2000) 4.92 mL/kg (Budavari, 2000) 4920 mg/kg (Clayton & Clayton, 1994; Hayes & Laws, 1991; ITI, 1995) 7180 mg/kg for 14D (OHM/TADS, 2002)
LDLo- (ORAL)CAT: LDLo- (INTRAVENOUS)DOG: LDLo- (ORAL)DOG: LDLo- (SUBCUTANEOUS)DOG: LDLo- (ORAL)HUMAN: LDLo- (ORAL)RABBIT: LDLo- (SUBCUTANEOUS)RABBIT: LDLo- (INTRATRACHEAL)RAT: TCLo- (INHALATION)DOG: 500 ppm for 4H, 8W-intermittent -- liver changes 3825 mg/m(3) for 8H, 6W- intermittent -- weight loss or decreased weight gain
TCLo- (INHALATION)GERBIL: 150 ppm for 24H, 30D- continuous -- degenerative brain changes; liver weight changes; effects on phosphatases 320 ppm for 24H, 90D- continuous -- degenerative changes to brain/coverings; effects on lipids
TCLo- (INHALATION)GUINEA_PIG: TCLo- (INHALATION)HAMSTER: TCLo- (INHALATION)HUMAN: 6900 mg/m(3) for 10M -- somnolence, hallucinations 160 ppm for 83M -- hallucinations, distorted perceptions 812 mg/kg -- somnolence; changes in gastro-intestinal tract; jaundice and other liver changes 500 ppm for 16.1Y-intermittent -- changes in kidney tubuli and glomeruli; proteinuria; effects on transferases 110 ppm for 8H -- hallucinations, distorted perceptions
TCLo- (INHALATION)MOUSE: 150 ppm for 24H, 30D- continuous -- liver weight changes; weight loss or decreased weight gain; effects on phosphatases 10,000 ppm for 1H, 12D-intermittent -- respiratory depression and other changes; death Female, 100 ppm for 7H, 5D before mating -- effects on spermatogenesis
TCLo- (INHALATION)RABBIT: 350 ppm for 4H, 12W- intermittent -- CNS changes 100 mg/m(3) for 4H, 39W- intermittent -- changes in urine composition; changes in white blood cell count; effects on esterases
TCLo- (INHALATION)RAT: Female, 100 ppm for 4H, 6-22D post -- teratogenic effects; postimplantation mortality; fetotoxicity (Lewis, 2000) 150 ppm for 7H, 2Y-intermittent -- carcinogenic effects (Lewis, 2000) 150 ppm for 24H, 3D-continuous -- liver weight changes 300 ppm for 24H, 12W-continuous -- changes in serum; change in liver weight; effect on lipids 2400 for 6H, 13W-intermittent -- change in acuity of sense organs 3200 ppm for 12H, 12W- intermittent -- CNS changes; changes in urine composition 4330 ppm for 4H, 2W-intermittent -- ataxia; changes in psychophysiological tests 50 mg/m(3) for 5H, 26W- intermittent -- CNS changes; changes in urine composition Female, 100 ppm for 4H, 8-21D preg -- musculoskeletal system developmental abnormalities Female, 1800 ppm for 6H, 1-20D preg -- urogenital system developmental abnormalities Female, 1800 ppm for 24H, 1-20D preg -- musculoskeletal system developmental abnormalities
TDLo- (ORAL)HUMAN: TDLo- (INTRAPERITONEAL)MOUSE: TDLo- (ORAL)MOUSE: 13 g/kg for 5D-intermittent -- weight loss or decreased weight gain; effects on hepatic microsomal mixed oxidase; death 48 g/kg for 4W-intermittent -- hepatitis; zonal changes to liver; effects on dehydrogenases and transaminases 182 g/kg for 26W-continuous -- changes in liver and bladder weight; weight loss or decreased weight gain 3360 mg/kg for 14D- intermittent -- liver weight changes 49,080 mg/kg for 17W- continuous -- bone marrow changes; decreased humoral immune response 455 g/kg for 78W-intermittent -- carcinogenic effects (Lewis, 2000)
TDLo- (ORAL)RAT: 24 g/kg for 6W-intermittent -- liver weight changes; effects on phosphatases 28 g/kg for 28D-intermittent -- liver weight changes; pigmented or nucleated red blood cells; effects on phosphatases 84 g/kg for 2W-continuous -- liver and bladder weight changes; effects on hepatic microsomal mixed oxidase 130 g/kg for 13W-intermittent -- weight loss or decreased weight gain; death 1160 mg/kg for 8W-intermittent -- demyelination in brain 2688 mg/kg for l-22D preg, 21D post -- reproductive effects; behaviooral abnormalities in newborn (Lewis, 2000) Female, 36 g/kg 15D before mating and 1-21D preg -- effects on weaning or lactation in newborn Female, 1140 mg/kg 14D before mating to 21D after birth -- CNS developmental abnormalities
TDLo- (SUBCUTANEOUS)RAT:
CALCULATIONS
1 ppm = 5.37 mg/m(3) (at 25 degrees C, 760 mmHg) (NIOSH , 2001) 1 ppm = 5.36 mg/m(3) (at 25 degrees C) (ACGIH, 1996a) 1 ppm = 5.38 mg/m(3) (at 25 degrees C, 760 mmHg) (HSDB , 2001) 1 mg/L = 185.8 ppm (HSDB , 2001) 1 mg/m(3) = 0.18 ppm (air at 20 degrees C) (ATSDR, 1997) 1 ppm = 5.46 mg/m(3) (air at 20 degrees C) (ATSDR, 1997) OTHER An equation was derived by Nomiyama (1971) to correlate exposure concentration (ppm) with concentration of chlorinated metabolites in urine samples collected on the t-day following the last 8-hour exposure. Note: This equation applies to urine samples collected from workers exposed 8 hours/day, 5 days/week to the same time-weighted exposure concentration.
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS79-01-6 (American Conference of Governmental Industrial Hygienists, 2010):
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.
- AIHA WEEL Values for CAS79-01-6 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS79-01-6 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS79-01-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
Listed as: Trichloroethylene Table Z-1 for Trichloroethylene: 8-hour TWA: ppm: mg/m3: Ceiling Value: Skin Designation: No Notation(s): Not Listed
Table Z-2 for Trichloroethylene (Z37.19-1967):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS79-01-6 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS79-01-6 (U.S. Environmental Protection Agency, 2010):
Listed as: Trichloroethylene Final Reportable Quantity, in pounds (kilograms): Additional Information: The following spent halogenated solvents used in degreasing; all spent solvent mixtures/blends used in degreasing containing, before use, a total of ten percent or more (by volume) of one or more of the halogenated solvents listed below or those solvents listed in F002, F004, and F005; and still bottoms from the recovery of these spent solvents and spent solvent mixtures. Listed as: Trichloroethylene Final Reportable Quantity, in pounds (kilograms): Additional Information: The following spent halogenated solvents; all spent solvent mixtures/ blends containing, before use, a total of ten percent or more (by volume) of one or more of the halogenated solvents listed below or those solvents listed in F001, F004, or F005; and still bottoms from the recovery of these spent solvents and spent solvent mixtures. Listed as: Trichloroethylene (D040) Final Reportable Quantity, in pounds (kilograms): Additional Information: Unlisted Hazardous Wastes Characteristic of Toxicity Listed as: Trichloroethylene Final Reportable Quantity, in pounds (kilograms): Additional Information: Listed as: Ethene, trichloro- Final Reportable Quantity, in pounds (kilograms): Additional Information:
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS79-01-6 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS79-01-6 (U.S. Environmental Protection Agency, 2010b):
Listed as: Ethene, trichloro- P or U series number: U228 Footnote: Listed as: Trichloroethylene P or U series number: U228 Footnote: Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.
- EPA SARA Title III, Extremely Hazardous Substance List for CAS79-01-6 (U.S. Environmental Protection Agency, 2010):
- EPA SARA Title III, Community Right-to-Know for CAS79-01-6 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
Listed as: Trichloroethylene Effective Date for Reporting Under 40 CFR 372.30: 1/1/87 Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:
- DOT List of Marine Pollutants for CAS79-01-6 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS79-01-6 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1710 (49 CFR 172.101, 2005):
- ICAO International Shipping Name for UN1710 (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS79-01-6 (NFPA, 2002):
-HANDLING AND STORAGE
STORAGE
Store trichloroethylene in light-resistant, sealed containers (Budavari, 2000). To minimize decomposition, store in cans or dark glass bottles (HSDB , 2001). Trichloroethylene may be stored in containers made of galvanized iron, black iron, or steel (HSDB , 2001). All trichloroethylene containers should bear a label giving the following or similar information: "TRICHLOROETHYLENE-WARNING: Vapor harmful. Use only with adequate ventilation" (ILO, 1983). Trichloroethylene is typically transported in drums, tank cars or tank trucks (OHM/TADS , 2001).
- ROOM/CABINET RECOMMENDATIONS
Storage areas should be cool, well-ventilated, and shielded from direct sunlight (ITI, 1995). Prevent prolonged exposure of this compound to excessive heat (Budavari, 2000). Handle and store this chemical away from operations that generate high temperatures (such as arc welding or cutting), unshielded resistance heating, open flames, and high intensity ultraviolet light (Sittig, 1991).
Keep separate from active metals, open flames, and combustible materials (NFPA, 1997). Prevent contact with hot metals because poisonous gases, such as phosgene and hydrochloric acid, may be released (Sittig, 1991). Prevent contact with strong alkalis because highly flammable, toxic liquid may be generated (Sittig, 1991). Prevent contact with aluminum and other chemically active metal (both in powdered form and as shavings) because violent reaction or explosion may occur (Sittig, 1991). Trichloroethylene is incompatible with (Pohanish & Greene, 1997): acids organic anhydrides isocyanates alkylene oxides aldehydes alcohols glycols phenols cresols caprolactam solution epichlorohydrin nitrogen tetroxide metal powders oxygen
See the REACTIVITY section of this document for more information.
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 160 (ERG, 2004)
Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. Structural firefighters' protective clothing will only provide limited protection.
EYE/FACE PROTECTION
- Chemical goggles are recommended (ITI, 1995).
- Should the chemical come in contact with the eyes, flush with plenty of water while holding eyelids open (CHRIS , 2001).
- Ensure that eyewash fountains are available to workers in areas where trichloroethylene is being used (NIOSH , 2001).
RESPIRATORY PROTECTION
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 79-01-6.
-PHYSICAL HAZARDS
FIRE HAZARD
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 160 (ERG, 2004) Some of these materials may burn, but none ignite readily. Most vapors are heavier than air. Air/vapor mixtures may explode when ignited. Container may explode in heat of fire.
Trichloroethylene usually is considered to be nonflammable; however, the chemical has wide flammability limits and an Auto Ignition Temperature of 410 degrees C. A flame or other intense heat source can ignite it (Urben, 1999). A flash point was not established in a conventional closed tester. Explosion may occur when vapors are exposed to a high energy source (NFPA, 1997). According to NIOSH (2001), the liquid is combustible, but burns with difficulty; however, AAR (2000) lists trichloroethylene as being noncombustible. Slightly flammable, except at elevated temperatures (OHM/TADS , 2001). This chemical may accumulate static electrical charges. This may result in ignition of its vapors (Pohanish & Greene, 1997). Toxic and flammable gas is released when exposed to caustics (Pohanish & Greene, 1997). "Nonflammable, but high concentrations of trichloroethylene vapor in high-temperature air can be made to burn mildly if plied with a strong flame" (Lewis, 2000). This compound is not flammable or explosive at room temperatures, and moderately flammable at high temperatures (Sittig, 1991). Trichloroethylene reacts with alkali and epoxides such as 1-chloro-2,3-epoxypropane, 1,4-butanediol mono-2,3-epoxypropylether, 1,4-butanediol di-2,3-epoxypropylether, 2,2-bis[(4(2'3'-epoxypropoxy)phenyl)propane]. In these reactions, the spontaneously flammable gas dichloroacetylene is formed (Lewis, 2000).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS79-01-6 (NFPA, 2002):
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 160 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 160 (ERG, 2004)
Dry chemical, CO2, alcohol-resistant foam or water spray. Move containers from fire area if you can do it without risk. Dike fire control water for later disposal; do not scatter the material.
- TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 160 (ERG, 2004)
Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire.
- NFPA Extinguishing Methods for CAS79-01-6 (NFPA, 2002):
- If material is involved in a fire, use fire extinguishing agent that is suitable for the surrounding fire (AAR, 2000; NFPA, 1997).
- Water spray can be used to cool containers that are exposed to the heat of a fire (NFPA, 1997; Sittig, 1991).
- Use dry chemical, carbon dioxide or foam to combat fire. Water fog may also be used (CHRIS , 2001; Sittig, 1991).
Hydrogen chloride and other toxic gases and irritants may result from trichloroethylene combustion (NFPA, 1997). When heated to decomposition, trichloroethylene emits toxic fumes of chlorine (Lewis, 2000).
EXPLOSION HAZARD
- If trichloroethylene is subjected to a high energy source, vapors in containers may explode (NFPA, 1997).
- When mixed with 1-chloro-2,3-epoxypropane, mono- and di-2,3-epoxypropyl ethers of 1,4-butanediol, and 2,2-bis(4(2',3'- epoxypropoxy)phenyl)propane, and in the presence of catalytic quantities of halide ions, trichloroethylene can dehydrochlorinate to dichloroacetylene. When the mixture is boiled under reflux, minor explosions can result (Urben, 1999).
- While distilling wet trichloroethylene at ambient pressure, a violent explosion occurred (Urben, 1999).
- Detonation may occur when trichloroethylene comes into contact with granular barium (Urben, 1999).
- Lithium shavings mixed with trichloroethylene are impact-sensitive and may explode violently (Urben, 1999).
- Dinitrogen tetraoxide mixed with trichloroethylene and subjected to a shock of 25 g TNT (or an equivalent) or less is explosive (Urben, 1999).
- Traces of the compound in a pipe exploded at ambient temperature under 27 bar pressure of oxygen (Urben, 1999).
- Trichloroethylene exploded violently when mixed with liquid oxygen, dichloromethane, 1,1,1-trichloroethane, and "chlorinated dye penetrants 1 and 2" (Urben, 1999).
- Trichloroethylene mixed with perchloric anhydrous acid reacts violently (Urben, 1999).
- A 0.5% impurity of trichloroethylene in tetrachloroethylene resulted in generation of dichloroacetylene when the tetrachloroethylene was dried under unheated conditions over solid sodium hydroxide. After subsequent fractional distillation, the volatile for-run exploded (Urben, 1999).
- Ignitable or explosive compounds are formed when trichloroethylene is brought in contact with metals (ITI, 1995).
- Explosive dichloroacetylene is formed when this compound is heated and exposed to potassium hydroxide (ITI, 1995).
DUST/VAPOR HAZARD
- Trichloroethylene is toxic by inhalation (Lewis, 1997).
- It is irritating to the nose and, if inhaled, will cause nausea, vomiting, breathing difficulty, or loss of consciousness (CHRIS , 2001).
- When heated to decomposition, trichloroethylene emits toxic fumes of chlorine (Lewis, 2000).
- Hydrogen chloride and other toxic gases and irritants may result from trichloroethylene combustion (NFPA, 1997).
- At high temperatures, trichloroethylene may decompose to hydrochloric acid, phosgene and other compounds. Photochemical degradation may also release chloroform (ILO , 1998).
REACTIVITY HAZARD
- In the presence of moisture, light slowly decomposes trichloroethylene, generating hydrochloric acid (Budavari, 2000).
- At high temperatures (e.g. arc welding, open flame) and in the presence of atmospheric oxygen, trichloroethylene decomposes to hydrochloric acid, phosgene and other compounds (Bingham et al, 2001; ILO , 1998; Sittig, 1991).
- When exposed to heat and pressure, trichloroethylene will react with water to form hydrogen chloride gas (Lewis, 2000).
- Trichloroethylene may react with moist, warm alkaline material (such as concrete) to yield dichloroacetylene, a highly reactive and very toxic chemical (Greim et al, 1984).
- Other products of decomposition are glycolic acid and hexachlorobenzol (Grant, 1986).
- When trichloroethylene was used to extract a strongly alkaline liquor, an emulsion decomposed with evolution of dichloroacetylene, a spontaneously flammable gas (Urben, 1999).
- Overalls soiled with aluminum dust were cleaned with trichloroethylene. While the garment was drying, "violent ignition" occurred (Urben, 1999).
- The following substances, when mixed with trichloroethylene, will flash or spark under heavy impact (Urben, 1999):
Powdered beryllium Powdered magnesium Titanium
- Trichloroethylene and perchloric anhydrous acid will react violently (ITI, 1995; Urben, 1999).
- Trichloroethylene can react violently with the following (Lewis, 2000):
- Phosgene, a highly toxic gas, was formed when trichloroethylene came in contact with iron, copper, zinc, or aluminum. Temperature range was 250 degrees C to 600 degrees C (HSDB , 2001).
- This compound is incompatible with caustics, aluminum and chemically active metals. Explosive dichloracetylene may be formed when this compound reacts with alkali (Sittig, 1991).
It reacts violently with metals such as lithium, magnesium, aluminum, titanium, barium, sodium (ILO , 1998; ITI, 1995).
- When this compound is brought in contact with aluminum, violent, self-accelerating polymerization may occur (Pohanish & Greene, 1997).
- Trichloroethylene is incompatible with (Pohanish & Greene, 1997):
acids organic anhydrides isocyanates alkylene oxides aldehydes alcohols glycols phenols cresols caprolactam solution epichlorohydrin nitrogen tetroxide metal powders oxygen
- Both dichloro- and monochloraacetylene were found in the air when trichloroethylene was reacted with hot alkalies such as soda lime (Grant & Schuman, 1993).
- Trichloroethylene reacts with alkali and epoxides such as 1-chloro-2,3-epoxypropane, 1,4-butanediol mono-2,3-epoxypropylether, 1,4-butanediol di-2,3-epoxypropylether, 2,2-bis[(4(2'3'-epoxypropoxy)phenyl)propane]. In these reactions, the spontaneously flammable gas dichloroacetylene is formed (Lewis, 2000).
- See the EXPLOSION HAZARD section of the Hazardtext document for more information.
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- LARGE SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 160 (ERG, 2004)
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 160 (ERG, 2004)
If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 160 (ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Many gases are heavier than air and will spread along ground and collect in low or confined areas (sewers, basements, tanks). Keep out of low areas. Ventilate closed spaces before entering.
- In spill situations, evacuate the area, don protective gear and spread sand or other absorbent material over the spilled material. Once the liquid is absorbed, shovel the material into a bucket and bring it to a safe place in the open. Spill area can be washed with soap and water (Sittig, 1991).
- AIHA ERPG Values for CAS79-01-6 (AIHA, 2006):
Listed as Trichloroethylene ERPG-1 (units = ppm): 100 ERPG-2 (units = ppm): 500 ERPG-3 (units = ppm): 5000 Under Ballot, Review, or Consideration: No Definitions: ERPG-1: The ERPG-1 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing more than mild, transient adverse health effects or perceiving a clearly defined objectionable odor. ERPG-2: The ERPG-2 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing irreversible or other serious health effects or symptoms that could impair an individual's ability to take protective action. ERPG-3: The ERPG-3 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing life-threatening health effects.
- DOE TEEL Values for CAS79-01-6 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Trichloroethylene TEEL-0 (units = ppm): 10 TEEL-1 (units = ppm): 130 TEEL-2 (units = ppm): 450 TEEL-3 (units = ppm): 3800 Definitions: TEEL-0: The threshold concentration below which most people will experience no adverse health effects. TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure. TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape. TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.
- AEGL Values for CAS79-01-6 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
Listed as: Trichloroethylene Proposed Value: AEGL-1 10 min exposure: 30 min exposure: 1 hr exposure: 4 hr exposure: 8 hr exposure:
Definitions: AEGL-1 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling, are transient, and are reversible upon cessation of exposure.
Listed as: Trichloroethylene Proposed Value: AEGL-2 10 min exposure: 30 min exposure: 1 hr exposure: 4 hr exposure: 8 hr exposure:
Definitions: AEGL-2 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting adverse health effects or an impaired ability to escape.
Listed as: Trichloroethylene Proposed Value: AEGL-3 10 min exposure: 30 min exposure: 1 hr exposure: 4 hr exposure: 8 hr exposure:
Definitions: AEGL-3 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening health effects or death.
- NIOSH IDLH Values for CAS79-01-6 (National Institute for Occupational Safety and Health, 2007):
IDLH: 1000 ppm Note(s): Ca
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 160 (ERG, 2004) ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). Stop leak if you can do it without risk.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 160 (ERG, 2004) Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. Structural firefighters' protective clothing will only provide limited protection.
ENVIRONMENTAL CONSIDERATIONS - LAND SPILL (AAR, 2000) To contain liquid or solid material, dig a pit, pond, lagoon, or holding area. Use soil, sand bags, foamed polyurethane, or foamed concrete to dike surface flow. Use fly ash or cement powder to absorb bulk liquid.
ENVIRONMENTAL CONSIDERATIONS - WATER SPILL (AAR, 2000) If the compound is dissolved in region of 10 ppm or greater concentration, apply activated carbon at 10 times the amount spilled. Use suction hoses to remove trapped material. Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates.
ENVIRONMENTAL CONSIDERATIONS - AIR SPILL (AAR, 2000) To knock down vapors, apply water spray or mist. Trichloroethylene combustion products include corrosive or toxic vapors.
Absorb on paper, evaporate on a glass dish in a hood, and then burn the paper (ITI, 1995). Remain upwind of the release. Stop or control the leak if it is safe to do so. Isolate any discharged material and then dispose of it properly (NFPA, 1997). In emergency situations, keep people out of the area. Avoid direct contact with the liquid and the vapor. Prevent leakage of the compound into water intakes, water sources and sewers. If necessary, build dikes to contain the spill. Notify local health and pollution control agencies and fire department (AAR, 2000; CHRIS , 2001).
Other treatment options for trichloroethylene are incineration (rotary kiln, fluidized bed, or liquid injection), activated carbon, stripping, biological treatment, chemical precipitation, and solvent extraction (HSDB , 2001). For cleanup procedures, this compound can be poured onto dry sand and allowed to evaporate in an isolated location (OHM/TADS , 2001). Other dispoal methods include purification by distillation or return to the supplier (ITI, 1995; OHM/TADS , 2001). Treatment methods capable of removing trichloroethylene from drinking water include (Verschueren, 2001): flocculation (Fe3+) and rapid filtration (17% removal); chlorination and flocculation (Fe3+) and rapid; filtration (36% removal); ozonation (99.5% removal); river bank filtration (6-25% removal); activated carbon (28-98% removal); aeration (75% removal).
Prior to land disposal of trichloroethylene or trichloroethylene-containing materials, authorization must be obtained from federal, state and local authorities (ATSDR, 1997). Transformation of trichloroethylene can be influenced by the presence of iron sulfide (FeS) or pyrite. The rate of this transformation, as well as the distribution of reaction products, has been shown to depend on the pH of the solution (increased rate with increase in pH from 6.3 and 9.3). Experimental results showed an increase in transformation rate when iron granules were pretreated with sodium hydrosulfide (NaHS), thereby aging the iron metal. No effect on the transformation rate was seen following the addition of manganese cloride (MnCl2), 2,2'-bipyridine or 2-propanol (Butler EC and Hayes KF, 2001). Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.
A fluidized bed bioreactor with attached-film technology was used in mixed culture anaerobic digestion to treat trichloroethene. The biofilm was attached to either diatomaceous earth or on granular activated carbon. The system was tested for four years and showed that attached-film methanotrophs are stable and useful in treating toxic chemicals (Fennell et al, 1992). The bacterium Xanthobactor (strain Py2) was grown on propylene as the carbon source. The resultant culture degraded several chlorinated alkenes of environmental concern, including trichloroethylene. This study confirmed that alkene monooxygenase was the active enzyme required to catalyze chlorinated alkene degradations (Ensign et al, 1992). In a laboratory study, radioactively labeled trichloroethylene was biodegraded in batch culture using a type II methane-utilizing bacterium, Methylocystis. The results showed that 32% of the radioactive carbon was converted to glyoxylic acid, dichloroacetic acid, and trichloroacetic acid (Uchiyama et al, 1992). Also, about 32% was converted to CO2 and CO after 140 hours of incubation in a pure culture experiment. The water-soluble products of this first stage were completely or partially degraded further and converted to CO2 by a mixed culture MU-18. A second bacterium identified in the mixed culture was Xanthobactor autotrophicus. It was this second bacterium that was important in completing the degradation (Uchiyama et al, 1992).
A constitutive reversion mutant of Pseudomonas was isolated which degraded trichloroethylene. The mutant was stable through 100 generations of nonselective growth (Shields & Reagin, 1992). The microorganism Burkholderia cepacia G4 5223-PR1 degrades trichloroethylene without aromatic induction. Its potential for bioremediation was tested within a simulated aquifer sediment system and groundwater microcosms. G4 5223-PR1 survived relatively well in sterilized groundwater. In non-sterile groundwater, no live cells could be detected at ten days after inoculation. The survival rate was greater in a non-sterile aquifer sediment microcosm; however, after 22 days of elution the number of live cells was low (Winkler et al, 1995). The IC50 for respiration inhibition in bench scale activated sludge is greater than 1,000 mg/L (Verschueren, 2001). Eighty-three to 91% of trichloroethylene was degraded from mixed organic wastes by a propane-fed bioreactor, under aerobic conditions within 21 days at 22 degrees C (Verschueren, 2001). More than 50% of this compound was biodegraded in a bioreactor containing a mixture of microorganisms that utilized methane as their primary carbon source. Influent concentration was 1 mg/L and the residence time was 50 minutes at 20 degrees C (Verschueren, 2001). Under methanogenic conditions and in the presence of fermenters, the carbon-carbon double bond of trichloroethylene can be hydrogenated, eventually generating chloroethane (Verschueren, 2001).
The half-life of this compound in a methanogenic aquifer at 17 degrees C was 12 weeks. After an incubation period of 16 weeks, the metabolites vinyl chloride and 1,2-dichloroethylene were detected in the water (Verschueren, 2001). After an 80-day incubation period, 33 to 47% of trichloroethylene was degraded by bacteria indigenous to a site contaminated with trichloroetylene, with aerobic and oligotrophic conditions. An initial lag time of 14 to 18 days was observed (Verschueren, 2001). Trichloroethylene's half-life in soil, based upon estimated aqueous aerobic biodegradation half-lives, is between 4320 hours (6 months) and 8640 hours (1 year) (Howard et al, 1991). Biodegradation half-life in soil suspensions that were shaken in the dark at 25 degrees C was found to range from 18 to >40 days. The highest degradation rate (80%) was found in a lotus field soil (Verschueren, 2001). Small amounts of trichloroethylene were mineralized by nonproliferating Mycobacterium vaccae grown on propane. When toluene was added to this process, an approximate 50% increase in mineralization was realized (Vanderberg et al, 1995). Reported biodegradation rates (Dragun, 1988): 51% in 7D -- static-culture flask biodegradation test, original culture; settled domestic waste water utilized as microbial inoculum 69% in 4D -- Soil-water or sediment-water incubation study; natural microbial flora under methanogenic conditions less than 3.5%/w -- soil incubation study; natural microbial flora used as inoculum 89% in 40W -- soil incubation study; natural microbial flora used as inoculum less than 1.2 to less than 2.3%/w -- soil incubation study; natural microbial flora used as inoculum
Trichloroethylene may be removed from water or aqueous waste by air stripping (Freeman, 1989). Incinerate trichloroethylene waste after mixing it with a combustible fuel. Ensure that combustion is complete so that phosgene formation does not occur. Use an acid scrubber to remove any halo acids that are produced (ATSDR, 1997; (HSDB , 2001). Pump or vacuum any undissolved material, and then apply carbon or peat. Do not heat (OHM/TADS , 2001). Other recommended incineration methods include (HSDB , 2001): Rotary kiln incineration at 820 to 1600 degrees C and a residence time of hours for solids and seconds for liquids and gases; Fluidized bed incineration at 450 to 980 degrees C with residence times of seconds for liquids and gases and longer for solids; Liquid injection incineration at temperatures of 650 to 1600 degrees C with residence times of 0.1 to 2 seconds.
For incineration, the temperature for 99% destruction of this chemical at 2-sec residence time under oxygen starved conditions is 865 degrees C (Verschueren, 2001).
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- INTRODUCTION INTO THE ENVIRONMENT
Trichloroethylene is released to the atmosphere primarily through evaporation from degreasing and metal finishing operations. It may also be released to the environment during its manufacture, use as chemical intermediate, and through solvent evaporation from adhesives, paints, and coatings (HSDB, 2005; ATSDR , 1997). Trichloroethylene is produced naturally by certain species of micro- and macroalgae. Rates of trichloroethylene production have been measured at 0.022 - 3400 mg/g fresh weight per hour. The overall significance of this source to atmospheric emissions is unknown (ATSDR , 1997). Trichloroethylene may also occur in the environment as a product of tetrachloroethylene decomposition (ATSDR , 1997). Trichloroethylene may be introduced to land, aquatic systems, and groundwater from industrial discharge landfill leachate (HSDB, 2005; ATSDR , 1997).
Workers may be exposed to trichloroethylene during its production, handling, and use. Workers involved in degreasing operations are generally exposed at the highest levels (ATSDR , 1997).
- GENERAL POPULATION EXPOSURE
People may be exposed to trichloroethylene through ingestion of contaminated foods or drinking water or through inhalation of ambient air containing the chemical (HSDB, 2005). It has been detected in meats, fish/seafood, grain-based foods, oils, fruits and vegetables, and in milk and dairy products. It has also been widely detected in drinking water and groundwater (HSDB, 2005; ATSDR , 1997). Trichloroethylene is frequently found in food and beverage plants (ILO , 1998).
Trichloroethylene is a volatile organic component of several household products and cleaning supplies. It has been detected in indoor air samples from numerous sites (HSDB, 2005).
ENVIRONMENTAL FATE AND KINETICS
Trichloroethylene is expected to exist solely as a vapor in the ambient atmosphere, based on its vapor pressure of 69 mmHg at 25 degrees C. Trichloroethylene released to the environment degrades through reaction with photochemically-produced hydroxyl radicals. It is moderately water soluble; experimental data indicate trichloroethylene may be rapidly scavenged by rain water and be removed from the atmosphere via wet deposition (HSDB, 2005; ATSDR , 1997). Assuming a hydroxyl radical concentration of 5 x 10(5) molecules/cm(3), trichloroethylene's half-life is 6.8 days; the estimated rate constant at 25 degrees C is 2.36 x 10(-12) cm(3)/molecule-sec (ATSDR , 1997). Degradation products of reaction with hydroxyl radicals include phosgene, dichloroacetyl chloride, chloroform, and formyl chloride (HSDB, 2005; Howard, 1990). Trichloroethylene in the atmosphere is degraded by photo-oxidation with a half-life of 7 days (Barceloux & Rosenberg, 1990). Photo-oxidation half-life in air is between 27 hours (1.1 day) and 272 hours (11.3 days), based upon measured rate for the vapor phase reaction with hydroxyl radicals in air (Howard et al, 1991).
Reaction with nitrate radicals has been measured at 2.93x10(-16) cm(3)/molecule-sec at 25 degrees C, which corresponds to at atmospheric half-live of 114 days at a nitrate concentration of 2.4 x 10(8) radicals/cm(3) (HSDB, 2005). Reaction with ozone is too slow to be a significant removal process for trichloroethylene from air (ATSDR , 1997). Because of its fairly high vapor pressure, trichloroethylene released to the air will react quickly, especially under smog conditions. Atmospheric residence time has been reported at 5 to 6 days (HSDB, 2005; Howard, 1990). Direct photolysis is not an important removal mechanism for trichloroethylene from the atmosphere, as the compound only weakly absorbs light at wavelengths >290 nm (HSDB, 2005).
SURFACE WATER The majority of trichloroethylene released to surface water is expected to volatilize rapidly. Amounts that do not volatilize immediately may submerge and undergo biodegradation. Neither hydrolysis nor photolysis appear to be significant removal mechanisms for trichloroethylene from aquatic systems (ATSDR , 1997). Hydrolysis half-lives for trichloroethylene at pH 7 and 25 degrees C have been estimated from 10.7 months to 1.3 x 10(6) years. The large range in values may be due to errors in extrapolation methods and transformation factors other than hydrolysis that were not accounted for in the lower measurement (ATSDR , 1997). Using an estimated Henry's Law constant of 9.85 x 10(-3) atm-m(3)/mole, volatilization half-lives for trichloroethylene have been estimated at 3.5 hours for a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec) and 5 days for a model lake (1 m deep, flowing 0.05 m/sec, wind velocity or 0.5 m/sec) (HSDB, 2005). First order rate constant for hydrolysis: k =0.065/month. First order hydrolysis half-life is 7704 hours (10.7 months), based upon first order rate constant (k) of 0.065/month (Howard et al, 1991).
Trichloroethylene is not expected to adsorb to suspended solids or sediment (HSDB, 2005; Howard, 1990).
GROUND WATER Half-life in groundwater, based upon hydrolysis half-lives and anaerobic sediment grab sample data, is between 7704 hours (10.7 months) and 39,672 hours (4.5 years) (Howard et al, 1991). Trichloroethylene was found to degrade to cis-1,2-dichloroethylene as an intermediate product in groundwater (Hirata et al, 1992). No sorption of trichloroethylene to organic carbon or mineral surfaces was observed in a sand aquifer groundwater field test (HSDB, 2005).
TERRESTRIAL Trichloroethylene released to soil surfaces will volatilize quickly due to its high vapor pressure. Liquid that does not volatilize will leach into subsurface soils where it can displace soil pore water. Trichloroethylene is relatively stable in soil, and does not appear to undergo chemical transformation or covalently bond with soil components (ATSDR , 1997; Howard, 1990). An EPA soil/sediment study showed that trichloroethylene vapor may sorb to soils. Linear sorption coefficients for trichloroethylene vapor were approximately 1 - 4 orders of magnitude greater than those from the aqueous phase (HSDB, 2005). Movement of trichloroethylene vapor through unsaturated soil was found to be lateral, based on density-induced advective flow of the contaminated soil gas. Vapor sorption may reduce the total volatilization in soil with increased water content and enhance total volatilization in soil with low water content at depth (HSDB, 2005).
Trichloroethylene's low adsorption coefficient suggests it is moderately to highly mobile in soil (HSDB, 2005; Howard, 1990). A study was conducted to determine the sorption and desorption characteristics of trichloroethylene in four granular media. The media were: sandy loam soil, organic top soil, peat moss, and granular activated carbon (GAC). The results were reasonably represented by Freundlich Isotherms and showed that organic carbon content is an important factor in both adsorption and desorption. The results suggest that trichloroethylene will migrate quickly through soil (Zytner, 1992).
ABIOTIC DEGRADATION
- Vapor phase trichloroethylene is degraded predominantly through reaction with photochemically-produced hydroxyl radicals. It may be removed from the atmosphere via wet deposition (ATSDR , 1997).
- Trichloroethylene in volatilizes from surface waters aquatic environments. It does not adsorb to sediment or suspended solids. Trichloroethylene reportedly does not hydrolyze under normal environmental conditions (ATSDR , 1997).
- In soil, trichloroethylene volatilizes from both dry and moist soil surfaces, though evaporation may be attenuated by vapor sorption. Amounts that do not volatilize quickly may leach to groundwater, as it is moderately to highly mobile in soils (ATSDR , 1997).
BIODEGRADATION
- Under most conditions trichloroethylene biodegrades very slowly in water. Significant biodegradation occurred in only a few studies and acclimation was slow. Under anaerobic conditions biodegradation has ranged from very little after 12 weeks to 40% after 8 weeks (Howard, 1990).
Half-life in surface water, based upon estimated aqueous aerobic biodegradation half-lives, is between 4320 hours (6 months) and 8640 hours (1 year) (Howard et al, 1991).
- Under aerobic conditions, a gram-negative, rod-shaped bacterium that was isolated from a water sample was able to degrade trichloroethylene to CO2 and unidentified, non-volatile compounds. This degradation required the presence of water from the site where the bacterium had been isolated (Verschueren, 2001).
- Biodegradation half-life in non-adapted, aerobic, clay subsoil from Oklahoma was found to be >485 days (Verschueren, 2001).
- Biodegradation half-life: 300 days (naturally-occuring soil-groundwater system; estimation based on field observation) (Dragun, 1988)
- Aqueous, unacclimated biodegradation half-life under aerobic conditions is between 4320 hours (6 months) and 8640 hours (1 year). This scientific judgement is based upon acclimated soil screening test data (Howard et al, 1991).
- Aqueous, unacclimated biodegradation half-life under anaerobic conditions is between 2352 hours (98 days) and 39,672 hours (4.5 years). This scientific judgement is based upon anaerobic sediment grab sample data (Howard et al, 1991).
BIOACCUMULATION
The following Bioconcentration Factors (BCF) have been reported for trichloroethylene (HSDB, 2005): Reported BCF in fish range between 10 and 100 for trichloroethylene in fish (ATSDR , 1997). The compound bioconcentrates moderately in marine life (2 to 25 times the concentration in water) (HSDB, 2005; Howard, 1990). BCF in algae (Chlorella fusca): 1160 (Verschueren, 2001) Killifish: BCF 2.71 (ATSDR , 1997) Blue mussel: BCF 4.52 (ATSDR , 1997)
ENVIRONMENTAL TOXICITY
EC0 - ALGAE (Microcystis aeruginosa): 63 mg/L for 8D (Verschueren, 2001) EC0 - ALGAE (Scenedesmus quadricauda): >1,000 mg/L for 7D (Verschueren, 2001) EC50 - ALGAE (Tetrahymena pyriformis): 410 mg/L for 24H (Verschueren, 2001) Toxicity threshold (cell multiplication inhibition test) - GREEN ALGAE (Scenedesmus quadricauda): greater than 1000 mg/L, time not specified, conditions of bioassay not specified (HSDB, 2005) Toxicity threshold (cell multiplication inhibition test) - ALGAE (Microcystis aeruginosa): 63 mg/L, time not specified, conditions of bioassay not specified (HSDB, 2005)
LC50 - CLAWED TOAD, at 3 to 4 weeks after hatching: 45 mg/L for 48H (Verschueren, 2001) LC50 - MEXICAN AXOLOTL SALAMANDER, at 3 to 4 weeks after hatching: 48 mg/L for 48H (Verschueren, 2001)
EC - FISH: 55 mg/L 0.6 hours; Freshwater toxicity test -- stupified effect (OHM/TADS, 2005) EC10 - FATHEAD MINNOW (Pimephales promelas): 15.2 mg/L for 24 hours -- loss of equilibrium, flow-through bioassay (HSDB, 2005) EC10 - FATHEAD MINNOW (Pimephales promelas): 16.9 mg/L for 48 hours -- loss of equilibrium, flow-through bioassay (HSDB, 2005) EC10 - FATHEAD MINNOW (Pimephales promelas): 15.5 mg/L for 72 hours -- loss of equilibrium, flow-through bioassay (HSDB, 2005) EC10 - FATHEAD MINNOW (Pimephales promelas): 13.7 mg/L for 96 hours -- loss of equilibrium, flow-through bioassay (HSDB, 2005) EC50 - FATHEAD MINNOW (Pimephales promelas): 23.0 mg/L for 24 hours -- loss of equilibrium (HSDB, 2005) EC50 - FATHEAD MINNOW (Pimephales promelas): 22.7 mg/L for 48 hours -- loss of equilibrium (HSDB, 2005) EC50 - FATHEAD MINNOW (Pimephales promelas): 22.2 mg/L for 72 hours -- loss of equilibrium (HSDB, 2005) EC50 - FATHEAD MINNOW (Pimephales promelas): 21.9 mg/L for 96 hours -- loss of equilibrium (HSDB, 2005) EC90 - FATHEAD MINNOW (Pimephales promelas): 36.2 mg/L for 24 hours -- loss of equilibrium (HSDB, 2005) EC90 - FATHEAD MINNOW (Pimephales promelas): 30.6 mg/L for 48 hours -- loss of equilibrium (HSDB, 2005) EC90 - FATHEAD MINNOW (Pimephales promelas): 31.8 mg/L for 72 hours -- loss of equilibrium (HSDB, 2005) EC90 - FATHEAD MINNOW (Pimephales promelas): 34.9 mg/L for 96 hours -- loss of equilibrium (HSDB, 2005) LC50 - BLUEGILL SUNFISH: 44,700 mcg/L for 96H, static bioassay (HSDB, 2005) LC50 - BLUEGILL (Lepomis macrochirus): 52 mg/L for 24H; static bioassay (Verschueren, 2001) LC50 - BLUEGILL (Lepomis macrochirus): 41 mg/L for 96H; static bioassay (Verschueren, 2001) LC50 - FATHEAD MINNOW (Pimephales promelas): 41 mg/L for 96 hours; flow-through test (Verschueren, 2001) LC50 - FATHEAD MINNOW (Pimephales promelas): 67 mg/L for 96 hours; static test (Verschueren, 2001) LC50 - GUPPY: 55 mg/L for 7D (Verschueren, 2001) LC50 - KILLIFISH (Oryzias latipes): 84 mg/L for 48H (Verschueren, 2001) LC50 - SHEEPSHEAD MINNOW: 20 mg/L for 96H (HSDB, 2005)
EC0 - BACTERIA (Pseudomonas putida): 65 mg/L for 16H (Verschueren, 2001) EC50 - BACTERIA: 260 mg/L; OECD 209 closed system inhibition (Verschueren, 2001)
LC - DAPHNIA: 660 mg/L for 40 hours; Freshwater toxicity test (CHRIS, 2005; OHM/TADS, 2005) LC50 - GRASS SHRIMP: 2 mg/L for 96H (HSDB, 2005) LC100 -WATER FLEA (Daphnia): 600 mg/L for 40H (Verschueren, 2001) NOEC - DAPHNIA: 99 mg/L for 40 hours; Freshwater toxicity test (OHM/TADS, 2005) NOEC - WATER FLEA (Daphnia): 100 mg/L for 49H (Verschueren, 2001)
LC0 - MIDGE (Chironomus riparius), 3rd instar larvae: 123 mg/L for 48H (Verschueren, 2001) LC50 - MIDGE (Chironomus riparius) 3rd instar larvae: 147 mg/L for 48H (Verschueren, 2001) LC50 - WORMS (Tubifex): 640 mg/L for 48H (Verschueren, 2001) LC100 - MIDGE (Chironomus riparius) 3rd instar larvae: 175 mg/L for 48H (Verschueren, 2001) NOEC - MIDGE (Chironomus riparius) 3rd instar larvae: <31 mg/L for 48H (Verschueren, 2001) NOLC - MIDGE (Chironomus riparius) 3rd instar larvae: 96 mg/L for 48H (Verschueren, 2001)
EC0 - PROTOZOA (Entosiphon sulcatum): 1,200 mg/L for 72H (Verschueren, 2001) EC0 - PROTOZOA (Uronema parduczi Chatton-Lwoff): >960 mg/L (Verschueren, 2001)
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- At 15 degrees C and 1 atm pressure, trichloroethylene is a clear, colorless, mobile liquid. It is non-flammable. Its odor is sweet and resembles chloroform (Budavari, 2000; CHRIS , 2001; Lewis, 2000; JEF Reynolds , 2000).
- The liquid is sometimes dyed blue (Harbison, 1998; ILO , 1998).
- It is a stable, photo-reactive liquid with low boiling point (Lewis, 1997).
VAPOR PRESSURE
- 100 mmHg (at 32 degrees C) (Lewis, 2000; OHM/TADS , 2001)
- 95 mm (at 30 degrees C) (Verschueren, 2001)
- 69 mmHg (at 25 degrees C) (Howard, 1990)
- 74 mmHg (at 25 degrees C) (ATSDR, 1997)
- 58 mmHg (at 20 degrees C) (ACGIH, 1996a; Hayes & Laws, 1991; NFPA, 1997; NIOSH , 2001)
- 60 mm (at 20 degrees C) (Verschueren, 2001)
- 20 mm (at 0 degrees C) (Verschueren, 2001)
- 19.9 mmHg (at 0 degrees C) (HSDB , 2001)
- 57.8 mmHg (at 20 degrees C) (HSDB , 2001)
SPECIFIC GRAVITY
- NORMAL TEMPERATURE AND PRESSURE
(25 degrees C; 77 degrees F and 760 mmHg) 1.4559 (at 25/4 degrees C) (Budavari, 2000) 1.456-1.462 (at 25/25 degrees C) (Lewis, 1997)
- OTHER TEMPERATURE AND/OR PRESSURE
1.4904 (at 4/4 degrees C) (Budavari, 2000) 1.4695 (at 15/4 degrees C) (Budavari, 2000) 1.4642 (at 20/4 degrees C) (Budavari, 2000) 1.46 (at 20/4 degrees C) (CHRIS , 2001; NIOSH , 2001) 1.4649 (at 20/4 degrees C) (ITI, 1995; Lewis, 2000)
- TEMPERATURE AND/OR PRESSURE NOT LISTED
DENSITY
- OTHER TEMPERATURE AND/OR PRESSURE
- TEMPERATURE AND/OR PRESSURE NOT LISTED
FREEZING/MELTING POINT
-99 degrees F (NIOSH , 2001) -87 degrees C (Ashford, 1994) -86.8 degrees C (Lewis, 2000) -86.4 degrees C; -123.5 degrees F; 186.8 K (CHRIS , 2001) -73 degrees C (Lewis, 1997) Solidifies at -83 degrees C (ITI, 1995) Solidifies at -84.8 degrees C (ACGIH, 1996a; Hayes & Laws, 1991)
-85 degrees C, -121 degrees F (NFPA, 1997) -84.8 degrees C (Budavari, 2000) -84 degrees C (Lewis, 2000) -83 degrees C (OHM/TADS , 2001) -87 degrees C (Verschueren, 2001) -87.1 degrees C (ATSDR, 1997) -73 degrees C (Howard, 1990; HSDB , 2001; ILO , 1998; ITI, 1995; Lewis, 1996)
BOILING POINT
- 86.9 degrees C (at 760 mmHg) (Budavari, 2000)
- 67.0 degrees C (at 400 mmHg) (Budavari, 2000)
- 48.0 degrees C (at 200 mmHg) (Budavari, 2000)
- 31.4 degrees C (at 100 mmHg) (Budavari, 2000)
- 20.0 degrees C (at 60 mmHg) (Budavari, 2000)
- -1.0 degrees C (at 20 mmHg) (Budavari, 2000)
- -12.4 degrees C (at 10 mmHg) (Budavari, 2000)
- -22.8 degrees C (at 5 mmHg) (Budavari, 2000)
- -43.8 degrees C (at 1 mmHg) (Budavari, 2000)
- 86-87 degrees C (Sittig, 1991)
- 86.7 degrees C (ATSDR, 1997; (Hayes & Laws, 1991; ITI, 1995; Lewis, 2000; Lewis, 1997; OHM/TADS , 2001)
- 87 degrees C(ACGIH, 1996a; Howard, 1990; HSDB , 2001; Verschueren, 2001)
- 87 degrees C; 189 degrees F (NFPA, 1997)
- 87 degrees C; 189 degrees F; 360 K (at 1 atm) (CHRIS , 2001)
- 86-98 dgrees C (Ashford, 1994)
- 189 degrees F (NIOSH , 2001)
FLASH POINT
- 89.6 degrees F (Lewis, 1996)
- 90 degrees F (closed cup); practically non-flammable (CHRIS , 2001)
- 32.1 degrees C (OHM/TADS , 2001)
- 32 degrees C (closed cup) (ITI, 1995)
- "There are a few halogenated hydrocarbons for which a flash point cannot be determined by standard tests, and these unfortunately are often described as non-flmmable, though they will burn if the ignition source is sufficiently intense" (Urben, 1999).
AUTOIGNITION TEMPERATURE
- 410 degrees C (ILO , 1998; ITI, 1995; OHM/TADS , 2001)
- 420 degrees C (Lewis, 1996)
- 420 degrees C; 788 degrees F (NFPA, 1997)
- 788 degrees F (Lewis, 2000)
EXPLOSIVE LIMITS
14.5% (at 35 degrees C) (Urben, 1999) 12.5% (ITI, 1995; Lewis, 1996; OHM/TADS , 2001) 8.5% (at 25 degrees C) (Urben, 1999) 8% (at 25 degrees C) (ATSDR, 1997; (CHRIS , 2001; NFPA, 1997; NIOSH , 2001; Sittig, 1991) 7.8% (at 100 degrees C) (NFPA, 1997; Sittig, 1991) 6.0-47% (at 150 degrees C) (Urben, 1999)
90% (ITI, 1995; Lewis, 1996; OHM/TADS , 2001) 10.5% (at 25 degrees C) (ATSDR, 1997; (CHRIS , 2001; NFPA, 1997; NIOSH , 2001; Sittig, 1991) 52% (at 100 degrees C) (NFPA, 1997; Sittig, 1991)
SOLUBILITY
1.070 g/L (at 20 degrees C) (ATSDR, 1997) 0.11 g/100 g (at 25 degrees C) (Budavari, 2000; HSDB , 2001; Verschueren, 2001) 1.366 g/L (at 25 degrees C) (ATSDR, 1997) 160 ppm (at 25 degrees C) (OHM/TADS , 2001) 0.1% (NIOSH , 2001) Insoluble in water (ACGIH, 1996a; Ashford, 1994; Hayes & Laws, 1991; Lewis, 2000; NFPA, 1997) Slightly soluble in water (Lewis, 1997) Immiscible with water (Lewis, 2000)
Miscible with oxygenated solvents (Ashford, 1994) It is miscible with the following (Budavari, 2000; Hayes & Laws, 1991; HSDB , 2001; Lewis, 2000): Acetone Alcohol Carbon tetrachloride Chloroform Ether
Dissolves most fixed and volatile oils (Budavari, 2000) Highly soluble in lipids (ACGIH, 1996a)
OCTANOL/WATER PARTITION COEFFICIENT
- log Kow = 2.42 (ATSDR, 1997; (Howard, 1990)
- log Kow = 2.61 (HSDB , 2001)
- log Poct = 2.42 (Verschueren, 2001)
HENRY'S CONSTANT
- 0.0070 atm-m(3)/mol(-1) (20 degrees C) (Tse et al, 1992)
- 0.0114 atm-m(3)/mol(-1) (30 degrees C) (Tse et al, 1992)
- 0.0173 atm-m(3)/mol(-1) (40 degrees C) (Tse et al, 1992)
- 1X10(-2) atm-m(3)/mole (HSDB , 2001)
- 1.03X10(-2) atm-m(3)/mole (Howard, 1990)
- 0.2 atm-L/mol (at 10 degrees C) (Verschueren, 2001)
- 0.3 atm-L/mol (at 18 degrees C) (Verschueren, 2001)
- 0.020 atm-m(3)/mol (at 20 degrees C) (ATSDR, 1997)
- 0.011 atm-m(3)/mol (at 25 degrees C) (ATSDR, 1997)
- 0.4 atm-L/mol (at 25 degrees C) (Verschueren, 2001)
- 0.6 atm-L/mol (at 35 degrees C) (Verschueren, 2001)
SPECTRAL CONSTANTS
OTHER/PHYSICAL
- LIQUID WATER INTERFACIAL TENSION
- NUCLEAR MAGNETIC RESONANCE
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