CHLOROFORM
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
 -IDENTIFICATION
SYNONYMS
CHLOROFORM CHLOROFORME (French) CHLOROFORMO (TRICLOROMETANO) (Spanish) CLOROFORMIO (Italian) FORMYL TRICHLORIDE FREON 20 METHANE TRICHLORIDE METHANE, TRICHLORO- METHENYL CHLORIDE METHENYL TRICHLORIDE METHYL TRICHLORIDE REFRIGERANT R20 R 20 (REFRIGERANT) TCM TRICHLOORMETHAAN (Dutch) TRICHLORMETHAN (Czech) TRICHLOROFORM TRICHLOROMETHANE TRICLOROMETANO (Italian) CHLOROFORMIO (ITALIAN) TRICHLOROMETANO (ITALIAN) TRICHLOROORMETHAAN (DUTCH)
IDENTIFIERS
4940311 (not elsewhere classified, technical grade) 4940310 (not elsewhere classified, other than technical grade)
BEILSTEIN HANDBOOK REFERENCE:4-01-00-00042 BEILSTEIN REFERENCE NUMBER:1731042 STANDARD INDUSTRIAL TRADE CLASSIFICATION NUMBER:51138
SYNONYM REFERENCE
- (Ariel GlobalView, 2001;(Ashford, 1994; Bingham et al, 2001; EPA, 1990; HSDB , 2001; Lewis, 2000; Lewis, 1998; RTECS , 2001)
USES/FORMS/SOURCES
Chloroform is used in the production of chlorodifluoromethane and fluoropolymers; as a solvent for alkaloids, fats, fixed and volatile oils, gulta-percha, and resins; in fire extinguishers as a heat-transfer medium; in analytical chemistry; in fumigants and insecticides; and in the rubber industry (ACGIH, 1991; Bingham et al, 2001; Budavari, 1996; Lewis, 1997; Lewis, 1998; Reynolds, 1982). Chloroform was introduced in 1847 as an inhalant anesthetic (Dykes, 1970). FDA ban prohibits the use of chloroform in cosmetics and medicines as a result of reported carcinogenicity in animals (JEF Reynolds , 1998). Applied topically, chloroform has a rubefacient action. It may be found in linaments as a counter irritant (JEF Reynolds , 1998). Applied topically in a clinical controlled study (n=41), chloroform reduced the time for scab formation when compared to placebo for herpes labialis (Reynolds, 1982). Cholesterol gallstones have been successfully removed by instilling 5 mL chloroform at a temperature of 40 degrees C (Reynolds, 1982). Hermann's Mixture containing 3 g chloroform, 2 g oil of eucalyptus, and 40 g castor oil was described in 1911 for the treatment of hookworm infestation (Dykes, 1970).
Chloroform is made from: acetone and bleaching powder by the addition of sulfuric acid; natural gas plus hydrogen chloride and anhydrous oxygen; hypochloride and aldehyde; methyl chloride plus chlorine; the reaction of chlorinated lime with acetone, acetaldehyde, or ethanol; or the chlorination of methane as a by-product(Ashford, 1994; Budavari, 1996; Lewis, 1997; Lewis, 1998).
SYNONYM EXPLANATION
- Editor's Note: Budavari (1996) noted that chloroform is improperly called "formyl trichloride".
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- USES: Chloroform is a halogenated hydrocarbon. Historically, it had been used as an inhaled anesthetic; however, it is not currently used clinically for this indication due to cardiotoxic and hepatotoxic effects. Rarely, it is used recreationally as an inhalant. Currently, chloroform is used commonly in industrial processes as a precursor for chemical production, as a solvent, in chemical fire extinguishers, in analytical chemistry, in fumigants and insecticides, and in the rubber industry.
- TOXICOLOGY: Chloroform toxicity occurs most commonly due to CNS depressant effects; as an inhaled anesthetic it causes inebriation, respiratory depression and hypoxia. The cardiotoxic effects due to chloroform are somewhat unclear in etiology, but are thought to be at least in part due to sensitization of the myocardium to catecholamines, leading to risk for developing dysrhythmias. The mechanism of chloroform-induced hepatic and renal toxicity is thought to be due to its toxic metabolites. The cytochrome system (unclear which isoenzymes) oxidizes chloroform to chloromethanol, which rapidly and spontaneously dechlorinates to create hydrochloric acid and phosgene. Phosgene in turn reacts with water to produce carbon dioxide and chloride ions and, with glutathione, to produce diglutathionyl dithiocarbonate. When glutathione is depleted to a critical level in the liver and kidney, excess phosgene covalently binds to tissue macromolecules, resulting in hepatic and renal necrosis.
- EPIDEMIOLOGY: Poisoning is rare and most often occurs by the inhalational route, although intentional ingestions have been reported.
MILD TO MODERATE TOXICITY: Common symptoms include nausea, vomiting, drowsiness, fatigue, headache, and nose and throat irritation. SEVERE TOXICITY: Common severe symptoms include CNS depression, myocardial depression, cardiac dysrhythmias, hypotension, respiratory depression, renal failure, hepatotoxicity, anoxia, and death. Dry mouth, hyperthermia, ataxia, chemical pneumonitis, dyspnea, delayed pulmonary edema, ARDS, hemolytic anemia, and leukocytosis may also be seen. Patients with chronic inhalational abuse may develop hallucinations, psychotic behavior, and white-matter degeneration. DERMAL EXPOSURE: Dermal contact results in irritation, reddening, burning pain, urticaria, vesiculation, and dermatitis via defatting. EYE EXPOSURE: Eye exposure to either the liquid or vapor forms of chloroform may cause conjunctivitis, blepharospasm, burning pain, and corneal epithelial injury.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin. Avoid any skin contact. Effects of contact or inhalation may be delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.
ACUTE CLINICAL EFFECTS
TOXICOLOGY: Chloroform toxicity occurs most commonly due to CNS depressant effects; as an inhaled anesthetic it causes inebriation, respiratory depression and hypoxia. The cardiotoxic effects due to chloroform are somewhat unclear in etiology, but are thought to be at least in part due to sensitization of the myocardium to catecholamines, leading to the risk of developing dysrhythmias. The mechanism of chloroform-induced hepatic and renal toxicity is thought to be due to its toxic metabolites. The cytochrome system (unclear which isoenzymes) oxidizes chloroform to chloromethanol, which rapidly and spontaneously dechlorinates to create hydrochloric acid and phosgene. Phosgene in turn reacts with water to produce carbon dioxide and chloride ions and, with glutathione, to produce diglutathionyl dithiocarbonate. When glutathione is depleted to a critical level in the liver and kidney, excess phosgene covalently binds to tissue macromolecules, resulting in hepatic and renal necrosis. EPIDEMIOLOGY: Poisoning is rare and most often occurs by the inhalational route, although intentional ingestions have been reported. MILD TO MODERATE TOXICITY: Common symptoms include nausea, vomiting, drowsiness, fatigue, headache, and nose and throat irritation. SEVERE TOXICITY: Common severe symptoms include CNS depression, myocardial depression, cardiac dysrhythmias, hypotension, respiratory depression, renal failure, hepatotoxicity, anoxia, and death. Dry mouth, hyperthermia, ataxia, chemical pneumonitis, dyspnea, delayed pulmonary edema, ARDS, hemolytic anemia, and leukocytosis may also be seen. Patients with chronic inhalational abuse may develop hallucinations, psychotic behavior, and white-matter degeneration. DERMAL EXPOSURE: Dermal contact results in irritation, reddening, burning pain, urticaria, vesiculation, and dermatitis via defatting. EYE EXPOSURE: Eye exposure to either the liquid or vapor forms of chloroform may cause conjunctivitis, blepharospasm, burning pain, and corneal epithelial injury.
- Chloroform is a CNS depressant, anesthetic, and hepatotoxin (ACGIH, 1991; Hathaway et al, 1991; Clayton & Clayton, 1994). Concentrations up to approximately 400 parts per million (ppm) can be tolerated for 30 minutes with no effect (Clayton & Clayton, 1994). Exposure to an airborne concentration of approximately 1000 ppm causes fatigue, headache, nausea, dizziness, and a sense of pressure in the head after a few minutes (Clayton & Clayton, 1994). With exposure to approximately 1500 ppm, dizziness and salivation may occur (Clayton & Clayton, 1994). Loss of consciousness (anesthesia) occurs with exposure to approximately 10,000 to 15,000 ppm, and concentrations in the range of 15,000 to 18,000 ppm may be lethal (ILO, 1983). Death occurs from cardiac or respiratory arrest (ILO, 1983).
- Symptoms of CNS depression include headache, nausea, dizziness, giddiness, euphoria, weakness, loss of coordination and judgement, coma, and death. With chloroform exposure, there is first a feeling of warmth, an irritation of mucous membranes, and nervousness in addition to the general symptoms.
- Chloroform can cause sudden death at high concentrations by predisposing the heart to the arrhythmogenic effects of epinephrine (adrenaline) (Clayton & Clayton, 1994). This cardiac effect has been produced in dogs (Hopkins & Krantz, 1968).
- Chloroform damages the liver and/or kidneys with either acute or chronic exposure (Clayton & Clayton, 1994). Liver damage may not be apparent for 24 to 48 hours (Hathaway et al, 1991). When applied to the skin, chloroform is irritating and can cause chemical burns (ILO, 1983; Hathaway et al, 1991). It is also irritating to the eye and can cause burning, pain, and reversible injury to the corneal epithelium (Hathaway et al, 1991).
- Small doses of chloroform, such as those obtained from exposure to tap water, are completely metabolized after ingestion and before entering the bloodstream, but the dose absorbed from other routes is dispersed throughout the body (Weisel & Jo, 1996).
CHRONIC CLINICAL EFFECTS
- Repeated chloroform exposure can cause damage to the liver, kidneys, and heart (Clayton & Clayton, 1994). Neurological and gastrointestinal symptoms resembling chronic alcoholism can also occur (ILO, 1983). The effects of chloroform on the liver have been known since 1912 (Davison & Wynne, 1970). Its hepatotoxic effects can manifest as liver enlargement (Bomski, 1967) or jaundice, which may be mistaken for infectious hepatitis (Hoong, 1975). Jaundice occurred with occupational exposure to an airborne concentration of approximately 250 ppm.
- With chronic exposure to airborne levels of approximately 200 ppm, no liver enlargement occurred, but there were symptoms of lassitude, mental dullness, and urinary and alimentary disturbances (Challen, 1958). With deliberate chloroform inhalation abuse, psychiatric symptoms including hallucinations can occur, as well as loss of appetite (Heilbrunn et al, 1945). Repeated application to the skin can produce defatting dermatitis (ILO, 1983).
- Repeated inhalation exposure to chloroform airborne concentrations in the range of 1 to 300 ppm, 6 hours per day for 7 consecutive days, produced complex changes, including new bone formation in the nasal passages of female rats. Female mice exposed under the same conditions had only increased cell proliferation. The no-observed-effect airborne level for various endpoints was in the range of 3 to 100 ppm (Mery et al, 1994).
- F344 rats given mixtures of low concentrations of chloroform, along with arsenic, phenol, benzene, chromium, lead, or trichloroethylene, showed hepatic proliferation after treatments up to 1 month (Constan et al, 1995).
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
- Prehospital gastrointestinal decontamination for chloroform ingestion is not recommended due to the potential for GI irritation, abrupt onset of CNS depression, and the risk for aspiration. INHALATIONAL EXPOSURE: Remove patient to fresh air. DERMAL EXPOSURE: Remove contaminated clothing and wash exposed area thoroughly with soap and water.
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance;give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. 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. Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
FIRST AID Immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Primary eye protection (spectacles or goggles), as defined by the Occupational Safety and Health Administration (OSHA), should be used when working with this chemical. Face shields should only be worn over primary eye protection. DERMAL EXPOSURE: Promptly wash the contaminated skin with soap and water. If this chemical penetrates the clothing, promptly remove the clothing and wash the skin with soap and water. Get medical attention promptly. INHALATION EXPOSURE: Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible. ORAL EXPOSURE: If this chemical has been swallowed, get medical attention immediately. TARGET ORGANS: Liver, kidneys, heart, eyes, skin and CNS [in animals: liver and kidney cancer] (National Institute for Occupational Safety and Health, 2007).
SUMMARY Move victims of inhalation exposure from the toxic environment and administer 100% humidified supplemental oxygen with assisted ventilation as required. Exposed skin and eyes should be copiously flushed with water. Because of the potential for rapid onset of CNS depression or seizures with possible aspiration of gastric contents, EMESIS SHOULD NOT BE INDUCED. Cautious gastric lavage followed by administration of activated charcoal may be of benefit if the patient is seen soon after the exposure.
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.
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.
ORAL EXPOSURE Because of the potential for gastrointestinal tract irritation and abrupt onset severe CNS depression and the risk of aspiration, GI decontamination is NOT recommended routinely. A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
The primary route of human exposure to chloroform is inhalation; most lethal dose information has been obtained from clinical reports of patients exposed to chloroform via anesthesia. Concentrations used for the induction of anesthesia were in the range of 20,000 to 40,000 ppm, followed by lower maintenance levels; continued exposure to 20,000 ppm resulted in respiratory failure, cardiac arrhythmia, and death. Acute hepatotoxicity was typically observed 24 to 48 hours post-exposure and often resulted in death (ATSDR, 1997; Hathaway et al, 1996). Unless brief, exposures to 40,000 ppm have been reported lethal (Bingham et al, 2001). Exposure to 14,000 ppm becomes dangerous to life in one hour (OHM/TADS , 2001).
Death has occurred following inhalation of chloroform from a handkerchief placed over the mouth and nose for anesthesia prior to surgery. On post-mortem examination the patient was found to have a diseased heart which was thought to have contributed to the death (Matsuki, 1973). Death due to central nervous system depression may result with acute ingestion of as little as 10 mL chloroform (Baselt, 2000). The oral lethal dose was estimated to be 0.5 to 5 g/kg (1 ounce to 1 pint) for an average 70 kg person (EPA, 1985).
MAXIMUM TOLERATED EXPOSURE
A man died of severe hepatic injury 9 days after ingesting approximately 6 ounces (3755 mg/kg) of chloroform; in contrast, a patient recovered from toxic hepatitis after ingesting approximately 4 ounces (2500 mg/kg) of chloroform (ATSDR, 1997). Experimental Human Exposure (Hathaway et al, 1996): Workers (17/68) exposed regularly to chloroform concentrations of 10 to 200 ppm for 1 to 4 years had hepatomegaly. In a different group of workers exposed to 50 ppm, no signs or symptoms were observed (Hathaway et al, 1996). According to Bingham et al (2001), concentrations of 70 to 80 mg/L are the narcotic limiting concentrations; 20 mg/L leads to vomiting and a sensation of fainting; 7.2 mg/L of chloroform leads to dizziness and salivation a few minutes after exposure; 5 mg/L leads to dizziness, intracranial pressure, and nausea 7 minutes after exposure, with fatigue and headache felt later (Bingham et al, 2001a). Acute hepatitis with encephalopathy occurred in a 24-year-old woman who was occupationally exposed to chloroform at a concentration of more than 15 ppm for 2 weeks (Lin et al, 2005).
- CASE REPORT: A 20-year-old woman became comatose with elevated liver enzyme levels and a prolonged prothrombin time after intentionally ingesting approximately 100 mL of chloroform. The patient gradually recovered following administration of n-acetylcysteine and supportive care (Choi et al, 2006).
- CASE REPORT: A 19-year-old man developed elevated liver enzyme concentrations and a prolonged prothrombin time after ingesting approximately 75 mL of chloroform. Following n-acetylcysteine therapy and supportive care, the patient recovered without sequelae (Dell'Aglio et al, 2010).
- CASE REPORT: A 31-year-old man developed acute renal failure and hepatotoxicity after ingesting 50 mL chloroform. With supportive care, including decontamination with activated charcoal and gastric lavage, 5 sessions of intermittent hemodialysis, and administration of N-acetylcysteine, the patient's condition improved and he was discharged on hospital day 10 (Sridhar et al, 2011).
- Carcinogenicity Ratings for CAS67-66-3 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Chloroform A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
EPA (U.S. Environmental Protection Agency, 2011): B2 ; Listed as: Chloroform 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): 2B ; Listed as: Chloroform 2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Chloroform MAK (DFG, 2002): Category 4 ; Listed as: Chloroform Category 4 : Substances with carcinogenic potential for which genotoxicity plays no or at most a minor part. No significant contribution to human cancer risk is expected provided the MAK value is observed. The classification is supported especially by evidence that increases in cellular proliferation or changes in cellular differentiation are important in the mode of action. To characterize the cancer risk, the manifold mechanisms contributing to carcinogenesis and their characteristic dose-time-response relationships are taken into consideration.
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 CAS67-66-3 (U.S. Environmental Protection Agency, 2011):
Oral: Slope Factor: RfD: 1x10(-2) mg/kg-day
Inhalation: Drinking Water:
References: ATSDR, 1997 Bingham et al, 2001 HSDB, 2001 IPCS, 1994 ITI, 1995 Lewis, 2000 OHM/TADS, 2001 RTECS, 2001 LC50- (INHALATION)DOG: LC50- (INHALATION)MOUSE: 28 g/m(3) (Lewis, 2000) Female, 4500 ppm for 9H (ATSDR, 1997) Male, 692 ppm for 1-3H (ATSDR, 1997)
LC50- (INHALATION)RAT: 47,702 mg/m(3) for 4H Female, 9770 ppm for 4H (ATSDR, 1997) 47,702 mg/m(3) for 4H (Lewis, 2000)
LCLo- (INHALATION)CAT: LCLo- (INHALATION)DOG: LCLo- (INHALATION)GUINEA_PIG: LCLo- (INHALATION)HUMAN: LCLo- (INHALATION)MOUSE: LCLo- (INHALATION)RABBIT: LCLo- (INHALATION)RAT: LD50- (INTRAPERITONEAL)DOG: LD50- (ORAL)DOG: LD50- (ORAL)GUINEA_PIG: LD50- (INTRAPERITONEAL)MOUSE: LD50- (ORAL)MOUSE: 1750 mg/kg (OHM/TADS, 2001) 118-1400 mg/kg (Bingham et al, 2001) 1100 mg/kg (ATSDR, 1997) 36 mg/kg Male, 1120 mg/kg (ATSDR, 1997) Female, 1400 mg/kg at 1 time/day for 14D (ATSDR, 1997)
LD50- (SUBCUTANEOUS)MOUSE: 3283 mg/kg (ITI, 1995) 704 mg/kg
LD50- (ORAL)RABBIT: LD50- (SKIN)RABBIT: LD50- (INTRAGASTRIC)RAT: LD50- (INTRAPERITONEAL)RAT: Female, 1379 mg/kg for 24H (IPCS, 1994) Female, 894 mg/kg for 14D (IPCS, 1994) 894 mg/kg
LD50- (ORAL)RAT: 444-2000 mg/kg (Bingham et al, 2001) 1875 mg/kg (OHM/TADS, 2001) 450 mg/kg (OHM/TADS, 2001) 300 mg/kg (OHM/TADS, 2001) Male, 14 days old, 450 mg/kg (IPCS, 1994) Male, 1200 mg/kg (IPCS, 1994) Male, 908 mg/kg (ATSDR, 1997; HSDB, 2001) Male, 908 mg/kg for 14D (IPCS, 1994) Male, 2000 mg/kg for 14D (IPCS, 1994) Male, young adult, 1337 mg/kg/once (ATSDR, 1997) Male, 14 days old, 446 mg/kg (ATSDR, 1997) Male, old adult, 1188 mg/kg (ATSDR, 1997) Male, 2000 mg/kg (ATSDR, 1997) Female, 2180 mg/kg (ATSDR, 1997) Female, 14 days old, 450 mg/kg (IPCS, 1994) Female, 1117 mg/kg (ATSDR, 1997; HSDB, 2001) Female, 1117 mg/kg for 14D (IPCS, 1994) Male, 908 mg/kg (HSDB, 2001; Lewis, 2000) 300 mg/kg (ITI, 1995) 695 mg/kg - change in motor activity; ataxia; respiratory stimulation
LDLo- (INTRAVENOUS)DOG: LDLo- (ORAL)DOG: LDLo- (ORAL)HUMAN: LDLo- (ORAL)MOUSE: LDLo- (ORAL)RABBIT: LDLo- (SUBCUTANEOUS)RABBIT: 800 mg/kg (ITI, 1995) 800 mg/kg
TCLo- (INHALATION)DOG: TCLo- (INHALATION)GUINEA_PIG: TCLo- (INHALATION)HUMAN: 10 mg/m(3) for 1Y -- central nervous system effects; gastrointestinal effects (Lewis, 2000) 5000 mg/m(3) for 7M -- hallucinations 10 mg/m(3) for 1Y -- anorexia, nausea
TCLo- (INHALATION)MOUSE: Female, 100 ppm for 7H at 1-7D of pregnancy -- changes in female fertility index; fetotoxicity (except death); post- implantation mortality Female, 100 ppm for 7H at 8-15D of pregnancy Female, 100 ppm for 7H at 8-15D of pregnancy -- craniofacial abnormalities 100 ppm for 6H/7D-intermittent -- weight loss/weight gain; changes in liver weight 12 ppm for 6H/13W-intermittent -- death
TCLo- (INHALATION)RABBIT: TCLo- (INHALATION)RAT: Female, 20,100 mcg/m(3) for 1H at 7-14D of pregnancy -- fetotoxicity; fetal death Female, 30 ppm for 7H at 6-15D of pregnancy -- fertility effects; fetotoxicity (except death); developmental abnormalities of the musculoskeletal system Female, 300 ppm for 7H at 6-15D of pregnancy -- decrease in female fertility index; post-implantation mortality Female, 100 ppm for 7H at 6-15D of pregnancy -- homeostasis; abnormalities of the gastrointestinal system Female, 20,100 mcg/m(3) for 1H at 7-14D of pregnancy - teratogenic (Lewis, 2000) 50 ppm for 7H/26W-intermittent -- fibrosis; pneumoconiosis; changes in bladder weight; liver changes 90 ppm for 6H/13W-intermittent -- hepatitis; acute renal failure; acute tubular necrosis; weight loss/decreased weight gain 300 ppm for 6H/7D-intermittent -- changes to sense organs; changes to musculoskeletal system 592 mg/m(3) for 2.5H/2W-intermittent -- changes in food intake; changes to liver; changes to kidney, ureter, and bladder
TD- (ORAL)MOUSE: 24,752 mg/kg for 2Y-continuous -- equivocal tumorigenic agent (liver tumors) 18 g/kg for 17W-intermittent -- tumorigenic (liver) 130 g/kg for 2Y-intermittent -- tumorigenic (liver; kidney, ureter, and bladder)
TD- (ORAL)RAT: 7020 mg/kg for 78W-intermittent -- carcinogenic 58,968 mg/kg for 2Y-continuous -- neoplastic; tumors of thyroid and blood 70 g/kg for 78W-intermittent -- neoplastic; kidney and thyroid tumors 98 g/kg for 78W-intermittent -- neoplastic; kidney and thyroid tumors
TDLo- (ORAL)MOUSE: 18 mg/kg for 120D-intermittent -- carcinogenic (ITI, 1995) 120 mg/kg (OHM/TADS, 2001) 1750 mg/kg for 14D-continuous -- weight loss; changes in liver and spleen weight 560 mg/kg for 4D-intermittent -- hepatitis; changes in kidney, ureter and bladder (includes acute renal failure and acute tubular necrosis) 9100 mg/kg for 13W-intermittent -- changes in liver and kidney weights; other changes to kidney, ureter, and bladder Male, 2177 mg/kg for 3W and 3W prior to mating-7D after birth prior to mating -- effects of growth statistics; biochemical and metabolic effects on the newborn Male, 2115 mg/kg for 3W and 3W prior to mating-5D after birth prior to mating-- postnatal effects 127 g/kg for 92W-intermittent -- tumorigenic (liver)
TDLo- (ORAL)RABBIT: TDLo- (ORAL)RAT: Female, 1260 mg/kg at 6-15D of pregnancy -- fetotoxicity (except death); post- implantation mortality; developmental abnormalities of the musculoskeletal system 13,832 mg/kg for 2Y-continuous -- carcinogenic; leukemia Female, 4 g/kg at 6-15D of pregnancy -- fetotoxicity (except death) 7560 mg/kg for 21D-intermittent -- effects on liver, biochemistry, and nutrition and metabolism 840 mg/kg for 28D-continuous -- changes in blood 5 mg/kg for 10D-intermittent -- biochemical and liver changes
CALCULATIONS
CONVERSION FACTORS 1 ppm = 4.89 mg/m(3) (at 25 degrees C and 760 mmHg) (Bingham et al, 2001) 1 ppm = 4.9 mg/m(3) (IPCS, 1994) 1 ppm (v/v) = 4.96 mg/m(3) (ATSDR, 1997) 1 mg/m(3) = 0.20 ppm (v/v) (ATSDR, 1997) 1 mg/m(3) = 0.204 ppm (at 25 degrees C and 760 mmHg) (IPCS, 1994) 1 mg/L = 206 ppm (Bingham et al, 2001)
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS67-66-3 (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 CAS67-66-3 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS67-66-3 (National Institute for Occupational Safety and Health, 2007):
Listed as: Chloroform REL: TWA: STEL: 2 ppm (9.78 mg/m(3)) [60-minute] Ceiling: Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards). Skin Designation: Not Listed Note(s): See Appendix A
IDLH:
- OSHA PEL Values for CAS67-66-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS67-66-3 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS67-66-3 (U.S. Environmental Protection Agency, 2010):
Listed as: Chloroform (D022) Final Reportable Quantity, in pounds (kilograms): Additional Information: Unlisted Hazardous Wastes Characteristic of Toxicity Listed as: Chloroform Final Reportable Quantity, in pounds (kilograms): Additional Information: Listed as: Methane, trichloro- Final Reportable Quantity, in pounds (kilograms): Additional Information:
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS67-66-3 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS67-66-3 (U.S. Environmental Protection Agency, 2010b):
Listed as: Chloroform P or U series number: U044 Footnote: Listed as: Methane, trichloro- P or U series number: U044 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 CAS67-66-3 (U.S. Environmental Protection Agency, 2010):
Listed as: Chloroform Reportable Quantity, in pounds: 10 Threshold Planning Quantity, in pounds: Note(s): f f: Chemicals on the original list that do not meet toxicity criteria but because of their acute lethality, high production volume and known risk are considered chemicals of concern ("Other chemicals"). (November 17, 1986, and February 15, 1990.)
- EPA SARA Title III, Community Right-to-Know for CAS67-66-3 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS67-66-3 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS67-66-3 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1888 (49 CFR 172.101, 2005):
- ICAO International Shipping Name for UN1888 (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS67-66-3 (NFPA, 2002):
-HANDLING AND STORAGE
SUMMARY
Chloroform may be a serious health hazard; handle chloroform containers with care and do not store this compound in areas of light, air, or heat, as doing so will cause chloroform to break down into phosgene, chlorine, and hydrochloric acid. Wash promptly with large amounts of soap and water if chloroform contacts the skin; speed in removing chloroform from the skin is critical. Contaminated clothing should be removed and isolated at the site (AAR, 2000; (Bingham et al, 2001; ITI, 1995; NFPA, 1997; Sittig, 1991). 0.6-1% ethanol is typically added to chloroform as a stabilizer (Bingham et al, 2001).
HANDLING
- Protect containers from any physical damage. Wear appropriate protective clothing (including gloves, boots, and goggles) and positive pressure self-contained breathing apparatus to prevent any reasonable probability of skin or eye contact (AAR, 2000; (ITI, 1995; NFPA, 1997; Sittig, 1991).
- Do not permit smoking or eating in areas where chloroform is stored, processed, or handled (HSDB , 2001).
STORAGE
Chloroform is usually shipped in drums, glass bottles, tank trucks, and tank cars; store chloroform in dark cans or bottles in a cool place. Keep containers of chloroform tightly-closed and in a dark place away from direct sunlight and moisture (ITI, 1995; NFPA, 1997; Sittig, 1991). Containers of chloroform should be labeled as "poison" (HSDB , 2001). "Glass containers should be dark green or amber. Technical-grade chloroform can be stored in lead-lined or mild steel containers of all-welded construction. When storage vessels are made of unlined steel, precautions are needed to prevent the entry of moisture" (HSDB , 2001).
- ROOM/CABINET RECOMMENDATIONS
Containers of chloroform should be stored in cool (temperature should not exceed 30 degrees C), dark, dry, and well-ventilated areas far from strong alkalies and strong mineral acids (HSDB , 2001; NFPA, 1997). Ensure that local exhaust measures are in place to control the concentration of chloroform in air (HSDB , 2001).
Reacts with strong alkalies, strong caustics, and chemically active metals such as aluminum powder, magnesium powder, sodium, and potassium (NFPA, 1997; Sittig, 1991). Please consult the 'Reactivity Hazards' section for more comprehensive incompatability information.
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
- Chloroform is a serious health hazard. It may be harmful if absorbed through the skin or inhaled; it is irritating to skin, eyes, and respiratory system and it will defat tissue. Wear personal protective clothing and a positive pressure self-contained breathing apparatus. Polyvinyl chloride and rubber are NOT suitable materials to protect against chloroform. Wash promptly with large amounts of soap and water if chloroform contacts the skin; speed in removing chloroform from the skin is critical. Clothing that has become contaiminated with chloroform should be removed and isolated at the site (AAR, 2000; (ITI, 1995; NFPA, 1997; NIOSH , 2001; Sittig, 1991).
- "Clothing wet with liquid chloroform should be placed in closed containers for storage until it can be discarded or until provision is made for the removal of chloroform from the clothing. If the clothing is to laundered or otherwise cleaned to remove the chloroform, the person performing the operation should be informed of chloroform's hazardous properties" (HSDB , 2001).
EYE/FACE PROTECTION
- Wear eye protection to prevent any reasonable probability of eye contact. If chloroform gets into the eyes, irrigate immediately for at least 15 minutes (AAR, 2000; (Sittig, 1991).
- Provide eyewash fountains in areas where workers may be exposed to chloroform (NIOSH , 2001).
- Do not wear contact lenses while working with chloroform (HSDB , 2001).
RESPIRATORY PROTECTION
- Avoid breathing vapors or dust; wear a positive pressure self-contained breathing apparatus (AAR, 2000; (NFPA, 1997; Sittig, 1991).
- 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 67-66-3.
-PHYSICAL HAZARDS
FIRE HAZARD
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004) Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes. Containers may explode when heated. Runoff may pollute waterways.
Although chloroform does not ignite easily, it has the capability of decomposing in fire to emit highly toxic gases, which are more hazardous than the chloroform itself. If it can be done without risk, move containers away from fire area, as heat may cause containers to explode. If it is involved in a fire, use an extinguishing agent suitable for the surrounding fire type and fight fire from as far as possible. Water spray should be used to keep fire-exposed containers cool. Wear protective equipment, including a self-containing breathing apparatus, and dike fire-control water so that chloroform does not enter water sources and sewers. Material should not be scattered (AAR, 2000; (CHRIS , 2001; HSDB , 2001; NFPA, 1997; Sittig, 1991). Accumulation of static electrical charges may cause its vapors to ignite (Pohanish & Greene, 1997).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS67-66-3 (NFPA, 2002):
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Water spray, fog or regular foam. Move containers from fire area if you can do it without risk. Dike fire control water for later disposal; do not scatter the material. Use water spray or fog; do not use straight streams.
- TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Do not get water inside containers. 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. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.
- NFPA Extinguishing Methods for CAS67-66-3 (NFPA, 2002):
Chloroform is a serious health hazard. When heated, chloroform's decomposition products include phosgene, hydrogen chloride, chlorine, and toxic and corrosive oxides of carbon and chlorine (HSDB , 2001; ITI, 1995; NFPA, 1997; Sittig, 1991). "On prolonged heating with water at 225 degrees C, decomposition to formic acid, carbon monoxide, and hydrogen chloride occurs" (HSDB , 2001).
EXPLOSION HAZARD
- Chloroform may explode if it comes in contact with the following (Lewis, 2000; NFPA, 1997; Urben, 2000):
acetone alkali metals aluminum powder 3-chloroperoxybenzoic acid (during evaporation of solvent) dibenzoyl peroxide dinitrogen tetraoxide (upon impact) fluorine lithium magnesium mangesium powder 2-nitrophenylacetyl chloride perchloric acid + phosphorus pentoxide perchloric acid + methanol peroxybenzoic acid potassium; silanes (in the presence of oxygen) sodium sodium-potassium alloy sodium + methanol sodium methoxide + methanol sodium methylate + methanol sodium hydroxide + methanol
DUST/VAPOR HAZARD
- Chloroform is a serious health hazard. When heated, chloroform's decomposition products include phosgene, hydrogen chloride, chlorine, and toxic and corrosive oxides of carbon and chlorine (Bingham et al, 2001; NFPA, 1997; Sittig, 1991).
REACTIVITY HAZARD
- Chloroform reacts violently with the following (Lewis, 2000; NFPA, 1997; Urben, 2000):
acetone acetone + alkali (such as sodium hydroxide, potassium hydroxide, or calcium hydroxide) strong alkalis aluminum carbon tetrachloride (reacts vigorously with incandescence) disilane fluorine lithium magnesium methanol + alkali nitrogen tetroxide perchloric acid + phosphorus pentoxide potassium-tert-butoxide sodium methylate sodium-potassium alloy triisopropyl phosphine
- Chloroform may explode if it comes in contact with the following (Lewis, 2000; NFPA, 1997; Urben, 2000):
acetone alkali metals aluminum powder 3-chloroperoxybenzoic acid (during evaporation of solvent) dibenzoyl peroxide dinitrogen tetraoxide (upon impact) fluorine lithium magnesium mangesium powder 2-nitrophenylacetyl chloride perchloric acid + phosphorus pentoxide perchloric acid + methanol peroxybenzoic acid potassium; silanes (in the presence of oxygen) sodium sodium-potassium alloy sodium + methanol sodium methoxide + methanol sodium methylate + methanol sodium hydroxide + methanol
- Chloroform may ignite when in contact with potassium-tert-butoxide (NFPA, 1997; Urben, 2000).
- Phosgene will slowly decompose in sunlight to produce phosgene and hydrogen chloride. The presence of iron or excess water or/at high temperatures may accelerate this reaction (ITI, 1995; Pohanish & Greene, 1997).
- Some plastics, rubber, and coatings are attacked by chloroform (HSDB , 2001; Pohanish & Greene, 1997).
- Chloroform becomes corrosive when in contact with water or high temperatures; it will attack iron or other metals (Pohanish & Greene, 1997).
- Formic acid is formed when chloroform is heated in the presence of a diluted caustic solution (IPCS, 1994).
- Chloroform undergoes oxidation when in the presence of strong oxidizing agents such as chromic acid; this results in the release of phosgene and chlorine gas (ATSDR, 1997).
- "Vacuum evaporation of 3-chloroperoxybenzoic acid of unheated conversion of the pyridine to its N-oxide with 5% excess of the peroxy acid in chloroform gave a residue which decomposed violently" (Urben, 2000).
- "The pyrolysis of chloroform vapor at temperatures above 450 degrees C produces tetrachloroethane, hydrochloric acid and various chlorinated hydrocarbons. In the presence of potassium amalgam or hot copper, acetylene is formed. The reaction with primary amines in an alkaline environment is known as the isonitrile reaction; aromatic hydroxyaldehydes are formed in the presence of phenolates (Reimer-Tiemann reaction). In the Friedel-Crafts reaction, chloroform and benzene produce triphenyl methane. Chlorination of the compound produces tetrachloromethane; bromination of chloroform vapor at 225-275 degrees C produces CCl2Br2 and CClBr3. Fluoroform is produced in the reaction with hydrogen fluoride in the presence of a metallic fluoride as a catalyst. Iodoform is produced by allowing chloroform to react with ethyl iodide in the presence of aluminium chloride. Unstabilized chloroform reacts with aluminium, zinc, and iron. Chloroform mixed with methanolic sodium hydroxide or acetone, in the presence of a base, gives a violent reaction" (IPCS, 1994).
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Increase, in the downwind direction, as necessary, the isolation distance of at least 25 to 50 meters (80 to 160 feet) in all directions.
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (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 151 (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 in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. Keep unauthorized personnel away. Stay upwind. Keep out of low areas.
- AIHA ERPG Values for CAS67-66-3 (AIHA, 2006):
Listed as Chloroform ERPG-1 (units = ppm): Not appropriate ERPG-2 (units = ppm): 50 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 CAS67-66-3 (U.S. Department of Energy, Office of Emergency Management, 2010):
- AEGL Values for CAS67-66-3 (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: Chloroform Proposed Value: AEGL-1 10 min exposure: ppm: insufficient data mg/m3:
30 min exposure: ppm: insufficient data mg/m3:
1 hr exposure: ppm: insufficient data mg/m3:
4 hr exposure: ppm: insufficient data mg/m3:
8 hr exposure: ppm: insufficient data mg/m3:
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: Chloroform 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: Chloroform 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 CAS67-66-3 (National Institute for Occupational Safety and Health, 2007):
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004) Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Cover with plastic sheet to prevent spreading. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004) Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
"Chloroform has been identified as a hazardous waste by the USEPA, and disposal is regulated under RCRA" (Bingham et al, 2001). Chloroform can be ultimately disposed through controlled incineration, preferable after being mixed with another combustible fuel. To prevent phosgene formation, ensure that complete combustion has taken place; use an acid scrubber to remove the haloacids produced (HSDB , 2001). OHM/TADS (2001) suggests using distillation or steam stripping in the recovery of chloroform.
Small spills should be taken up with an absorbent material, such as dry sand, earth, or vermiculate, and placed into containers for later disposal. The spill area should be flushed with water (AAR, 2000; (HSDB , 2001; Sittig, 1991).
Keep unnecessary people away by isolating the spill area and denying entry. Approach spilled chloroform from upwind and stay out of low areas; closed spaces should be ventilated before entering them. Wear appropriate protective clothing (including a self-contained breathing apparatus); do not touch spilled chloroform. If it can be done without risk, attempt to stop or control the leak. Control runoff with dikes far ahead of the spill and isolate for proper disposal (NFPA, 1997; Sittig, 1991). LAND SPILL: If chloroform is spilled onto land, a holding area should be created and the surface flow diked through the use of sand bags, soil, foamed concrete, or foamed polyurethane. Fly ash or cement powder can be used to absorb bulk liquid. Immobilize the spill through the use of "universal" gelling agent (AAR, 2000). WATER SPILL: If chloroform is spilled into water, the material should be trapped at bottom (use sand bags, excavated lagoons, or deep water pockets) and then removed using suction hoses. If spilled in concentrations of 10 ppm or greater, activated carbon should be applied at 10 times the spilled amount. Immobilized masses can be removed through the use of mechanical dredges or lifts (AAR, 2000).
Mix chloroform with another combustible material and incinerate. Exercise care to assure complete combustion and to prevent the formation of phosgene. An acid scrubber is necessary to remove the halo acids produced during incineration (Sittig, 1991). Absorb spilled chloroform on paper, evaporate on a glass dish in a hood, and then burn the paper (ITI, 1995).
Chloroform is a candidate for liquid injection, rotary kiln, or fluidized bed incineration (HSDB , 2001): Liquid Injection Incineration: Temperature range of 650 to 1600 degrees C; Residence time of 0.1 to 2 seconds Rotary Kiln Incineration: Temperature ranging from 820 to 1600 degrees C; Residence time of seconds for liquids and gases, hours for solids Fluidized Bed Incineration: Temperature ranging from 450 to 980 degrees C; Residence time of seconds for liquids and gases, longer for solids
Chloroform in aqueous wastes may be treated by a countercurrent gas-liquid desorption process known as packed-tower air stripping (Freeman, 1989). Chloroform in liquid, sludge, and solid wastes may be destroyed in a fluidized-bed thermal oxidation system; destruction and removal efficiencies were greater than 99.99% at bed temperatures of 950 degrees C with 2-s residence times (Freeman, 1989). 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.
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- Chloroform is both a synthetic and naturally-occurring substance, with anthropogenic sources contributing most of the chloroform entering the environment. The major sources of release into the environment include releases resulting from its manufacture and use as an industrial solvent, extractant, and chemical intermediate; its formation in the chlorination of drinking water, industrial and municipal waste water, and swimming pool water; and from other water treatment processes involving chlorination. Bacteria can release chloroform by dehalogenating carbon tetrachloride under anaerobic conditions (ATSDR, 1997).
- Most of the chloroform released into the environment will eventually enter the atmosphere. Releases to water and land evaporate into the atmosphere (ATSDR, 1997; Howard, 1990).
ENVIRONMENTAL FATE AND KINETICS
Chloroform released into the atmosphere will exist predominantly in the vapor phase based upon a vapor pressure of 159 mmHg at 20 degrees and 197 mmHg at 25 degrees C. It will degrade by reaction with photochemically-produced hydroxyl radicals with a half-life of 80 to 180 days. Under photochemical smog conditions, it is more reactive with a half-life of 11 days. Chemical hydrolysis is not expected to be a significant removal process. Chloroform can be transported over long distances (it has been detected in ambient air in locations far from anthropogenic sources) and, because it is significantly soluble in water, will be partially returned to the earth in the form of precipatation (ATSDR, 1997; Howard, 1990; HSDB , 2001; IPCS, 1994). 623 to 6231 hours is the photooxidation half-life for chloroform in air; this is based upon chloroform's vapor phase reaction with hydroxyl radicals present in air (Howard et al, 1991).
SURFACE WATER Due to its volatility, chloroform released into water will primarily evaporate into the atmosphere. The experimental evaporation half-life is several hours; the volatilization half-life is estimated to be 9-10 days in a lake, 36 hours in a river, and 40 hours in a pond. Experimentally determined half-lives ranging from 1850 to 3650 years at pH 7 and 25 to 37 years at pH 9 indicate that hydrolysis is not a significant degradation process in water; direct photolysis is also an unimportant degradation process in surface waters (ATSDR, 1997; Howard, 1990; IPCS, 1994). Based upon its Koc values, chloroform is not expected to absorb to suspended solids or sediment in water (HSDB , 2001). The half-life of chloroform in surface water is 672 to 4320 hours, based upon the aqueous aerobic biodegradation half-life (Howard et al, 1991). The scientific judgment for the half-life of chloroform in ground water ranges from 1344 to 43,200 hours (Howard et al, 1991). 78.5 to 3140 years is the photooxidation half-life of chloroform in water, as indicated by the reaction rate of hydroxyl radicals in aqueous solution (Howard et al, 1991).
TERRESTRIAL Due to its high vapor pressure, chloroform released to soil is expected to rapidly evaporate into the atmosphere from near-surface soils. With Koc values ranging from 45 to 80, it will adsorb poorly to soil, especially soil with low organic carbon content; it can leach into ground water (ATSDR, 1997; Howard, 1990). "If released to soil, chloroform is expected to have moderate mobility based upon a Koc value ranging from 153-196. Volatilization from moist soil surfaces is expected to be an important fate process based upon a Henry's Law constant of 3.67x10(-3) atm-m(3)/mol. Chloroform may volatilize from dry soil surfaces based upon its vapor pressure. Under normal environmental conditions, chloroform is not expected to undergo biodegradation in soil. However, several studies have demonstrated that at low concns, chloroform can be anaerobically degraded by methanogenic bacteria in the presence of a primary substrate such as acetic acid" (HSDB , 2001). Chloroform spilled onto land may enter the soil and replace water as the primary solvent in localized situations; therefore, the basic principles of water migration in soil also apply to chloroform migration. Chloroform will penetrate the soil surface along the most permeable path. It may temporarily pond on the soil surface if the soil has a low permeability and a very high clay content; sandy soil may allow rapid infiltration. Chloroform will migrate downward in unsaturated zone soil due to gravity and capillary forces and, since chloroform is more dense than water, it will continue to migrate downward through groundwater. Downward migration will stop when chloroform is converted into residual saturation or when it reaches an impermeable bed (Dragun, 1988). Once released to soil, the half-life of chloroform ranges from 672 to 4320 hours; this is based upon an estimated aqueous biodegradation half-life (Howard et al, 1991).
ABIOTIC DEGRADATION
- Chloroform hydrolyzes at a negligible rate; photodegradation is also not a significant loss process (Howard, 1990).
The maximal rate of anaerobic biodegradation for chloroform was determined in a study using computer controlled reactors. Propionate, hydrogen, and acetate, known to be important anaerobic intermediates, were used as primary substrates. Chloroform was degraded from 89-99% using the enriched cultures (Rhee & Speece, 1992). An anaerobic, expanded-bed granular activated carbon (GAC) reactor removed chloroform in excess of 97% from a waste stream, but was found to inhibit degradation of acetate and acetone. COD removal was near complete for systems without a source of chloroform in the feed (Narayanan et al, 1993). High concentrations of three chlorinated aliphatic chemicals were subjected to anaerobic biodegradation in this study. The chemicals were dichloromethane, chloroform, and 1,1,1-trichloroethane. Feeding mixtures of the chemicals to the digester caused a decrease in the degradation of 1,1,1-trichloroethane and an increase in the degradation of dichloromethane. When fed high levels of acetate, the system showed an increased ability to transform all the chlorinated aliphatic chemicals (Hughes & Parkin, 1992).
BIODEGRADATION
- Slow but substantial biodegradation may occur when there are proper microbial populations which are acclimated to chloroform (Howard, 1990).
A bioreactor was developed that uses a mixed culture of bacteria to oxidize trichloroethylene and chloroform. The bacteria used methane as the carbon and energy source (Alvarezcohen et al, 1992). A laboratory scale packed-bed reactor was used to degrade chloroform. The reactor was seeded with the methanotroph, Methylosinus trichosporium OB3b. Chloroform was added in a solution containing 100 mcg/L and was degraded to greater than 90% with a bed retention time of about 90 minutes. A formate supplement enhanced the rate and stability of the reactor (Speitel & Leonard, 1992). Using Methylosinus trichosporium OB3b with the addition of methane in the system reduced the chloroform rate constants, through competitive inhibition. The predominant degradation product from chloroform was carbon dioxide (Speitel et al, 1993).
BIOACCUMULATION
Chloroform body burden resulting from exposure to various concentrations of chloroform in water and air of an indoor swimming pool was measured in 11 male swimmers. The results of the study indicated that approximately 24% of body burden resulted from dermal absorption. The authors conclude that swimming in indoor pools may be an important source of exposure to chloroform (Levesque et al, 1994).
Bluegill (Lepomis macrochirus): 1.6-2.5 (Howard, 1990) Bluegill Sunfish (Lepomis macrochirus): 6-8 (ATSDR, 1997; Howard, 1990) Catfish (Ictalurus punctatus): 3.3-3.7 (Howard, 1990) Fathead Minnow: 14 (calculated) (ATSDR, 1997) Largemouth Bass (Micropterus salmoides): 2.9-3.1 (Howard, 1990) Rainbow Trout (Salmo gairdneri): 3.34-10.35 (Howard, 1990) Selenastrum capricornutum (green algae): 690 (experimentally determined) (ATSDR, 1997)
ENVIRONMENTAL TOXICITY
- No information found at the time of this review.
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Chloroform is a heavy, colorless, clear, highly refractive, nonflammable, volatile liquid. It has a sweet taste and a characteristic, pleasant, sweet odor (AAR, 2000; (ACGIH, 1991; Budavari, 1996) Lewis, 1997; (Lewis, 2000; Lewis, 1998).
To avoid photochemical transformation to hydrogen chloride and phosgene, reagent grade chloroform typically contains 0.75% ethanol, which acts as a stabilizer (IPCS, 1994).
PH
VAPOR PRESSURE
- 20 mmHg (at -19 degrees C) (OHM/TADS , 2001)
- 100 mmHg (at 10.4 degrees C) (Lewis, 2000)
- 159 mmHg (at 20 degrees C) (ACGIH, 1991; Bingham et al, 2001)
- 160 mmHg (at 20 degrees C) (NFPA, 1997; NIOSH , 2001)
- 160 mmHg (Harbison, 1998)
- 197 mmHg (at 25 degrees C) (HSDB , 2001)
- 200 mmHg (at 25 degrees C) (Bingham et al, 2001)
- 246 mmHg (at 25 degrees C) (Howard, 1990)
- 8.13 kPa (at 0 degrees C) (IPCS, 1994)
- 21.28 kPa (at 20 degrees C) (IPCS, 1994)
- 15 psig (at 84 degrees C) (OHM/TADS , 2001)
- 60 psig (at 120 degrees C) (OHM/TADS , 2001)
SPECIFIC GRAVITY
- NORMAL TEMPERATURE AND PRESSURE
- OTHER TEMPERATURE AND/OR PRESSURE
1.484 (at 20/20 degrees C) (Budavari, 1996) 1.485 (at 20/20 degrees C) (Lewis, 1997) 1.489 (at 20/4 degrees C) (ITI, 1995) 1.49845 (at 15/4 degrees C) (Bingham et al, 2001)
- TEMPERATURE AND/OR PRESSURE NOT LISTED
DENSITY
- NORMAL TEMPERATURE AND PRESSURE
- OTHER TEMPERATURE AND/OR PRESSURE
1.485 g/cm(3) (at 20 degrees C) (ATSDR, 1997) 1.49 g/mL (at 20 degrees C) (CHRIS , 2001)
- TEMPERATURE AND/OR PRESSURE NOT LISTED
1.474-1.478 g/mL (U.S.P. chloroform that contains 0.5-1% ethanol as a stabilizer) (Budavari, 1996) 1.48 g/mL (NFPA, 1997) 1.4832 g/cm(3) (ATSDR, 1997) 1.49 g/mL (Dragun, 1988)
FREEZING/MELTING POINT
-63.5 degrees C; -82.3 degrees F; 209.7 K (CHRIS , 2001; ITI, 1995; Lewis, 1997) -82 degrees F (NIOSH , 2001)
-63 degrees C; -82 degrees F (NFPA, 1997) -63.2 degrees C (ACGIH, 1991; ATSDR, 1997; Bingham et al, 2001; Lewis, 2000) -63.5 degrees C (Budavari, 1996; Howard, 1990) -64 degrees C (ATSDR, 1997)
BOILING POINT
- 61 degrees C (Ashford, 1994; OHM/TADS , 2001)
- 61.2 degrees C; 142 degrees F; 334.4 K (at 1 atm) (CHRIS , 2001; ITI, 1995; Lewis, 1997)
- 61.3 degrees C (ACGIH, 1991; IPCS, 1994; Lewis, 2000)
- 61.7 degrees C (at 760 mmHg) (Howard, 1990; Sittig, 1991)
- 61-62 degrees C (Budavari, 1996)
- 62 degrees C; 143 degrees F (NFPA, 1997; NIOSH , 2001)
- Chloroform forms a constant boiling mixture at 59 degrees C with 7% alcohol (Budavari, 1996).
FLASH POINT
- None (ATSDR, 1997; Lewis, 2000)
AUTOIGNITION TEMPERATURE
- >1000 degrees C (ATSDR, 1997; IPCS, 1994)
EXPLOSIVE LIMITS
SOLUBILITY
not soluble (Ashford, 1994; NFPA, 1997) slightly soluble in water (AAR, 2000; (ITI, 1995; Lewis, 2000) 0.5% (at 77 degrees F) (NIOSH , 2001) 0.822 mL/100 mL water (at 20 degrees C) (ACGIH, 1991) 1 mL/200 mL water (at 25 degrees C) (Budavari, 1996) 1.0 g/100 mL water (at 15 degrees C) (Bingham et al, 2001) 3.81 g/kg (at 25 degrees C) (HSDB , 2001) 7710 mg/L (at 25 degrees C) (HSDB , 2001) 7.22x10(3) mg/L (at 25 degrees C) (ATSDR, 1997) 7.43x10(3) mg/L (ATSDR, 1997) 7950 mg/L (Howard, 1990) 7.5-9.3 g/L (IPCS, 1994) 9.3x10(3) mg/L (ATSDR, 1997)
Chloroform has been described as being miscible or soluble with acetone, alcohol, benzene, carbon disulfide, carbon tetrachloride, ether, organic solvents, petroleum ether, solvent naptha or fixed and volatile oils (Bingham et al, 2001; Budavari, 1996; HSDB , 2001; ITI, 1995)
OCTANOL/WATER PARTITION COEFFICIENT
- log Kow = 1.97 (ATSDR, 1997; Howard, 1990)
HENRY'S CONSTANT
- 1.7x10(2) atm (at 20 degrees C) (Freeman, 1989)
- 3.0x10(-3)atm-m(3)/mol (at 20 degrees C) (ATSDR, 1997)
- 3.67x10(-3)atm-m(3)/mol (at 24.8 degrees C) (ATSDR, 1997)
- 4.06x10(-3) atm-m(3)/mol (at 25 degrees C) (ATSDR, 1997)
- 4.35x10(-3)atm-m(3)/mol (at 25 degrees C) (Howard, 1990)
SPECTRAL CONSTANTS
445 (Atlas of Mass Spectral Data, John Wiley & Sons, New York) (HSDB , 2001) Intense Mass Spectral Peaks: 83 m/z, 118 m/z (HSDB , 2001)
OTHER/PHYSICAL
2.4 ppm (w/v) (in water) (ATSDR, 1997) 85 ppm (v/v) (in air) (ATSDR, 1997) 3.30 mg/L (in air) (HSDB , 2001) 250 mg/m(3) (Low); 1000 mg/m(3) (High) (HSDB , 2001) 205-307 ppm (CHRIS , 2001) 50 ppm (Baselt, 1997) 200-300 ppm (OHM/TADS , 2001) 200-300 ppm; this concentration may act as an exposure warning to acutely hazardous amounts, but is not low enough to be considered a warning for chronic exposure (Bingham et al, 2001; Sittig, 1991).
1.4422 (at 25 degrees C) (Lewis, 1997) 1.4467 (at 20 degrees C) (IPCS, 1994; ITI, 1995) 1.4476 (at 20 degrees C) (Budavari, 1996)
- LIQUID WATER INTERFACIAL TENSION
- NUCLEAR MAGNETIC RESONANCE
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