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ETHYLENE DICHLORIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Ethylene dichloride is a colorless liquid with an odor typical of chlorinated hydrocarbons (pleasant and chloroform-like). Its primary use is in the manufacture of vinyl chloride monomer.
    B) The vapor is heavier than air and may travel a significant distance to a source of ignition and flash back. When heated to decomposition, toxic fumes of carbon monoxide, carbon dioxide, hydrogen chloride gas, and phosgene are emitted.

Specific Substances

    1) 1,2-Bichloroethane
    2) 1,2-Dichlorethane
    3) Dichloro-1,2-ethane
    4) Alpha-beta-dichloroethane
    5) Sym-dichloroethane
    6) 1,2-Dichloroethane
    7) EDC
    8) Ethane dichloride
    9) Ethylene chloride
    10) 1,2-Ethylene dichloride
    11) Glycol dichloride
    12) DCE
    13) Molecular Formula: C2-H4-Cl2
    14) CAS 107-06-2
    15) DCE (ETHYLENE DICHLORIDE)
    16) EDC (ETHYLENE DICHLORIDE)
    17) FREON 150
    1.2.1) MOLECULAR FORMULA
    1) C2-H4-Cl2

Available Forms Sources

    A) FORMS
    1) Ethylene dichloride is a heavy colorless liquid with a sweet taste and an odor typical of chlorinated hydrocarbons (pleasant and chloroform-like) (Bingham et al, 2001; Lewis, 2000; Budavari, 1996).
    2) Editor's note: Ethylene dichloride, together with ethylidene chloride (also known as 1,1-dichloroethane) [CAS number 75-34-3], can be categorically referred to as dichloroethane [CAS number 1300-21-6] (HSDB , 2001) Budavari, 1996).
    B) USES
    1) Its primary use is in the manufacture of vinyl chloride monomer (Bingham et al, 2001). It is an intermediate in the manufacture of trichloroethane and fluorocarbons (Budavari, 1996) Allentown & Barcelona, 1988). Ethylene dichloride was formerly used as a solvent for fats, glues, gums, oils, resins, rubber, and waxes, in the manufacturing of acetyl cellulose and tobacco extract, and as a soil fumigant. Due to its toxicity and flammability, usage as a solvent has decreased significantly (Bingham et al, 2001; Budavari, 1996; Jacobziner & Raybin, 1961).
    2) Ethylene dichloride is a pesticide and a priority pollutant (Lewis, 2000).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) INGESTION - Initial effects seen after ethylene dichloride (EDC) ingestion are gastrointestinal; vomiting is common. Cyanosis, dyspnea, and coma may be delayed in onset. In severe cases, CNS signs appear first within several hours of exposure, followed by a quiescent period. On the second day, oliguria and hepatic transaminasemia may develop. Subsequently, hepatorenal failure can occur over the next several days. Gastrointestinal bleeding may occur. Pulmonary edema may develop. Death may be due to cardiovascular, respiratory, or hepatorenal failure.
    1) Neurologic effects have been reported including headache, weakness, vertigo, tremor, and dizziness.
    B) INHALATION - Vapors may produce irritation of respiratory tract and conjunctiva, corneal clouding, CNS depression, and liver, kidney and adrenal gland impairment.
    C) DERMAL - Ethylene dichloride is a skin and severe eye irritant, and strong local irritant. The liquid is readily absorbed through the skin, thus systemic effects may occur.
    D) EYE - Contact with either the liquid or with high concentrations of vapor causes immediate discomfort with conjunctival hyperemia and slight corneal injury; corneal burns from splashes recover quickly with no scarring.
    E) When heated to decomposition, toxic fumes of carbon monoxide, carbon dioxide, hydrogen chloride gas, and phosgene are emitted.
    0.2.4) HEENT
    A) Vapor exposure may result in respiratory tract irritation and a burning sensation. Corneal burns, with rapid recovery, have occurred following splash contact.
    0.2.5) CARDIOVASCULAR
    A) Acute inhalation of high concentrations may result in ventricular fibrillation.
    0.2.6) RESPIRATORY
    A) Coughing progressing to pulmonary edema, tachypnea, and cyanosis may occur.
    0.2.7) NEUROLOGIC
    A) Ethylene dichloride is a CNS depressant. Dizziness, headache, mental confusion, lethargy, coma or seizures may occur. In severe exposures, CNS depression leading to respiratory arrest may occur.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, anorexia, and abdominal pain may be noted.
    0.2.9) HEPATIC
    A) Liver toxicity may be noted as a late finding.
    0.2.10) GENITOURINARY
    A) Oliguria, anuria, and renal failure may be noted as a late finding. Complete recovery is usual.
    0.2.12) FLUID-ELECTROLYTE
    A) Hypercalcemia may be noted as a late finding.
    0.2.14) DERMATOLOGIC
    A) EDC produced raw, red, scalded appearing hands of workers after 4 hours of intermittent immersion. The hands appeared dry, shiny with a "cigarette-paper" appearance 2 weeks after exposure.
    0.2.16) ENDOCRINE
    A) Hypoglycemia may occur secondary to liver necrosis. Chronic exposures may result in damage to the adrenal glands.
    0.2.20) REPRODUCTIVE
    A) There are no human or convincing animal data to suggest that ethylene dichloride is a reproductive hazard.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no studies were found on the possible carcinogenic activity of ethylene dichloride in humans. However, a 2-year study in rats and mice showed a dose dependent increase of both benign and malignant tumors.

Laboratory Monitoring

    A) Plasma levels of ethylene dichloride are not useful.
    B) Monitor serum glucose, electrolytes, liver function, and renal function in severe cases. Monitor INR in symptomatic cases.
    C) Monitor for CNS depression. In symptomatic cases with respiratory compromise, chest x-ray may be obtained.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) EMESIS
    1) Oral ingestion of EDC may result in burns of the oropharynx. Emesis is not recommended.
    B) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    C) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    D) Consider insertion of a small, flexible nasogastric or orogastric tube to suction gastric contents after recent large ingestions; the risk of further mucosal injury must be weighed against potential benefits.
    E) MONITOR VITAL SIGNS, ECG, and urine output.
    F) 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.
    G) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    H) N-Acetylcysteine and vitamin E have been described as potential antidotes in Russian studies, but there is insufficient evidence to recommend their use.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) MONITOR VITAL SIGNS, ECG, and urine output.
    C) 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.
    D) N-Acetylcysteine and vitamin E have been described as potential antidotes in Russian studies, but there is insufficient evidence to recommend their use.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) Fatalities in adults have been reported after ingestion of 30 to 70 grams, and in an adolescent after ingestion of 15 mL. Death is usually due to circulatory or respiratory collapse, but may occur due to hepatorenal failure.
    B) After ingesting 15 mL and 50 mL of ethylene dichloride, two adult patients recovered following supportive care and treatment with intravenous N-acetylcysteine and alprostadil.

Clinical Effects

Summary Of Exposure

    A) INGESTION - Initial effects seen after ethylene dichloride (EDC) ingestion are gastrointestinal; vomiting is common. Cyanosis, dyspnea, and coma may be delayed in onset. In severe cases, CNS signs appear first within several hours of exposure, followed by a quiescent period. On the second day, oliguria and hepatic transaminasemia may develop. Subsequently, hepatorenal failure can occur over the next several days. Gastrointestinal bleeding may occur. Pulmonary edema may develop. Death may be due to cardiovascular, respiratory, or hepatorenal failure.
    1) Neurologic effects have been reported including headache, weakness, vertigo, tremor, and dizziness.
    B) INHALATION - Vapors may produce irritation of respiratory tract and conjunctiva, corneal clouding, CNS depression, and liver, kidney and adrenal gland impairment.
    C) DERMAL - Ethylene dichloride is a skin and severe eye irritant, and strong local irritant. The liquid is readily absorbed through the skin, thus systemic effects may occur.
    D) EYE - Contact with either the liquid or with high concentrations of vapor causes immediate discomfort with conjunctival hyperemia and slight corneal injury; corneal burns from splashes recover quickly with no scarring.
    E) When heated to decomposition, toxic fumes of carbon monoxide, carbon dioxide, hydrogen chloride gas, and phosgene are emitted.

Heent

    3.4.1) SUMMARY
    A) Vapor exposure may result in respiratory tract irritation and a burning sensation. Corneal burns, with rapid recovery, have occurred following splash contact.
    3.4.3) EYES
    A) IRRITANT - At high concentrations, EDC is a severe eye irritant (Bingham et al, 2001; Lewis, 2000). Exposures may cause severe corneal effects (Lewis, 2000). Corneal burns from splashes generally recover quickly with no scarring.
    1) HUMANS/SPLASH CONTACT - Twenty cases of corneal burns were reported from splash contact in the workplace, with rapid recovery (McLaughlin, 1946).
    B) Impaired vision has been reported in clean-up workers with chronic exposure to 1,2-dichloroethane (Bowler et al, 2003).
    C) ANIMALS -
    1) SPLASH/VAPOR CONTACT - Experimental exposure to drops or concentrated vapors resulted in immediate discomfort, conjunctival hyperemia, and slight corneal epithelial disturbance, with recovery in 1 to 2 days. The reaction was graded 3 on a scale of 1 to 10 (Grant & Schuman, 1993).
    2) INHALATION/SUBCUTANEOUS EXPOSURE - Corneal opacification has been reported following inhalation and subcutaneous exposure to ethylene dichloride in animals (Jacobziner & Raybin, 1961). This effect is highly selective for the canine species, presumably due to differences in the amount of EDC entering the aqueous humor from the blood, and has not been reported in humans or primate species (Grant & Schuman, 1993).
    3.4.5) NOSE
    A) At high concentrations, EDC is a nasal irritant (Bingham et al, 2001; Lewis, 2000).
    3.4.6) THROAT
    A) At high concentrations, EDC is a nose and throat irritant (Bingham et al, 2001; Lewis, 2000)
    B) CASE REPORT - A 2-year-old had some burning of the mouth and throat after he swallowed some toy airplane glue containing ethylene dichloride (Jacobziner & Raybin, 1961).
    C) METALLIC TASTE has been described after inhalation exposure (HSDB , 2001).

Cardiovascular

    3.5.1) SUMMARY
    A) Acute inhalation of high concentrations may result in ventricular fibrillation.
    3.5.2) CLINICAL EFFECTS
    A) VENTRICULAR FIBRILLATION
    1) Inhalation of high concentrations of EDC may result in death from ventricular fibrillation (Procter et al, 1988; (Nouchi, 1984).
    B) HYPOTENSIVE EPISODE
    1) Acute exposure may lead to reduced blood pressure and cardiac impairment (HSDB , 2001). Ingestion of higher concentrations of EDC is very likely to cause shock, then death by multiple organ failure (Jacobziner & Raybin, 1961).
    C) ACUTE CARDIAC PULMONARY EDEMA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - After ingesting 50 mL of ethylene dichloride, a 28-year-old man developed nausea, black vomiting, abdominal pain, elevated liver enzymes (ASAT 37136 IU/L, ALAT 17083 IU/L), hypoprothrombinemia (INR 4.43), hyperbilirubinemia (bilirubin 75.2 mcmol/L), and elevated creatinine (219.2 mcmol/L). Echocardiography revealed abnormal left ventricle contractility. In addition, he experienced 2 episodes of cardiogenic pulmonary edema. The patient recovered following supportive care and treatment with intravenous N-acetylcysteine and alprostadil (Payen et al, 2002).

Respiratory

    3.6.1) SUMMARY
    A) Coughing progressing to pulmonary edema, tachypnea, and cyanosis may occur.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Ethylene dichloride may cause irritation to the upper respiratory tract and burning in the nose.
    B) ACUTE LUNG INJURY
    1) Respiratory tract irritation may progress to pulmonary edema, characterized by cough, then production of frothy sputum. Pulmonary edema may appear immediately, or it may be delayed (Yodaiken & Babcock, 1973) Marraccini et al, 1983; (Lewis, 2000; HSDB , 2001; Bingham et al, 2001).
    C) ACUTE RESPIRATORY INSUFFICIENCY
    1) Respiratory depression, dyspnea, and cyanosis may occur (Jacobziner & Raybin, 1961).

Neurologic

    3.7.1) SUMMARY
    A) Ethylene dichloride is a CNS depressant. Dizziness, headache, mental confusion, lethargy, coma or seizures may occur. In severe exposures, CNS depression leading to respiratory arrest may occur.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Exposure to high concentrations results in symptoms largely related to CNS depression. In severe cases, CNS signs appear first within several hours of exposure and are followed by a quiescent period. Dizziness, ataxia, vertigo, confusion, malaise, lethargy, stupor, and coma have been reported (Bingham et al, 2001; HSDB , 2001; Lewis, 2000; Jacobziner & Raybin, 1961). In severe cases, respiratory arrest may occur (HSDB , 2001). CNS depression results from both acute and chronic exposure to lower concentrations (Bingham et al, 2001).
    B) IMPAIRED COGNITION
    1) WITH POISONING/EXPOSURE
    a) The clinical neuropsychological study of clean-up workers (n=137), with chronic exposure to 1,2-dichloroethane, revealed lower neuropsychological functioning in the domains of processing speed, attention, cognitive flexibility, motor coordination and speed, verbal memory, verbal fluency, and visuo-spatial abilities. In addition, these workers experienced disturbed mood and impaired vision. Dose-response relationships between exposure to 1,2-dichloroethane and test scores were noted (Bowler et al, 2003).
    C) FLACCID PARALYSIS
    1) Flaccid paralysis, without anesthesia (usually neuromuscular blockade), has been reported following both ingestion and inhalation exposures to higher concentrations (Lewis, 2000).
    D) HEADACHE
    1) Headache has been reported (Payen et al, 2002; HSDB , 2001).
    E) SEIZURE
    1) Seizures as well as excitability may occur (Jacobziner & Raybin, 1961).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, anorexia, and abdominal pain may be noted.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Nausea and vomiting may commonly occur following ingestion, inhalation or dermal absorption (Payen et al, 2002; Proctor et al, 1988) Watrous, 1942; (Jacobziner & Raybin, 1961; Yodaiken & Babcock, 1973) Letz et al, 1984; (Lewis, 2000; HSDB , 2001; Bingham et al, 2001).
    B) DIARRHEA
    1) Diarrhea may occur following ingestion of EDC (Hubbs & Prusmack, 1955; Lewis, 2000; HSDB , 2001).
    C) ABDOMINAL PAIN
    1) Cramping and abdominal pain were reported following inhalational and dermal exposure to EDC (Payen et al, 2002; Wirtschafter & Schwartz, 1939).
    D) GASTRIC ULCER
    1) Following ingestions of higher concentrations, gastric ulcerations with bleeding may occur (Lewis, 2000).

Hepatic

    3.9.1) SUMMARY
    A) Liver toxicity may be noted as a late finding.
    3.9.2) CLINICAL EFFECTS
    A) HEPATIC NECROSIS
    1) A later toxic effect is liver necrosis. The necrosis is midzonal, rather than centrilobular, and is accompanied by fatty degeneration (Yodaiken & Babcock, 1973; Lewis, 2000; HSDB , 2001).
    B) INJURY OF LIVER
    1) Ethylene dichloride clearly belongs in the group of hepatotoxic halogenated hydrocarbons, as opposed to those with primarily narcotic effects (Payen et al, 2002; ACGIH, 1986). At EDC levels that do not cause acute CNS toxicity, liver damage may also occur (Bingham et al, 2001).
    2) CASE SERIES - Male workers (n = 251) exposed to low to moderate levels of ethylene dichloride and vinyl chloride monomer displayed increased aminotransferase levels. The authors concluded that relatively low levels of exposure are sufficient to cause hepatotoxicity (Cheng et al, 1999).

Genitourinary

    3.10.1) SUMMARY
    A) Oliguria, anuria, and renal failure may be noted as a late finding. Complete recovery is usual.
    3.10.2) CLINICAL EFFECTS
    A) HEPATORENAL SYNDROME
    1) Following exposure to higher concentrations, oliguria and hepatic transaminasemia may develop. Subsequently, hepatorenal failure can occur over the next several days (Payen et al, 2002; HSDB , 2001).
    B) CRUSH SYNDROME
    1) Acute tubular necrosis may occur following ethylene dichloride ingestion (Jacobziner & Raybin, 1961; Yodaiken & Babcock, 1973; HSDB , 2001).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) PROTHROMBIN TIME LOW
    1) Hypoprothrombinemia has been reported in severe cases, secondary to liver necrosis (Payen et al, 2002; Yodaiken & Babcock, 1973; HSDB , 2001).

Dermatologic

    3.14.1) SUMMARY
    A) EDC produced raw, red, scalded appearing hands of workers after 4 hours of intermittent immersion. The hands appeared dry, shiny with a "cigarette-paper" appearance 2 weeks after exposure.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Dermal exposures have resulted in dermatitis, burning, and dermatographia. Repeated skin contact may result in defatting of skin, severe irritation, and moderate edema (Lewis, 2000; HSDB , 2001).
    2) EDC produced raw, red, scalded appearing hands of workers after 4 hours of intermittent immersion. The hands appeared dry, shiny with a "cigarette-paper" appearance 2 weeks after exposure despite application of emollient ointment (Wirtschafter & Schwartz, 1939).
    B) DISCOLORATION OF SKIN
    1) Heavy dermal exposure results in a bluish purple skin discoloration (NIOSH, 1978; HSDB , 2001).
    C) SKIN ABSORPTION
    1) Prolonged skin exposure, as from contact with soaked clothing, produces severe irritation, moderate edema, and necrosis; systemic effects may ensue, as the liquid is readily absorbed through the skin (Proctor et al, 1988; HSDB , 2001; Bingham et al, 2001).

Endocrine

    3.16.1) SUMMARY
    A) Hypoglycemia may occur secondary to liver necrosis. Chronic exposures may result in damage to the adrenal glands.
    3.16.2) CLINICAL EFFECTS
    A) HYPOGLYCEMIA
    1) Hypoglycemia may occur in severe cases secondary to liver impairment (HSDB , 2001). Hypoglycemia was reported in one severe case; onset was the second day postingestion; etiology was secondary to massive liver necrosis (Yodaiken & Babcock, 1973).
    B) ADRENAL CORTICAL HYPOFUNCTION
    1) Chronic or repeated exposure to subacute EDC levels produces a pathological picture of injury to the liver, kidneys and adrenals (Bingham et al, 2001; HSDB , 2001). Ingestion of a significant amount has resulted in necrosis of the liver, kidneys, and adrenal glands (HSDB , 2001).

Reproductive

    3.20.1) SUMMARY
    A) There are no human or convincing animal data to suggest that ethylene dichloride is a reproductive hazard.
    3.20.2) TERATOGENICITY
    A) HUMANS
    1) Increased frequencies of heart defects have occurred in children of women living in areas where trichloroethylene and EDC occur in the drinking water (Dawson et al, 1993). It is not clear if these effects are due to EDC, however.
    B) ANIMAL STUDIES
    1) EDC does not appear to adversely affect the reproductive or developmental process in experimental animals, except at doses which are toxic to the mother (19; p 350; Hathaway et al, 1991). In rats, it can pass through the placenta to the fetus (Withey & Karpinski, 1985; Vozovaya & Malyarova, 1975). No effects on fertility were observed in rats and rabbits, and ethylene dichloride was not teratogenic at concentrations in the range of 100 to 300 ppm (Rao, 1980). Inhalation of an airborne concentration of 208 mg/(m)3/6H in female rats affected pre-implantation mortality. Inhalation of 300 ppm/7H in female rats affected post-implantation mortality (RTECS , 2001).
    2) Trichloroethylene and EDC administered during gestation produced heart defects in fetal rats; either compound given only prior to conception was not teratogenic (Dawson et al, 1993).
    3.20.3) EFFECTS IN PREGNANCY
    A) HUMANS
    1) EDC has been found in fetal tissues, and there were problems with pregnancies in women exposed to both EDC and benzene (Mukhametova & Vozovaya, 1972).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) HUMANS
    1) An average concentration of 0.074 +/- 0.046 mg/kg was reported in breast milk of workers exposed to EDC at the workplace (Mukhametova & Vozovaya, 1972). This compound was still detectable in breast milk at 17 hours after exposure was discontinued.
    B) ANIMAL STUDIES
    1) EDC is found in the milk of nursing rats (Vozovaya & Malyarova, 1975) and people (Barlow & Sullivan, 1982). Levels reported in breast milk from occupational exposures were in the range of 5.4 to 6.4 ppm, with residual chemical present for at least 18 hours after exposure (Davidson et al, 1982). NIOSH recommends that nursing mothers not be exposed to EDC (HSDB).
    3.20.5) FERTILITY
    A) ANIMAL STUDIES
    1) EDC has also been found to affect fertility and development in rats exposed to an airborne concentration of only 14 ppm by inhalation (Vozovaya, 1974) with decreased litter size (Barlow & Sullivan, 1982). However; it appears that up to 500 ppm in the diet had no effect on reproduction in male and female rats fed mash with 250 or 500 ppm of EDC for up to 2 years. There was no significant effect on numbers mating, numbers carrying to term, mean litter size, stillbirths, postnatal mortality, or body weight of the young (Barlow & Sullivan, 1982).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS107-06-2 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: 1,2-Dichloroethane
    b) Carcinogen Rating: 2B
    1) 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.
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no studies were found on the possible carcinogenic activity of ethylene dichloride in humans. However, a 2-year study in rats and mice showed a dose dependent increase of both benign and malignant tumors.
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Ethylene dichloride has been carcinogenic in rats and mice in several studies (Nagano et al, 2006; Mitoma, 1977; Anon, 1978; Fishbein, 1979; Van Duuren, 1979; Ward, 1980), but not carcinogenic in one study in rats and mice (Maltoni, 1980).
    B) DRUG INTERACTION
    1) The addition of disulfiram to the diet of rats exposed to 50 ppm ethylene dichloride for 2 years resulted in a significant increase in the incidence of bile duct cholangiomas, subcutaneous fibromas, neoplastic nodules, interstitial cell testicle tumors, and mammary adenocarcinomas (Cheever et al, 1990).
    2) Disulfiram also increases the hepatotoxic potential of EDC, presumably due to inhibition of microsomal mixed-function oxidase-mediated metabolism of ethylene dichloride, and a compensatory increase in metabolism to reactive metabolites formed by glutathione-EDC conjugation (Igwe et al, 1986).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Plasma levels of ethylene dichloride are not useful.
    B) Monitor serum glucose, electrolytes, liver function, and renal function in severe cases. Monitor INR in symptomatic cases.
    C) Monitor for CNS depression. In symptomatic cases with respiratory compromise, chest x-ray may be obtained.
    4.1.2) SERUM/BLOOD
    A) COAGULATION STUDIES
    1) Monitor prothrombin time or INR in severe cases.
    B) BLOOD/SERUM CHEMISTRY
    1) Monitor serum glucose, electrolytes, liver function, and renal function in severe cases.
    2) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count and liver and kidney function tests is suggested for patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.
    2) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) If respiratory tract irritation is present, monitor chest x-ray.

Methods

    A) OTHER
    1) Ethylene dichloride is detectable in expired air. This may be useful in monitoring exposed workers.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Plasma levels of ethylene dichloride are not useful.
    B) Monitor serum glucose, electrolytes, liver function, and renal function in severe cases. Monitor INR in symptomatic cases.
    C) Monitor for CNS depression. In symptomatic cases with respiratory compromise, chest x-ray may be obtained.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED
    1) Oral ingestion of ethylene dichloride may result in burns of the oropharynx. Emesis is not recommended.
    B) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS
    1) Oral ingestion of EDC may result in burns of the oropharynx. Emesis is not recommended.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    C) ACTIVATED CHARCOAL
    1) Activated charcoal has been shown to adsorb ethylene dichloride in in animals (Laass, 1975).
    2) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    3) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    D) GASTRIC LAVAGE
    1) Consider insertion of a small, flexible nasogastric or orogastric tube to suction gastric contents after recent large ingestions; the risk of further mucosal injury must be weighed against potential benefits.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Respiratory and cardiovascular function should be followed carefully. Onset of symptoms may be delayed and sudden in onset.
    2) Monitor ECG for potential cardiac dysrhythmias.
    3) Monitor seizure activity with EEG following severe, acute exposures.
    4) Monitor liver and kidney function following significant exposure or repeated exposures.
    B) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    C) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    D) ANTIDOTE
    1) N-ACETYLCYSTEINE
    a) N-ACETYLCYSTEINE: Has been suggested as a potential antidote for ethylene dichloride poisoning, but its efficacy has not been documented in the English literature (Kurashov et al, 1989). It had no apparent clinical effect in another study (Luzhnikov et al, 1985).
    1) CASE REPORT - After ingesting 15 mL of ethylene dichloride, an 18-year-old man developed headache, vomiting, oliguria, elevated liver enzymes, hyperbilirubinemia, elevated creatinine, and hypoprothrombinemia. The patient did not present to medical care until 36 hours after ingestion, and recovered following supportive care and treatment with intravenous N-acetylcysteine and alprostadil (Payen et al, 2002).
    2) CASE REPORT - After ingesting 50 mL of ethylene dichloride, a 28-year-old man developed nausea, black vomiting, abdominal pain, elevated liver enzymes, hypoprothrombinemia, hyperbilirubinemia, and elevated creatinine. Echocardiography revealed abnormal left ventricle contractility. In addition, he experienced 2 episodes of cardiogenic pulmonary edema. The patient did not present to medical care until 36 hours after ingestion, and recovered following supportive care and treatment with intravenous N-acetylcysteine and alprostadil (Payen et al, 2002).
    2) VITAMIN E
    a) VITAMIN E: Has been tried based on the presumption that toxicity is secondary to generation of free chlorine radicals (Luzhnikov et al, 1989).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

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

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) BURN
    1) BURNS should be treated as appropriate for any chemical burn.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Abstracts

Case Reports

    A) ADULT
    1) After ingesting 15 mL of ethylene dichloride, an 18-year-old man developed headache, vomiting, oliguria, elevated liver enzymes (ASAT 1603 IU/L (<43), ALAT 3014 IU/L (<36)), hyperbilirubinemia (bilirubin 171 mcmol/L (<17.1)), elevated creatinine (326.2 mcmol/L (<106)), and hypoprothrombinemia (INR 6.26). The patient recovered following supportive care and treatment with intravenous N-acetylcysteine and alprostadil (Payen et al, 2002).
    2) After ingesting 50 mL of ethylene dichloride, a 28-year-old man developed nausea, black vomiting, abdominal pain, elevated liver enzymes (ASAT 37136 IU/L, ALAT 17083 IU/L), hypoprothrombinemia (INR 4.43), hyperbilirubinemia (bilirubin 75.2 mcmol/L), and elevated creatinine (219.2 mcmol/L). Echocardiography revealed abnormal left ventricle contractility. In addition, he experienced 2 episodes of cardiogenic pulmonary edema. The patient recovered following supportive care and treatment with intravenous N-acetylcysteine and alprostadil (Payen et al, 2002).
    B) PEDIATRIC
    1) ROUTE OF EXPOSURE
    a) ORAL: A 14-year-old boy drank 15 mL of EDC for recreational purposes. Onset of symptoms was within 2 hours, including severe headache, staggering, lethargy, and vomiting. Oliguria was noted initially and persisted. Hypoglycemia was noted on the second day. On the third day dyspnea and somnolence were noted. Liver function tests were slightly abnormal on admission and steadily worsened. Hypoprothrombinemia occurred on the third day, secondary to depletion of liver-dependent clotting factors. Aspiration occurred secondary to endotracheal intubation attempt. Pulmonary edema was then documented, which resolved over the next 36 hours. The serum calcium level began to rise on the fourth day to 14.5 mg/dL. Sinus tachycardia and ST-T wave changes were reported. Refractory hypotension developed on the fifth day, followed by death on the sixth day (Yodaiken & Babcock, 1973).

Range Of Toxicity

Summary

    A) Fatalities in adults have been reported after ingestion of 30 to 70 grams, and in an adolescent after ingestion of 15 mL. Death is usually due to circulatory or respiratory collapse, but may occur due to hepatorenal failure.
    B) After ingesting 15 mL and 50 mL of ethylene dichloride, two adult patients recovered following supportive care and treatment with intravenous N-acetylcysteine and alprostadil.

Minimum Lethal Exposure

    A) CASE REPORTS
    1) ADULTS - Fatalities in adults have been reported after ingestion of 30 to 70 grams (Jacobziner & Raybin, 1961). Death is usually due to circulatory or respiratory collapse.
    2) ADOLESCENTS - Death resulted from ingestion of 15 milliliters by a 14-year-old boy, secondary to hepatorenal failure (Yodaiken & Babcock, 1973).
    B) ACUTE
    1) LDLo - (ORAL) HUMAN: 286 mg/kg (RTECS, 2001)
    2) LDLo - (ORAL) HUMAN, Male 714 mg/kg (RTECS, 2001)

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) Inhalation and dermal exposure to 4 to 60 parts per million resulted in symptoms in 90 of 118 workers, including conjunctivitis, weakness, metallic taste, headache, dermatographism, nausea, liver pain, tachycardia, dyspnea, and bronchial or pharyngeal irritation. Abnormal LFT were found in 40 of 56 workers (HSDB , 2001).
    2) Exposure to 5 to 40 parts per million emitted from aircraft glue was associated with liver and bile duct disease, neurosis, dystonia, asthenia, goiter, and hyperthyroidism (HSDB , 2001).
    3) CASE REPORT - After ingesting 15 mL of ethylene dichloride, an 18-year-old man developed headache, vomiting, oliguria, elevated liver enzymes (ASAT 1603 IU/L (<43), ALAT 3014 IU/L (<36)), hyperbilirubinemia (bilirubin 171 mcmol/L (<17.1)), elevated creatinine (326.2 mcmol/L (<106)), and hypoprothrombinemia (INR 6.26). The patient recovered following supportive care and treatment with intravenous N-acetylcysteine and alprostadil (Payen et al, 2002).
    4) CASE REPORT - After ingesting 50 mL of ethylene dichloride, a 28-year-old man developed nausea, black vomiting, abdominal pain, elevated liver enzymes (ASAT 37136 IU/L, ALAT 17083 IU/L), hypoprothrombinemia (INR 4.43), hyperbilirubinemia (bilirubin 75.2 mcmol/L), and elevated creatinine (219.2 mcmol/L). Echocardiography revealed abnormal left ventricle contractility. In addition, he experienced 2 episodes of cardiogenic pulmonary edema. The patient recovered following supportive care and treatment with intravenous N-acetylcysteine and alprostadil (Payen et al, 2002).
    B) ACUTE
    1) TDLo - (ORAL) HUMAN: 428 mg/kg (RTECS, 2001)
    2) TCLo - (INHL) HUMAN, Male: 4000 ppm for 1H (RTECS, 2001)

Workplace Standards

    A) ACGIH TLV Values for CAS107-06-2 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Ethylene dichloride
    a) TLV:
    1) TLV-TWA: 10 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: Not Listed
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    c) TLV Basis - Critical Effect(s): Liver dam; nausea
    d) Molecular Weight: 98.96
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS107-06-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Ethylene dichloride
    2) REL:
    a) TWA: 1 ppm (4 mg/m(3))
    b) STEL: 2 ppm (8 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix A; See Appendix C (Chloroethanes)
    3) IDLH:
    a) IDLH: 50 ppm
    b) Note(s): Ca
    1) Ca: NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A).

    C) Carcinogenicity Ratings for CAS107-06-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Ethylene dichloride
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) EPA (U.S. Environmental Protection Agency, 2011): B2 ; Listed as: 1,2-Dichloroethane
    a) B2 : Probable human carcinogen - based on sufficient evidence of carcinogenicity in animals.
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 2B ; Listed as: 1,2-Dichloroethane
    a) 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.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Ethylene dichloride
    a) Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    5) MAK (DFG, 2002): Category 2 ; Listed as: 1,2-Dichloroethane
    a) Category 2 : Substances that are considered to be carcinogenic for man because sufficient data from long-term animal studies or limited evidence from animal studies substantiated by evidence from epidemiological studies indicate that they can make a significant contribution to cancer risk. Limited data from animal studies can be supported by evidence that the substance causes cancer by a mode of action that is relevant to man and by results of in vitro tests and short-term animal studies.
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): R ; Listed as: 1,2-Dichloroethane (Ethylene Dichloride)
    a) R : RAHC = Reasonably anticipated to be a human carcinogen

    D) OSHA PEL Values for CAS107-06-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Ethylene dichloride (1,2-Dichloroethane)
    2) Table Z-1 for Ethylene dichloride (1,2-Dichloroethane):
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3:
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed
    3) Table Z-2 for Ethylene dichloride (Z37.21-1969):
    a) 8-hour TWA:50 ppm
    b) Acceptable Ceiling Concentration: 100 ppm
    c) Acceptable Maximum Peak above the Ceiling Concentration for an 8-hour Shift:
    1) Concentration: 200 ppm
    2) Maximum Duration: 5 min. in any 3 hrs
    d) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2001 Lewis, 2000
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 470 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 489 mg/kg
    3) LD50- (INTRAPERITONEAL)RAT:
    a) 807 mg/kg
    4) LD50- (ORAL)RAT:
    a) 670 mg/kg
    5) LD50- (SUBCUTANEOUS)RAT:
    a) 1 g/kg
    6) TCLo- (INHALATION)HUMAN:
    a) 4000 ppm for 1H
    7) TCLo- (INHALATION)MOUSE:
    a) 5 ppm/7H for 78W
    8) TCLo- (INHALATION)RAT:
    a) 300 ppm/7h
    b) 5 ppm for 7H for 78W

Pharmacology Toxicology

Toxicologic Mechanism

    A) The major toxic effects of ethylene dichloride are: 1) pulmonary edema, 2) increased myocardial irritability, 3) CNS depression, 4) dermal irritation and necrosis, 5) liver injury, and 6) renal damage.
    B) Although some dechlorination occurs in vivo, it is excreted mainly in the expired air.

Physicochemical

Physical Characteristics

    A) It is a heavy liquid with pleasant odor and sweet taste; vapors produce irritation (Bingham et al, 2001; Budavari, 1996; CHRIS , 1989).

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) 98.96 (Budavari, 1996; RTECS , 2001)

Other

    A) ODOR THRESHOLD
    1) 100 ppm (CHRIS , 2002).

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.
    5) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    6) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    7) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    9) 66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.
    10) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
    11) 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
    12) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
    13) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, 5th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1986, pp 252-253.
    14) ACGIH: Documentation of the Treshold Limit Values and Biological Exposure Indices, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991, pp 609-611.
    15) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
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