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1,1-DICHLOROETHANE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) 1,1-Dichloroethane is a colorless, mobile, oily, flammable liquid with a chloroform- or ether-like odor and a saccharin taste (ACGIH, 1996; Ashford, 1994; Budavari, 2000; Lewis, 2001; Lewis, 2000).
    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

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C2-H4-Cl2

Available Forms Sources

    A) FORMS
    1) 1,1-Dichloroethane is a colorless, mobile, oily, flammable liquid which has a chloroform-like odor and a saccharin-like taste (ACGIH, 1996; Ashford, 1994; Budavari, 2000; Lewis, 2001; Lewis, 2000).
    B) SOURCES
    1) 1,1-Dichloroethane is produced by the addition of anhydrous hydrogen chloride to vinyl chloride, by the addition of hydrogen chloride to acetylene, or by the chlorination of monochloromethane (Ashford, 1994; HSDB , 2002)
    2) Though it does not occur as a natural product, 1,1-dichloroethane appears to be an environmental breakdown product of some commonly used chlorinated solvents (Bingham et al, 2001; Howard, 1990).
    C) USES
    1) 1,1-Dichloroethane is primarily used as a chemical intermediate. It is also used as a grain fumigant, coupling agent in antiknock gasoline, paint and varnish remover, metal degreaser, and ore flotation agent. It has limited use as a solvent for plastics, oils, and fats (ACGIH, 1996; Bingham et al, 2001; Hathaway et al, 1996; Howard, 1990; Lewis, 2001).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) At the time of this review, no studies of acute oral toxic effects in humans were found. Overall toxicity is thought to be less than its isomer 1,2-dichloroethane. Animal studies indicated that 1,1-dichloroethane is well absorbed by ingestion. The central nervous system (CNS), cardiovascular, hepatic and renal systems may be adversely affected. Death may be due to cardiac dysrhythmias, or aspiration. Neurologic effects have been reported including headache, weakness, vertigo, tremor, and dizziness.
    B) INHALATION - Vapors may produce irritation of the respiratory tract and conjunctiva, CNS depression, and cardiac dysrhythmias.
    C) DERMAL - 1,1-dichloroethane is a skin, mucous membrane and eye 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. Conjunctival and corneal injury may occur.
    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.
    0.2.5) CARDIOVASCULAR
    A) Acute inhalation of high concentrations may result in cardiac dysrhythmias such as ventricular fibrillation.
    0.2.6) RESPIRATORY
    A) Coughing progressing to acute lung injury, tachypnea, and cyanosis may occur.
    0.2.7) NEUROLOGIC
    A) 1,1-dichloroethane is s 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.
    0.2.14) DERMATOLOGIC
    A) Dermal exposure may result in skin burns or red scaly rash.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no studies were found on the potential human reproductive effects of 1,1-dichloroethane.
    B) Skeletal abnormalities were noted in the offspring of pregnant rats exposed to 6000 ppm of days 6-15 of gestation.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no reports of carcinogenicity in humans were found.
    B) The ACGIH states that 1,1-dichloroethane is not classifiable as a human carcinogen (ACGIH, 1996a).

Laboratory Monitoring

    A) Plasma levels of 1,1-dichloroethane are not useful. Monitor cardiac function. Obtain electrocardiogram in symptomatic cases. Monitor serum glucose, electrolytes, liver function, and renal function in severe cases. Monitor INR in symptomatic cases. 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 1,1-dichloroethane may result in irritation or 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.
    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.
    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) The minimal lethal dose of this compound has not been delineated. 1,1-dichloroethane is thought to possess less toxicity than 1,2-dichloroethane.

Clinical Effects

Summary Of Exposure

    A) At the time of this review, no studies of acute oral toxic effects in humans were found. Overall toxicity is thought to be less than its isomer 1,2-dichloroethane. Animal studies indicated that 1,1-dichloroethane is well absorbed by ingestion. The central nervous system (CNS), cardiovascular, hepatic and renal systems may be adversely affected. Death may be due to cardiac dysrhythmias, or aspiration. Neurologic effects have been reported including headache, weakness, vertigo, tremor, and dizziness.
    B) INHALATION - Vapors may produce irritation of the respiratory tract and conjunctiva, CNS depression, and cardiac dysrhythmias.
    C) DERMAL - 1,1-dichloroethane is a skin, mucous membrane and eye 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. Conjunctival and corneal injury may occur.
    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.
    3.4.3) EYES
    A) IRRITANT - 1,1-dichlorethane is an eye irritant and lacrimator (HSDB , 2002; ACGIH, 1996; Bingham et al, 2001).
    3.4.5) NOSE
    A) At high concentrations, 1,1-dichloroethane is a nasal irritant (Bingham et al, 2001; HSDB , 2002).
    3.4.6) THROAT
    A) At high concentrations, 1,1-dichloroethane is a nose and throat irritant (Bingham et al, 2001; HSDB , 2002).

Cardiovascular

    3.5.1) SUMMARY
    A) Acute inhalation of high concentrations may result in cardiac dysrhythmias such as ventricular fibrillation.
    3.5.2) CLINICAL EFFECTS
    A) VENTRICULAR FIBRILLATION
    1) Acute exposures to high airborne concentrations of 1,1-dichloroethane can produce cardiac arrhythmias that may lead to ventricular fibrillation (ATSDR, 1990) ATSDR, 2002).

Respiratory

    3.6.1) SUMMARY
    A) Coughing progressing to acute lung injury, tachypnea, and cyanosis may occur.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) 1,1-dichloroethane may cause irritation to the upper respiratory tract and burning in the nose. Aspiration and acute lung injury is possible.

Neurologic

    3.7.1) SUMMARY
    A) 1,1-dichloroethane is s 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) Exposure to high concentrations results in symptoms largely related to CNS depression. 1,1-dichloroethane was used for a time as a general anesthetic agent, but this use was discontinued because of an increased incidence of cardiac dysrhthmais at anesthetic doses ((ATSDR, 2002)) ASTDR, 1990) Decreased level of consciousness and dizziness have been reported (HSDB , 2002).

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 (HSDB , 2002).

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).

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) ABNORMAL RENAL FUNCTION
    1) Renal damage may occur (HSDB , 2002).

Dermatologic

    3.14.1) SUMMARY
    A) Dermal exposure may result in skin burns or red scaly rash.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Dermal exposures have resulted in dermatitis and burning. A scaly red rash may be seen (HSDB , 2002).
    B) SKIN ABSORPTION
    1) Systemic absorption from dermal exposure may occur (HSDB , 2002; Bingham et al, 2001).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no studies were found on the potential human reproductive effects of 1,1-dichloroethane.
    B) Skeletal abnormalities were noted in the offspring of pregnant rats exposed to 6000 ppm of days 6-15 of gestation.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) An increased incidence of delayed ossification of the sternum was noted in the offspring of pregnant rats exposed to an air concentration of 6000 ppm during days 6 through 15 of gestation. No other abnormalities were noted (Schwetz et al, 1974).
    2) Delayed ossification of the fetal sternebrae and decreased weight gain in the dams were noted in exposed experimental animals (Hathaway et al, 1996) RTECS, 1997). Retarded fetal development without any significant toxic effect was observed in rats with maternal inhalation exposure on days 6 to 15 of gestation (Schwetz et al, 1974).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS75-34-3 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no reports of carcinogenicity in humans were found.
    B) The ACGIH states that 1,1-dichloroethane is not classifiable as a human carcinogen (ACGIH, 1996a).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) In mice and rats, 1,1-dichloroethane caused marginal increases in mammary adenocarcinomas and hemangiosarcomas and a statistically significant increase in the incidence of endometrial stromal polyps; however, there was no conclusive evidence for the carcinogenicity of this agent (ACGIH, 1996).
    2) A positive dose-related trend was seen in female rats for the incidence of hemangiosarcomas and mammary adenocarcinomas. An increased incidence in hepatocellular carcinomas was seen in male mice. The incidence of endometrial polyps was statistically significant when compared to controls in female mice. Although the animals were expsoed to the maximum tolerated dose for mice (3,331 mg/kg/day) and rats (475 mg/kg/day), overall animal survival was low and the meaning of the results questioned (ASTDR, 1990).
    3) Klaunig et al (1986) studied the effect on liver and lung tumor incidence of continuous treatment of 1,1-dichloroethane (835 mg/L and 2500 mg/L) administered in drinking water to 70 male 4-week old B6C3F1 mice using a two-stage (initiation/promotion) treatment protocol. Of these mice, 35 were initiated by treatment with diethylnitrosamine (DENA) (10 mg/L) in the drinking water for 4 weeks. The remaining 35 received deionized drinking water.
    4) Each group was subsequently treated with one of the two dose concentrations 1,1-dichloroethane in drinking water for 52 weeks. The positive control group received phenobarbital (500 mg/L) as a liver tumor promoter. Mice were sampled after 24 weeks (10 mice) and 52 weeks (25 mice). The number of lung or liver tumors did not increase over the positive controls in the 1,1-dichloroethane exposed mice. By themselves 1,1-DCE and 1,2-DCE did not affect the incidence or number of liver or lung tumors in the DENA-initiated animals.

Genotoxicity

    A) At the time of this review, no human genotoxicity data following exposure to 1,1-dichloroethane was available. 1,1-dichloroethane may bind to proteins, RNA, and DNA in experimental animals.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Plasma levels of 1,1-dichloroethane are not useful. Monitor cardiac function. Obtain electrocardiogram in symptomatic cases. Monitor serum glucose, electrolytes, liver function, and renal function in severe cases. Monitor INR in symptomatic cases. 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.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Plasma levels of 1,1-dichloroethane are not useful. Monitor cardiac function. Obtain electrocardiogram in symptomatic cases. Monitor serum glucose, electrolytes, liver function, and renal function in severe cases. Monitor INR in symptomatic cases. 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 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 1,1-dichloroethane may result in irritation or 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 adsosrb 1,1-dichloroethane.
    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).

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.

Range Of Toxicity

Summary

    A) The minimal lethal dose of this compound has not been delineated. 1,1-dichloroethane is thought to possess less toxicity than 1,2-dichloroethane.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.
    2) Available data on 1,1-dichloroethane indicate that it is rather low in toxicity. At high concentrations, it is irritating to the eyes and respiratory tract and causes CNS depression and anesthesia, but it has a relatively low capacity to cause liver or kidney injury even with repeated exposures (ACGIH, 1996; Bingham et al, 2001; Hathaway et al, 1996).
    3) In the past, 1,1-dichloroethane was used as an anesthetic at approximately 25,000 ppm; however, there are no reported cases of human overexposure by inhalation (Hathaway et al, 1996).

Workplace Standards

    A) ACGIH TLV Values for CAS75-34-3 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) 1,1-Dichloroethane
    a) TLV:
    1) TLV-TWA: 100 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): URT and eye irr; liver and kidney dam
    d) Molecular Weight: 98.97
    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 CAS75-34-3 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: 1,1-Dichloroethane
    2) REL:
    a) TWA: 100 ppm (400 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix C (Chloroethanes)
    3) IDLH:
    a) IDLH: 3000 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS75-34-3 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: 1,1-Dichloroethane
    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): C ; Listed as: 1,1-Dichloroethane
    a) C : Possible human carcinogen.
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: 1,1-Dichloroethane
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS75-34-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: 1,1-Dichloroethane
    2) Table Z-1 for 1,1-Dichloroethane:
    a) 8-hour TWA:
    1) ppm: 100
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 400
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: CHRIS, 2002 HSDB, 2002 Lewis, 2000 RTECS, 2002
    1) LD50- (ORAL)RAT:
    a) 0.5 to 5 g/kg (CHRIS, 2002)
    b) 14.1 g/kg (HSDB, 2002)
    c) 725 mg/kg
    2) TCLo- (INHALATION)RAT:
    a) 6000 ppm for 7H at 6-15D of pregnancy -- developmental abnormalities of the musculoskeletal system

Physicochemical

Physical Characteristics

    A) 1,1-Dichloroethane is a colorless, mobile, oily, flammable liquid with a chloroform- or ether-like odor and a saccharin taste (ACGIH, 1996; Ashford, 1994; Budavari, 2000; Lewis, 2001; Lewis, 2000).

Ph

    A) It is a neutral liquid (Lewis, 2001).
    1) Editor's Note: Strictly speaking this compound does not possess a pH, as it does not have an ionizable hydrogen atom. In water, the pH would be neutral, approximately pH 7.

Molecular Weight

    A) 98.97

Other

    A) ODOR THRESHOLD
    1) 100-200 ppm (ACGIH, 1996)

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