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EPICHLOROHYDRIN

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Epichlorohydrin is a major raw material used in the manufacture of epoxy resins.

Specific Substances

    1) 3-Chloro-1, 2-epoxy propane
    2) (Chloromethyl) ethylene oxide
    3) Chloromethyloxirane
    4) Chloropropylene oxide
    5) Gamma-chloropropylene oxide
    6) 3-chloro-1, 2-propylene oxide
    7) 2-chloromethyl-oxirane
    8) Alpha-epichlorohydrin
    9) Epichlorophydrin
    10) Glycidyl chloride
    11) ECH
    12) Oxirane (chloromethyl)
    13) CAS 106-89-8
    14) ECH (EPICHLOROHYDRIN)
    1.2.1) MOLECULAR FORMULA
    1) C3-H5-Cl-O

Available Forms Sources

    A) FORMS
    1) Epichlorohydrin is a mobile, colorless, flammable, and reactive liquid. Its odor has been described as sweet and pungent or chloroform-like (Ashford, 2001; Bingham et al, 2001; Budavari, 1996; Lewis, 2000; Lewis, 2001; Lewis, 1998; Raffle et al, 1994; Verschueren, 1983).
    B) SOURCES
    1) It is produced by dehydrochlorination (glycerol-1,3-dichlorohydrin + calcium hydroxide) and by chlorination/dehydrochlorination (allyl alcohol + chlorine) (Ashford, 2001).
    C) USES
    1) Epichlorohydrin is used as a solvent for resins, gums, cellulose esters and ethers, paints, varnishes, nail enamels, and laquers; in the manufacture of glycerol and glycidol derivatives; in the manufacture of epoxy and phenoxy resins; and as a stabilizer in chlorine-containing materials (Bingham et al, 2001; Budavari, 1996; Lewis, 2001; Lewis, 1998).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Inhalation of vapors, the major route of exposure, causes systemic effects; it is also toxic by ingestion and skin absorption. Epichlorohydrin is a strong irritant to skin, producing burning, itching, deep pain, redness, swelling, burns and blisters, and to the eyes and respiratory system. Exposure may result in nausea, vomiting, abdominal pain, shortness of breath, cyanosis, dizziness and suffocation. Effects may be delayed for several hours.
    B) Epichlorohydrin is toxic to kidneys. Central nervous system and respiratory depression are possible.
    C) There have been few serious reactions to epichlorohydrin following industrial exposures. Repeated, chronic exposure may damage lung, liver and kidney, with symptoms of enervation, dermatitis and disturbances in the stomach and kidneys.
    0.2.3) VITAL SIGNS
    A) Hypotension and apnea have been reported in animal studies.
    0.2.4) HEENT
    A) Facial swelling and eye and nasal mucosal irritation may be seen after exposure.
    0.2.6) RESPIRATORY
    A) Irritation of the respiratory tract, bronchitis, and dyspnea are possible, but have not been seen in industrial exposures.
    0.2.7) NEUROLOGIC
    A) CNS depression has been the primary cause of death in poisoned laboratory animals.
    0.2.8) GASTROINTESTINAL
    A) Vomiting, nausea, and abdominal pain have been seen in exposed workers.
    0.2.9) HEPATIC
    A) Hepatomegaly has been seen in both animal studies and human exposures. Liver function abnormalities have been reported in humans up to 2 years after exposure to an unknown concentration.
    0.2.10) GENITOURINARY
    A) Kidney lesions were seen in humans briefly exposed to 100 ppm.
    0.2.14) DERMATOLOGIC
    A) ECH is irritating on contact. Burns may result. Vesiculation has occurred several hours after direct contact with the skin.
    B) Sensitization may occur.
    0.2.20) REPRODUCTIVE
    A) Fetotoxicity was seen in mice.

Laboratory Monitoring

    A) No toxic serum levels have been established.
    B) Liver and kidney function should be monitored.
    C) Monitor for CNS and/or respiratory depression in symptomatic patients following a massive acute exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) EMESIS: Ipecac-induced emesis is not recommended because there is so little information about the effects of overdose in humans.
    B) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    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) 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.
    E) 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.
    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) Toxic levels have not been established in humans.
    B) The no-effect air level in humans is estimated at 9 ppm.

Clinical Effects

Heent

    3.4.1) SUMMARY
    A) Facial swelling and eye and nasal mucosal irritation may be seen after exposure.
    3.4.2) HEAD
    A) Facial swelling may be seen after exposures to epichlorohydrin vapors (NIOSH, 1976).
    3.4.3) EYES
    A) CONJUNCTIVITIS - ECH is very irritating to the eyes, producing a burning sensation at 20 ppm of the vapor.
    1) If instilled into the eyes, it is markedly irritating, causing blepharospasm, hyperemia of the mucous membranes, tearing, pupillary constriction, clouded cornea and lid edema (NIOSH, 1976; ACGIH, 1991) Proctor & Hughes, 1977).
    3.4.5) NOSE
    A) RHINORRHEA - ECH may cause a burning sensation of the nasal mucosa as well as rhinorrhea at concentrations of 20 ppm (ACGIH, 1986; NIOSH, 1976).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) Has been seen in animal studies, but has not been seen in human exposures (Clayton & Clayton, 1982).

Respiratory

    3.6.1) SUMMARY
    A) Irritation of the respiratory tract, bronchitis, and dyspnea are possible, but have not been seen in industrial exposures.
    3.6.2) CLINICAL EFFECTS
    A) PNEUMONITIS
    1) Irritation of the respiratory tract, bronchitis, and dyspnea are possible, but have not been seen in industrial exposures (ACGIH, 1991; Bingham et al, 2001; Clayton & Clayton, 1982).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) APNEA
    a) Respiratory depression leading to apnea has been seen in animals. Cyanosis has also been present (Clayton & Clayton, 1982).

Neurologic

    3.7.1) SUMMARY
    A) CNS depression has been the primary cause of death in poisoned laboratory animals.
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CNS DEPRESSION
    a) CNS depression has been a primary cause of death in poisoned laboratory animals, but has not been reported in humans (Clayton & Clayton, 1982).

Gastrointestinal

    3.8.1) SUMMARY
    A) Vomiting, nausea, and abdominal pain have been seen in exposed workers.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Nausea, vomiting, and abdominal pain have been seen in exposed workers (ACGIH, 1986; Hathaway et al, 1996).

Hepatic

    3.9.1) SUMMARY
    A) Hepatomegaly has been seen in both animal studies and human exposures. Liver function abnormalities have been reported in humans up to 2 years after exposure to an unknown concentration.
    3.9.2) CLINICAL EFFECTS
    A) LARGE LIVER
    1) Hepatomegaly has been seen in both animal studies and human exposures (ACGIH, 1986). Liver function abnormalities have been reported in humans up to 2 years after a single exposure of unknown concentration (NIOSH, 1976).

Genitourinary

    3.10.1) SUMMARY
    A) Kidney lesions were seen in humans briefly exposed to 100 ppm.
    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) Kidney lesions were seen in humans briefly exposed to approximately 100 ppm (ACGIH, 1986).

Hematologic

    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEMOLYSIS
    a) Hemolysis has been reported in rabbit's blood, but has NOT been reported in humans (Clayton & Clayton, 1982).

Dermatologic

    3.14.1) SUMMARY
    A) ECH is irritating on contact. Burns may result. Vesiculation has occurred several hours after direct contact with the skin.
    B) Sensitization may occur.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) ECH is irritating on contact. Absorption and systemic toxicity may occur by way of the skin (ACGIH, 1986). This chemical penetrates leather and rubber (Clayton & Clayton, 1982).
    B) BULLOUS ERUPTION
    1) Skin contact may result in a transient burning sensation, followed several hours later by blistering, pain, and possibly necrosis (Proctor & Hughes, 1978; Lane, 1979).
    C) CONTACT DERMATITIS
    1) ECH is a strong irritant and sensitizer (Windholz et al, 1983).
    2) CASE SERIES - Of 6 patients with occupational contact dermatitis, 2 produced positive patch tests for ECH and 4 reacted to epoxy resin (van Jost, 1988).
    3) The prevalence of occupational sensitization to ECH in a larger study was 3.5% (Prens et al, 1986).

Reproductive

    3.20.1) SUMMARY
    A) Fetotoxicity was seen in mice.
    3.20.2) TERATOGENICITY
    A) FETOTOXICITY
    1) ECH was fetotoxic in mice at a relatively high oral dose (RTECS, 2002).
    3.20.5) FERTILITY
    A) FERTILITY DECREASED MALE
    1) Impairment of male fertility was seen in animal tests.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS106-89-8 (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: Epichlorohydrin
    b) Carcinogen Rating: 2A
    1) The agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.
    3.21.3) HUMAN STUDIES
    A) HUMANS
    1) Enterline et al (1990) studied the incidence of all cancers in two plants using epichlorhydrin. The SMR for all cancers at 20 or more years post following first exposure was 112.2, with a statistically significant SMR of 500 for leukemia.
    2) This work was questioned by Tsia et al (1990) as to its validity. A follow-up study of this cohort of U.S. epichlorohydrin workers demonstrated overall and cancer mortality lower than that seen in surrounding communities (Tsai et al, 1996).
    3) Other case control studies of ECH workers were not considered to have a positive correlation with lung cancer (Hagmar et al, 1986; Bond et al, 1986) Olsen et al, 1994).
    4) Barbone et al (1994) reported an association between epichlorohydrin exposure and central nervous system neoplasms. However, three of the four reported cases also had exposure to intermediates of anthraquinone dye production.
    3.21.4) ANIMAL STUDIES
    A) ANIMAL STUDIES
    1) ECH has been carcinogenic in rats and mice by the oral and inhalation routes (RTECS, 2002).
    B) CARCINOMA
    1) MICE - Cancers were produced in mice via dermal application and subcutaneous injection. Concentrations greater than 30 ppm produced nasal cavity carcinoma in rats (ACGIH, 1991; Bingham et al, 2001).
    2) There is sufficient evidence to classify ECH as an animal carcinogen by IARC criteria (RTECS, 2002).
    3) MICE - Tumors of the respiratory system were seen in mice given ECH by the IP route (RTECS, 2002).
    4) MICE - Tumors at the site of application were produced in mice by ECH given SC; lymphomas were produced by an unspecified route.
    a) Tumors of the respiratory system and nose were found in rats treated by inhalation, and of the gastrointestinal tract from oral dosing (RTECS, 2002).
    5) ECH is listed in the NTP Ninth Annual Report on Carcinogens in 2000 (RTECS, 2002).

Genotoxicity

    A) ECH has induced DNA damage or repair, unscheduled DNA synthesis, DNA inhibition, mutations, chromosome aberrations, sex chromosome loss and nondisjunction, gene conversion and mitotic recombination.
    1) Sister chromatid exchanges, micronuclei, abnormal sperm morphology, and oncogenic transformation in a variety of cells and species have been reported.

Summary Of Exposure

    A) Inhalation of vapors, the major route of exposure, causes systemic effects; it is also toxic by ingestion and skin absorption. Epichlorohydrin is a strong irritant to skin, producing burning, itching, deep pain, redness, swelling, burns and blisters, and to the eyes and respiratory system. Exposure may result in nausea, vomiting, abdominal pain, shortness of breath, cyanosis, dizziness and suffocation. Effects may be delayed for several hours.
    B) Epichlorohydrin is toxic to kidneys. Central nervous system and respiratory depression are possible.
    C) There have been few serious reactions to epichlorohydrin following industrial exposures. Repeated, chronic exposure may damage lung, liver and kidney, with symptoms of enervation, dermatitis and disturbances in the stomach and kidneys.

Vital Signs

    3.3.1) SUMMARY
    A) Hypotension and apnea have been reported in animal studies.
    3.3.4) BLOOD PRESSURE
    A) Hypotension has been seen in animal studies, but has not been seen in human exposures (Clayton & Clayton, 1982).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No toxic serum levels have been established.
    B) Liver and kidney function should be monitored.
    C) Monitor for CNS and/or respiratory depression in symptomatic patients following a massive acute exposure.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) No toxic serum levels have been established.
    2) This agent may cause liver failure. Monitor liver functions for several days after an exposure.
    3) This agent may cause kidney damage. Monitor kidney function tests.
    4.1.3) URINE
    A) URINALYSIS
    1) This agent may cause kidney damage. Monitor renal function and urinalysis.
    2) Occupational exposure to epichlorohydrin correlates with urinary excretion of 3-chloro-2-hydroxylpropylpercapturic acid (CHMPA) and 2,3-dihydroxypropylmercapturic acid (De Rooij et al, 1997).
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Animal studies show CNS and respiratory depression are possible in high dose acute exposures; monitor for CNS and respiratory depression after high dose exposure and in symptomatic patients.
    b) Hemoglobin adducts have been utilized to monitor occupational exposure to epichlorohydrin and are said to reflect exposure for the preceding four month period (Landin et al, 1997).

Methods

    A) CHROMATOGRAPHY
    1) Epichlorhydrin can be detected in water using gas chromatography with electron capture (Pesselman & Feit, 1988).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) No toxic serum levels have been established.
    B) Liver and kidney function should be monitored.
    C) Monitor for CNS and/or respiratory depression in symptomatic patients following a massive acute exposure.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED -
    1) EMESIS: Ipecac-induced emesis is not recommended because there is so little information about the effects of overdose in humans.
    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) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) There is no antidote for epichlorohydrin poisoning. Treatment is symptomatic and supportive. CNS depression and respiratory depression have not been reported in human, but are anticipated based upon animal studies. Monitoring for CNS and respiratory depression should be done for all symptomatic patients. Airway management should be provided for patients with respiratory compromise.
    B) ACUTE LUNG INJURY
    1) Pulmonary edema has not yet been seen in human cases, but is a probable effect extrapolated from animal data.
    2) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    3) 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)
    4) 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).
    5) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    6) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    7) 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).
    8) 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) Hypotension has not been seen in human cases but may occur in significant exposures.
    2) 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.
    3) 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).
    4) 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.

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) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    2) Contaminated clothing should be decontaminated by thorough washing with soap and water. ECH will penetrate leather or rubber objects. Contaminated shoes or belts should be discarded.
    6.9.2) TREATMENT
    A) BURN
    1) Dermal reactions are often delayed several hours.
    2) Prolonged contact with leather soaked with ECH may cause severe blistering and necrosis (NIOSH, 1976).
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) Toxic levels have not been established in humans.
    B) The no-effect air level in humans is estimated at 9 ppm.

Minimum Lethal Exposure

    A) ADULT
    1) The minimum lethal human dose to this agent has not been delineated.
    2) Epichlorohydrin is severely irritating to the eyes and respiratory tract, and to the skin. Exposure to 20 ppm for 1 hour reportedly causes temporary burning; exposure to 40 ppm reportedly causes 48 hours of irritation and exposure to 100 ppm may result in pulmonary edema and renal lesions. Skin contact with epichlorohydrin reportedly causes itching, erythema, edema, and sensitization depending upon exposure levels. Severe burns may also result from the use of improper protective clothing; epichlorohydrin easily penetrates leather shoes and gloves and may result in chemical burns (Baxter, 2000; (Bingham et al, 2001; Clayton & Clayton, 1993; Grant, 1993; Harbison, 1998; Hathaway et al, 1996; Lewis, 2000; Raffle et al, 1994).

Maximum Tolerated Exposure

    A) ADULT
    1) The maximum tolerated human exposure to this agent has not been delineated.
    2) Epichlorohydrin can damage the lungs, liver, and kidneys after chronic exposure; however, no statistically significant increases in cancer rates in cohort studies of exposed factory workers were found. Epichlorohydrin is listed as carcinogenic by several references based on animal studies (Hathaway et al, 1996; IARC, 1987; ILO, 1998; Lewis, 2000; Lewis, 2001; Lewis, 1998).

Workplace Standards

    A) ACGIH TLV Values for CAS106-89-8 (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) Epichlorohydrin
    a) TLV:
    1) TLV-TWA: 0.5 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A3
    2) Codes: Skin
    3) Definitions:
    a) A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    b) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): URT irr; male repro
    d) Molecular Weight: 92.53
    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 CAS106-89-8 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Epichlorohydrin
    2) REL:
    a) TWA:
    b) STEL:
    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
    3) IDLH:
    a) IDLH: 75 ppm
    b) Note(s): Ca
    1) Ca: NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A).

    C) Carcinogenicity Ratings for CAS106-89-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Epichlorohydrin
    a) A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    2) EPA (U.S. Environmental Protection Agency, 2011): B2 ; Listed as: Epichlorohydrin
    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): 2A ; Listed as: Epichlorohydrin
    a) 2A : The agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Epichlorohydrin
    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: Epichlorohydrin
    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: Epichlorohydrin
    a) R : RAHC = Reasonably anticipated to be a human carcinogen

    D) OSHA PEL Values for CAS106-89-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Epichlorohydrin
    2) Table Z-1 for Epichlorohydrin:
    a) 8-hour TWA:
    1) ppm: 5
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 19
    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: Yes
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: (RTECS, 2002)
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 170 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 195 mg/kg -- behavioral changes
    3) LD50- (SKIN)MOUSE:
    a) 250 mg/kg
    4) LD50- (INTRAPERITONEAL)RAT:
    a) 133 mg/kg -- increased urine volume
    5) LD50- (ORAL)RAT:
    a) 90 mg/kg -- increased urine volume
    6) LD50- (SUBCUTANEOUS)RAT:
    a) 150 mg/kg -- increased urine volume
    7) TCLo- (INHALATION)HUMAN:
    a) 20 ppm -- affected sense organs
    b) 40 ppm for 2H -- affected respiratory system
    8) TCLo- (INHALATION)MOUSE:
    a) 25 ppm for 6H/90D-I -- caused changes in sense organs and liver
    9) TCLo- (INHALATION)RAT:
    a) Female, 100 ppm for 7H at 6-15D of pregnancy -- affected fertility
    b) Male, 50 ppm for 6H at 50D prior to mating -- affected fertility
    c) 100 ppm for 6H/30D-C -- induced tumors
    d) 20 mg/m3 for 24H/14W-C -- affected brain, behavior, and blood
    e) 170 mg/m(3) for 3H/17W-C -- caused respiratory and renal changes

Pharmacology Toxicology

Toxicologic Mechanism

    A) Epichlorohydrin is an alkylating agent which causes a delayed reaction (NIOSH, 1976).

Physicochemical

Physical Characteristics

    A) Epichlorohydrin is a mobile, colorless, flammable, and reactive liquid. Its odor has been described as sweet and pungent or chloroform-like (Ashford, 2001; Budavari, 1996; Bingham et al, 2001; Lewis, 2000; Lewis, 2001; Lewis, 1998; Raffle et al, 1994; Verschueren, 1983).

Molecular Weight

    A) 92.53

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