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ETHANOLAMINE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Ethanolamine is an alkanolamine compound with wide industrial use.

Specific Substances

    A) Ethanolamine
    1) Aethanolamin
    2) Aminoethanol
    3) Ethanol, 2-amino-
    4) Aethanolamin (German)
    5) 2-Aminoaethanol (German)
    6) 2-Aminoetanolo (Italian)
    7) 2-Aminoethanol
    8) beta-Aminoethyl alcohol
    9) Colamine
    10) Etanolamina
    11) Etanolamina (Italian)
    12) Ethanol, 2-amino- (solution)
    13) beta-Ethanolamine
    14) Ethylolamine
    15) Glycinol
    16) beta-Hydroxyethylamine
    17) 2-hydroxyethanamine
    18) 2-Hydroxyethylamine
    19) Kolamin
    20) MEA
    21) Monoaethanolamin
    22) Monoaethanolamin (German)
    23) Monoethanolamine
    24) Monoethanolamine solution
    25) Olamine
    26) Thiofaco M-50
    27) USAF EK-1596
    28) USAF EK-1597
    29) Molecular Formula: C2-H7-N-O
    30) NIOSH/RTECS KJ 5775000
    31) CAS 141-43-5
    32) References: RTECS, 1988; Sax, 1984; Budavari, 1989
    ETHANOLAMINE OLEATE
    1) Aethanolaminum oleate
    2) Monoethanolamine oleate
    3) Olamine oleate
    4) 2-hydroxyethylamine oleate
    5) 2-Aminoethanol oleate
    6) Molecular Formula: C20-H41-N-O3

    1.2.1) MOLECULAR FORMULA
    1) C2-H7-N-O

Available Forms Sources

    A) FORMS
    1) Ethanolamine is a clear, colorless, viscous, hygroscopic liquid with a slightly ammonia-like odor (AAR, 2000; Budavari, 2000; Lewis, 2001; Verschueren, 2001).
    2) Ethanolamine is available in NF and technical grades (Lewis, 2001).
    a) NF grade material is 85 percent ethanolamine and 15 percent water (CHRIS , 2002).
    b) The commercial grade material is 99 plus percent ethanolamine (CHRIS , 2002).
    3) Ethamolin(R), ethanolamine oleate 5% injection for local intravenous use is available from Glaxo Pharmaceuticals as a 2 mL ampule (Prod Info, 1989).
    B) SOURCES
    1) Reaction of ammonia with ethylene oxide results in a mixture of mono-, di-, and triethanolamines (Lewis, 2001).
    2) Large-scale production is done by ammonolysis of ethylene oxide. Ethanolamine can also be prepared from nitromethane and formaldehyde (Budavari, 2000).
    3) Ethanolamine is found in small amounts in normal human urine; excretion rates range from 5 to 23 mg/day (Lewis, 1998; Zenz, 1994).
    4) It is excreted by the algae Ochromonas danica (Verschueren, 2001).
    C) USES
    1) Ethanolamine is an alkanolamine compound with wide industrial use (Clayton & Clayton, 1982): for purification of natural gas and other gases through removal of acidic compounds such as carbonyl sulfide, hydrogen, carbon monoxide, and hydrogen sulfide (ITI, 1995; Sittig, 1991; Verschueren, 2001); a corrosion inhibitor and rubber accelerator (ITI, 1995; Lewis, 2001; Verschueren, 2001); in the process of softening hides and as an alkaline conditioning agent (Proctor & Hughes, 1978; Sittig, 1991; Lewis, 2001); as an intermediate compound in chemical synthesis (especially for ammonia, where it is a scrubber for the gas streams), in the manufacture of pharmaceutical agents (antibiotics) and non-ionic surfactants (ITI, 1995; Proctor & Hughes, 1978) ACGIH, 1986; (Sittig, 1991; Lewis, 2001; Verschueren, 2001) (These non-ionic surfactants are then used in dry cleaning, wool treatment, emulsion paints, polishes, and agricultural sprays (Lewis, 2001).); as a dispersing agent for various agricultural chemicals (Gosselin et al, 1984) ACGIH, 1986; (Lewis, 2001); as an antimicrobial in metalworking fluids, where its effects are greatly enhanced by keeping the fluids at high pH (Sandin et al, 1990).
    2) Ethanolamine, in dilute solutions, has also been considered for use as an initial skin decontaminant following military chemical warfare agent exposure (Klain et al, 1985).
    3) Ethanolamine is found as an emulsifier in polishes and hair wave solutions and in detergents, dyes, and textiles (Gosselin et al, 1984; Anon, 1968) ACGIH, 1986; (Lewis, 2001; Sittig, 1991), but is usually present as a neutral salt of one of a number of acids in consumer products (Lewis, 1998).
    4) It is used therapeutically as an injectable sclerosing agent in humans (Harbison, 1998).
    5) Ethanolamine is a metabolic intermediate in some animal species, aiding in the formation of phospholipids and choline (Howard, 1990).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Ethanolamine is a sclerosing agent used primarily for the treatment of esophageal varices with recent bleeding. It also has widespread use in industry.
    B) PHARMACOLOGY: Ethanolamine and oleic acid trigger an inflammatory response resulting in fibrosis and possible occlusion of the vein both in intravascularly and extravascularly. Oleic acid also activates coagulation in vivo by releasing tissue factor and activation of Hageman factor (Factor XII), but the ethanolamine component does not inhibit fibrin clot formation by chelating calcium so that a procoagulant action has not been demonstrated.
    C) EPIDEMIOLOGY: Overdose is rare.
    D) WITH THERAPEUTIC USE
    1) ADVERSE EFFECTS: COMMON: Pleural effusion, esophageal ulcer, pyrexia, retrosternal pain, esophageal stricture. LESS COMMON: Esophagitis, tearing of the esophagus, sloughing of the mucosa overlying the injected varix, necrosis, periesophageal abscess and perforation. RARE: bacteremia, anaphylactic shock, acute renal failure and disseminated intravascular coagulation.
    E) WITH POISONING/EXPOSURE
    1) TOXICITY: Injection of too large a volume of ethanolamine can result in intramural necrosis of the esophagus with complications leading to death. It is a pulmonary, GI, skin and eye irritant.
    0.2.3) VITAL SIGNS
    A) WITH THERAPEUTIC USE
    1) PYREXIA
    a) Pyrexia has been reported with ethanolamine therapy (incidence 1.8%) (Prod Info ETHAMOLIN(R) IV injection, 2006).
    0.2.4) HEENT
    A) WITH POISONING/EXPOSURE
    1) Eye, nose, and throat irritation may occur.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Severe respiratory tract irritation or acute lung injury can develop.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) Evidence from animal studies indicate that CNS depression may occur following acute intoxication.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Burns or irritation of the esophagus or GI tract may occur following acute intoxication.
    0.2.9) HEPATIC
    A) WITH POISONING/EXPOSURE
    1) Hepatotoxicity has been observed following acute exposure.
    0.2.10) GENITOURINARY
    A) WITH THERAPEUTIC USE
    1) Nephrotoxicity has been reported with therapy.
    0.2.14) DERMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Dermal irritation or burns may occur following acute exposure.
    0.2.19) IMMUNOLOGIC
    A) WITH THERAPEUTIC USE
    1) Anaphylactic shock developed following local IV injection of ethanolamine oleate.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no reproductive studies were found for monoethanolamine in humans.

Laboratory Monitoring

    A) Monitor liver and kidney function tests and urinalysis in patients with significant exposure.
    B) Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for respiratory tract irritation, bronchitis, anaphylaxis or pneumonitis.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    B) MUCOSAL DECONTAMINATION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact 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. Patients should not be forced to drink after ingestion of an acid, nor should they be allowed to drink larger volumes since this may induce vomiting, and thereby re-exposure of the injured tissues to the corrosive acid. Dilution may only be helpful if performed in the first seconds to minutes after ingestion.
    C) GASTRIC DECONTAMINATION: Ipecac contraindicated. Activated charcoal is not recommended as it may interfere with endoscopy and will not reduce injury to GI mucosa. Consider insertion of a small, flexible nasogastric or orogastric tube to suction gastric contents after recent large ingestion of a strong acid; the risk of further mucosal injury or iatrogenic esophageal perforation must be weighed against potential benefits of removing any remaining acid from the stomach.
    D) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    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) 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).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    0.4.6) PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Support respiratory, cardiovascular, and renal function.
    C) DECONTAMINATION
    1) PREHOSPITAL: GI dilution is recommended for decontamination due to the irritative effects of ethanolamine. Immediately dilute with 4 to 8 ounces (120 to 240 mL) of water or milk (not to exceed 4 ounces/120 mL in a child) after oral exposure.
    2) HOSPITAL: GI dilution is recommended for decontamination due to the irritative effects of ethanolamine. Immediately dilute with 4 to 8 ounces (120 to 240 mL) of water or milk (not to exceed 4 ounces/120 mL in a child) after oral exposure.
    D) AIRWAY MANAGEMENT
    1) Ensure adequate ventilation and preform endotracheal intubation early in patients with pulmonary toxicity.
    E) ANTIDOTE
    1) None.
    F) ENHANCED ELIMINATION PROCEDURE
    1) The role of hemodialysis is unknown for ethanolamine overdose.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic patients with inadvertent exposure may be monitored at home.
    2) OBSERVATION CRITERIA: Patients with pulmonary irritation, or persistent eye, skin or GI irritation should be referred to a healthcare facility.
    3) ADMISSION CRITERIA: Admit any individuals who are persistently symptomatic. Patients exhibiting symptoms of pulmonary distress (eg, stridor, chest retractions, dysphagia, cyanosis, choking, signs or symptoms of aspiration), cardiovascular compromise, unexplained or exacerbated bleeding or acute renal failure should be admitted for further evaluation and treatment.
    4) CONSULT CRITERIA: Consult a medical toxicologist or poison center for assistance in managing severe toxicity or if diagnosis is unclear.
    H) PITFALLS
    1) Failure to consider delayed toxicity.
    I) PHARMACOKINETICS
    1) Ethanolamine oleate disappears from the portal vein within 5 minutes of injection. In cases of overdose (ie, injections above 20 mL or 0.4 mL/kg), ethanolamine oleate can flow into the azygos vein through the periesophageal vein, causing the following effects: neutrophil infiltration (4 days), hemorrhage (6 days), granulation of the tissue (10 days), red thrombi closing the varices (20 days) and sclerosis of the vein (2.5 months). The maximum lethal dose for rabbits is 130 mg/kg. When 1 ml/kg injected over one minute into the right atrium of dogs, an increase of extravascular lung water was observed.
    J) DIFFERENTIAL DIAGNOSIS
    1) Includes other agents that may cause sclerosis (eg, polidocanol) or exposure to other ethanolamines (ie, triethanolamine and diethanolamine).

Range Of Toxicity

    A) TOXICITY: Injection of too large a volume of ethanolamine can result in intramural necrosis of the esophagus with complications leading to death. Ambient concentrations of 30 ppm are considered immediately dangerous to life and health.
    B) THERAPEUTIC DOSE: The usual local intravenous dose for sclerotherapy of esophageal varices is 1.5 to 5 mL of ethanolamine oleate 5% solution per varix. Do not exceed a total dose of 20 mL per session. Patients with significant liver dysfunction or concomitant cardiopulmonary disease should usually receive a maximum dose per session of less than 20 mL

Clinical Effects

Summary Of Exposure

    A) USES: Ethanolamine is a sclerosing agent used primarily for the treatment of esophageal varices with recent bleeding. It also has widespread use in industry.
    B) PHARMACOLOGY: Ethanolamine and oleic acid trigger an inflammatory response resulting in fibrosis and possible occlusion of the vein both in intravascularly and extravascularly. Oleic acid also activates coagulation in vivo by releasing tissue factor and activation of Hageman factor (Factor XII), but the ethanolamine component does not inhibit fibrin clot formation by chelating calcium so that a procoagulant action has not been demonstrated.
    C) EPIDEMIOLOGY: Overdose is rare.
    D) WITH THERAPEUTIC USE
    1) ADVERSE EFFECTS: COMMON: Pleural effusion, esophageal ulcer, pyrexia, retrosternal pain, esophageal stricture. LESS COMMON: Esophagitis, tearing of the esophagus, sloughing of the mucosa overlying the injected varix, necrosis, periesophageal abscess and perforation. RARE: bacteremia, anaphylactic shock, acute renal failure and disseminated intravascular coagulation.
    E) WITH POISONING/EXPOSURE
    1) TOXICITY: Injection of too large a volume of ethanolamine can result in intramural necrosis of the esophagus with complications leading to death. It is a pulmonary, GI, skin and eye irritant.

Vital Signs

    3.3.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) PYREXIA
    a) Pyrexia has been reported with ethanolamine therapy (incidence 1.8%) (Prod Info ETHAMOLIN(R) IV injection, 2006).

Heent

    3.4.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Eye, nose, and throat irritation may occur.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Eye irritation may occur (Sittig, 1991). Severe eye irritation occurs with direct liquid contact (Lewis, 2000; Grant, 1986; ACGIH, 1991; Anon, 1968).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) Irritation of the mucosa of the nose and throat may occur (Sittig, 1991).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) Irritation of the mucosa of the nose and throat may develop (Sittig, 1991).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Severe respiratory tract irritation or acute lung injury can develop.
    3.6.2) CLINICAL EFFECTS
    A) PULMONARY ASPIRATION
    1) WITH THERAPEUTIC USE
    a) Elderly patients undergoing esophageal variceal sclerotherapy have developed fatal aspiration pneumonia, which is likely related to the procedure, not the ethanolamine (Prod Info ETHAMOLIN(R) IV injection, 2006).
    B) PLEURAL EFFUSION
    1) WITH THERAPEUTIC USE
    a) Pleural effusion and infiltration has been reported with ethanolamine therapy (incidence 2.1%)(Prod Info ETHAMOLIN(R) IV injection, 2006).
    C) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Although reported to date only in experimental animals, it is expected that severe pulmonary irritation or acute lung injury would occur in heavily exposed humans (Proctor & Hughes, 1978; Hathaway et al, 1991).
    D) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 65-year-old man intentionally ingested 600 mL of an alkaline detergent (pH 11.7) that contained 3.3% monoethanolamine (MEA). He presented 1.5 hours later with complaints of dyspnea, and he reported vomiting with choking several times. Respiratory function continued to decline, necessitating intubation 6 hours later, and imaging was consistent with acute lung injury. Liver and renal damage was evident, and the patient expired on hospital day 4 due to ARDS progression. The patient had ingested approximately 0.3 grams/kg of MEA. Autopsy findings were suggestive of significant aspiration of the detergent (necrotic respiratory mucous membranes and hemorrhagic congestion of the lungs) (Kamijo et al, 2004).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) Respiratory tract irritation may occur, and was the main effect of inhalation exposure in experimental animals (Grant, 1986; Sittig, 1985).
    2) GRANULOMATOUS LESION
    a) Pulmonary lesions were found in animals exposed chronically to high concentrations of vapor and mist (ACGIH, 1986).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Evidence from animal studies indicate that CNS depression may occur following acute intoxication.
    3.7.2) CLINICAL EFFECTS
    A) PARALYSIS
    1) WITH THERAPEUTIC USE
    a) Spinal cord paralysis due to anterior spinal artery occlusion was reported in a child 8 hours after ethanolamine administration (Prod Info ETHAMOLIN(R) IV injection, 2006).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CNS DEPRESSION
    a) Central nervous system depression, lethargy, and apathy have been noted in exposed experimental animals, preceded by CNS stimulation at low doses ACGIH, 1986; (Sittig, 1985; Clayton & Clayton, 1982; Proctor & Hughes, 1978).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Burns or irritation of the esophagus or GI tract may occur following acute intoxication.
    3.8.2) CLINICAL EFFECTS
    A) GASTROENTERITIS
    1) WITH POISONING/EXPOSURE
    a) Although not reported, irritation or burns of the esophagus or gastrointestinal tract may be predicted to occur following ingestion based on this agent's irritant properties and its alkalinity (Gosselin et al, 1984).
    b) CASE REPORT: Esophagogastritis and acute respiratory distress syndrome developed in a 65-year-old man who ingested 600 mL of an alkaline detergent (pH 11.7) that contained 3.3% monoethanolamine (approximately 0.3 grams/kg). Upper gastrointestinal endoscopy showed diffuse erosion and ulceration in the esophagus and stomach (Kamijo et al, 2004).
    B) STRICTURE OF ESOPHAGUS
    1) WITH THERAPEUTIC USE
    a) Esophageal stricture, tearing of the esophagus, retrosternal pain and perforation have been infrequently reported (incidence less than 5%) with therapeutic use of ethanolamine(Prod Info ETHAMOLIN(R) IV injection, 2006).
    C) VASCULAR INSUFFICIENCY OF INTESTINE
    1) WITH THERAPEUTIC USE
    a) Extensive esophageal necrosis and death have been reported from direct injection of sclerosing agents (Prod Info ETHAMOLIN(R) IV injection, 2006).
    b) Complications of submucosally injected ethanolamine oleate have included delayed esophageal perforation, necrosis, and ulceration (Prod Info ETHAMOLIN(R) IV injection, 2006).

Hepatic

    3.9.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Hepatotoxicity has been observed following acute exposure.
    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: One case of acute hepatic involvement has been reported in a worker exposed to concentrated ethanolamine vapors in an unventilated room for 6 hours while filling drums with a hand pump (Jindrichova & Urban, 1970).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) Nonspecific hepatic lesions were noted in animal experiments ACGIH, 1986; (Sittig, 1985; Anon, 1968).

Genitourinary

    3.10.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) Nephrotoxicity has been reported with therapy.
    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL FAILURE SYNDROME
    1) WITH THERAPEUTIC USE
    a) CASE REPORTS: Two women who had received 15 to 20 mL of ethanolamine oleate injection developed acute renal failure, followed by spontaneous recovery within 3 weeks (Prod Info ETHAMOLIN(R) IV injection, 2006; Maling & Cretney, 1975).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NEPHROPATHY TOXIC
    a) Nonspecific renal lesions were noted in animal experiments ACGIH, 1986; (Sittig, 1985; Anon, 1968). This effect has not been reported in exposed humans.

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) DISSEMINATED INTRAVASCULAR COAGULATION
    1) WITH THERAPEUTIC USE
    a) One case of disseminated intravascular coagulation has occurred with ethanolamine use (Prod Info ETHAMOLIN(R) IV injection, 2006).
    B) BACTEREMIA
    1) WITH THERAPEUTIC USE
    a) Bacteremia has been infrequently reported (incidence less than 0.4%) with ethanolamine use (Prod Info ETHAMOLIN(R) IV injection, 2006).

Dermatologic

    3.14.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Dermal irritation or burns may occur following acute exposure.
    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) WITH POISONING/EXPOSURE
    a) Although ethanolamine is quite irritating to the skin in animal experiments, human experiments with direct exposure showed only dermal redness (Sittig, 1985).
    b) Marked erythema occurred in humans when the concentrated liquid was applied to the skin for an 1.5 hours (Hathaway et al, 1996).
    c) The irritant and necrotic effects on the skin may not be due simply to the alkalinity of this agent (ACGIH, 1991).
    B) SKIN ABSORPTION
    1) WITH POISONING/EXPOSURE
    a) Percutaneous absorption may be expected to occur following acute exposure (Gosselin et al, 1984; Anon, 1968).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ERUPTION
    a) Exposure to vapor concentrations between 5 and 12 ppm caused dermal irritation in animals (Grant, 1986).

Immunologic

    3.19.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) Anaphylactic shock developed following local IV injection of ethanolamine oleate.
    3.19.2) CLINICAL EFFECTS
    A) ANAPHYLACTOID REACTION
    1) WITH THERAPEUTIC USE
    a) Fatal anaphylactic shock has been reported following injection of larger than normal volume of ethanolamine oleate 5% injection (Prod Info ETHAMOLIN(R) IV injection, 2006).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no reproductive studies were found for monoethanolamine in humans.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) CONGENITAL ANOMALY
    a) Monoethanolamine was teratogenic and fetotoxic in rats when given by gavage at doses up to 500 mg/kg/day on days 6 to 15 of gestation (Mankes, 1986). Abnormalities of skeletal and urogenital development were noted in the offspring of exposed rats (RTECS , 2002).
    b) Monoethanolamine was not teratogenic in rats or rabbits exposed dermally to doses as high as 225 mg/kg/day on days 6 through 15, or 75 mg/kg/day on days 6 through 18 of gestation, respectively. Dose-related maternal toxicity was present in the form of skin irritation or lesions and changes in maternal body weight (Liberacki et al, 1996).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS141-43-5 (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

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor liver and kidney function tests and urinalysis in patients with significant exposure.
    B) Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for respiratory tract irritation, bronchitis, anaphylaxis or pneumonitis.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) 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.
    4.1.3) URINE
    A) URINALYSIS
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring urinalysis is suggested for patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.
    2) MONITORING
    a) Monitor cardiorespiratory status in patients with cardiac and/or respiratory disease (Prod Info ETHAMOLIN(R) IV injection, 2006).
    b) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.

Radiographic Studies

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

Methods

    A) CHROMATOGRAPHY
    1) Ethanolamine air concentration can be measured by absorption on silica gel, elution with methanolic acid, derivitization with benzaldehyde, and analysis with gas chromatography (Sittig, 1991).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) ADMISSION CRITERIA: Admit any individuals who are persistently symptomatic. Patients exhibiting symptoms of pulmonary distress (eg, stridor, chest retractions, dysphagia, cyanosis, choking, signs or symptoms of aspiration), cardiovascular compromise, unexplained or exacerbated bleeding or acute renal failure should be admitted for further evaluation and treatment.
    6.3.1.2) HOME CRITERIA/ORAL
    A) HOME CRITERIA: Asymptomatic patients with inadvertent exposures can be observed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) CONSULT CRITERIA: Consult a medical toxicologist or poison center for assistance in managing severe toxicity or if diagnosis is unclear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) OBSERVATION CRITERIA: Patients with pulmonary irritation, or persistent eye, skin or GI irritation should be referred to a healthcare facility.

Monitoring

    A) Monitor liver and kidney function tests and urinalysis in patients with significant exposure.
    B) Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for respiratory tract irritation, bronchitis, anaphylaxis or pneumonitis.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) DO NOT induce emesis.
    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 (Caravati, 2004).
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Monitor liver enzymes and kidney function tests and urinalysis in patients with significant exposure.
    2) Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for respiratory tract irritation, bronchitis, anaphylaxis or pneumonitis.
    B) IRRITATION SYMPTOM
    1) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    C) OBSERVATION REGIMES
    1) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    D) ANAPHYLAXIS
    1) SUMMARY
    a) Mild to moderate allergic reactions may be treated with antihistamines with or without inhaled beta adrenergic agonists, corticosteroids or epinephrine. Treatment of severe anaphylaxis also includes oxygen supplementation, aggressive airway management, epinephrine, ECG monitoring, and IV fluids.
    2) BRONCHOSPASM
    a) ALBUTEROL
    1) ADULT: 2.5 to 5 milligrams in 2 to 4.5 milliliters of normal saline delivered per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 2.5 to 10 mg every 1 to 4 hours as needed, or 10 to 15 mg/hr by continuous nebulization as needed (National Heart,Lung,and Blood Institute, 2007). CHILD: 0.15 milligram/kilogram (minimum 2.5 milligrams) per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 0.15 to 0.3 mg/kg (up to 10 mg) every 1 to 4 hours as needed, or 0.5 mg/kg/hr by continuous nebulization (National Heart,Lung,and Blood Institute, 2007).
    3) CORTICOSTEROIDS
    a) Consider systemic corticosteroids in patients with significant bronchospasm.
    b) PREDNISONE: ADULT: 40 to 80 milligrams/day. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 to 2 divided doses divided twice daily (National Heart,Lung,and Blood Institute, 2007).
    4) MILD CASES
    a) DIPHENHYDRAMINE
    1) SUMMARY: Oral diphenhydramine, as well as other H1 antihistamines can be used as indicated (Lieberman et al, 2010).
    2) ADULT: 50 milligrams orally, or 10 to 50 mg intravenously at a rate not to exceed 25 mg/min or may be given by deep intramuscular injection. A total of 100 mg may be administered if needed. Maximum daily dosage is 400 mg (Prod Info diphenhydramine HCl intravenous injection solution, intramuscular injection solution, 2013).
    3) CHILD: 5 mg/kg/24 hours or 150 mg/m(2)/24 hours. Divided into 4 doses, administered intravenously at a rate not exceeding 25 mg/min or by deep intramuscular injection. Maximum daily dosage is 300 mg (Prod Info diphenhydramine HCl intravenous injection solution, intramuscular injection solution, 2013).
    5) MODERATE CASES
    a) EPINEPHRINE: INJECTABLE SOLUTION: It should be administered early in patients by IM injection. Using a 1:1000 (1 mg/mL) solution of epinephrine. Initial Dose: 0.01 mg/kg intramuscularly with a maximum dose of 0.5 mg in adults and 0.3 mg in children. The dose may be repeated every 5 to 15 minutes, if no clinical improvement. Most patients respond to 1 or 2 doses (Nowak & Macias, 2014).
    6) SEVERE CASES
    a) EPINEPHRINE
    1) INTRAVENOUS BOLUS: ADULT: 1 mg intravenously as a 1:10,000 (0.1 mg/mL) solution; CHILD: 0.01 mL/kg intravenously to a maximum single dose of 1 mg given as a 1:10,000 (0.1 mg/mL) solution. It can be repeated every 3 to 5 minutes as needed. The dose can also be given by the intraosseous route if IV access cannot be established (Lieberman et al, 2015). ALTERNATIVE ROUTE: ENDOTRACHEAL ADMINISTRATION: If IV/IO access is unavailable. DOSE: ADULT: Administer 2 to 2.5 mg of 1:1000 (1 mg/mL) solution diluted in 5 to 10 mL of sterile water via endotracheal tube. CHILD: DOSE: 0.1 mg/kg to a maximum of 2.5 mg administered as a 1:1000 (1 mg/mL) solution diluted in 5 to 10 mL of sterile water via endotracheal tube (Lieberman et al, 2015).
    2) INTRAVENOUS INFUSION: Intravenous administration may be considered in patients poorly responsive to IM or SubQ epinephrine. An epinephrine infusion may be prepared by adding 1 mg (1 mL of 1:1000 (1 mg/mL) solution) to 250 mL D5W, yielding a concentration of 4 mcg/mL, and infuse this solution IV at a rate of 1 mcg/min to 10 mcg/min (maximum rate). CHILD: A dosage of 0.01 mg/kg (0.1 mL/kg of a 1:10,000 (0.1 mg/mL) solution up to 10 mcg/min (maximum dose 0.3 mg) is recommended for children (Lieberman et al, 2010). Careful titration of a continuous infusion of IV epinephrine, based on the severity of the reaction, along with a crystalloid infusion can be considered in the treatment of anaphylactic shock. It appears to be a reasonable alternative to IV boluses, if the patient is not in cardiac arrest (Vanden Hoek,TL,et al).
    7) AIRWAY MANAGEMENT
    a) OXYGEN: 5 to 10 liters/minute via high flow mask.
    b) INTUBATION: Perform early if any stridor or signs of airway obstruction.
    c) CRICOTHYROTOMY: Use if unable to intubate with complete airway obstruction (Vanden Hoek,TL,et al).
    d) BRONCHODILATORS are recommended for mild to severe bronchospasm.
    e) ALBUTEROL: ADULT: 2.5 to 5 milligrams in 2 to 4.5 milliliters of normal saline delivered per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 2.5 to 10 mg every 1 to 4 hours as needed, or 10 to 15 mg/hr by continuous nebulization as needed (National Heart,Lung,and Blood Institute, 2007).
    f) ALBUTEROL: CHILD: 0.15 milligram/kilogram (minimum 2.5 milligrams) per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulization (National Heart,Lung,and Blood Institute, 2007).
    8) MONITORING
    a) CARDIAC MONITOR: All complicated cases.
    b) IV ACCESS: Routine in all complicated cases.
    9) HYPOTENSION
    a) If hypotensive give 500 to 2000 milliliters crystalloid initially (20 milliliters/kilogram in children) and titrate to desired effect (stabilization of vital signs, mentation, urine output); adults may require up to 6 to 10 L/24 hours. Central venous or pulmonary artery pressure monitoring is recommended in patients with persistent hypotension.
    1) VASOPRESSORS: Should be used in refractory cases unresponsive to repeated doses of epinephrine and after vigorous intravenous crystalloid rehydration (Lieberman et al, 2010).
    2) DOPAMINE: Initial Dose: 2 to 20 micrograms/kilogram/minute intravenously; titrate to maintain systolic blood pressure greater than 90 mm Hg (Lieberman et al, 2010).
    10) H1 and H2 ANTIHISTAMINES
    a) SUMMARY: Antihistamines are second-line therapy and are used as supportive therapy and should not be used in place of epinephrine (Lieberman et al, 2010).
    1) DIPHENHYDRAMINE: ADULT: 25 to 50 milligrams via a slow intravenous infusion or IM. PEDIATRIC: 1 milligram/kilogram via slow intravenous infusion or IM up to 50 mg in children (Lieberman et al, 2010).
    b) RANITIDINE: ADULT: 1 mg/kg parenterally; CHILD: 12.5 to 50 mg parenterally. If the intravenous route is used, ranitidine should be infused over 10 to 15 minutes or diluted in 5% dextrose to a volume of 20 mL and injected over 5 minutes (Lieberman et al, 2010).
    c) Oral diphenhydramine, as well as other H1 antihistamines, can also be used as indicated (Lieberman et al, 2010).
    11) DYSRHYTHMIAS
    a) Dysrhythmias and cardiac dysfunction may occur primarily or iatrogenically as a result of pharmacologic treatment (epinephrine) (Vanden Hoek,TL,et al). Monitor and correct serum electrolytes, oxygenation and tissue perfusion. Treat with antiarrhythmic agents as indicated.
    12) OTHER THERAPIES
    a) There have been a few reports of patients with anaphylaxis, with or without cardiac arrest, that have responded to vasopressin therapy that did not respond to standard therapy. Although there are no randomized controlled trials, other alternative vasoactive therapies (ie, vasopressin, norepinephrine, methoxamine, and metaraminol) may be considered in patients in cardiac arrest secondary to anaphylaxis that do not respond to epinephrine (Vanden Hoek,TL,et al).

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) IRRITATION SYMPTOM
    1) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    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) OBSERVATION REGIMES
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    D) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    E) 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).
    6.8.2) TREATMENT
    A) INJURY OF CORNEA
    1) If severe eye irritation or corneal burns are present, prolonged initial flushing and early ophthalmologic consultation are advisable.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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).
    6.9.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    B) SKIN ABSORPTION
    1) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) HEMODIALYSIS
    1) The role of hemodialysis in the treatment of ethanolamine overdose is unknown.

Abstracts

Case Reports

    A) ADULT
    1) One case of acute hepatic involvement has been reported in a worker exposed to concentrated ethanolamine vapors in an unventilated room for 6 hours while filling drums with a hand pump (Jindrichova & Urban, 1970).

Range Of Toxicity

Summary

    A) TOXICITY: Injection of too large a volume of ethanolamine can result in intramural necrosis of the esophagus with complications leading to death. Ambient concentrations of 30 ppm are considered immediately dangerous to life and health.
    B) THERAPEUTIC DOSE: The usual local intravenous dose for sclerotherapy of esophageal varices is 1.5 to 5 mL of ethanolamine oleate 5% solution per varix. Do not exceed a total dose of 20 mL per session. Patients with significant liver dysfunction or concomitant cardiopulmonary disease should usually receive a maximum dose per session of less than 20 mL

Therapeutic Dose

    7.2.1) ADULT
    A) The usual local intravenous dose for sclerotherapy of esophageal varices is 1.5 to 5 mL of ethanolamine oleate 5% solution per varix. Do not exceed a total dose of 20 mL per session. Patients with significant liver dysfunction or concomitant cardiopulmonary disease should usually receive a maximum dose per session of less than 20 mL (Prod Info Ethamolin(R) intravenous injection solution, 2012).
    B) Therapy to obliterate the varix includes local injections at the time of the acute bleeding episode and then after 1 week, 6 weeks, 3 months, and 6 months (Prod Info Ethamolin(R) intravenous injection solution, 2012).
    C) Ethanolamine oleate should only be administered by a physician who is familiar with an acceptable injection technique (Prod Info Ethamolin(R) intravenous injection solution, 2012).
    7.2.2) PEDIATRIC
    A) GENERAL
    1) The safety and effectiveness have not been established in children (Prod Info Ethamolin(R) intravenous injection solution, 2012).

Minimum Lethal Exposure

    A) Six grams is an estimated fatal dose of ethanolamine for a 150 pound adult (Sittig, 1991).
    B) CASE REPORT: A 65-year-old man intentionally ingested 600 mL of an alkaline detergent (pH 11.7) that contained 3.3% monoethanolamine (MEA). He presented 1.5 hours later with complaints of dyspnea, and he reported vomiting with choking several times. Respiratory function continued to decline, necessitating intubation 6 hours later, and imaging was consistent with acute respiratory distress syndrome (ARDS). Liver and renal damage was evident, and the patient expired on hospital day 4 due to ARDS progression. The patient had ingested approximately 0.3 grams/kg of MEA (Kamijo et al, 2004).
    C) ANIMAL DATA
    1) Four of six guinea pigs died when exposed to a 233 ppm concentration for one hour (Anon, 1968; Hathaway et al, 1996).
    2) Exposure to a concentration of 75 ppm for 24 days killed 75% of a group of guinea pigs. Eighty-three percent of a group of rats exposed to 66 ppm for 28 days died (Anon, 1968).
    3) Deaths occurred in a group of rats fed 1.28 grams/kg/day for 90 days (ACGIH, 1991).

Maximum Tolerated Exposure

    A) Ethanolamine is irritating to skin, eyes, and mucous membranes. It is toxic by ingestion, dermal contact, subcutaneous, intravenous, and intramuscular routes. It is poisonous through intraperitoneal administration (HSDB , 2002; Lewis, 2000).
    B) Exposure to ethanolamine or its vapors can cause wheezing, laryngitis, shortness of breath, skin and eye redness and burns, dermatitis, blurred vision, sore throat, coughing and respiratory distress, headache, lethargy, increased blood pressure (but hypotension at high concentrations), diuresis, salivation, pupillary dilation, and necrosis. Ingestion can cause burns to the mouth and esophagus, abdominal pain, nausea, vomiting, central nervous system depression, coma, kidney and liver damage ((ICSC, 2001); NTP , 2001; Snyder et al, 1990; Zenz, 1994).
    C) Persons suffering from asthma, pre-existing skin disorders, or impaired liver, kidney, or pulmonary function may be more susceptible to the effects of exposure to ethanolamine (NTP , 2001).
    D) The undiluted liquid caused redness and swelling similar to a first degree burn when applied directly to the skin for 1.5 hours (ACGIH, 1986; (Proctor & Hughes, 1978; Snyder et al, 1990).
    E) The standard local intravenous dose for sclerotherapy of esophageal varices is 1.5 to 5 mL of ethanolamine oleate 5% solution per varix, not to exceed a total dose of 20 mL per session. Patients with significant liver dysfunction or concomitant cardiopulmonary disease should usually receive a maximum dose per session of less than 20 mL(Prod Info ETHAMOLIN(R) IV injection, 2006).
    F) ANIMAL DATA
    1) RATS: Ethanolamine fed to rats at 320 mg/kg/day for 90 days caused no observable effects (ACGIH, 1991).
    2) Chronic inhalation exposures of 100 ppm for 30 days resulted in dermal irritation, apathy, hair loss, and poor appetites in dogs, rats, or guinea pigs; similar exposure to 12 to 26 ppm for 90 days caused similar, but less severe, symptoms (ACGIH, 1991; Proctor & Hughes, 1978).
    3) RABBITS: One drop of undiluted liquid caused severe eye irritation in rabbits. Undiluted liquid applied to the skin caused redness and swelling (ACGIH, 1991).
    4) DOGS: Dogs exposed to 5 ppm for 90 days resulted in slight and temporary weight loss, and a minor decrease in activity and alertness (ACGIH, 1991).
    5) DOGS/CATS: Dogs and cats survived exposure to 900 ppm for 4 days (Hathaway et al, 1996).

Workplace Standards

    A) ACGIH TLV Values for CAS141-43-5 (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) Ethanolamine
    a) TLV:
    1) TLV-TWA: 3 ppm
    2) TLV-STEL: 6 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): Eye and skin irr
    d) Molecular Weight: 61.08
    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 CAS141-43-5 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Ethanolamine
    2) REL:
    a) TWA: 3 ppm (8 mg/m(3))
    b) STEL: 6 ppm (15 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 30 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS141-43-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Ethanolamine
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    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: Ethanolamine
    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 CAS141-43-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Ethanolamine
    2) Table Z-1 for Ethanolamine:
    a) 8-hour TWA:
    1) ppm: 3
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 6
    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: ACGIH, 1991 Budavari, 2000 CHRIS, 2002 NTP, 2001 OHM/TADS, 2002 RTECS, 2002 Snyder et al, 1990
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 50 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 700 mg/kg -- somnolence, dyspnea, muscle spasticity
    b) 1475 mg/kg (OHM/TADS, 2002)
    3) LD50- (INTRAMUSCULAR)RAT:
    a) 1750 mg/kg
    4) LD50- (INTRAPERITONEAL)RAT:
    a) 67 mg/kg
    b) 981 mg/kg (ACGIH, 1991; Snyder et al, 1990)
    5) LD50- (ORAL)RAT:
    a) 1720 mg/kg
    b) 2050 mg/kg (NTP, 2001; OHM/TADS, 2002)
    c) 3.32 g/kg (ACGIH, 1991)
    d) 0.5 to 5 g/kg (CHRIS, 2002)
    e) 2100 mg/kg (OHM/TADS, 2002)
    f) 3320 mg/kg (OHM/TADS, 2002; Snyder et al, 1990)
    g) 2140 mg/kg (OHM/TADS, 2002)
    h) 10,200 mg/kg for 14D (Budavari, 2000; OHM/TADS, 2002)
    i) 2740 mg/kg (Snyder et al, 1990)
    j) male, 1970 mg/kg (Snyder et al, 1990)
    k) female, 1720 mg/kg (Snyder et al, 1990)
    6) LD50- (SKIN)RAT:
    a) 1 mg/kg (ACGIH, 1991)
    7) LD50- (SUBCUTANEOUS)RAT:
    a) 1500 mg/kg
    8) TCLo- (INHALATION)RAT:
    a) 66 ppm for 24H/30D: continuous -- somnolence, irritative dermatitis, death
    b) 300 mg/m(3) for 5H/26W: intermittent -- proteinuria, changes in urine composition, weight loss or decreased weight gain
    c) 400 mg/m(3) for 5H/26W: intermittent -- respiratory depression, impaired liver function, proteinuria

Pharmacology Toxicology

Toxicologic Mechanism

    A) Ethanolamine is a direct irritant of eyes, skin, and mucous membranes (Sittig, 1991; Anon, 1968). It has caused liver and renal injury by undetermined mechanisms.

Physicochemical

Physical Characteristics

    A) Ethanolamine is a clear, colorless, viscous, hygroscopic liquid with a slightly ammonia-like odor (AAR, 2000; Budavari, 2000; Lewis, 2001; Verschueren, 2001).

Ph

    A) 12.1 (for a 25% aqueous solution) (Budavari, 2000)
    B) 12.05 (for a 0.1 N aqueous solution) (Budavari, 2000)

Molecular Weight

    A) 61.08

References

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