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GLYCOLS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Glycols are dihydroxy alcohol derivatives of the aliphatic hydrocarbons. They are distinguished as glycols because of their sweet taste.
    B) This document contains information on dioxane, hexylene glycol, pentaethylene glycol, tetraethylene glycol, and triethylene glycol. Information on the following agents are available in separate documents: "DIETHYLENE GLYCOL", "DIPROPYLENE GLYCOL", "ETHYLENE GLYCOL", "ETHYLENE GLYCOL ETHYL ETHER", "ETHYLENE GLYCOL METHYL ETHER", "GLYCOL ETHERS", "POLYETHYLENE GLYCOL", "PROPYLENE GLYCOL".

Specific Substances

    A) DIOXANE
    1) 1,4-Dioxan
    2) 1,4-Dioxan, tetrahydro-
    3) 1,4-Diethylene dioxide
    4) 1,4-Dioxanne
    5) 1,4-Dioxacyclohexane
    6) Diethylene oxide
    7) Diethylene dioxide
    8) Diethylene ether
    9) Dioxan
    10) Dioxyethylene ether
    11) Glycol ethylene ether
    12) Para-Dioxane
    13) Tetrahydro-1,4-dioxan
    14) Tetrahydro-1,4-dioxin
    15) Tetrahydro-parap-dioxin
    16) p-Dioxan
    17) p-Dioxan, tetrahydro-
    18) Para-Dioxan
    19) Tetrahydro-p-dioxane
    20) Molecular Formula: C4-H8-O2
    21) CAS 123-91-1
    HEXYLENE GLYCOL
    1) 2,4-dihydroxy-2-methylpentane
    2) 1,2-Hexanediol
    3) 2-Methyl pentane-2,4-diol
    4) 2-Methyl-2,4-Pentanediol
    5) Molecular Formula: C6-H14-O2
    6) CAS 107-41-5
    PENTAETHYLENE GLYCOL
    1) Pentaglycol
    2) 3,6,9,12-Tetraoxatetradecane-1,14-diol
    3) Molecular Formula: C10-H22-O6
    4) CAS 4792-15-8
    TETRAETHYLENE GLYCOL
    1) 3,6,9-Trioxaundecane-1,11-diol
    2) Ethanol,2,2'-(oxybis(2,1-ethanediyloxy))Bis-
    3) Ethanol,2,2'-(oxybis(ethyleneoxy))Di-
    4) Tetraglycol
    5) 2,2'-(Oxybis(ethyleneoxy))diethanol
    6) Molecular Formula: C8-H18-O5
    7) CAS 112-60-7
    TRIETHYLENE GLYCOL
    1) 1,2-Bis(2-hydroxyethoxy)ethane
    2) 2,2-(1,2-Ethanediylbis-(oxy))bisethanol
    3) 2,2'-Ethylenedioxybis(ethanol)
    4) 2,2'-Ethylenedioxyethanol
    5) 3,6-Dioxa-1,8-octanediol
    6) 3,6-Dioxaoctane-1,8-diol
    7) Ethylene glycol dihydroxydiethyl ether
    8) Triglycol
    9) Molecular Formula: C6-H14-O4
    10) CAS 112-27-6

Available Forms Sources

    A) FORMS
    1) DIOXANE: Is a flammable, colorless liquid. It is available in reagent, technical, spectrophotometric, and scintillation grades (Lewis, 1993).
    2) HEXYLENE GLYCOL: Is a colorless liquid with mild sweetish odor (HSDB - Hazardous Substances Data Bank, 2007; Lewis, 2008).
    3) PENTAETHYLENE GLYCOL: Is a colorless liquid (Lewis, 2008).
    4) TETRAETHYLENE GLYCOL: Is a colorless to straw-colored oily liquid with pleasant mild odor (HSDB - Hazardous Substances Data Bank, 2007; Lewis, 2008).
    5) TRIETHYLENE GLYCOL: Is an odorless, tasteless, clear liquid (Lewis, 2008).
    B) SOURCES
    1) DIOXANE: Is commonly produced by dehydration and ring closure of diethylene glycol, by dehydrohalogenation of 2-chloro-2'-hydroxydiethyl ether, or by dimerizing ethylene oxide (HSDB - Hazardous Substances Data Bank, 2007; Clayton & Clayton, 1994; Lewis, 1993).
    C) USES
    1) This document contains information on dioxane, hexylene glycol, pentaethylene glycol, tetraethylene glycol, and triethylene glycol. Information on the following agents are available in separate documents: "DIETHYLENE GLYCOL", "DIPROPYLENE GLYCOL", "ETHYLENE GLYCOL", "ETHYLENE GLYCOL ETHYL ETHER", "ETHYLENE GLYCOL METHYL ETHER", "GLYCOL ETHERS", "POLYETHYLENE GLYCOL", "PROPYLENE GLYCOL".
    2) DIOXANE: Is used mainly as a solvent for a wide range of organic products such as paints, lacquers, varnishes, plastics, waxes, resins, fats, oils, and cellulose esters and ethers. As a wetting agent, it is used in textile processing, stains, dye baths, and printing. It is also used as a stabilizer in chlorinated solvents. It has also been used in detergent and cleaning preparations, cosmetics, fumigants, deodorants, cements, polishing products, and in scintillation counters (ACGIH, 1991; Lewis, 1993; Budavari, 1996; Clayton & Clayton, 1994).
    3) HEXYLENE GLYCOL: Is used in cosmetics, textile dye vehicles. It is also used as a cement additive, solvent in petroleum refining, a coupling agent in hydraulic brake fluids and printing inks, and gasoline anti-icer additive (HSDB - Hazardous Substances Data Bank, 2007).
    4) TRIETHYLENE GLYCOL: Has been used as a solvent, ingredient of perfume, in various plastics to increase pliability, and in aerosol form as a disinfectant (Budavari, 1996a; Polderman, 1947). It is also used as automotive brake fluid, and has been reported in a concentration of 99.9% in Caltex(R) brake fluid (Vassiliadis et al, 1999). It is also used in various plastics to increase pliability, and as an air disinfectant (Budavari, 1996a).
    5) TETRAETHYLENE GLYCOL: Is used as a solvent for nitrocellulose, plasticizer, lacquers, coating compositions, ceramic paste/printing ink binder, lubricant, softening agent (paper tissue), and as a liquid desiccant for natural gas (HSDB - Hazardous Substances Data Bank, 2007).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) This document contains information on dioxane, hexylene glycol, pentaethylene glycol, tetraethylene glycol, and triethylene glycol. Information on the following agents are available in separate documents: "DIETHYLENE GLYCOL", "DIPROPYLENE GLYCOL", "ETHYLENE GLYCOL", "ETHYLENE GLYCOL ETHYL ETHER", "ETHYLENE GLYCOL METHYL ETHER", "GLYCOL ETHERS", "POLYETHYLENE GLYCOL", "PROPYLENE GLYCOL".
    B) USES: Glycols are used as solvents for a wide range of products such as paints, lacquers, varnishes, plastics, waxes, resins, fats, oils, and ethers. They are also used in cosmetics, automotive brake fluid, textile processing, stains, dye baths, and printing.
    C) EPIDEMIOLOGY: Limited data. Exposure rarely causes significant toxicity.
    D) WITH POISONING/EXPOSURE
    1) Glycols included in this management may cause irritation of eyes, skin, and mucous membranes.
    2) DIOXANE: Exposure to dioxane may cause irritation of eyes, skin, and mucous membranes. Dermatitis has been reported following the direct contact of the skin with liquid dioxane. Exposure to high concentrations of dioxane vapor may result in nausea and vomiting.
    a) CNS depression with headache, dizziness, drowsiness, and coma have been reported following exposure to high concentrations of dioxane. Hemorrhagic nephritis, centrilobular liver necrosis, severe epigastric pain, convulsion, and coma developed in workers who died following inhalational exposure to high concentrations of dioxane; however, the causal relationship to dioxane is not clear.
    0.2.4) HEENT
    A) Eye irritation may occur with any of the glycols.
    0.2.11) ACID-BASE
    A) WITH POISONING/EXPOSURE
    1) Metabolic acidosis has been reported in a patient exposed to triethylene glycol. However, the causal relationship to triethylene glycol is not clear.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no reproductive studies were found in humans.
    0.2.21) CARCINOGENICITY
    A) DIOXANE: Dioxane did not appear to cause cancer in workers exposed for 10 years. In the German MAK/BAT Values, 1,4-dioxane is listed in Category 4 of carcinogens (those known to act typically by nongenotoxic mechanisms). Dioxane may act as a promoter to produce skin tumors.
    B) TRIETHYLENE GLYCOL: At the time of this review, no studies were found on the possible carcinogenic effects of triethylene glycol in humans.
    C) HEXYLENE GLYCOL: At the time of this review, no studies were found on the possible carcinogenic activity of hexylene glycol in humans.

Laboratory Monitoring

    A) Monitor serum electrolytes in symptomatic patients, those with large, deliberate ingestions, and patients with severe vomiting.
    B) DIOXANE: Monitor vital signs, renal function, liver enzymes, mental status, pulse oximetry in symptomatic patients.
    C) Serum concentrations of these glycols are not widely available or helpful in clinical management.

Treatment Overview

    0.4.2) ORAL/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. Symptomatic patients may require airway management. Closely monitor neurologic function. Treat seizures with intravenous benzodiazepines or barbiturates.
    C) DECONTAMINATION
    1) PREHOSPITAL: Because of the potential for CNS depression (eg, drowsiness, sedation) with dioxane exposure, prehospital GI decontamination is NOT recommended. If there is a dermal or eye exposure, it would be reasonable to perform simple decontamination with water at home.
    2) HOSPITAL: Activated charcoal may be considered in patients with large, recent ingestions who are alert or in whom the airway is protected.
    D) AIRWAY MANAGEMENT
    1) Most likely unnecessary. Patients with severe CNS depression may require airway management; intubate and ventilate as needed.
    E) ANTIDOTE
    1) None.
    F) ACIDOSIS
    1) TRIETHYLENE GLYCOL: Metabolic acidosis has been reported in a patient exposed to triethylene glycol. However, the causal relationship to triethylene glycol is not clear. Monitor blood gases to assess the severity of acidosis in symptomatic patients. Correct severe acidosis (pH < 7.1) with IV sodium bicarbonate (ADULT: 1 to 2 mEq/kg; CHILDREN: 1 mEq/kg). Monitor blood gases to guide bicarbonate therapy.
    G) ENHANCED ELIMINATION
    1) Most likely unnecessary and there is no data on whether it enhances elimination of these substances. Hemodialysis may correct metabolic acidosis, electrolyte abnormalities, and maintains fluid balance.
    H) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic children with unintentional ingestions can be monitored at home with telephone follow up.
    2) OBSERVATION CRITERIA: All symptomatic patients (beyond minor irritation) and those with with deliberate self-harm ingestions should be evaluated in a healthcare facility and monitored until symptoms resolve.
    3) ADMISSION CRITERIA: Patients demonstrating seizure activity, or other persistent neurotoxicity should be admitted.
    4) CONSULT CRITERIA: Call a Poison Center for assistance in managing patients with severe toxicity or in whom the diagnosis is unclear.
    I) PITFALLS
    1) When managing a suspected glycol poisoning, the possibility of coingestants should be considered.
    J) DIFFERENTIAL DIAGNOSIS
    1) CNS depression: Other toxic alcohols, benzodiazepines, opiates/opioids, antipsychotic medications.
    2) Elevated anion gap metabolic acidosis: Ketones, uremia, lactic acidosis, other toxins (eg; ethylene glycol, iron, methanol, etc.), or alcoholic ketoacidosis.
    3) Renal injury: Other nephrotoxic agents (eg, ethylene glycol, NSAIDs, aminoglycoside antibiotics), dehydration.
    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) A worker died after exposure to dioxane levels ranging from 208 to 605 ppm for one week. The probable oral lethal dose of hexylene glycol ranges from 0.5 to 15 g/kg, or 1 oz (28.35 g) to 1 qt (946 mL) for a 70 kg (150 lb) person. Brake oil or brake fluid is composed of a mixture of several glycols, such as ethylene glycol, polyethylene glycol, diethylene glycol, polypropylene glycol and glycol ethers. Survival has occurred after ingestion of 40 to 100 mL of brake fluid.

Clinical Effects

Summary Of Exposure

    A) This document contains information on dioxane, hexylene glycol, pentaethylene glycol, tetraethylene glycol, and triethylene glycol. Information on the following agents are available in separate documents: "DIETHYLENE GLYCOL", "DIPROPYLENE GLYCOL", "ETHYLENE GLYCOL", "ETHYLENE GLYCOL ETHYL ETHER", "ETHYLENE GLYCOL METHYL ETHER", "GLYCOL ETHERS", "POLYETHYLENE GLYCOL", "PROPYLENE GLYCOL".
    B) USES: Glycols are used as solvents for a wide range of products such as paints, lacquers, varnishes, plastics, waxes, resins, fats, oils, and ethers. They are also used in cosmetics, automotive brake fluid, textile processing, stains, dye baths, and printing.
    C) EPIDEMIOLOGY: Limited data. Exposure rarely causes significant toxicity.
    D) WITH POISONING/EXPOSURE
    1) Glycols included in this management may cause irritation of eyes, skin, and mucous membranes.
    2) DIOXANE: Exposure to dioxane may cause irritation of eyes, skin, and mucous membranes. Dermatitis has been reported following the direct contact of the skin with liquid dioxane. Exposure to high concentrations of dioxane vapor may result in nausea and vomiting.
    a) CNS depression with headache, dizziness, drowsiness, and coma have been reported following exposure to high concentrations of dioxane. Hemorrhagic nephritis, centrilobular liver necrosis, severe epigastric pain, convulsion, and coma developed in workers who died following inhalational exposure to high concentrations of dioxane; however, the causal relationship to dioxane is not clear.

Heent

    3.4.1) SUMMARY
    A) Eye irritation may occur with any of the glycols.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) IRRITATION - Ocular exposure to any of the glycols may result in immediate discomfort with mild temporary conjunctival inflammation, blepharospasm, and lacrimation, but no significant corneal damage (HSDB - Hazardous Substances Data Bank, 2007; US Department of Labor Occupational Safety & Health Administration, 2003; S Sweetman , 2001; Grant & Schuman, 1993; Reinhardt et al, 1978; Carpenter & Smyth, 1946; Carpenter et al, 1956; McLaughlin, 1946).
    2) DIOXANE: Eye irritation has been reported following exposure to the following concentrations of 1,4-dioxane: 200 or 300 ppm for 15 minutes, 1600 ppm for 10 minutes, or 5500 ppm for 1 minute (HSDB - Hazardous Substances Data Bank, 2007; DeRosa et al, 1996). Another study reported mild eye irritation following exposure to 50 ppm of 1,4-dioxane for 6 hours (Young et al, 1977).
    3.4.5) NOSE
    A) IRRITATION - Nasal irritation has been noted during industrial exposures to some glycol vapors (HSDB - Hazardous Substances Data Bank, 2007; Carpenter et al, 1956).
    B) DIOXANE: Nasal irritation has been reported following exposure to the following 1,4-dioxane concentrations: 200 or 300 ppm for 15 minutes, 1600 ppm for 10 minutes, or 5500 ppm for 1 minute (HSDB - Hazardous Substances Data Bank, 2007; DeRosa et al, 1996).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) DIOXANE: Throat irritation has been reported following exposure to the following 1,4-dioxane concentrations: 200 or 300 ppm for 15 minutes, 1600 ppm for 10 minutes, or 5500 ppm for 1 minute (HSDB - Hazardous Substances Data Bank, 2007; DeRosa et al, 1996).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) INJURY OF UPPER RESPIRATORY TRACT
    1) Irritation and burning cough may occur following inhalation of glycols (HSDB - Hazardous Substances Data Bank, 2007; US Department of Labor Occupational Safety & Health Administration, 2003; Wills et al, 1974).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) DIOXANE: CNS depression with headache, dizziness, drowsiness, and coma have been reported following exposure to high concentrations of dioxane (S Sweetman , 2001); however, the causal relationship to dioxane is not clear.
    b) DIOXANE: Hemorrhagic nephritis, centrilobular liver necrosis, severe epigastric pain, convulsion, and coma developed in workers who died following inhalational exposure to high concentrations of dioxane (DeRosa et al, 1996); however, the causal relationship to dioxane is not clear.

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) DIOXANE: Exposure to high concentrations of dioxane vapor may result in nausea and vomiting (S Sweetman , 2001).
    b) GLYCOL MIXTURE: Nausea and vomiting occurred immediately in 3 patients following ingestion of brake oil containing a mixture of several glycols (Sharma & Jain, 2002).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) TOXIC LIVER DISEASE
    1) WITH POISONING/EXPOSURE
    a) DIOXANE: Liver toxicity was reported in 6 of 74 workers exposed to 1,4-dioxane concentrations (0.02 to 47.8 mg/m(3) (0.006 to 13.3 ppm) for an average duration of 25 years (a cumulative potential exposure of 1840 man-years) (DeRosa et al, 1996).
    B) HEPATIC NECROSIS
    1) WITH POISONING/EXPOSURE
    a) DIOXANE: Hemorrhagic nephritis, centrilobular liver necrosis, severe epigastric pain, convulsion, and coma developed in workers who died following inhalational exposure to high concentrations of dioxane (DeRosa et al, 1996); however, the causal relationship to dioxane is not clear.

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) NEPHRITIS
    1) WITH POISONING/EXPOSURE
    a) DIOXANE: Hemorrhagic nephritis, centrilobular liver necrosis, severe epigastric pain, convulsion, and coma developed in workers who died following inhalational exposure to high concentrations of dioxane (DeRosa et al, 1996); however, the causal relationship to dioxane is not clear.

Acid-Base

    3.11.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Metabolic acidosis has been reported in a patient exposed to triethylene glycol. However, the causal relationship to triethylene glycol is not clear.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) TRIETHYLENE GLYCOL: Severe metabolic acidosis (pH 7.03, PCO2 44 mmHg, PO2 265 mmHg, bicarbonate 11 mmol/L, base excess -20, lactate 2 mmol/L) developed in a 23-year-old woman who ingested an unknown quantity of brake fluid containing triethylene glycol. She recovered following supportive care and ethanol infusion. It is believed that triethylene glycol is metabolized by alcohol dehydrogenase to acidic products resulting in metabolic acidosis (Vassiliadis et al, 1999). Although the study reported that the brake fluid contained 99.9% of triethylene glycol, the following ingredients were listed on the MSDS: 30% to 60% polyglycol ethers, 30% to 60% borate of triethylene glycol monomethyl ether; and 30% to 60% polyglycol (HSDB - Hazardous Substances Data Bank, 2007).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Skin irritation may occur following exposures to glycols (US Department of Labor Occupational Safety & Health Administration, 2003; Clayton & Clayton, 1994c; Johanson & Boman, 1991).
    b) DIOXANE: Dermatitis has been reported following the direct contact of the skin with liquid dioxane (S Sweetman , 2001).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no reproductive studies were found in humans.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) DIOXANE: Dioxane was not teratogenic in rats, (Giavini, 1985; RTECS , 1996). It was teratogenic in chick embryos (Franceschini, 1964). The implications of this study for human reproduction are unclear.
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) DIOXANE: Dioxane was fetotoxic at the highest dose level where some maternal toxicity was also seen and produced specific developmental abnormalities of the musculoskeletal system in the offspring (Giavini, 1985; RTECS , 1996).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) DIOXANE: A physiologically-based pharmacokinetic (PBPK) model has been developed which suggests that a nursing infant might receive more than the US EPAs non-cancer drinking water ingestion rate of 1,4-dioxane in breast milk if the nursing mother was exposed to this chemical in the workplace (Fisher et al, 1997).
    3.20.5) FERTILITY
    A) ANIMAL STUDIES
    1) HEXYLENE GLYCOL: Hexylene glycol did not affect male fertility in rats when given orally at a dose of 148 to 190 mg/kg/day for 130 days (Clayton & Clayton, 1982).
    2) TRIETHYLENE GLYCOL: Monkeys and rats exposed to high levels by inhalation for 12 to 18 months experienced no obvious adverse effects, and had normal fertility (Robertson, 1947).
    3) TETRAETHYLENE GLYCOL:Reproductive studies on tetraethylene glycol in mice have found no embryotoxic or teratogenic activity when given orally to pregnant dams at the very high dose of 11,270 mg/kg during days 7-14 of pregnancy (Piccirillo, 1983).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS107-21-1 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) DIOXANE: Dioxane did not appear to cause cancer in workers exposed for 10 years. In the German MAK/BAT Values, 1,4-dioxane is listed in Category 4 of carcinogens (those known to act typically by nongenotoxic mechanisms). Dioxane may act as a promoter to produce skin tumors.
    B) TRIETHYLENE GLYCOL: At the time of this review, no studies were found on the possible carcinogenic effects of triethylene glycol in humans.
    C) HEXYLENE GLYCOL: At the time of this review, no studies were found on the possible carcinogenic activity of hexylene glycol in humans.
    3.21.3) HUMAN STUDIES
    A) CARCINOGENS
    1) DIOXANE: In the German MAK/BAT Values, 1,4-dioxane is listed in Category 4 of carcinogens (those known to act typically by nongenotoxic mechanisms) (Neumann et al, 1998a).
    B) SKIN TUMORS
    1) DIOXANE: Dioxane may act as a promoter to produce skin tumors (King, 1973).
    C) LACK OF EFFECT
    1) DIOXANE: Dioxane did not appear to cause cancer in workers exposed for 10 years (Buffler, 1978).
    3.21.4) ANIMAL STUDIES
    A) LEUKEMIA AND LYMPHOMA
    1) DIOXANE: Dioxane induced leukemias and lymphomas in rats (RTECS, 2003).
    B) LACK OF EFFECT
    1) DIOXANE: p-Dioxane has been extensively studied for its ability to cause cancer in laboratory animals. Inhalation exposure did not cause liver or nasal cavity tumors in rats (Torkelson, 1974).
    2) DIOXANE: In mice, dioxane did not cause lung tumors following inhalation exposure (Stoner, 1986).
    3) TRIETHYLENE GLYCOL: Was not carcinogenic in rats or monkeys (Fitzhugh & Nelson, 1946; Robertson, 1947).

Genotoxicity

    A) DIOXANE: No increase in chromosome aberrations was seen in workers with chronic dioxane exposure (Thiess et al, 1976). Dioxane produced sister chromatid exchange in hamster ovary cells (RTECS , 1996). It produced DNA inhibition in HeLa cells and DNA damage in rat liver cells (RTECS , 1996). It was not mutagenic in the Ames Salmonella/microsome assay (Nestmann, 1984), or in yeast (Zimmermann, 1985). Dioxane was not mutagenic in five different in vitro assays and in mouse peripheral blood, but was mutagenic in the mouse liver micronucleus assay (Morita & Hayashi, 1998). This could indicate that dioxane might be mutagenic or that it acts by a nongenotoxic mechanism such as errors in repair following cell proliferation (Morita & Hayashi, 1998).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor serum electrolytes in symptomatic patients, those with large, deliberate ingestions, and patients with severe vomiting.
    B) DIOXANE: Monitor vital signs, renal function, liver enzymes, mental status, pulse oximetry in symptomatic patients.
    C) Serum concentrations of these glycols are not widely available or helpful in clinical management.

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) A simple extraction and derivatization procedure for the analysis of eight different glycols (ethylene glycol, diethylene glycol, triethylene glycol, 1,2-propanediol, 1,3-propanediol, 1,2-butanediol, 2,3-butanediol and hexylene glycol) using a blood sample is described by Gembus et al (2002). Glycols were detected using gas chromatography-electron impact mass spectrometry following deproteinisation with acetonitrile and derivatization to its mono or di TMS derivative. Other chromatographic methods have been described, but are only able to determine ethylene glycol alone or use specific equipment to detect several different glycols (Gembus et al, 2002).

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) Patients demonstrating seizure activity, or other persistent neurotoxicity should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Asymptomatic children with unintentional ingestions can be managed at home with telephone follow up.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Call a Poison Center for assistance in managing patients with severe toxicity or in whom the diagnosis is unclear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) All symptomatic patients (beyond minor irritation) and those with deliberate self-harm ingestions should be evaluated in a healthcare facility and monitored until symptoms resolve.

Monitoring

    A) Monitor serum electrolytes in symptomatic patients, those with large, deliberate ingestions, and patients with severe vomiting.
    B) DIOXANE: Monitor vital signs, renal function, liver enzymes, mental status, pulse oximetry in symptomatic patients.
    C) Serum concentrations of these glycols are not widely available or helpful in clinical management.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Severe toxicity from these agents is rare, and absorption of liquids is generally rapid. Activated charcoal should be considered in the rare case of a recent, large ingestion in a patient who is awake and alert or in whom the airway is protected.
    B) ACTIVATED CHARCOAL
    1) 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.
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) Activated charcoal may be considered in patients who are alert or in whom the airway is protected after a large, recent ingestion.
    2) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    3) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    B) ACIDOSIS
    1) TRIETHYLENE GLYCOL: Metabolic acidosis has been reported in a patient exposed to triethylene glycol. However, the causal relationship to triethylene glycol is not clear.
    2) Monitor blood gases to assess the severity of acidosis in symptomatic patients.
    3) METABOLIC ACIDOSIS: Treat severe metabolic acidosis (pH less than 7.1) with sodium bicarbonate, 1 to 2 mEq/kg is a reasonable starting dose(Kraut & Madias, 2010). Monitor serum electrolytes and arterial or venous blood gases to guide further therapy.
    C) MONITORING OF PATIENT
    1) Monitor serum electrolytes in symptomatic patients, those with large ingestions, and those with severe vomiting.
    2) DIOXANE: Monitor vital signs, renal function, liver enzymes, mental status, pulse oximetry in symptomatic patients.

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) 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).

Enhanced Elimination

    A) HEMODIALYSIS
    1) Most likely unnecessary and there is no data on whether it enhances elimination of these substances. Hemodialysis may correct metabolic acidosis, electrolyte abnormalities, and maintains fluid balance.

Range Of Toxicity

Summary

    A) A worker died after exposure to dioxane levels ranging from 208 to 605 ppm for one week. The probable oral lethal dose of hexylene glycol ranges from 0.5 to 15 g/kg, or 1 oz (28.35 g) to 1 qt (946 mL) for a 70 kg (150 lb) person. Brake oil or brake fluid is composed of a mixture of several glycols, such as ethylene glycol, polyethylene glycol, diethylene glycol, polypropylene glycol and glycol ethers. Survival has occurred after ingestion of 40 to 100 mL of brake fluid.

Minimum Lethal Exposure

    A) DIOXANE: A worker died after exposure to dioxane levels ranging from 208 to 605 ppm for one week (Hathaway et al, 1996).
    B) HEXYLENE GLYCOL: The probable oral lethal dose of hexylene glycol ranges from 0.5 to 15 g/kg, or 1 oz (28.35 g) to 1 qt (946 mL) for a 70 kg (150 lb) person (HSDB , 1997).

Maximum Tolerated Exposure

    A) Brake oil or brake fluid is composed of a mixture of several glycols, such as ethylene glycol, polyethylene glycol, diethylene glycol, polypropylene glycol and glycol ethers. Survival has occurred after ingestion of 40 to 100 mL of brake fluid (Sharma & Jain, 2002).
    B) ANIMAL STUDIES
    1) HEXYLENE GLYCOL: Rats exposed to 590 mg/kg/day for 8 months experienced no adverse effects (Clayton & Clayton, 1994a).
    2) HEXYLENE GLYCOL: Rabbits exposed for 90 days by inunction of 0.92 g/kg/day to the skin experienced no effects (Clayton & Clayton, 1994a).

Workplace Standards

    A) ACGIH TLV Values for CAS107-21-1 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Ethylene glycol
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling: 100 mg/m(3)
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: H
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) H: Aerosol only
    c) TLV Basis - Critical Effect(s): URT and eye irr
    d) Molecular Weight: 62.07
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS107-21-1 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Ethylene glycol
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix D
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS107-21-1 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Ethylene glycol
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Ethylene glycol
    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: Ethylene glycol
    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 CAS107-21-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) DIOXANE
    1) LD50- (ORAL)MOUSE:
    a) 5300 mg/kg (RTECS, 2003)
    2) LD50- (ORAL)RAT:
    a) 4200 mg/kg (RTECS, 2003)
    B) HEXYLENE GLYCOL
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 1299 mg/kg (RTECS, 2003; HSDB , 1997; Hathaway et al, 1996; Clayton & Clayton, 1994a)
    2) LD50- (ORAL)MOUSE:
    a) 3097 mg/kg (RTECS, 2003; HSDB , 1997; Hathaway et al, 1996; Clayton & Clayton, 1994a)
    b) 3.5 g/kg (RTECS, 2003; HSDB , 1997; Hathaway et al, 1996; Clayton & Clayton, 1994a)
    3) LD50- (ORAL)RAT:
    a) 3696 mg/kg (RTECS, 2003; HSDB , 1997; Hathaway et al, 1996; Clayton & Clayton, 1994a)
    b) 3700 mg/kg (RTECS, 2003; HSDB , 1997; Hathaway et al, 1996; Clayton & Clayton, 1994a)
    c) 4760 mg/kg (RTECS, 2003; HSDB , 1997; Hathaway et al, 1996; Clayton & Clayton, 1994a)
    d) 31,640 mg/kg/14D (RTECS, 2003; HSDB , 1997; Hathaway et al, 1996; Clayton & Clayton, 1994a)
    e) 4.79 g/kg (RTECS, 2003; HSDB , 1997; Hathaway et al, 1996; Clayton & Clayton, 1994a)
    f) 4.70 g/kg (RTECS, 2003; HSDB , 1997; Hathaway et al, 1996; Clayton & Clayton, 1994a)

Physicochemical

Molecular Weight

    A) Dioxane: 88.11 (S Sweetman , 2001)
    B) Triethylene glycol: 150.17 (HSDB , 2000)

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