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MALEIC ANHYDRIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Maleic anhydride is an important industrial chemical used as a chemical intermediate or in the production of resins and coatings. It hydrolyzes rapidly in water to the acid, so it quickly degrades to maleic acid if spilled in water (HSDB , 1994).
    B) Exposure to maleic anhydride would be primarily limited to occupational settings. Human exposure would usually be from contact with spills, fugitive emissions, or vent gases (HSDB , 1994).
    C) This management does NOT cover toxicity of styrene maleic anhydride.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C4-H2-O3 OCOCH:CHCO

Available Forms Sources

    A) FORMS
    1) Maleic anhydride has been described as: fused black or white crystals; colorless needles; and, orthorhombic needles from chloroform, also readily by sublimation (ACGIH, 1986; Budavari, 1989; Lewis, 1992; Sax & Lewis, 1987).
    2) Commercial grades are furnished in fused form, as briquettes (Budavari, 1989).
    B) USES
    1) It is used: in Diels-Alder syntheses (as a dienophile); in co-polymerization reactions; in manufacture of alkyd-type of resins; as dye intermediates; in pharmaceuticals; in agricultural chemicals (maleic hydrazide, Malathion); as a pesticide; in fumaric and tartaric acid manufacture; as preservative for oils and fats; in manufacture of polyester resins; and, in permanent press fabrics (ACGIH, 1986; Budavari, 1989; Lewis, 1992; Sax & Lewis, 1987).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) INHALATION may produce coughing, nausea, nervousness, respiratory difficulties, cardiovascular system disorders, nosebleed, headache, sneezing, throat irritation.
    1) Workers exposed to vapors from heated maleic anhydride developed an intense burning sensation in the eyes and throat, with cough and vomiting.
    2) Pulmonary edema may develop.
    B) DERMAL - Skin contact causes irritation, and redness.
    C) EYE - Vapors cause severe eye irritation and conjunctivitis, photophobia, and double vision, temporary visual impairment.
    1) Exposure to high fume concentrations caused photophobia, double vision, and a visual phenomenon of seeing rings around lights.
    0.2.4) HEENT
    A) Headache may occur.
    B) Eye irritation may lead to conjunctivitis, keratitis, photophobia, double vision, and visual impairment.
    C) Irritation may lead to nosebleed.
    0.2.6) RESPIRATORY
    A) Chronic exposure to maleic anyhdride may lead to bronchitis or to development of occupational asthma.
    0.2.8) GASTROINTESTINAL
    A) Nauesa and/or anorexia may occur after exposure.
    0.2.9) HEPATIC
    A) Animal data would indicate possible hemorrhage in the liver with serious exposures.
    0.2.13) HEMATOLOGIC
    A) Hemolytic anemia and pulmonary hemorrhage have been attributed to maleic anhydride toxicity, but the relationship is not clearcut.
    0.2.14) DERMATOLOGIC
    A) Maleic anhydride is a sensitizing agent which may cause erythema, vesiculation, or dermatitis, depending on concentration and length of exposure.
    0.2.15) MUSCULOSKELETAL
    A) Exposed animals developed weakness.
    0.2.19) IMMUNOLOGIC
    A) No clinically significant effects seen.
    0.2.20) REPRODUCTIVE
    A) Human data not available. Rats tested with up to 140 mg/kg did not develop effects.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

    A) Monitor pulse oximetry and/or ABGs, chest x-ray, and pulmonary function tests in symptomatic patients.
    B) Monitor CBC, urinalysis, and liver and kidney function tests in patients with significant exposure.

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) After dilution care is symptomatic and supportive. Patients should be observed for potential irritant/corrosive damage.
    C) NOT RECOMMENDED -
    1) Induced emesis, gastric lavage, and administration of activated charcoal/cathartic are NOT recommended.
    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) INHALATION: Administer oxygen. If respiratory symptoms develop obtain chest x-ray, monitor pulse oximetry and/or blood gases. Treat bronchospasm with inhaled beta2-adrenergic agonists. If acute lung injury develops, consider PEEP. Evaluate for esophageal, dermal and eye burns as indicated.
    0.4.4) EYE EXPOSURE
    A) CAUSTIC EYE DECONTAMINATION: Immediately irrigate each affected eye with copious amounts of water or sterile 0.9% saline for about 30 minutes. Irrigating volumes up to 20 L or more have been used to neutralize the pH. After this initial period of irrigation, the corneal pH may be checked with litmus paper and a brief external eye exam performed. Continue direct copious irrigation with sterile 0.9% saline until the conjunctival fornices are free of particulate matter and returned to pH neutrality (pH 7.4). Once irrigation is complete, a full eye exam should be performed with careful attention to the possibility of perforation.
    B) EYE ASSESSMENT: The extent of eye injury (degree of corneal opacification and perilimbal whitening) may not be apparent for 48 to 72 hours after the burn.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) The minimum lethal human dose to this agent has not been delineated.
    B) Maleic anhydride dust or vapor is an acute skin, eye, and respiratory tract irritant at concentrations of approximately 2 parts per million.

Clinical Effects

Summary Of Exposure

    A) INHALATION may produce coughing, nausea, nervousness, respiratory difficulties, cardiovascular system disorders, nosebleed, headache, sneezing, throat irritation.
    1) Workers exposed to vapors from heated maleic anhydride developed an intense burning sensation in the eyes and throat, with cough and vomiting.
    2) Pulmonary edema may develop.
    B) DERMAL - Skin contact causes irritation, and redness.
    C) EYE - Vapors cause severe eye irritation and conjunctivitis, photophobia, and double vision, temporary visual impairment.
    1) Exposure to high fume concentrations caused photophobia, double vision, and a visual phenomenon of seeing rings around lights.

Heent

    3.4.1) SUMMARY
    A) Headache may occur.
    B) Eye irritation may lead to conjunctivitis, keratitis, photophobia, double vision, and visual impairment.
    C) Irritation may lead to nosebleed.
    3.4.2) HEAD
    A) HEADACHE has been reported after exposure (Keith & Walters, 1985).
    3.4.3) EYES
    A) IRRITATION - Eye irritation may lead to conjunctivitis, keratitis, photophobia, double vision, and visual impairment.
    1) Workers reported eye irritation within 15 minutes at a concentration of 1.5 to 2 ppm. Levels of 2.5 ppm and higher are extremely irritating. One source states eye irritation may be possible at 0.25 ppm (HSDB , 1994).
    B) KERATITIS - Chronic eye irritation, conjunctivitis, and keratitis may result from continued exposure (Rosenberg et al, 1988) Hawthaway, 1991; (Keith & Walters, 1985).
    C) VISION CHANGES - Photophobia, double vision, and temporary visual impairment may occur (Keith & Walters, 1985; HSDB , 1994).
    D) ANIMALS - Both the powder and solutions produced persistent congestion and vascularization of rabbit corneas (Clayton & Clayton, 1981).
    1) Maleic anhydride was corrosive to the rabbit eye when 45 mg of finely ground maleic anhydride was placed into the conjunctival sac of New Zealand albino rabbits (Randall & Healy, 1990).
    3.4.5) NOSE
    A) IRRITATION - Workers reported nasal irritation within 1 minute at a concentration of 1.5 to 2 ppm. Levels of 2.5 ppm and higher are extremely irritating. Some sources say there is a faint odor without irritation at 0.5 ppm (HSDB , 1994).
    B) NOSEBLEED has been reported after exposure (Keith & Walters, 1985; Titiova & Zakirova, 1977).

Respiratory

    3.6.1) SUMMARY
    A) Chronic exposure to maleic anyhdride may lead to bronchitis or to development of occupational asthma.
    3.6.2) CLINICAL EFFECTS
    A) BRONCHITIS
    1) The frequency of chronic bronchitis amoung workers exposed over many years to maleic anhydride is much greater than amoung those with similar exposures to phthalic anhydride (HSDB , 1994).
    B) BRONCHOSPASM
    1) Maleic anhydride is thought to induce occupational asthma, the physiopathology of which is similar to that due to isocyanates (Guerin, 1980; Lee et al, 1991).
    2) CASE REPORT - A 34-year-old heavy smoking male developed cough, rhinitis, dyspnea, and wheezing after a month of exposure to chemicals at an alkyd polyester section of a urea-formaldehyde factory. He had exposure to glue, polystyrene, and alkyd and polystyrene resins.
    a) Symptoms developed within a few minutes of exposure to alkyd or polyurethane resins. He was transferred to another area of the plant after an acute asthma attack. His symptoms completely disappeared.
    b) Two months later he was accidently exposed to maleic anhydride and phthalic-anhydride and developed an immediate acute asthma attack. He reported having no personal or family history of asthma. Bronchoprovocation challenge and skin prick testing was conducted. The patient demonstrated a dual asthmatic reaction maleic anhydride.
    c) The authors conclude that the patient had occupational asthma due to maleic anhydride. The role of smoking and atopy in this case is unclear (HSDB , 1994).
    C) ACUTE LUNG INJURY
    1) Pulmonary edema may develop (Budavari, 1989)
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Rats given fatal oral doses and rabbits exposed dermally showed hemorrhagic or inflammed areas of the lung (Randall & Healy, 1990).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nauesa and/or anorexia may occur after exposure.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA
    1) Nausea has been reported after exposure (Keith & Walter, 1985).
    B) LOSS OF APPETITE
    1) ANIMALS - Anorexia was seen in both rats given oral doses and rabbits dermally exposed (Randall & Healy, 1990). Autopsy of showed fatally exposed animals in both groups showed gastrointestinal tract inflammation.
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CHOLECYSTITIS
    a) ANIMALS - Rabbits exposed dermally were found on autopsy to have enlarged gall bladder and discoloration of spleen and kidneys (Randall & Healy, 1990).

Hepatic

    3.9.1) SUMMARY
    A) Animal data would indicate possible hemorrhage in the liver with serious exposures.
    3.9.2) CLINICAL EFFECTS
    A) HEMORRHAGE OF LIVER
    1) ANIMALS - Rats given fatal oral doses and rabbits exposed dermally showed hyperemic, discolored, or hemorrhagic areas of the liver (Randall & Healy, 1990).

Hematologic

    3.13.1) SUMMARY
    A) Hemolytic anemia and pulmonary hemorrhage have been attributed to maleic anhydride toxicity, but the relationship is not clearcut.
    3.13.2) CLINICAL EFFECTS
    A) HEMOLYTIC ANEMIA
    1) Hemolytic anemia and pulmonary hemorrhage has been seen after exposure, but the actual relationship of maleic anhydride to autoimmune hemolytic anemia is unclear (Jackson & Jones, 1993) Ganon et al, 1992; (Rosenberg et al, 1988).
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ERYTHROCYTES ABNORMAL
    a) IN-VITRO STUDIES
    1) Human red cells treated with maleic anhydride developed increased potassium permeability, increased sodium permeability (less extent), and decreased sulfate and chloride permeability (RTECS , 1994).
    2) Rats given 0,10,32, and 100 mg/kg/day for 2 years developed red blood cell count (at 6 months, decreased in males at all dose levels, females at high and low dose levels; at 12 months, decreased for males at low dose), and hematocrit levels (at 6 months, decreased for males at high and low doses) (HSDB , 1994).

Dermatologic

    3.14.1) SUMMARY
    A) Maleic anhydride is a sensitizing agent which may cause erythema, vesiculation, or dermatitis, depending on concentration and length of exposure.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Skin testing has shown sensitizing action (HSDB , 1994; Hathaway et al, 1991).
    B) CHEMICAL BURN
    1) On dry skin the dust may result in a delayed burning sensation, but on moist skin the sensation is almost immediate, producing erythema, which may progress to vesiculation.
    2) Prolonged or repeated exposure also may cause dermatitis (Hathaway et al, 1991).
    3) Causes smarting of the skin and first-degree burns on short exposure; may cause secondary burns on long exposure (CHRIS , 1994).
    C) SKIN IRRITATION
    1) ANIMAL STUDIES
    a) Maleic anhydride was corrosive to New Zealand albino rabbit skin when responses were scored in accordance with the Federal Hazardous Substances Act (HSDB , 1994).
    b) Maleic anhydride was not corrosive to New Zealand albino rabbit skin when responses were scored in accordance with Classification of Corrosive Hazards - Department of Transportation (Randall & Healy, 1990).

Musculoskeletal

    3.15.1) SUMMARY
    A) Exposed animals developed weakness.
    3.15.2) CLINICAL EFFECTS
    A) MUSCLE WEAKNESS
    1) ANIMALS - Rabbits exposed dermally and rats given oral doses developed weakness (Randall & Healy, 1990).

Immunologic

    3.19.1) SUMMARY
    A) No clinically significant effects seen.
    3.19.2) CLINICAL EFFECTS
    A) DECREASED IMMUNOGLOBULIN
    1) Maleic anhydride caused the complete disappearance of precipitating activity of human gamma-globulins (HSDB , 1994).

Reproductive

    3.20.1) SUMMARY
    A) Human data not available. Rats tested with up to 140 mg/kg did not develop effects.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) Human data not available. Rats tested with up to 140 mg/kg did not develop effects.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    B) ANIMAL STUDIES
    1) RATS - Up to 140 mg per kilogram was given to rats on days 6 to 15. No treatment related fetal effects were noted. No ill effects were seen in a two generation study with doses of 55 mg per kilogram (Short et al, 1986).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS108-31-6 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    B) ANIMAL STUDIES
    1) Oncogenicity was evaluated in male and female Fischer 344 rats (504 males, 501 females; number/group not reported) exposed orally to maleic anhydride in the diet at 0, 10, 32 and 100 mg/kg/day for 2 yrs.
    a) Thyroid clear cell ademomas and hyperplasia were seen in females at all dose, but were not considered to be treatment related (HSDB , 1994).

Genotoxicity

    A) At the time of this review, no data were available to assess the mutagenic or genotoxic potential of this agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor pulse oximetry and/or ABGs, chest x-ray, and pulmonary function tests in symptomatic patients.
    B) Monitor CBC, urinalysis, and liver and kidney function tests in patients with significant exposure.
    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, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    B) PULMONARY FUNCTION TESTS
    1) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.
    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.

Radiographic Studies

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

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor pulse oximetry and/or ABGs, chest x-ray, and pulmonary function tests in symptomatic patients.
    B) Monitor CBC, urinalysis, and liver and kidney function tests in patients with significant exposure.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Maleic anhydride is irritating to tissues. Methods to decrease absorption such as activated charcoal or gastric lavage are not likely to be beneficial. Dilution with small amounts of water may be useful soon after exposure.
    B) EMESIS/NOT RECOMMENDED
    1) Emesis is CONTRAINDICATED due to the irritant nature of this material.
    C) ACTIVATED CHARCOAL
    1) Not recommended due to the irritant nature of this material.
    6.5.3) TREATMENT
    A) SUPPORT
    1) There is no specific antidote. Treatment is symptomatic and supportive for potential skin, eye, or oral irritation. Irrigation and dilution may be indicated.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).

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) SUPPORT
    1) CAUSTIC INHALATION: Administer humidified oxygen, and remove from exposure. Monitor patient for respiratory distress; if a cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, and pneumonitis.
    2) Patients with upper airway burns may develop significant edema abruptly; early intubation is advised.
    3) Determine pulse oximetry and/or blood gases, obtain chest x-ray, perform endotracheal intubation and provide mechanical ventilation as clinically indicated.
    4) Administer inhaled beta2-adrenergic agonists in patients with bronchospasm (National Heart,Lung,and Blood Institute, 2007). If acute lung injury develops, consider PEEP (Haas, 2011; Leaver & Evans, 2007; Stolbach & Hoffman, 2011).
    5) Evaluate for esophageal, dermal and eye burns as indicated.
    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) 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) GENERAL TREATMENT
    1) CAUSTICS - MEDICAL FACILITY IRRIGATION -
    a) Begin irrigation immediately with copious amounts of water or sterile 0.9% saline, which ever is more rapidly available. Lactated Ringer's solution may also be effective. Once irrigation has begun, instill a drop of local anesthetic (eg, 0.5% proparacaine) for comfort; switching from water to slightly warmed sterile saline may also improve patient comfort (Singh et al, 2013; Spector & Fernandez, 2008; Ernst et al, 1998; Grant & Schuman, 1993). In one study, isotonic saline, lactated Ringer's solution, normal saline with bicarbonate, and balanced saline plus (BSS Plus) were compared and no difference in normalization of pH were found; however, BSS Plus was better tolerated and more comfortable (Fish & Davidson, 2010).
    1) Continue irrigation for at least an hour or until the superior and inferior cul-de-sacs have returned to neutrality (check pH every 30 minutes), pH of 7.0 to 8.0, and remain so for 30 minutes after irrigation is discontinued (Spector & Fernandez, 2008; Brodovsky et al, 2000a). After severe alkaline burns, the pH of the conjunctival sac may only return to a pH of 8 or 8.5 even after extensive irrigation (Grant & Schuman, 1993). Irrigating volumes up to 20 L or more have been used to neutralize the pH (Singh et al, 2013; Fish & Davidson, 2010). Immediate and prolonged irrigation is associated with improved visual acuity, shorter hospital stay and fewer surgical interventions (Kuckelkorn et al, 1995; Saari et al, 1984).
    2) Search the conjunctival sac for solid particles and remove them while continuing irrigation (Grant & Schuman, 1993).
    3) For significant alkaline or concentrated acid burns with evidence of eye injury irrigation should be continued for at least 2 to 3 hours, potentially as long as 24 to 48 hours if pH not normalized, in an attempt to normalize the pH of the anterior chamber (Smilkstein & Fraunfelder, 2002). Emergent ophthalmologic consultation is needed in these cases (Spector & Fernandez, 2008).
    2) DAMAGE ASSESSMENT -
    a) ASSESSMENT CAUSTIC EYE BURNS: It may take 48 to 72 hours after the burn to assess correctly the degree of ocular damage (Brodovsky et al, 2000).
    b) The 1965 Roper-Hall classification uses the size of the corneal epithelial defect, the degree of corneal opacification and extent of limbal ischemia to evaluate the extent of the chemical ocular injury (Brodovsky et al, 2000; Singh et al, 2013):
    1) GRADE 1 (prognosis good): Corneal epithelial damage; no limbal ischemia.
    2) GRADE 2 (prognosis good): Cornea hazy; iris details visible, ischemia less than one-third of limbus.
    3) GRADE 3 (prognosis guarded): Total loss of corneal epithelium; stromal haze obscures iris details; ischemia of one-third to one-half of limbus.
    4) GRADE 4 (prognosis poor): Cornea opaque; iris and pupil obscured, ischemia affects more than one-half of limbus.
    c) A newer classification (Dua) is based on clock hour limbal involvement as well as a percentage of bulbar conjunctival involvement (Singh et al, 2013):
    1) GRADE 1 (prognosis very good): 0 clock hour of limbal involvement and 0% conjunctival involvement.
    2) GRADE 2 (prognosis good): Less than 3 clock hour of limbal involvement and less than 30% conjunctival involvement.
    3) GRADE 3 (prognosis good): Greater than 3 and up to 6 clock hour of limbal involvement and greater than 30% to 50% conjunctival involvement.
    4) GRADE 4 (prognosis good to guarded): Greater than 6 and up to 9 clock hour of limbal involvement and greater than 50% to 75% conjunctival involvement.
    5) GRADE 5 (prognosis guarded to poor): Greater than 9 and less than 12 clock hour of limbal involvement and greater than 75% and less than 100% conjunctival involvement.
    6) GRADE 6 (very poor): Total limbus (12 clock hour) involved and 100% conjunctival involvement.
    3) MINOR DAMAGE -
    a) SUMMARY
    1) If ocular damage is minor, artificial tears/lubricants, topical cycloplegics, and antibiotics may be all that are needed.
    b) ARTIFICIAL TEARS
    1) To promote re-epithelization, preservative-free artificial tears/lubricants (eg, hyaluronic acid hourly) may be used (Fish & Davidson, 2010; Tuft & Shortt, 2009).
    c) TOPICAL CYCLOPLEGIC
    1) Use to guard against development of posterior synechiae and ciliary spasm (Brodovsky et al, 2000b; Grant & Schuman, 1993). Cyclopentolate 0.5% or 1% eye drops may be administered 4 times daily to control pain (Tuft & Shortt, 2009; Spector & Fernandez, 2008).
    d) TOPICAL ANTIBIOTICS
    1) An antibiotic ophthalmic ointment or drops should be used for as long as epithelial defects persist (Brodovsky et al, 2000b; Grant & Schuman, 1993). Topical erythromycin or tetracycline ointment may be used (Spector & Fernandez, 2008).
    e) PAIN CONTROL
    1) If pain control is required, oral or parenteral NSAIDs or narcotics are preferred to topical ocular anesthetics, which may cause local corneal epithelial damage if used repeatedly (Spector & Fernandez, 2008; Grant & Schuman, 1993). However, topical 0.5% proparacaine has been recommended (Spector & Fernandez, 2008).
    4) EXTENSIVE DAMAGE -
    a) SUMMARY
    1) If the damage is minor, the above may be all that is needed. For grade 3 or 4 injuries, one or more of the following may be used, only with ophthalmologic consultation: acetazolamide, topical timolol, topical steroids, citrate, ascorbate, EDTA, cysteine, NAC, penicillamine, tetracycline, or soft contact lenses.
    b) ARTIFICIAL TEARS
    1) To promote re-epithelization, preservative-free artificial tears/lubricants (eg, hyaluronic acid hourly) may be used (Fish & Davidson, 2010; Tuft & Shortt, 2009).
    c) PAIN CONTROL
    1) If pain control is required, oral or parenteral NSAIDs or narcotics are preferred to topical ocular anesthetics, which may cause local corneal epithelial damage if used repeatedly (Spector & Fernandez, 2008; Grant & Schuman, 1993). However, topical 0.5% proparacaine has been recommended (Spector & Fernandez, 2008).
    d) CARBONIC ANHYDRASE INHIBITOR
    1) Acetazolamide (250 mg orally 4 times daily) may be given to control increased intraocular pressure (Singh et al, 2013; Tuft & Shortt, 2009; Spector & Fernandez, 2008).
    e) TOPICAL STEROIDS
    1) DOSE: Dexamethasone 0.1% ointment 4 times daily to reduce inflammation. If persistent epithelial defect is present, discontinue dexamethasone by day 14 to reduce the risk of stromal melt (Tuft & Shortt, 2009). Other sources suggest that corticosteroids should be stopped if the epithelium has not covered surface defects by 5 to 7 days (Grant & Schuman, 1993a).
    2) Topical prednisolone 0.5% has also been used. A further increase in corneoscleral melt may occur if topical steroids are used alone. In one study, topical prednisolone 0.5% was used in combination with topical ascorbate 10%; no increase in corneoscleral melt was observed when topical steroids were used until re-epithelization (Singh et al, 2013; Fish & Davidson, 2010).
    3) In one retrospective study, fluorometholone 1% drops were administered every 2 hours initially, then decreased to four times daily when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete (Brodovsky et al, 2000a).
    a) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000a).
    f) ASCORBATE
    1) Oral or topical ascorbate may be used to promote epithelial healing and reduce the risk of stromal necrosis (Fish & Davidson, 2010).
    2) DOSE: Ascorbate 10% 4 times daily topically or 1 g orally (2 g/day) (Singh et al, 2013; Tuft & Shortt, 2009).
    3) Ascorbate is needed for the formation of collagen and the concentration of ascorbate in the anterior chamber is decreased when the ciliary body is damaged by alkali burns (Tuft & Shortt, 2009; Grant & Schuman, 1993a). In one retrospective study, ascorbate drops (10%) were administered every 2 hours, then decreased to 4 times a day when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete. These patients also received 500 mg of oral ascorbate 4 times daily, until discharge from the hospital (Brodovsky et al, 2000a).
    a) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000a).
    g) CITRATE
    1) Topical citrate may be used to promote epithelial healing and reduce the risk of stromal necrosis (Fish & Davidson, 2010).
    2) DOSE: Potassium citrate 10% 4 times daily topically (Tuft & Shortt, 2009).
    3) Citrate chelates calcium, and thereby interferes with the harmful effects of neutrophil accumulation, such as release of proteolytic enzymes and superoxide free radicals, phagocytosis and ulceration (Grant & Schuman, 1993a). In one retrospective study, 10% citrate drops were administered every 2 hours, then decreased to 4 times a day when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete. These patients also received a urinary alkalinizer containing 720 mg of citric acid anhydrous and 630 mg of sodium citrate anhydrous 3 times daily, until discharge from the hospital (Brodovsky et al, 2000a).
    a) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000a).
    h) COLLAGENASE INHIBITORS
    1) Inhibitors of collagenase can inhibit collagenolytic activity, prevent stromal ulceration, and promote wound healing. Several effective agents, such as cysteine, n-acetylcysteine, sodium ethylenediamine tetra acetic acid (EDTA), calcium EDTA, penicillamine, and citrate, have been recommended (Singh et al, 2013; Tuft & Shortt, 2009; Perry et al, 1993; Seedor et al, 1987).
    2) TETRACYCLINE: Has been found to have an anticollagenolytic effect. Systemic tetracycline 50 mg/kg/day reduced the incidence of alkali-induced corneal ulcerations in rabbits (Seedor et al, 1987).
    3) DOXYCYCLINE: Decreased epithelial defects and collagenase activity in a rabbit model of alkali burns to the eye (Perry et al, 1993). DOSE: 100 mg twice daily (Tuft & Shortt, 2009).
    i) ANTIBIOTICS
    1) An antibiotic ophthalmic ointment or drops should be used for as long as epithelial defects persist (Brodovsky et al, 2000b; Grant & Schuman, 1993). Topical erythromycin or tetracycline ointment may be used (Spector & Fernandez, 2008). In patients with severe burns, a topical fluoroquinolone antibiotic drop 4 times daily may also be used (Tuft & Shortt, 2009). A topical fourth generation fluoroquinolone has been recommended as an antimicrobial prophylaxis in patients with large epithelial defect (Fish & Davidson, 2010).
    j) TOPICAL CYCLOPLEGIC
    1) Cyclopentolate 0.5% or 1% eye drops may be administered 4 times daily to control pain (Tuft & Shortt, 2009; Spector & Fernandez, 2008).
    k) SOFT CONTACT LENSES
    1) A bandage contact lens (eg, silicone hydrogel) may make the patient more comfortable and protect the surface (Fish & Davidson, 2010; Tuft & Shortt, 2009). Hydrophilic high oxygen permeability lenses are preferred (Singh et al, 2013). Soft lenses with intermediate water content and inherent rigidity may facilitate reepithelialization. The use of 0.5 normal sodium chloride drops hourly and artificial tears or lubricant eyedrops instilled 4 times a day may help maintain adequate hydration and lens mobility.
    5) LATE TREATMENT -
    a) SURGICAL THERAPY CAUSTIC EYE INJURY
    1) Early insertion of methylmethacrylate ring or suturing saran wrap over palpebral and cul-de-sac conjunctiva may prevent fibrinosis adhesions and reduce fibrotic contracture of conjunctiva, but the advantage of such treatments is not clear.
    2) Limbal stem cell transplantation has been used successfully in both the acute stage of injury and the chronically scarred healing phase in patients with persistent epithelial defects after chemical burns (Azuara-Blanco et al, 1999; Morgan & Murray, 1996; Ronk et al, 1994).
    3) In some patients, amniotic membrane transplantation (AMT) has been successful in improving corneal healing and visual acuity in patients with persistent epithelial defects after chemical burns. It can restore the conjunctival surface and decrease limbal stromal inflammation (Fish & Davidson, 2010; Sridhar et al, 2000; Su & Lin, 2000; Meller et al, 2000; Azuara-Blanco et al, 1999).
    4) Control glaucoma. Remove any cataracts formed (Fish & Davidson, 2010; Tuft & Shortt, 2009).
    5) In patients with severe injury, tenonplasty can be performed to promote epithelialization and prevent melting (Tuft & Shortt, 2009).
    6) A keratoprosthesis placement has also been indicated in severe cases (Fish & Davidson, 2010). Penetrating keratoplasty is usually delayed as long as possible as results appear to be better with a greater lag time between injury and keratoplasty (Grant & Schuman, 1993).
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) IRRIGATION (WATER ONLY) -
    a) Remove contaminated clothing and jewelry and irrigate exposed areas with copious amounts of water. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) BURN
    1) APPLICATION
    a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.
    2) DEBRIDEMENT
    a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
    b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
    c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).
    3) TREATMENT
    a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
    b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
    c) WOUND DRESSING:
    1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
    2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.
    d) DRESSING CHANGES:
    1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
    2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.
    e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.
    4) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EFFICACY
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.

Range Of Toxicity

Summary

    A) The minimum lethal human dose to this agent has not been delineated.
    B) Maleic anhydride dust or vapor is an acute skin, eye, and respiratory tract irritant at concentrations of approximately 2 parts per million.

Minimum Lethal Exposure

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

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) Exposure of humans to a concentration of 1.5 to 2 ppm resulted in nasal irritation within 1 minute and eye irritation after 15 to 20 minutes (Hathaway et al, 1991).
    2) Among workers repeatedly exposed to 1.25 to 2.5 ppm, effects were ulceration of nasal mucous membranes, chronic bronchitis, and, in some cases, asthma (Hathaway et al, 1991).
    3) Levels of 2.5 ppm and higher are extremely irritating (ACGIH, 1986).
    4) Workers exposed to vapors from heated maleic anhydride developed an intense burning sensation in the eyes and the throat, with cough and vomiting. Exposure to high fume concentrations caused photophobia, double vision, and a visual phenomenon of seeing rings around lights (Hathaway et al, 1991).
    B) ANIMAL DATA
    1) An inhalation study of rats, hamsters, and monkeys exposed to 1.1, 3.3, or 9.8 mg/m(3), 6 hours/day, 5 days/week for 6 months, revealed dose-related signs of nasal and ocular irritations including discharge, sneezing, gasping, and coughing for all species (Hathaway et al, 1991).

Workplace Standards

    A) ACGIH TLV Values for CAS108-31-6 (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) Maleic anhydride
    a) TLV:
    1) TLV-TWA: (0.1 ppm)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: SEN
    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) SEN: The designation SEN refers to the potential for an agent to produce sensitization, as confirmed by human or animal data. The notation does not imply that this is the critical effect or that this is the sole basis for the TLV. Although, for those TLVs that are based on sensitization, the TLV is meant to protect workers from induction of this effect, but cannot protect workers who have already become sensitized. The notation should be used to assist in identifying sensitization hazards and reducing respiratory, dermal, and conjunctival exposures to sensitizing agents in the workplace. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): (Eye, URT, and skin irr)
    d) Molecular Weight: 98.06
    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:
    1) See Notice of Intended Changes; Adopted values enclosed in parentheses are those for which changes are proposed in the Notice of Intended Changes.
    b) Notice of Intended Changes
    1) Maleic anhydride
    a) TLV:
    1) TLV-TWA: 0.01 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: IFV, SEN
    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) IFV: Inhalable fraction and vapor.
    c) SEN: The designation SEN refers to the potential for an agent to produce sensitization, as confirmed by human or animal data. The notation does not imply that this is the critical effect or that this is the sole basis for the TLV. Although, for those TLVs that are based on sensitization, the TLV is meant to protect workers from induction of this effect, but cannot protect workers who have already become sensitized. The notation should be used to assist in identifying sensitization hazards and reducing respiratory, dermal, and conjunctival exposures to sensitizing agents in the workplace. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): Resp sens
    d) Molecular Weight: 98.06
    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 CAS108-31-6 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Maleic anhydride
    2) REL:
    a) TWA: 1 mg/m(3) (0.25 ppm)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 10 mg/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS108-31-6 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Maleic anhydride
    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) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Maleic anhydride
    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.
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Maleic anhydride
    4) 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
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Maleic anhydride
    6) MAK (DFG, 2002): Not Listed
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS108-31-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Maleic anhydride
    2) Table Z-1 for Maleic anhydride:
    a) 8-hour TWA:
    1) ppm: 0.25
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 1
    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: Lewis, 1992 RTECS, 1993
    1) LD50- (ORAL)MOUSE:
    a) 465 mg/kg
    2) LD50- (INTRAPERITONEAL)RAT:
    a) 97 mg/kg
    3) LD50- (ORAL)RAT:
    a) 400 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Toxicity may be attributed to a conjugated double bond system which is hightly reactive and may cause enzyme inhibition and protein denaturation (Grant, 1986).

Physicochemical

Physical Characteristics

    A) This compound exists as fused black or white crystals or colorless needles (Lewis, 1992; Sax & Lewis, 1987; ACGIH, 1986). It has a penetrating, acrid, choking odor (CHRIS , 1993; NFPA, 1991). It is generally colorless in solution (OHM/TADS , 1994). Orthorhomic needles are derived from chloroform (HSDB , 1994). The commercial grades are furnished in fused form, as briquettes (Budavari, 1989).

Ph

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

Molecular Weight

    A) 98.06 (Budavari, 1989)

References

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