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METHYL ISOCYANATE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Methyl isocyanate (MIC) is one of a series of agents sharing a similar isocyanate (N=C=O) moiety. MIC is a chemical intermediate in the manufacturing of the carbamate insecticides.
    B) MIC is toxic by inhalation, ingestion, and contact (skin, eyes) with liquid, dust and vapors. Even brief exposure at high concentrations may cause severe injury, burns, or death (Lewis, 2000; Sittig, 1991).

Specific Substances

    1) MIC
    2) Isocyanic acid, methyl ester
    3) CAS 624-83-9
    4) METHYLISOCYANAT (GERMAN)
    5) METHYLISOKYANAT (POLISH)
    6) MIC (METHYL ISOCYANATE)
    1.2.1) MOLECULAR FORMULA
    1) C2-H3-N-O

Available Forms Sources

    A) FORMS
    1) Methyl isocyanate is a colorless liquid with a sharp, pungent odor (NFPA, 1991; (HSDB , 2001).
    B) SOURCES
    1) Methyl isocyanate is produced by heating metal cyanates or by heating N,N-Diphenyl-N'-methylurea (HSDB , 2001).
    C) USES
    1) Methyl isocyanate is primarily used as a chemical intermediate in the production of carbamate insecticides, herbicides, pharmaceuticals. It is also used in the manufacture of polyurethane foams and plastics (Seifter, 1985; HSDB , 2001).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Methyl isocyanate (MIC) is a severe eye, skin, and mucous membrane irritant. MIC exposure, especially large doses, may produce an immunologic response. It may be absorbed through the skin. MIC and its trimer are absorbed via inhalation.
    B) Most deaths from methyl isocyanate are a result of lung tissue damage. Cyanide poisoning does NOT occur following exposure to pure MIC, and empiric antidotal therapy is not warranted. Effects of cyanide poisoning have been noted but this is most likely due to impurities (Sax & Lewis, 1989).
    C) Immediate and persistent respiratory symptoms occurred in about 200,000 local inhabitants of Bhopal, India following an inadvertent release of MIC in 1984. Severe irritation of the eyes, nose, and throat, choking sensation, and cough were the initial symptoms reported from these survivors. Some of those exposed became weak, fainted, and died within minutes. Defecation, urination, and vomiting with colicky abdominal pains occurred.
    1) Survivors sought treatment for symptoms of intense burning of the eyes, photophobia, blepharospasm, profuse lacrimation, lid edema, and superficial corneal ulceration.
    2) Severe dyspnea was common and considered due to focal atelectasis, local inflammation, and acute lung injury.
    3) Respiratory function and visual acuity has remained abnormal among the persons exposed in the Bhopal incident for at least two years (Kamat et al, 1992) and longer in those of close proximity to the 1984 accident (Cullinan & Acquilla, 1997).
    0.2.3) VITAL SIGNS
    A) Acute exposure may cause dyspnea.
    0.2.4) HEENT
    A) Contact with the eye is extremely irritating and may cause permanent damage with cataract formation, trachoma and chronic blepharitis.
    0.2.6) RESPIRATORY
    A) Low concentrations may produce mild respiratory irritation. High concentrations result in cough, dyspnea, increase secretions, chest pain, tightness and asthmatic episodes. Acute lung injury may be seen. Chronic exposures may result in chronic obstructive lung disease.
    0.2.7) NEUROLOGIC
    A) Acute lung injury-induced hypoxia may produce CNS depression.
    0.2.8) GASTROINTESTINAL
    A) Gastrointestinal irritation and vomiting may occur.
    0.2.9) HEPATIC
    A) Decreased liver function may occur.
    0.2.10) GENITOURINARY
    A) Renal tubular necrosis and edema may be noted.
    0.2.11) ACID-BASE
    A) Metabolic acidosis may occur.
    0.2.13) HEMATOLOGIC
    A) Cherry-red blood may be observed.
    0.2.14) DERMATOLOGIC
    A) Skin irritation is likely. Contact can cause chemical burns (Sittig, 1991; HSDB , 2001).
    0.2.19) IMMUNOLOGIC
    A) The immunologic system has been suggested as a mechanism of persistent respiratory and eye effects. Antibodies specific to methyl isocyanate have been demonstrated in the blood of exposed patients in Bhopal, India.
    0.2.20) REPRODUCTIVE
    A) There is conflicting data as to whether methyl isocyanate is fetotoxic, however, it crosses the placental barrier. Reports from Bhopal, India and animal studies suggest a high degree of adverse reproductive effects and teratogenicity.
    0.2.22) OTHER
    A) Cholinesterase inhibition was not found in animals poisoned with methyl isocyanate.

Laboratory Monitoring

    A) Monitor ECG, chest x-ray, pulse oximetry, peak air flows, arterial blood gases, serum electrolytes, and renal and hepatic function in symptomatic patients.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    0.4.3) INHALATION EXPOSURE
    A) Treatment is primarily supportive, with attention directed to treating pulmonary irritation and maintaining adequate ventilation and oxygenation.
    B) Hospitalization and observation for 72 hours is advisable to detect a late onset of acute lung injury (pulmonary edema).
    C) Evaluate chest x-ray, FEV 1, and arterial blood gases.
    D) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    E) BRONCHOSPASM: Treat symptomatically with oxygen, bronchodilators, and steroids.
    0.4.4) EYE EXPOSURE
    A) The liquid in contact with the eye is extremely irritating and may cause permanent damage.
    B) 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.
    C) Topical antibiotics may be useful in secondary infection.
    D) Severe iritis may be treated with topical atropine or homatropine.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

Range Of Toxicity

    A) MAXIMUM TOLERATED EXPOSURE - Two ppm, no odor was detected but irritation and lacrimation were noted. Symptoms were more marked at 4 ppm and unbearable at 21 ppm. Exposures to breathing zone concentrations of 0.5 ppm are likely to produce a respiratory response.

Clinical Effects

Summary Of Exposure

    A) Methyl isocyanate (MIC) is a severe eye, skin, and mucous membrane irritant. MIC exposure, especially large doses, may produce an immunologic response. It may be absorbed through the skin. MIC and its trimer are absorbed via inhalation.
    B) Most deaths from methyl isocyanate are a result of lung tissue damage. Cyanide poisoning does NOT occur following exposure to pure MIC, and empiric antidotal therapy is not warranted. Effects of cyanide poisoning have been noted but this is most likely due to impurities (Sax & Lewis, 1989).
    C) Immediate and persistent respiratory symptoms occurred in about 200,000 local inhabitants of Bhopal, India following an inadvertent release of MIC in 1984. Severe irritation of the eyes, nose, and throat, choking sensation, and cough were the initial symptoms reported from these survivors. Some of those exposed became weak, fainted, and died within minutes. Defecation, urination, and vomiting with colicky abdominal pains occurred.
    1) Survivors sought treatment for symptoms of intense burning of the eyes, photophobia, blepharospasm, profuse lacrimation, lid edema, and superficial corneal ulceration.
    2) Severe dyspnea was common and considered due to focal atelectasis, local inflammation, and acute lung injury.
    3) Respiratory function and visual acuity has remained abnormal among the persons exposed in the Bhopal incident for at least two years (Kamat et al, 1992) and longer in those of close proximity to the 1984 accident (Cullinan & Acquilla, 1997).

Vital Signs

    3.3.1) SUMMARY
    A) Acute exposure may cause dyspnea.
    3.3.2) RESPIRATIONS
    A) Acute exposure may cause dyspnea.

Heent

    3.4.1) SUMMARY
    A) Contact with the eye is extremely irritating and may cause permanent damage with cataract formation, trachoma and chronic blepharitis.
    3.4.3) EYES
    A) IRRITATION - The liquid in contact with the eye is extremely irritating and may cause permanent damage (Rye, 1973). A 40 percent increased incidence of trachoma, 36 percent increased risk of other lid infection and 45 percent increased incidence of irritant symptoms were noted in the exposed population of Bhopal resulting in a "Bhopal eye syndrome" (Andersson et al, 1990).
    B) BLINDNESS - However, no cases of blindness or evidence of permanent damage were found in a survey of 261 patients exposed to methyl isocyanate gas (Andersson et al, 1984). There is a possibly higher incidence of cataracts after exposure (Andersson et al, 1990).
    C) ACUTE EFFECTS - Lacrimation, photophobia, profuse lid edema, and superficial corneal ulcerations, mostly circular, occur immediately after exposure to vapors (Hathaway et al, 1996).
    D) CORNEAL EROSIONS - An animal study indicated eye changes (erosions of the corneal epithelium) were most severe at intermediate levels of exposure (Salmon et al, 1985).
    E) CORNEAL ULCERATION - Corneal ulceration was one of the most common severe effects seen in the Bhopal disaster; secondary infection may occur. Photophobia may persist for a week or longer. In Bhopal survivors, corneal ulcerations healed without scarring in most cases (Bucher, 1987; Grant & Schuman, 1993).
    F) OTHER OCULAR FINDINGS include inferior punctate keratopathy, conjunctival chemosis, iritis, and corneal pigmentation. Cataracts are a potential long-term complication (Harding & Rixon, 1985).
    G) PERSISTENT EYE WATERING - Irritation and persistent eye watering have been reported up to one year following methyl isocyanate gas exposure (Andersson et al, 1986).
    1) A follow-up study three years after the Bhopal methyl isocyanate exposure demonstrated an excess of eyelid infection, decreased visual acuity, cataracts, and eye irritation among survivors as compared to controls. Whether these findings are the result of some generalized condition or strictly primary eye effects from the acute exposure remains unknown (Andersson et al, 1990).

Cardiovascular

    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEART DISORDER
    a) Addition of methyl isocyanate to rabbit cardiac tissue in vitro resulted in a dose-dependent inhibition of sodium-potassium ATPase (Jeevarantam, 1995).

Respiratory

    3.6.1) SUMMARY
    A) Low concentrations may produce mild respiratory irritation. High concentrations result in cough, dyspnea, increase secretions, chest pain, tightness and asthmatic episodes. Acute lung injury may be seen. Chronic exposures may result in chronic obstructive lung disease.
    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) LOW CONCENTRATIONS may produce mild respiratory symptoms which mimic upper respiratory infection. Prolonged exposure to very low levels of methyl isocyanate (0.02 ppm) in an occupational setting did not result in any identifiable pulmonary impairment (Avashia et al, 1996).
    2) HIGH CONCENTRATIONS result in cough, dyspnea, increased secretions, chest pain, tightness, and asthmatic episodes. Sloughing of bronchial epithelium may occur in ventilation-perfusion mismatch and hypoxia (Dhara, 1992). Animal studies have shown extensive necrosis and loss of epithelial cells in the proximal airways with low concentrations and widespread alveolar damage after exposure to high concentrations (Nemery et al, 1985).
    3) LONG-TERM EFFECTS - Evidence of persistent lung changes were present in Bhopal survivors up to 53 days post-exposure (Bucher, 1987). One follow-up study found that there was significant small airways obstruction 10 years after the accident (Cullinan & Acquilla, 1997).
    a) Up to 50% of the patients from Bhopal, India had fluctuations in forced vital capacity, maximum expiratory flow rates, peak expiratory flow rates and Vo2 two-four years after the accident. Lung function showed mainly restrictive changes with small airway obstruction and interstitial deposits (Kamat et al, 1992).
    b) Pulmonary function testing performed 1-7 years after the Bhopal accident demonstrated that deterioration in respiratory function occurred in gas-exposed patients as a consequence of accumulation of inflammatory cells (macrophages and lymphocytes). The intensity of the inflammatory response was greatest in the most severely exposed patients (Vijayan & Sandaru, 1996).
    B) COUGH
    1) In one study, the frequency of cough closely followed the death rate (Andersson et al, 1988).
    C) ACUTE LUNG INJURY
    1) Acute lung injury (pulmonary edema) may occur and was the most common severe effect noted in the accident at Bhopal, India where at least 2000 people were killed (Anon, 1984; Lewis, 2000). Acute respiratory distress syndrome may cause severe pulmonary damage.
    D) BRONCHOSPASM
    1) Asthmatic episodes may occur at low concentrations in sensitized patients, although this has yet to be documented from mono-isocyanates. Respiratory irritant symptoms will develop 4 to 8 hours after onset of exposure, depending on level of concentration, and persist 3 to 7 days. Incidence of methyl isocyanate induced occupational asthma is similar to that of other industrial allergens (Malo et al, 1992).
    E) RESPIRATORY FINDING
    1) CHRONIC TOXICITY
    a) Chronic exposure may result in chronic obstructive lung disease (Peters & Murphy, 1970). Long-term effects on the lungs due to extensive cell destruction may occur from heavy exposure (Anon, 1984). Emphysema, bronchiolitis and pulmonary fibrosis are the most likely long-term effects (Anon, 1985). Chronic exposure to very low levels of methyl isocyanate (0.02ppm) in the occupational setting results in no identifiable pulmonary impairment (Avashia et al, 1996).
    F) ACUTE RESPIRATORY INSUFFICIENCY
    1) Respiratory depression may result from the sensory irritant effect of methyl isocyanate (Ferguson et al, 1986).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RESPIRATORY DISORDER
    a) RATS exposed to 3 to 15 ppm methyl isocyanate for 4 to 8 days showed increased lung weights, pseudostratified regenerative epithelium in the bronchi, and submucosal fibroplasia on necropsy (Dodd & Fowler, 1986).
    b) Radiolabeled methyl isocyanate undergoes selective reactions in specific areas of the airway dependent on respiratory region and cell type. It does not penetrate to the level of the alveoli in guinea pigs (Kennedy et al, 1993).
    c) Animal studies have shown extensive necrosis and loss of epithelial cells in the proximal airways with low concentrations and widespread alveolar damage after exposure to high concentrations (Nemery et al, 1985).
    d) A single exposure to methyl isocyanate caused injury to the pulmonary parenchyma which was reflected by an increase in polymorphonuclear neutrophils, total protein, sialic acids, lactic acid and lactate dehydrogenase in the bronchoalveolar fluid of rats (Gupta, 1993).
    e) In the subacute phase, the intra-alveolar and interstitial edema are prominent in rats exposed to a single high inhalational dose of methyl isocyanate culminating in the long-term development of interstitial pneumonitis and pulmonary fibrosis (Sriramachari, 1994).

Neurologic

    3.7.1) SUMMARY
    A) Acute lung injury-induced hypoxia may produce CNS depression.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) Decreased level of consciousness may result from hypoxia secondary to acute lung injury.
    B) SUBARACHNOID HEMORRHAGE
    1) Hemorrhages and cerebral edema were noted on autopsy of Bhopal victims (Zaidi, 1986).

Gastrointestinal

    3.8.1) SUMMARY
    A) Gastrointestinal irritation and vomiting may occur.
    3.8.2) CLINICAL EFFECTS
    A) GASTROINTESTINAL IRRITATION
    1) Minimal gastrointestinal irritation occurs with very high doses (Rye, 1973).
    B) VOMITING
    1) Vomiting may be a common effect of exposures and may occur as a result of ingestion or inhalation (Bucher, 1987; Sittig, 1991; ILO , 1998).
    C) DIARRHEA
    1) Although reported rarely, in one study diarrhea was correlated positively with increasing death rates (Andersson et al, 1988).

Hepatic

    3.9.1) SUMMARY
    A) Decreased liver function may occur.
    3.9.2) CLINICAL EFFECTS
    A) ABNORMAL LIVER FUNCTION
    1) Decreased liver function may be noted (Anon, 1985). Fatty infiltration of the liver was noted on autopsy of Bhopal victims (Zaidi, 1986).

Genitourinary

    3.10.1) SUMMARY
    A) Renal tubular necrosis and edema may be noted.
    3.10.2) CLINICAL EFFECTS
    A) CRUSH SYNDROME
    1) Renal tubular necrosis and edema may be noted (Anon, 1985; Zaidi, 1986; Bucher, 1987).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL FUNCTION ABNORMAL
    a) The inhibitory effects of methyl isocyanate on glutathione reductase coupled with the propensity to react spontaneously with oxidized glutathione combine to deplete significantly intracellular stores of oxidized glutathione (Kassahun et al, 1994).

Acid-Base

    3.11.1) SUMMARY
    A) Metabolic acidosis may occur.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) Metabolic acidosis has been reported following toxic exposures (Bucher, 1987).

Hematologic

    3.13.1) SUMMARY
    A) Cherry-red blood may be observed.
    3.13.2) CLINICAL EFFECTS
    A) ABNORMAL COLOR
    1) CHERRY-RED BLOOD - Zaidi (1986) reported cherry-red blood of all body organs the most striking feature of postmortem examination of Bhopal, India victims.

Dermatologic

    3.14.1) SUMMARY
    A) Skin irritation is likely. Contact can cause chemical burns (Sittig, 1991; HSDB , 2001).
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Skin irritation is likely. Contact can cause chemical burns (Sittig, 1991; HSDB , 2001).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SKIN NECROSIS
    a) Subcutaneous injection of methyl isocyanate in rabbits resulted in significant increases in hemoglobin concentration, erythrocyte volume and leucocyte number as well as total plasma proteins and urea (Jeevaratnam et al, 1993).
    b) RABBIT - Erythema and edema, followed by necrosis and perforation, occurred following a 30 minute application to rabbit's ears. A few drops resulted in tissue corrosion (HSDB , 2001).

Immunologic

    3.19.1) SUMMARY
    A) The immunologic system has been suggested as a mechanism of persistent respiratory and eye effects. Antibodies specific to methyl isocyanate have been demonstrated in the blood of exposed patients in Bhopal, India.
    3.19.2) CLINICAL EFFECTS
    A) DISORDER OF IMMUNE FUNCTION
    1) Immunologic system has been suggested as a mechanism of persistent respiratory and eye effects observed in Bhopal gas victims (Gassert et al, 1986). Antibodies specific to methyl isocyanate were detected in 12 of 144 exposed persons in Bhopal, India. Titres were low and the antibody response was transient (Karol, 1987; (Karol & Kamat, 1988). Methyl isocyanate will activate complement in human serum in vitro (Kolb, 1987).
    3.19.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) WBC ABNORMAL
    a) Animal studies of the effect of methyl isocyanate exposure on the immune system have been reported. No change was seen in humoral immunity or lymphoproliferative responses to mitogens. Dose-related suppression was seen in splenic lymphocytes exposed to allogeneic leukocytes in a mixed leukocyte response (Luster et al, 1986). Antibodies specific to methyl isocyanate were raised in guinea pigs after injection but the titres were low and the response was transient (Karol et al, 1987) Karol & Kolb, 1988). Methyl isocyanate will activate complement in guinea pig serum in vivo (Kolb et al, 1987).

Reproductive

    3.20.1) SUMMARY
    A) There is conflicting data as to whether methyl isocyanate is fetotoxic, however, it crosses the placental barrier. Reports from Bhopal, India and animal studies suggest a high degree of adverse reproductive effects and teratogenicity.
    3.20.2) TERATOGENICITY
    A) HUMANS
    1) ABORTION
    a) The fetal loss rate by gas-affected women in the Bhopal area of India was abnormally high (26.3%) compared with a control group (7.8%) from a nearby area not affected by the gas at five years after the accident (Kapoor, 1991). A study of pregnant women residing near the Union Carbide pesticide plant in Bhopal, India was undertaken at nine months after the accident (Varma, 1987).
    b) Twenty-nine of 38 pregnant women (from a sample of 100 women of childbearing age living within 10 km of the Bhopal release) had spontaneous abortions and 2 had premature deliveries. Both surviving infants were born with multiple anomalies. Lung disease and severe pulmonary changes were found at autopsy of the infants exposed in utero (Mehta et al, 1990).
    B) ANIMAL STUDIES
    1) SKELETAL MALFORMATION
    a) Specific developmental abnormalities of the musculoskeletal, as well as extra embryonic structures, were observed in the mouse with exposure to methyl isocyanate via inhalation (RTECS , 2002). Methyl isocyanate will complex with glutathione to suppress embryonic growth, yolk sac and limb bud formation in the mouse primarily by an inhibition of nutrient uptake (Guest & Varma, 1993).
    b) Female Charles Foster rats exposed to 0.212, 0.265, and 0.353 ppm MIC vapor and mated with normal males of the same strain resulted in fetal teratologic abnormalities (wrist drop, everted claw, valgus deformity, syndactyly, blood clot formation, liver enlargement, cleft palate and unequal ribs) (Singh, 1996).
    3.20.3) EFFECTS IN PREGNANCY
    A) HUMANS
    1) STILLBIRTH
    a) Following the Bhopal, India MIC release, of 865 observed pregnancies in potentially exposed women, 43 percent did NOT result in a live infant and there was a 14 percent death rate amongst live-born infants (Varma, 1987). It is not known if these observations represent direct fetotoxicity; severe maternal-fetal hypoxia secondary to maternal noncardiogenic pulmonary edema may have been responsible.
    2) ABORTION
    a) Twenty-nine out of 38 pregnant women (from a sample of 100 women of childbearing age living within 10 km of the Bhopal plant) had spontaneous abortions and 2 had premature deliveries. Both surviving infants were born with multiple anomalies. Lung disease and severe pulmonary changes were found on autopsy of the infants exposed in utero (Mehta et al, 1990). Reduction of litter size and an increase in stillbirths were seen with exposure to this agent (RTECS , 2002).
    b) Following the Bhopal, India MIC release, the spontaneous abortion rate was found to be nearly four times higher in the affected areas compared to a control area (24.2% versus 5.6%; p<0.0001) (Bajaj, 1993).
    B) ANIMAL STUDIES
    1) In experimental animal studies, methyl isocyanate was found to cross the placenta and enter the fetus. Reduction of litter size and an increase in stillbirths were seen with exposure to this agent (RTECS , 2002).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS624-83-9 (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
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) In experimental animals, no long-term neoplastic lesions were significantly associated with methyl isocyanate exposure; however, male rats had marginally increased rates of pheochromocytomas of the adrenal medulla and adenomas of pancreatic acinar cells (HSDB , 2001).

Genotoxicity

    A) Mutations were seen in S. typhimurium and mouse lymphocytes with exposure to this agent. The people exposed to methyl isocyanate during the Bhopal accident repeatedly display Robertsonian translocations. Other types of translocations involving chromosomes 5,9,11,14 and 16 have a statistically significant association with exposure to methyl isocyanate.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor ECG, chest x-ray, pulse oximetry, peak air flows, arterial blood gases, serum electrolytes, and renal and hepatic function in symptomatic patients.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitor serum electrolytes and renal and hepatic function in symptomatic patients.
    B) ACID/BASE
    1) High-performance liquid chromatography (HPLC) is specific and sensitive for the detection of methyl isocyanate in blood (Venkateswaran et al, 1992).
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor ECG and pulse oximetry.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Obtain chest x-ray in symptomatic patients.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor ECG, chest x-ray, pulse oximetry, peak air flows, arterial blood gases, serum electrolytes, and renal and hepatic function in symptomatic patients.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Covering the face with a wet cloth immediately during exposure may minimize toxicity.
    B) 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.
    C) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    D) 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.
    E) Commercially available air-purifying cartridges were found to provide inadequate protection from high concentrations of MIC (Moyer & Berardinelli, 1987).
    F) Only supplied air respirators should be used when MIC is a suspected contaminant (Moyer & Berardinelli, 1987).
    6.7.2) TREATMENT
    A) OBSERVATION REGIMES
    1) Observation for 72 hours is advisable to detect delayed onset of acute lung injury.
    B) MONITORING OF PATIENT
    1) Monitor chest x-ray, spirometry, pulse oximetry and arterial blood gases.
    C) 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).
    D) BRONCHOSPASM
    1) BRONCHOSPASM SUMMARY
    a) Administer beta2 adrenergic agonists. Consider use of inhaled ipratropium and systemic corticosteroids. Monitor peak expiratory flow rate, monitor for hypoxia and respiratory failure, and administer oxygen as necessary.
    2) ALBUTEROL/ADULT DOSE
    a) 2.5 to 5 milligrams diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response, administer 2.5 to 10 milligrams every 1 to 4 hours as needed OR administer 10 to 15 milligrams every hour by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.5 milligram by nebulizer every 30 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    3) ALBUTEROL/PEDIATRIC DOSE
    a) 0.15 milligram/kilogram (minimum 2.5 milligrams) diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.25 to 0.5 milligram by nebulizer every 20 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    4) ALBUTEROL/CAUTIONS
    a) The incidence of adverse effects of beta2-agonists may be increased in older patients, particularly those with pre-existing ischemic heart disease (National Asthma Education and Prevention Program, 2007). Monitor for tachycardia, tremors.
    5) CORTICOSTEROIDS
    a) Consider systemic corticosteroids in patients with significant bronchospasm. PREDNISONE: ADULT: 40 to 80 milligrams/day in 1 or 2 divided doses. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 or 2 divided doses (National Heart,Lung,and Blood Institute, 2007).
    E) EXPERIMENTAL THERAPY
    1) ANIMAL STUDY: In an effort to determine if cyanide poisoning was involved, one experimenter exposed rats to methyl isocyanate and then treated with saline and sodium thiosulfate. No clinical difference was seen (Nemery et al, 1985a).
    F) 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) ANTIBIOTIC
    1) Topical antibiotics may be useful in secondary infection.
    B) ATROPINE
    1) Severe iritis may be treated with topical atropine or homatropine (Anon, 1985).
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Abstracts

Case Reports

    A) ACUTE EFFECTS
    1) In an accidental release of methyl isocyanate gas, producing a cloud 2 to 3 miles wide, in Bhopal, India, fatality rates were estimated at 3 percent of those exposed to the highest concentrations. The 2 most frequently noted initial symptoms were coughing and burning of the eyes and throat, followed by vomiting in those closest to the factory. Choking and shortness of breath were also common. Collapse, unconsciousness and marked respiratory distress occurred in those close to the factory (Andersson et al, 1984).
    B) CHRONIC EFFECTS
    1) Irritation and persistent watering of the eyes was a common complaint one year following methyl isocyanate gas exposure in Bhopal (Andersson et al, 1986). Chronic pulmonary obstruction 10 years after the accident was found to decrease as the distance increased from the plant (Cullinan & Acquilla, 1997).

Range Of Toxicity

Summary

    A) MAXIMUM TOLERATED EXPOSURE - Two ppm, no odor was detected but irritation and lacrimation were noted. Symptoms were more marked at 4 ppm and unbearable at 21 ppm. Exposures to breathing zone concentrations of 0.5 ppm are likely to produce a respiratory response.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    2) No adverse effects were seen after prolonged exposure to 0.02 parts per million methyl isocyanate in an occupational setting (Avashia et al, 1996). The NIOSH/OSHA Exposure limit (TWA) is 0.02 parts per million. IDLH is 3 parts per million.

Maximum Tolerated Exposure

    A) ACUTE
    1) HUMANS -
    a) Humans exposed to 0.4 parts per million for 1 to 5 minutes detected no odor and experienced no irritation. At 2 parts per million no odor was detected but irritation and lacrimation were noted. Symptoms were more marked at 4 parts per million and unbearable at 21 parts per million (Rye, 1973). Exposures to breathing zone concentrations of 0.5 parts per million are likely to produce a respiratory response.
    2) ANIMALS -
    a) No effect was observed in rats following exposure to 2 parts per million for 2 hours. High concentration (25-3506 parts per million) exposure for a short duration (15 minutes) resulted in lacrimation, blepharospasm and mouth breathing in rats and guinea pigs. None of the subjects died (Dodd et al, 1987).

Workplace Standards

    A) ACGIH TLV Values for CAS624-83-9 (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) Methyl isocyanate
    a) TLV:
    1) TLV-TWA: 0.02 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Skin
    3) Definitions:
    a) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): URT irr
    d) Molecular Weight: 57.05
    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) Under Study
    1) Methyl isocyanate
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s):
    d) Molecular Weight:
    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 CAS624-83-9 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Methyl isocyanate
    2) REL:
    a) TWA: 0.02 ppm (0.05 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: [skin]
    1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.
    f) Note(s):
    3) IDLH:
    a) IDLH: 3 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS624-83-9 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Methyl isocyanate
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Methyl isocyanate
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Methyl isocyanate
    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: Methyl isocyanate
    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 CAS624-83-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Methyl isocyanate
    2) Table Z-1 for Methyl isocyanate:
    a) 8-hour TWA:
    1) ppm: 0.02
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.05
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: Yes
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Lewis, 2000 RTECS, 2002
    1) LD50- (ORAL)MOUSE:
    a) 120 mg/kg
    2) LD50- (SKIN)MOUSE:
    a) 1820 mg/kg
    3) LD50- (SUBCUTANEOUS)MOUSE:
    a) 81900 mcg/kg -- flaccid paralysis without anesthesia, somnolence, respiratory depression
    4) LD50- (ORAL)RAT:
    a) 51500 mcg/kg -- flaccid paralysis without anesthesia, somnolence, respiratory depression
    b) 69 mg/kg
    c) Male, 140 mg/kg
    5) LD50- (SKIN)RAT:
    a) 2780 mg/kg
    6) LD50- (SUBCUTANEOUS)RAT:
    a) 261 mg/kg -- flaccid paralysis without anesthesia, somnolence, respiratory depression
    7) TCLo- (INHALATION)HUMAN:
    a) 2 ppm -- conjunctive irritation
    8) TCLo- (INHALATION)MOUSE:
    a) Female, 1 ppm for 6H at 14-17D of pregnancy-- stillbirth
    b) Female, 3 ppm for 6H at 14-17D of pregnancy
    c) 3 ppm for 6H/4D-intermittent
    d) Female, 9 ppm for 3H at 8D of pregnancy -- musculoskeletal system abnormalities, post-implantation mortality, fetotoxicity
    9) TCLo- (INHALATION)RAT:
    a) 3 ppm for 6H/4D-intermittent (Lewis, 2000)
    b) Female, 9 ppm for 3H at 10D of pregnancy -- post-implantation mortality, fetotoxicity

Pharmacology Toxicology

Toxicologic Mechanism

    A) The direct irritant response is due to triggering of normal protective mechanisms of the upper respiratory tract similar to other respiratory irritants. The second type of response is allergic and usually does not develop with the initial exposure.
    B) Controversy exists regarding the actual gaseous component that caused the toxicity seen with methyl isocyanate release in Bhopal, India, in 1984.
    1) Evidence that hydrogen cyanide gas was NOT the toxic component includes: no HCN residue was detected in or around the plant or in the most severely affected neighborhoods surrounding it; no cyanide was reported in tissue samples of victims; and the temporal pattern of mortality was not consistent with death due to hydrogen cyanide poisoning (Varma, 1989).
    2) Evidence that hydrogen cyanide gas WAS the toxic component includes: reported cherry-red color of victims' viscera and blood; increased thiocyanate levels in the urine of some survivors; and reports of symptomatic relief after administration of sodium thiosulfate (Mehta et al, 1990).
    3) Other possible toxic substances liberated when MIC decomposes include carbon monoxide, ammonia, and N,N'-dimethylcarbodiimide. MIC itself has demonstrated toxicity in animals. Any of these substances may have caused substantial toxicity (Mangla, 1989).

Physicochemical

Physical Characteristics

    A) Methyl isocyanate is a colorless liquid with a sharp, pungent odor (NFPA, 1991; (HSDB , 2001).

Ph

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

Molecular Weight

    A) 57.05 (Budavari, 1996)

Other

    A) ODOR THRESHOLD
    1) Currently not available (CHRIS , 2002)

References

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