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METHYL IODIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Methyl iodide is a naturally occurring substance with many industrial uses. Humans are exposed in ambient air since it is probably formed in the sea. Exposure would also occur from ingesting marine seafood, and from various industrial processes (HSDB , 1994).

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C-H3-I

Available Forms Sources

    A) FORMS
    1) Methyl iodide is a colorless, transparent liquid; it turns brown upon exposure to light (Budavari, 1989).
    B) SOURCES
    1) ROUTES OF EXPOSURE - Humans are exposed to methyl iodide in ambient air since it is probably formed in the sea. Exposure would also occur from ingesting marine seafood (HSDB , 1994).
    a) Industrial processes (see Available Forms/Sources section of this document for types)
    b) Average Daily Air Intake (assume median conc of 3.5 parts/trillion): 0.41 microgram (HSDB , 1994)
    C) USES
    1) It is used in methylations of pharmaceuticals; in microscopy because of its high refractive index; as imbedding material for examining diatoms; and, in testing for pyridine (Budavari, 1989).
    2) Chemical intermediate
    3) Fumigant to control internal fungi of grain sorghum
    4) Is used chemically as an alkylatating agent
    5) Building block for radioactive tracer synthesis
    6) Reacts with dimethyl ethyl amine to yield quaternary ammonium compounds.
    7) References: (Budavari, 1989; HSDB , 1994)

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) SYSTEMIC EFFECTS: Methyl Iodide is a strong narcotic and anesthetic. Massive exposure has led to pulmonary edema. Prolonged or repeated exposure may cause central nervous system effects. The latency period between exposure and onset of symptoms ranges from hours to days.
    1) Initial symptoms are lethargy, somnolence, slurred speech, ataxia, dysmetria, and visual disturbances. Neurologic dysfunction may progress to convulsions, coma, and death.
    2) If recovery occurs, neurologic findings recede over several weeks and are followed by psychiatric disturbances such as paranoia, delusions, and hallucination.
    3) In severe poisoning, the primary target organs were the lungs, liver, kidney, and brain.
    B) SKIN: A human skin irritant which may cause burns with repeated exposure.
    0.2.3) VITAL SIGNS
    A) Dyspnea may occur due to pulmonary irritation.
    0.2.4) HEENT
    A) Headache may occur after exposure. Diplopia and nystagmus have been reported in serious poisonings. Animal exposures have demonstrated eye irritation and lacrimation.
    0.2.6) RESPIRATORY
    A) Acute exposures may produce lung irritation leading to congestion and pulmonary edema.
    0.2.7) NEUROLOGIC
    A) Irritability, headache, and syncope have been reported. Cerebellar and parkinsonian neurologic dysfunction may progress to paralysis, convulsions, coma, and death.
    B) If recovery occurs, neurologic findings recede over several weeks and may be followed by psychiatric disturbances such as paranoia, delusions, and hallucination.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, and diarrhea have been reported after exposure.
    0.2.10) GENITOURINARY
    A) Acute exposures may produce oliguric renal failure.
    0.2.14) DERMATOLOGIC
    A) Exposure to the liquid may produce erythema and blister the skin, especially with prolonged contact. A case of partial-thickness burns has been reported. Animal experiments have demonstrated depigmentation.
    0.2.17) METABOLISM
    A) Human abnormalities not reported.
    B) Animal experiments have demonstrated increased insulin, decreased plasma glucose, abnormal responses to glucose tolerance tests, elevated triglycerides and lipids, and changes in ATP, creatinine phosphate, lactate, phosphatidylserine and phosphatidylcholine in rabbit brain tissues.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    0.2.21) CARCINOGENICITY
    A) Methyl iodide is a suspected carcinogen with experimental neoplastigenic and tumorigenic data. Human mutation data have been reported. The overall IARC evaluation is group 3 (agent is not classifiable as to its human carcinogenicity).

Laboratory Monitoring

    A) Monitor pulse oximetry and/or ABGs, chest x-ray, and pulmonary function tests in symptomatic patients.
    B) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    C) Exposure to methyl iodide has increased serum lipids, especially triglycerides. A blood panel, especially of serum lipids, and liver and kidney function testing might be predictive of methyl iodide poisoning.
    D) If respiratory tract irritation is present, monitor chest x-ray.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) There is no specific antidote. Care is symptomatic and supportive for CNS depression and skin, eye, pulmonary, and gastrointestinal irritation. Because of its irritant nature, emesis is NOT recommended. Dilution, followed by lavage and activated charcoal may be of some use in significant exposures.
    B) Significant esophageal or gastrointestinal tract irritation or burns may occur following ingestion. The possible benefit of early removal of some ingested material by cautious gastric lavage must be weighed against potential complications of bleeding or perforation.
    C) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    D) 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.
    E) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    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.
    C) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    0.4.4) EYE EXPOSURE
    A) 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).
    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) The minimum lethal human dose to this agent has not been delineated.
    B) The maximum tolerated human exposure to this agent has not been delineated.
    C) The following lethal doses have been reported in animal studies:
    1) ORAL - Single oral doses of 70 milligrams per kilogram were lethal to rabbits, but several oral doses of 50 milligrams per kilogram were necessary before they caused death.
    2) INHALATION - Inhalation of 54 parts per million (0.31 milligrams per liter) was fatal to mice within 24 hours.
    D) The following nontoxic doses have been reported in animal studies:
    1) ORAL - Repeated oral doses of 30 to 50 mg/kg of methyl iodide caused minimal effect in mice.

Clinical Effects

Neurologic

    3.7.1) SUMMARY
    A) Irritability, headache, and syncope have been reported. Cerebellar and parkinsonian neurologic dysfunction may progress to paralysis, convulsions, coma, and death.
    B) If recovery occurs, neurologic findings recede over several weeks and may be followed by psychiatric disturbances such as paranoia, delusions, and hallucination.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) Irritability, headache, and syncope have been reported. Cerebellar and parkinsonian neurologic dysfunction may progress to paralysis, seizures, coma, and death.
    b) If recovery occurs, neurologic findings recede over several weeks and may be followed by psychiatric disturbances such as paranoia, delusions, and hallucination.
    c) Various signs of cerebellar and parkinsonian neurologic damage may occur after exposure (IARC, 1977). Slurred speech and shaking has been reported (Mackison et al, 1981).
    d) CASE REPORT: A case of cerebellar and parkinsonian signs and symptoms occurred after an industrial exposure (Appel et al, 1975).
    e) CASE REPORT: A 50-year-old man presented with stroke-like symptoms (sudden onset of slurred speech, double vision, nystagmus, headache, drowsiness, heaviness on the right side of his body and unsteadiness of gait) and visual and auditory hallucinations. Initially, a diagnosis of stroke was made, however, methyl iodide poisoning following occupational exposure was suspected. CT and MRI of the brain were normal. Following supportive care, his symptoms improved gradually (Nair & Chatterjee, 2010).
    f) COMBINATION EXPOSURE: A 37-year-old chemist with a 5-year history of headaches, dizziness, and fatigue due to a long-term inhalational exposure to dichloromethane and iodomethane, presented with ataxia, increasing inhibition, dizziness, dysarthria, and a confusional and delirious state a day after distilling dichloromethane and iodomethane at work. His symptoms deteriorated in the next several hours and his lethargy progressed to stupor and shallow coma, with episodes of confusion, restlessness, and aggression. All laboratory tests and a CT scan were normal. An MRI scan of the brain revealed the presence of a T2-hyperintense lesion in the splenium of the corpus callosum, suggestive of myelinolysis. His symptoms gradually improved and a repeat MRI of the brain 16 days later revealed complete resolution of all lesions in the corpus callosum as well as in the cerebellar hemispheres (Ehler et al, 2011).
    B) COMA
    1) Serious exposures may proceed from drowsiness to coma (Ehler et al, 2011; Hathaway et al, 1991; Mackison et al, 1981).
    C) SEIZURE
    1) Serious exposures may result in seizures (Appel et al, 1975).
    D) SYNCOPE
    1) Dizziness and giddiness have occurred after exposure (Mackison et al, 1981; Anon, 1984).
    2) CASE REPORT: An adult exposed to methyl iodide vapors felt dizzy and weak (HSDB , 1994).
    E) CENTRAL STIMULANT ADVERSE REACTION
    1) Patients may experience irritability after exposure (Mackison et al, 1981).
    F) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache has been reported after exposure (Ehler et al, 2011; Nair & Chatterjee, 2010; Anon, 1984).
    G) ATAXIA
    1) WITH POISONING/EXPOSURE
    a) Ataxia may occur with exposure (Ehler et al, 2011; Nair & Chatterjee, 2010; Anon, 1984).
    H) SEQUELA
    1) Four months after exposure to methyl iodide, a 49-year-old male began to experience problems with memory, concentration, performance of tasks, and changes in his behavior and personality. He was referred to a toxicology clinic for evaluation of possible chronic methyl iodide toxicity. He demonstrated toxin-related deficits in recent memory function, visual complex memory, focused-auditory complex attention, and decreased ability for information processing, and dual task performance. At follow-up 2 months later, he was noticing small improvements in his mental acuity and ability to concentrate (Schwartz et al, 2005).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Poisoned rabbits manifested increased susceptibility to d-tubocurarine (Hasegawa et al, 1971).
    1) Animals injected with methyl iodide showed that acetylcholine liberation at neuromuscular junctions of cervical muscle decreased and was minimal at 48 hours after the administration of the poison.
    2) The changes in the amount of ATP, lactic acid, ammonia, glutamine, creatine phosphate, and inorganic phosphate in the brain were greatest at 48 hours after administration (Hasegawa et al, 1967).
    b) Systemic administration to guinea pigs and rabbits caused CNS disturbances (Grant, 1986).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, and diarrhea have been reported after exposure.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA, VOMITING AND DIARRHEA
    1) Nausea, vomiting, and diarrhea have been reported after exposure (Mackison et al, 1981).

Genitourinary

    3.10.1) SUMMARY
    A) Acute exposures may produce oliguric renal failure.
    3.10.2) CLINICAL EFFECTS
    A) RENAL FAILURE SYNDROME
    1) Acute exposure may produce oliguric renal failure which was reported after an industrial exposure (Appel et al, 1975).

Dermatologic

    3.14.1) SUMMARY
    A) Exposure to the liquid may produce erythema and blister the skin, especially with prolonged contact. A case of partial-thickness burns has been reported. Animal experiments have demonstrated depigmentation.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Exposure to the liquid may produce erythema and blisters, especially with prolonged contact.
    B) ERUPTION
    1) Experimental application to volunteers produced early stinging and erythema, with significant erythema and vesicles after prolonged contact.
    2) CASE: Experimental application of the liquid to human skin produced a stinging sensation and slight reddening in 10 minutes. After 6 hours of contact, there was spreading erythema followed by formation of vesicles (Hathaway et al, 1991).
    C) BURN OF SKIN
    1) A 49-year-old male was hand carrying and loading tanks of newly manufactured methyl iodide onto a truck. He was wearing a chemical protective suit and a full face respirator with air hose, but did not recall wearing outer boots and believed he may have damaged the soles of his chemical protective suit while walking. At the end of the shift, he noticed the suit breach on the soles of his suit.
    a) He went home and showered. An erythematous rash developed on his genitalia, inner thighs, and groin. He developed syncope and was brought to the emergency department where he began to manifest burns over his torso, back, and lower extremities. He was transferred to a burn unit with partial thickness burns over 50% of his body which required several split-thickness skin grafts to his left lower extremity. At follow-up, the skin grafts were noted to be healing well (Schwartz et al, 2005).
    D) BULLOUS ERUPTION
    1) Prolonged contact with the liquid may cause blisters.
    2) May blister the skin; prolonged contact with the liquid may cause vesication (HSDB , 1994; Mackison et al, 1981).
    3) CASE SERIES
    a) When one milliliter was applied under a gauze dressing to a volunteer for 0.5 hours, erythema was seen, followed by vesicles 19 hours after application (IARC, 1977).
    b) A woman wearing rubber gloves while handling methyl iodide developed skin reactions but no systemic reaction. The gloves allowed for skin contact, but not for evaporation from under the gloves (Skutilova, 1975).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Depigmentation was produced in mice injected intradermally with 50 micrograms of methyl iodide (Aw & Boyland, 1981).

Summary Of Exposure

    A) SYSTEMIC EFFECTS: Methyl Iodide is a strong narcotic and anesthetic. Massive exposure has led to pulmonary edema. Prolonged or repeated exposure may cause central nervous system effects. The latency period between exposure and onset of symptoms ranges from hours to days.
    1) Initial symptoms are lethargy, somnolence, slurred speech, ataxia, dysmetria, and visual disturbances. Neurologic dysfunction may progress to convulsions, coma, and death.
    2) If recovery occurs, neurologic findings recede over several weeks and are followed by psychiatric disturbances such as paranoia, delusions, and hallucination.
    3) In severe poisoning, the primary target organs were the lungs, liver, kidney, and brain.
    B) SKIN: A human skin irritant which may cause burns with repeated exposure.

Vital Signs

    3.3.1) SUMMARY
    A) Dyspnea may occur due to pulmonary irritation.
    3.3.2) RESPIRATIONS
    A) Dyspnea may occur due to pulmonary irritation (HSDB , 1994).

Heent

    3.4.1) SUMMARY
    A) Headache may occur after exposure. Diplopia and nystagmus have been reported in serious poisonings. Animal exposures have demonstrated eye irritation and lacrimation.
    3.4.2) HEAD
    A) SUMMARY: Headache may occur after exposure.
    B) HEADACHE: A few cases of headache have been seen after industrial exposure (Anon, 1994).
    3.4.3) EYES
    A) Diplopia and nystagmus have been reported in serious poisonings. Animal exposures have demonstrated eye irritation and lacrimation.
    B) DIPLOPIA: Has occurred after exposure.
    1) CASE: An adult exposed to methyl iodide vapor developed horizontal and vertical diplopia. Intermittent subjective "blindness" with stumbling over obstacles was present. When examined 8 days after exposure the eyes were found to be normal and the patient was asymptomatic (Grant, 1986).
    C) NYSTAGMUS: Has been reported (Nair & Chatterjee, 2010; Grant, 1986). Headache was reported in one fatal poisoning, associated with right internal strabismus (Grant, 1986).
    D) ANIMAL EXPERIMENTS: Mice exposed to lethal concentrations of vapor (25 to 85 mg/L in air) developed immediate eye irritation and lacrimation. Exposure to 5 mg/L for 10 minutes produced no signs of eye irritation in most animals, although all died within 24 hours (Grant, 1986).

Respiratory

    3.6.1) SUMMARY
    A) Acute exposures may produce lung irritation leading to congestion and pulmonary edema.
    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) Acute exposures may produce lung irritation leading to congestion and pulmonary edema.
    B) IRRITATION SYMPTOM
    1) Acute exposure may produce lung irritation (HSDB , 1994) and pulmonary congestion (Appel et al, 1975).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) Rats exposed for 15 minutes to 22 mg/L in air (3790 ppm), died within 11 days. Lung irritation and pulmonary edema were seen at necropsy (Clayton & Clayton, 1982).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    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.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS74-88-4 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: Methyl iodide
    b) Carcinogen Rating: 3
    1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    3.21.2) SUMMARY/HUMAN
    A) Methyl iodide is a suspected carcinogen with experimental neoplastigenic and tumorigenic data. Human mutation data have been reported. The overall IARC evaluation is group 3 (agent is not classifiable as to its human carcinogenicity).
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) IARC SUMMARY AND EVALUATION - No data are available in humans, but there is limited evidence of carcinogenicity in animals.
    2) IARC OVERALL EVALUATION (Group 3) - The agent is not classifiable as to its carcinogenicity to humans (IARC, 1987).
    B) CARCINOMA
    1) Methyl iodide is a suspected carcinogen with experimental neoplastigenic and tumorigenic data. Human mutation data have been reported. The overall IARC evaluation is group 3 (the agent is not classifiable as to its human carcinogenicity).
    C) OCCUPATIONAL
    1) POTENTIAL OCCUPATIONAL CARCINOGENIC (NIOSH) - The monohalomethanes are alkylating agents which have the potential for inducing mutations and cancer. All compounds tested were found to be direct acting mutagens in the Ames test. They also demonstrated the ability to produce cancer in mice and rats. Because of these data, NIOSH recommends that methyl iodide be considered as a postential occupational carcinogen (Anon, 1984).
    2) Human mutation data have been reported (Lewis, 1992).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) SUMMARY - Methyl iodide is generally regarded to be carcinogenic in animals (USEPA, 1980).
    2) MICE - In one study, methyl iodide was NOT shown to be carcinogenic.
    a) Doses of 8.5, 21.3 and 44.0 mg/kg body weight were given to 3 groups of 10 male and 10 female 6 to 8 week old mice IP 3 times per week in tricaprylin for a total of 24 doses. Survivors of each group were 19/20, 20/20 & 11/20, respectively.
    b) The numbers of mice with lung tumors were 4, 6 and 5 in each respective group. The average number of lung tumors in untreated mice was 0.21 per animal (6/29 mice), and that in tricaprylin treated controls was 0.22/animal (34/154) (IARC, 1977).
    3) RATS - About 100 day old rats were injected subcutaneously weekly with 10 mg/kg and 20 mg/kg respectively. Subcutaneous sarcomas occurred in 9 of 16 and 6 of 8 rats (IARC, 1977).
    a) Rats were given single injections of 50 mg/kg body weight. In 4 of 14, local tumors occurred between 500 and 700 days after the first injection. Pulmonary metastases were observed. No tumors were seen in the control group injected with vegetable oil alone (IARC, 1977).

Genotoxicity

    A) Experimentally, methyl iodide has been shown to be mutagenic, causing chromosomal and DNA alternations.

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) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    C) Exposure to methyl iodide has increased serum lipids, especially triglycerides. A blood panel, especially of serum lipids, and liver and kidney function testing might be predictive of methyl iodide poisoning.
    D) If respiratory tract irritation is present, monitor chest x-ray.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Exposure to methyl iodide has increased serum lipids, especially triglycerides. A blood panel, especially of serum lipids, and liver and kidney function testing might be predictive of methyl iodide poisoning (Hasegawa et al, 1971).
    2) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    3) GLUCOSE - Animal studies have shown abnormalities in glucose and insulin metabolism. Monitor blood sugar in significant exposures.
    B) ACID/BASE
    1) BLOOD GASES
    a) Monitor arterial blood gases and/or pulse oximetry in patients with significant exposure.
    4.1.3) URINE
    A) URINALYSIS
    1) There have been a few cases of renal failure after significant exposure. Monitor renal function tests and urinalysis.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.

Radiographic Studies

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

Methods

    A) SPECTROSCOPY/SPECTROMETRY
    1) Serum concentrations of methyl iodide may be measured by mass spectroscopy (Robertz-Vaupel et al, 1991); however, the clinical utility of each measurement is uncertain.
    B) CHROMATOGRAPHY
    1) Concentrations of methyl idodide in air samples are determined by adsorption of methyl iodide vapours on activated carbon and desorption with toluene. Analysis of the resulting solution chromatographically is done with the use of a column containing 10% SE-30 on Chromosorb W-AW-DMCS. The sensitivity range is from 3 to 30mg/m3 (Miazek-Kula, 1986).

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) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    C) Exposure to methyl iodide has increased serum lipids, especially triglycerides. A blood panel, especially of serum lipids, and liver and kidney function testing might be predictive of methyl iodide poisoning.
    D) If respiratory tract irritation is present, monitor chest x-ray.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) If swallowed, have the victim drink water. Do not induce vomiting (CHRIS , 1994). For significant oral exposures gastric lavage and activated charcoal may be useful.
    B) EMESIS/NOT RECOMMENDED
    1) Do not induce emesis.
    C) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    D) ACTIVATED CHARCOAL/CATHARTIC
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) There is no specific antidote. Mild to moderate exposures will produce irritation. More extensive exposures may produce CNS depression, seizures, and pulmonary edema. Care should be directed at supportive and symptomatic measures.
    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).
    C) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) 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) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) INJURY OF GLOBE OF EYE
    1) EVALUATION
    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.
    2) 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).
    3) MINOR INJURY
    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) SEVERE INJURY
    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) SURGICAL THERAPY
    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) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) 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) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Abstracts

Case Reports

    A) ROUTE OF EXPOSURE
    1) ROUTE-OTHER
    a) An adult suicidal patient self-administered approximately 14 grams of methyl iodide IV. Upon admission to the hospital, somnolence and agitation were noted, followed by a seizure and severe hypotension.
    b) Treatment consisted of therapy with acetylcysteine and hemoperfusion. The serum concentration of methyl iodide was significantly reduced following these treatments. The patient survived and was discharged from the hospital a week after the exposure (Robertz-Vaupel et al, 1991).
    2) INHALATION: A chemical worker accidently exposed to an unknown concentration of the vapor developed giddiness, diarrhea, sleepiness, and irritability, with recovery in a week. When re-exposed three months later, he experienced drowsiness, vomiting, pallor, incoordination, slurred speech, muscular twitching, oliguria, coma, and death (Hathaway et al, 1991).

Range Of Toxicity

Summary

    A) The minimum lethal human dose to this agent has not been delineated.
    B) The maximum tolerated human exposure to this agent has not been delineated.
    C) The following lethal doses have been reported in animal studies:
    1) ORAL - Single oral doses of 70 milligrams per kilogram were lethal to rabbits, but several oral doses of 50 milligrams per kilogram were necessary before they caused death.
    2) INHALATION - Inhalation of 54 parts per million (0.31 milligrams per liter) was fatal to mice within 24 hours.
    D) The following nontoxic doses have been reported in animal studies:
    1) ORAL - Repeated oral doses of 30 to 50 mg/kg of methyl iodide caused minimal effect in mice.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    B) ANIMAL DATA
    1) HISTORICAL DATA - Single oral doses of 70 mg/kg were lethal to rabbits, but several oral doses of 50 mg/kg were necessary before they caused death (Bucknell, 1950).
    2) HISTORICAL DATA - Inhalation of 54 ppm was fatal to mice within 24 hours (Bucknell, 1950).

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) A chemical worker accidently exposed to an unknown concentration of the vapor developed giddiness, diarrhea, sleepiness, and irritability, with recovery in a week. When re-exposed three months later, he experienced drowsiness, vomiting, pallor, incoordination, slurred speech, muscular twitching, oliguria, coma, and death (Hathaway et al, 1991).
    2) Experimental application of the liquid to human skin produced a stinging sensation and slight reddening in 10 minutes. After 6 hours of contact there was spreading erythema followed by formation of vesicles (Hathaway et al, 1991).
    3) The liquid splashed in the eyes causes conjunctivitis (Hathaway et al, 1991).
    B) ANIMAL DATA
    1) HISTORICAL DATA - Repeated oral doses of 30 to 50 mg/kg methyl iodide caused minimal effect in mice (Bucknell, 1950).

Workplace Standards

    A) ACGIH TLV Values for CAS74-88-4 (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 iodide
    a) TLV:
    1) TLV-TWA: 2 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): Eye dam; CNS impair
    d) Molecular Weight: 141.95
    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 CAS74-88-4 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Methyl iodide
    2) REL:
    a) TWA: 2 ppm (10 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    e) Skin Designation: [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): See Appendix A
    3) IDLH:
    a) IDLH: 100 ppm
    b) Note(s): Ca
    1) Ca: NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A).

    C) Carcinogenicity Ratings for CAS74-88-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Methyl iodide
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Methyl iodide
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 3 ; Listed as: Methyl iodide
    a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Methyl iodide
    a) Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    5) MAK (DFG, 2002): Category 2 ; Listed as: Methyl iodide
    a) Category 2 : Substances that are considered to be carcinogenic for man because sufficient data from long-term animal studies or limited evidence from animal studies substantiated by evidence from epidemiological studies indicate that they can make a significant contribution to cancer risk. Limited data from animal studies can be supported by evidence that the substance causes cancer by a mode of action that is relevant to man and by results of in vitro tests and short-term animal studies.
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS74-88-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Methyl iodide
    2) Table Z-1 for Methyl iodide:
    a) 8-hour TWA:
    1) ppm: 5
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 28
    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, 1992 RTECS, 1993
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 172 mg/kg
    2) LD50- (SUBCUTANEOUS)MOUSE:
    a) 110 mg/kg
    3) LD50- (INTRAPERITONEAL)RAT:
    a) 101 mg/kg
    4) LD50- (SUBCUTANEOUS)RAT:
    a) 110 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Methly iodide depletes glutathione (Di Simplicio et al, 1984)
    1) It was studied in primary dissociated neuronal and glial murine cell cultures to determine its mechanism of neurotoxicity (Bonnefoi, 1992; Bonnefoi et al, 1991). An intracellular glutathione (GSH) depleting effect was measured in vivo and was correlated with neurotoxicity.
    2) Methyl iodide has both an enzymatic and non-enzymatic action on glutathione.
    3) (REFERENCES - Hallier et al, 1990; (Gandy et al, 1990) Toxicologic and metabolic similarities among the monohalomethanes suggest a common mechanism of toxic action, probably methylation and disturbance or inactivation of essential proteins (rather than presence of the parent compound or free halide per se) (USEPA/OTS, 1977).

Physicochemical

Physical Characteristics

    A) Methyl iodide is a colorless, transparent liquid; it turns brown upon exposure to light (Budavari, 1989).
    B) ODOR: Has been described as pungent, sweet, or ethereal (HSDB , 1994).

Molecular Weight

    A) 141.95 (Budavari, 1989)

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