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METHYLENE IODIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Methylene iodide is a halogenated hydrocarbon used as a separating mixture for minerals, in organic synthesis, and in x-ray contrast media. It may be used by jewelers to analyze the quality of gems.
    B) It is probably an irritant and narcotic in high concentrations. Human systemic effects may include acute pulmonary edema and somnolence. It is metabolized to carbon monoxide following systemic absorption and may cause elevated carboxyhemoglobin levels, although the significance of this is not well established.

Specific Substances

    1) Methylene iodide
    2) Diiodomethane
    3) Dijodomethan
    4) Methane, diiodo-
    5) Methylene diiodide
    6) Methylenjodid
    7) Mi-Gee
    8) NIOSH/RTECS PA 8575000
    9) Molecular Formula: C-H2-I2
    10) CAS 75-11-6
    11) References: RTECS, 1998
    12) DIJODMETHAN
    1.2.1) MOLECULAR FORMULA
    1) C-H2-I2

Available Forms Sources

    A) FORMS
    1) Methylene iodide is a yellow, light straw-colored, or clear heavy refractive liquid (Lewis, 1996).
    B) USES
    1) Methylene iodide is a halogenated hydrocarbon used as a separating mixture for minerals, in organic synthesis, and in x-ray contrast media (Lewis, 1996; Budavari, 1996).
    2) It may be used by jewelers to analyze the quality of gems (Weimerskirch et al, 1990).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Methylene iodide is an irritant which has narcotic properties. It is metabolized to carbon monoxide following systemic absorption in both experimental animals and humans. The contribution of this metabolic carbon monoxide release to acute human poisoning is difficult to evaluate.
    B) In the only reported case of human poisoning, initial symptoms were vomiting, lethargy, and incoordination. Elevated carboxyhemoglobin levels were noted, peaking at 11 hours following ingestion. Hepatic injury and bone marrow suppression were noted, and pulmonary and cerebral edema were late manifestations of a generalized multiorgan system failure.
    0.2.4) HEENT
    A) Irritation of the eyes, nose, and throat may occur.
    0.2.6) RESPIRATORY
    A) Respiratory tract irritation may occur. Noncardiogenic pulmonary edema developed after ingestion in one fatal case. Death may result due to respiratory failure from CNS depression.
    0.2.7) NEUROLOGIC
    A) CNS depression, lethargy, and incoordination may occur. Cerebral edema was a premorbid finding in one fatal case following ingestion exposure.
    0.2.8) GASTROINTESTINAL
    A) Nausea and vomiting may occur.
    0.2.9) HEPATIC
    A) Fatal hepatotoxicity developed in one case after ingestion.
    0.2.13) HEMATOLOGIC
    A) Bone marrow suppression was a late development in one fatal case with ingestion exposure.
    0.2.14) DERMATOLOGIC
    A) Skin irritation could follow direct contact.
    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) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

    A) Monitor carboxyhemoglobin levels, complete blood count, platelet count, prothrombin time or INR, and liver function tests.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    B) 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.
    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.
    D) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    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) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) Respiratory tract irritation, if severe, can progress to pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    D) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    E) 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.
    F) Administer supplemental oxygen. The place of hyperbaric oxygen therapy is controversial. (See main section for details.)
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

Range Of Toxicity

    A) Ingestion of 25 mL of pure methylene iodide was fatal to a 20-month-old child.

Clinical Effects

Summary Of Exposure

    A) Methylene iodide is an irritant which has narcotic properties. It is metabolized to carbon monoxide following systemic absorption in both experimental animals and humans. The contribution of this metabolic carbon monoxide release to acute human poisoning is difficult to evaluate.
    B) In the only reported case of human poisoning, initial symptoms were vomiting, lethargy, and incoordination. Elevated carboxyhemoglobin levels were noted, peaking at 11 hours following ingestion. Hepatic injury and bone marrow suppression were noted, and pulmonary and cerebral edema were late manifestations of a generalized multiorgan system failure.

Heent

    3.4.1) SUMMARY
    A) Irritation of the eyes, nose, and throat may occur.
    3.4.3) EYES
    A) Ocular exposures may result in eye irritation (MSDS, 1998; Lewis, 1997).
    3.4.5) NOSE
    A) IRRITATION of the nose and throat may develop (Lewis, 1997).
    3.4.6) THROAT
    A) IRRITATION of the nose and throat may develop (Lewis, 1997).

Respiratory

    3.6.1) SUMMARY
    A) Respiratory tract irritation may occur. Noncardiogenic pulmonary edema developed after ingestion in one fatal case. Death may result due to respiratory failure from CNS depression.
    3.6.2) CLINICAL EFFECTS
    A) ACUTE LUNG INJURY
    1) CASE REPORT - Pulmonary edema was noted as a late complication of multiorgan system failure following ingestion of methylene iodide in one reported human case (Weimerskirch et al, 1990).
    B) IRRITATION SYMPTOM
    1) Inhalation may result in irritation of the respiratory tract (MSDS, 1998; Lewis, 1997).
    C) ACUTE RESPIRATORY INSUFFICIENCY
    1) Following a significant ingestion or inhalation, CNS depression leading to central respiratory depression and possible respiratory failure may develop (MSDS, 1998).

Neurologic

    3.7.1) SUMMARY
    A) CNS depression, lethargy, and incoordination may occur. Cerebral edema was a premorbid finding in one fatal case following ingestion exposure.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) Ingestions may result in toxic effects of CNS depression, characterized by excitement, followed by headache, dizziness, and drowsiness. If untreated, symptoms may progress to collapse, unconsciousness, coma and possible death due to respiratory failure (MSDS, 1998).
    2) CASE REPORT - Methylene iodide has caused initial lethargy and incoordination following ingestion in one reported human case (Weimerskirch et al, 1990).
    B) CEREBRAL EDEMA
    1) CASE REPORT - Cerebral edema was noted as a late complication of multiorgan system failure following ingestion of methylene iodide in one reported human case (Weimerskitch et al, 1990).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CNS DEPRESSION
    a) Methylene iodide has narcotic effects in experimental animals (Lewis, 1996).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea and vomiting may occur.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) Irritation of the digestive tract may occur following an ingestion (MSDS, 1998).
    2) CASE REPORT - Vomiting was noted shortly after ingestion in one reported human case (Weimerskirch et al, 1990).

Hepatic

    3.9.1) SUMMARY
    A) Fatal hepatotoxicity developed in one case after ingestion.
    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) CASE REPORT - Severe hepatotoxicity with elevated transaminase, serum ammonia, and bilirubin levels associated with a prolonged prothrombin time developed between days 2 and 4 following ingestion in one reported human case (Weimerskirch et al, 1990). This child died while a suitable donor liver was being sought.
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) In MICE, subcutaneous administration of methylene iodide caused delayed deaths which were felt to be due to hepatotoxicity (Kutob & Plaa, 1962).

Hematologic

    3.13.1) SUMMARY
    A) Bone marrow suppression was a late development in one fatal case with ingestion exposure.
    3.13.2) CLINICAL EFFECTS
    A) MYELOSUPPRESSION
    1) Bone marrow suppression with decreased WBC and platelet counts was noted following fatal ingestion in one reported human case (Weimerskirch et al, 1990).
    B) METABOLIC FINDING
    1) Methylene iodide is metabolized to carbon monoxide following systemic absorption in both experimental animals and humans (Stevens et al, 1980; Kubic & Anders, 1978; Rodkey & Collison, 1977; Ahmed et al, 1980; Weimerskirch et al, 1990). The contribution of this metabolic carbon monoxide release to acute human poisoning is difficult to evaluate.

Dermatologic

    3.14.1) SUMMARY
    A) Skin irritation could follow direct contact.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Dermal exposures may result in skin irritation (MSDS, 1998; Lewis, 1997). Irritation and dermatitis may occur following prolonged or repeated contact.

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 CAS75-11-6 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Genotoxicity

    A) Methylene iodide was positive for inducing mutations in the E coli bacterial assay (RTECS , 2001) and one strain of S typhimurium (Osterman-Golkar et al, 1983).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor carboxyhemoglobin levels, complete blood count, platelet count, prothrombin time or INR, and liver function tests.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    4.1.2) SERUM/BLOOD
    A) HEMATOLOGIC
    1) Complete blood count including platelets should be monitored in cases of significant exposure.
    2) Monitoring carboxyhemoglobin levels may be useful as an index of exposure. Carboxyhemoglobin levels may not peak until up to 11 hours after ingestion (Weimerskirch et al, 1990).
    B) BLOOD/SERUM CHEMISTRY
    1) Monitor liver enzymes, serum ammonia, and bilirubin levels in cases of significant exposure.
    C) COAGULATION STUDIES
    1) Prothrombin time or INR, should be monitored in cases of significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.
    2) MONITORING
    a) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.

Radiographic Studies

    A) ABDOMINAL RADIOGRAPH
    1) In one reported case, ingested methylene iodide was shown to be radiopaque on abdominal radiography (Weimerskirch et al, 1990).
    B) CHEST RADIOGRAPH
    1) If respiratory tract irritation or pulmonary edema occurs, monitor chest x-ray.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.
    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.
    6.3.5) DISPOSITION/DERMAL EXPOSURE
    6.3.5.5) OBSERVATION CRITERIA/DERMAL
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

Monitoring

    A) Monitor carboxyhemoglobin levels, complete blood count, platelet count, prothrombin time or INR, and liver function tests.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

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) 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.
    B) 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) MONITORING OF PATIENT
    1) Monitor complete blood count and liver function tests in patients with significant exposure. Monitor for CNS depression and respiratory depression. Provide airway management as required.
    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) GENERAL TREATMENT
    1) Methylene iodide may be converted to carbon monoxide. See inhalation section for information on CO treatment.
    2) 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) MONITORING OF PATIENT
    1) Determine a carboxyhemoglobin level. Methylene iodide is converted in part to carbon monoxide.
    2) Monitor complete blood count and liver function tests in patients with significant exposure.
    3) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    B) OXYGEN
    1) Administer oxygen, 100% humidification, for short periods, then concentrations comfortable to the patient.
    C) AIRWAY MANAGEMENT
    1) If significant CNS or respiratory depression are present, ensure adequacy of respirations and oxygenation. Endotracheal intubation with assisted ventilation could be required.
    D) HYPERBARIC OXYGEN THERAPY
    1) No cases of methylene iodide poisoning treated with hyperbaric oxygen therapy have been described. The following data pertains to hyperbaric oxygen therapy of patients poisoned with the similar agent, methylene chloride.
    a) Two patients who used a methylene chloride (25%) paint, sprayed in a semienclosed area, developed coma and peak carboxyhemoglobin levels of 11.5% and 13%. Psychometric testing showed severe dysfunction in both, which improved after HBO therapy. Repeated dives were needed in the patient with the highest level 9 days later due to persistence of cognitive dysfunction (Rioux & Myers, 1989).
    b) The carboxyhemoglobin half-life in these 2 patients was shorter (4.75 and 6.5 hours) than that reported in untreated patients (13 hours) (Ratney et al, 1974), but comparable to that reported after 100% normobaric oxygen (5.8 hours) (Sturmann et al, 1985).
    2) The comparative efficacy between 100% normobaric oxygen and HBO has not been studied in animals or humans.
    E) OBSERVATION REGIMES
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    F) IRRITATION SYMPTOM
    1) Respiratory tract irritation, if severe, can progress to noncardiogenic pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    2) There are no controlled studies indicating that early administration of corticosteroids can prevent the development of noncardiogenic pulmonary edema in patients with inhalation exposure to respiratory irritant substances, and long-term use may cause adverse effects (Boysen & Modell, 1989).
    a) However, based on anecdotal experience, some clinicians do recommend early administration of corticosteroids (such as methylprednisolone 1 gram intravenously as a single dose) in an attempt to prevent the later development of pulmonary edema.
    1) Anecdotal experience with dimethyl sulfate inhalation showed possible benefit of methylprednisolone in the TREATMENT of noncardiogenic pulmonary edema (Ip et al, 1989).
    3) Anecdotal experience also indicated that systemic corticosteroids may have possible efficacy in the TREATMENT of drug-induced noncardiogenic pulmonary edema (Zitnik & Cooper, 1990; Stentoft, 1990; Chudnofsky & Otten, 1989) or noncardiogenic pulmonary edema developing after cardiopulmonary bypass (Maggart & Stewart, 1987).
    4) It is not clear from the published literature that administration of systemic corticosteroids early following inhalation exposure to respiratory irritant substances can PREVENT the development of noncardiogenic pulmonary edema. The decision to administer or withhold corticosteroids in this setting must currently be made on clinical grounds.
    G) 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).
    H) 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).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    B) SKIN ABSORPTION
    1) It is currently unknown whether or not systemic toxicity can result from dermal contact with methylene iodide.
    2) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    3) If systemic absorption results from dermal exposure, refer to treatment recommendations under INHALATION EXPOSURE above.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

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

Abstracts

Case Reports

    A) PEDIATRIC
    1) Only one case of human poisoning has been reported in the literature (Weimerskirch et al, 1990).
    2) A 20-month-old child ingested 25 mL of pure methylene iodide intended for use by jewelers for gem quality analysis. Initial symptoms were vomiting, lethargy, and incoordination. Radiopaque material in the intestinal tract was noted on initial KUB. At 11 hours following ingestion, a peak carboxyhemoglobin concentration of 14.2 percent was measured, indicating metabolic conversion of the methylene iodide to carbon monoxide.
    3) Multiorgan system failure rapidly developed. Elevated hepatic transaminases, serum ammonia, and bilirubin levels with a prolonged prothrombin time indicating serious hepatotoxicity developed between days 2 and 4 after ingestion. Bone marrow suppression with decreased WBC and platelet counts was also noted. Pulmonary and cerebral edema were late complications, and the child expired 9 days after ingestion while a suitable donor for a liver transplant was being sought.

Range Of Toxicity

Summary

    A) Ingestion of 25 mL of pure methylene iodide was fatal to a 20-month-old child.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) Ingestion of 25 milliliters of pure methylene iodide was fatal to a 20-month-old child (Weimerskirch et al, 1990).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CONCENTRATION LEVEL
    a) A peak carboxyhemoglobin level of 14.2 percent was noted 11 hours after ingestion of 25 milliliters of the pure material by a 20-month-old child (Weimerskirch et al, 1990).

Workplace Standards

    A) ACGIH TLV Values for CAS75-11-6 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS75-11-6 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS75-11-6 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS75-11-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2001 Kutob & Plaa, 1962
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 467 mg/kg
    2) LD50- (SUBCUTANEOUS)MOUSE:
    a) 830 mg/kg
    3) LD50- (INTRAPERITONEAL)RAT:
    a) 403 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Methylene iodide directly causes CNS depression (Weimerskirch et al, 1990; Lewis, 1996). It may also have irritant properties (Lewis, 1996), especially if ingested (Weimerskirch et al, 1990).
    B) Methylene iodide can cause hepatotoxicity and bone marrow suppression (Weimerskirch et al, 1990).
    1) In rats, the injury seems to be especially to the hepatic endoplasmic reticulum (Reynolds, 1972). Alterations in protein synthesis and decreased activity of glucose-6-phosphatase were noted (Reynolds, 1972).
    C) Methylene iodide is metabolized to carbon monoxide following systemic absorption in both experimental animals and humans (Stevens et al, 1980; Kubic & Anders, 1978; Rodkey & Collison, 1977; Ahmed et al, 1980; Weimerskirch et al, 1990). The contribution of this metabolic carbon monoxide release to acute human poisoning is difficult to evaluate.
    D) Methylene iodide is mutagenic in some bacterial species, which is most likely not due to its conversion to formaldehyde (Osterman-Golkar et al, 1983).

Physicochemical

Physical Characteristics

    A) Methylene iodide is a yellow, light straw-colored, or clear heavy refractive liquid (MSDS, 1998; Lewis, 1997; Lewis, 1996).

Molecular Weight

    A) 267.83 (RTECS , 2001)

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