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METHYL MERCAPTAN

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Methyl mercaptan, also called methanethiol, is a sulfhydryl compound.

Specific Substances

    1) Methyl mercaptan
    2) Mercaptan methylique (French)
    3) Mercaptomethane
    4) Methaanthiol (Dutch)
    5) Methanethiol
    6) Methaneethiol
    7) Methanthiol (German)
    8) Methvtiolo (Italian)
    9) Methylmercaptaan (Dutch)
    10) Methylmercaptan
    11) Methyl sulfhydrate
    12) Metilmercaptano (Italian)
    13) Thiomethanol
    14) Thiolmethyl alcohol
    15) CAS 74-93-1
    16) References: AAR, 1987; Budavari, 1996; CHRIS, 1996; RTECS, 2000; HSDB, 2000
    17) CYKLOHEXYLMERKAPTAN (GERMAN)
    1.2.1) MOLECULAR FORMULA
    1) C-H4-S

Available Forms Sources

    A) FORMS
    1) Methyl mercaptan is a colorless, flammable gas that liquefies at 6 degrees C; it is shipped as a liquefied gas (98% pure) under its vapor pressure (AAR, 1998; ACGIH, 1991; (Ashford, 1994; Budavari, 1996; CGA, 1990; Clayton & Clayton, 1994) Hathaway et al, 1996; (ILO, 1998; Lewis, 1996; Lewis, 1997; NFPA, 1997) Raffle et al, 1994; (Verschueren, 1983).
    B) SOURCES
    1) Methyl mercaptan is produced from methanol and hydrogen sulfide, from sodium methyl sulfate and potassium hydrosulfide, and from methyl chloride and sodium hydrosulfide. It is also found as an emission from paper and pulp mills. Methyl mercaptan occurs naturally in a wide variety of vegetables (e.g., onions and garlic), in "sour" gas in West Texas oil fields, in coal tar and petroleum distillates, and it is a major contributor to normal human mouth odor (ACGIH, 1991; (Ashford, 1994; Clayton & Clayton, 1994; Lewis, 1997).
    C) USES
    1) Methyl mercaptan is used as an intermediate in the production of pesticides, fungicides, jet fuel and plastics, in the synthesis of methionine, as a catalyst, and as a gas odorant for natural gas, propane, and butane (ACGIH, 1991; (Budavari, 1996; CGA, 1990; Clayton & Clayton, 1994) Hathaway et al, 1996; (Lewis, 1997; Lewis, 1998).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Methyl mercaptan, also called methanethiol, is a sulfhydryl compound, used as an intermediate in the production of pesticides, fungicides, jet fuel and plastics, in the synthesis of methionine, as a catalyst, and as a gas odorant for natural gas, propane, and butane.
    B) TOXICOLOGY: Methyl mercaptan is a colorless, flammable gas that liquefies at 6 degrees C. It is shipped as a cryogenic liquefied gas (98% pure). Methyl mercaptan causes CNS depression and depresses the respiratory center in a fashion similar to hydrogen sulfide. It appears to have a mechanism of toxicity similar to that of hydrogen sulfide in that it reversibly impairs rat mitochondrial respiration by inhibiting cytochrome C oxidase. One human study has suggested that exposure to methyl mercaptan and inorganic mercaptans may impair heme synthesis by interfering with the activities of enzymes involved in the biosynthetic heme pathway.
    C) EPIDEMIOLOGY: Exposure is rare.
    D) WITH POISONING/EXPOSURE
    1) Lower-level exposure produces eye, skin, and respiratory tract irritation, and signs of CNS depression such as headache, weakness, dizziness, and loss of coordination and judgement. Contact with the liquid or compressed gas may cause frostbite injury. Other symptoms of acute exposure include fever, cough, dyspnea, a feeling of tightness and burning in the chest, nausea, vomiting, diarrhea, tachycardia, hypertension, restlessness, renal dysfunction, proteinuria, and hematuria.
    2) Inhalation of the gas may cause CNS depression, respiratory irritation, respiratory paralysis, pulmonary edema, tremors, and seizures. Pulmonary embolism and pneumonia have rarely been reported in humans. Methemoglobinemia and severe hemolytic anemia with hematuria and proteinuria have been reported in a patient with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency.
    0.2.20) REPRODUCTIVE
    A) There is insufficient information to determine possible reproductive effects of methyl mercaptan in humans or animals.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no studies were found on the possible carcinogenic activity of methyl mercaptan in humans.

Laboratory Monitoring

    A) Serum methyl mercaptan concentrations are not widely available or clinically useful.
    B) Monitor vital signs, mental status, and renal function in symptomatic patients.
    C) Monitor CBC and methemoglobin concentration in patients with cyanosis. If hemolysis is suspected, monitor hemoglobin, hematocrit, plasma free hemoglobin, urinalysis, and perhaps other tests for hemolysis.
    D) Monitor serum electrolyte status in patients with significant vomiting.
    E) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with respiratory symptoms.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment of mild to moderate toxicity consists of predominantly symptomatic and supportive care. For mild/moderate asymptomatic hypertension (no end organ damage), pharmacologic treatment is generally not necessary.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. HYPERTENSION: For severe hypertension, nitroprusside is preferred. Labetalol, nitroglycerin, and phentolamine are alternatives. METHEMOGLOBINEMIA: Symptomatic patients should be treated with methylene blue. Rarely, pediatric patients with severe methemoglobinemia not responsive to methylene blue therapy may require exchange transfusion; patients may be temporized while awaiting transfusion with hyperbaric oxygen therapy. Contraindications to treatment with methylene blue include known G-6-PD deficiency (may cause hemolysis), known hypersensitivity to methylene blue, and methemoglobin reductase deficiency. SEIZURES: Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur.
    C) DECONTAMINATION
    1) PREHOSPITAL: Prehospital gastrointestinal decontamination is generally not recommended because of the potential for CNS depression or persistent seizures and subsequent aspiration.
    2) HOSPITAL: Consider activated charcoal if the overdose is recent, the patient is not vomiting, and is able to maintain airway.
    D) AIRWAY MANAGEMENT
    1) Ensure adequate ventilation and perform endotracheal intubation early in patients with significant CNS and respiratory depression, repeated seizure activity, or functional hypoxia due to methemoglobinemia.
    E) ANTIDOTE
    1) None. Patients with methemoglobinemia should be treated with methylene blue.
    F) ACUTE LUNG INJURY
    1) Supplemental oxygen; PEEP and mechanical ventilation may be needed.
    G) METHEMOGLOBINEMIA
    1) Initiate oxygen therapy. Treat with methylene blue if patient is symptomatic (usually at methemoglobin concentrations greater than 20% to 30% or at lower concentrations in patients with anemia, underlying pulmonary or cardiovascular disease). METHYLENE BLUE: INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules and 10 mg/1 mL (1% solution) vials. Additional doses may sometimes be required. Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection. NEONATES: DOSE: 0.3 to 1 mg/kg.
    H) ENHANCED ELIMINATION
    1) If methemoglobinemia is not corrected with IV methylene blue in a severely symptomatic patient, exchange transfusion should be considered, especially in infants and children.
    I) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients who are asymptomatic or with minimal symptoms after inadvertent exposure to low concentration products and are otherwise improving may be managed at home.
    2) OBSERVATION CRITERIA: Patients with deliberate ingestions, eye exposure, or symptoms should be sent to a healthcare facility for observation until they are clearly improving and clinically stable.
    3) ADMISSION CRITERIA: Patients with worsening symptoms or severe systemic symptoms should be admitted to the hospital for further evaluation.
    4) CONSULT CRITERIA: Consult a medical toxicologist or poison center for any patient with systemic symptoms, severe exposure, or in whom the diagnosis is unclear.
    J) PITFALLS
    1) Missing an ingestion of another chemical or other possible etiologies for a patient’s symptoms. History of exposure may be difficult to obtain in some settings.
    K) TOXICOKINETICS
    1) Absorbed rapidly via inhalation. Absorption via skin and eye exposure is minimal.
    L) DIFFERENTIAL DIAGNOSIS
    1) Includes other agents that can cause respiratory irritation, hypertension, seizures, or methemoglobinemia.
    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) Refer to Oral overview for specific treatment information.
    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.
    3) PREHOSPITAL
    a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).
    4) REWARMING
    a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
    b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
    c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
    d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).
    5) WOUND CARE
    a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
    b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
    c) The injured extremities should be elevated and should not be allowed to bear weight.
    d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
    e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
    f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
    g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
    h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
    i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
    j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
    k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
    l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
    m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
    n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).

Range Of Toxicity

    A) TOXICITY: Human toxicity data are insufficient to be definitive, but methyl mercaptan should be treated as dangerously toxic. Exposure to 4 ppm for several hours caused nausea and headache. Fatalities have been reported after exposure.

Clinical Effects

Summary Of Exposure

    A) USES: Methyl mercaptan, also called methanethiol, is a sulfhydryl compound, used as an intermediate in the production of pesticides, fungicides, jet fuel and plastics, in the synthesis of methionine, as a catalyst, and as a gas odorant for natural gas, propane, and butane.
    B) TOXICOLOGY: Methyl mercaptan is a colorless, flammable gas that liquefies at 6 degrees C. It is shipped as a cryogenic liquefied gas (98% pure). Methyl mercaptan causes CNS depression and depresses the respiratory center in a fashion similar to hydrogen sulfide. It appears to have a mechanism of toxicity similar to that of hydrogen sulfide in that it reversibly impairs rat mitochondrial respiration by inhibiting cytochrome C oxidase. One human study has suggested that exposure to methyl mercaptan and inorganic mercaptans may impair heme synthesis by interfering with the activities of enzymes involved in the biosynthetic heme pathway.
    C) EPIDEMIOLOGY: Exposure is rare.
    D) WITH POISONING/EXPOSURE
    1) Lower-level exposure produces eye, skin, and respiratory tract irritation, and signs of CNS depression such as headache, weakness, dizziness, and loss of coordination and judgement. Contact with the liquid or compressed gas may cause frostbite injury. Other symptoms of acute exposure include fever, cough, dyspnea, a feeling of tightness and burning in the chest, nausea, vomiting, diarrhea, tachycardia, hypertension, restlessness, renal dysfunction, proteinuria, and hematuria.
    2) Inhalation of the gas may cause CNS depression, respiratory irritation, respiratory paralysis, pulmonary edema, tremors, and seizures. Pulmonary embolism and pneumonia have rarely been reported in humans. Methemoglobinemia and severe hemolytic anemia with hematuria and proteinuria have been reported in a patient with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) IRRITATION: Methyl mercaptan is an eye and mucous membrane irritant (Clayton & Clayton, 1994).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Elevated blood pressure occurred in a man fatally exposed to methyl mercaptan (Shults et al, 1970).
    B) TACHYCARDIA
    1) WITH POISONING/EXPOSURE
    a) Tachycardia was noted in man exposed to an unknown concentration leaking from cylinders (Shults et al, 1970).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) PULMONARY EMBOLISM
    1) WITH POISONING/EXPOSURE
    a) A man who developed coma, hemolytic anemia, and methemoglobinemia died 28 days later of a massive embolus which occluded both main pulmonary arteries (Shults et al, 1970).
    B) PNEUMONIA
    1) WITH POISONING/EXPOSURE
    a) Bronchopneumonia was reported in a worker exposed to unknown concentrations (Spacilova, 1971).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RESPIRATORY DEPRESSION
    a) Respiratory depression and apnea were reported in fatally poisoned experimental animals (Gosselin et al, 1984). The respirations are first stimulated, then paralyzed (Ljunggren & Norberg, 1943).
    2) PULMONARY EDEMA
    a) Pulmonary edema occurred in fatally poisoned experimental animals (Gosselin et al, 1984).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) WITH POISONING/EXPOSURE
    a) Irreversible coma developed in a man exposed to an unknown concentration for 1 hour. The man expired 28 days after exposure (Shults et al, 1970).
    B) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Staggering, headache, and dizziness can occur (Clayton & Clayton, 1994; Pickler, 1918).
    b) Headache (statistically significant), dizziness, and decreased ability to concentrate were reported more frequently in workers exposed to methyl mercaptan, hydrogen sulfide, dimethyl sulfide and dimethyl disulfide in the pulp industry, as compared to controls (Kangas et al, 1984).
    C) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Seizures developed in a man 4 days after a one-hour exposure to an unknown concentration of methyl mercaptan (Shults et al, 1970).
    D) FEELING NERVOUS
    1) Restlessness was reported more frequently (not statistically significant) in workers exposed to methyl mercaptan, hydrogen sulfide, dimethyl sulfide and dimethyl disulfide in the pulp industry than in controls (Kangas et al, 1984).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) COMA
    a) Coma occurred in 50% of rats exposed for 15 minutes to a 0.16% concentration. All animals recovered in 30 minutes (Gosselin et al, 1984).
    2) NERVOUSNESS
    a) Restlessness has been reported in fatally poisoned experimental animals (Gosselin et al, 1984).
    3) SEIZURES
    a) Seizures developed in fatally poisoned experimental animals (Ljunggren & Norberg, 1943).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting may occur (Clayton & Clayton, 1994; Pickler, 1918).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) BLOOD IN URINE
    1) WITH POISONING/EXPOSURE
    a) Hematuria and proteinuria were seen in one case of methyl mercaptan poisoning with severe hemolytic anemia and methemoglobinemia (Shults et al, 1970).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) METHEMOGLOBINEMIA
    1) WITH POISONING/EXPOSURE
    a) Methemoglobinemia and severe hemolytic anemia, both of brief duration and associated with a deficiency in red blood cell glucose-6-phosphate dehydrogenase (G-6-PD), occurred in a man exposed to an unknown concentration of methyl mercaptan for about an hour (Shults et al, 1970).
    B) ERYTHROCYTE ENZYME DEFICIENCY
    1) WITH POISONING/EXPOSURE
    a) A study of 17 workers reported decreased delta-aminolevulinic acid synthetase and heme synthetase activities in 8 and 6 workers, respectively. Erythrocyte protoporphyrin was also below the normal range in 7 cases. Eight hour time weighted average (TWA) exposure concentrations included 0.07 to 2.0 ppm methyl mercaptan (ACGIH 8 hour TWA 0.5 ppm), 0.05 to 5.2 ppm (ACGIH 8 hour TWA 10 ppm), and 0.03 to 3.2 ppm dimethyl sulfide (Tenhunen et al, 1983; ACGIH, 1996).
    b) Decreased activities of heme synthase and delta-aminolevulinic acid synthetase were reported in another study involving workplace exposure to low mean concentrations of methyl mercaptan (less than 0.2 ppm), dimethylsulfide and dimethyldisulfide (less than 0.05 ppm). Compared to enzyme activities in unexposed controls, these decreases were not statistically significant (Klingberg et al, 1988).
    C) DISORDER OF IRON METABOLISM
    1) WITH POISONING/EXPOSURE
    a) Concentrations of serum iron and transferrin were significantly higher and ferritin significantly lower in 5 workers with high exposure to methyl mercaptan, dimethylsulfide, and dimethyldisulfide as compared to an unexposed referent group, possibly indicating that methyl mercaptan and sulfide exposure disturbs iron metabolism (Klingberg et al, 1988).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Dermatitis has developed in workers exposed to chronic, low level concentrations (Kvartovkina & Meerson, 1974).
    B) FROSTBITE
    1) WITH POISONING/EXPOSURE
    a) Frostbite injury can result from dermal exposure to liquid methyl mercaptan (Chemsoft(R) , 1996; OHM/TADS , 1996).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) INCREASED MUSCLE TONE
    1) WITH POISONING/EXPOSURE
    a) Muscular rigidity of the extremities occurred in one man exposed to an unknown concentration of methyl mercaptan (Shults et al, 1970).

Reproductive

    3.20.1) SUMMARY
    A) There is insufficient information to determine possible reproductive effects of methyl mercaptan in humans or animals.
    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.
    3.20.5) FERTILITY
    A) OCCUPATIONAL EXPOSURE
    1) Reproductive function disorders were reported in female workers exposed to chronic, low level concentrations (Kvartovkina & Meerson, 1974). Details were not available. Exposure to other chemicals, such as carbon disulfide, also occurred.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS74-93-1 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no studies were found on the possible carcinogenic activity of methyl mercaptan in humans.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Serum methyl mercaptan concentrations are not widely available or clinically useful.
    B) Monitor vital signs, mental status, and renal function in symptomatic patients.
    C) Monitor CBC and methemoglobin concentration in patients with cyanosis. If hemolysis is suspected, monitor hemoglobin, hematocrit, plasma free hemoglobin, urinalysis, and perhaps other tests for hemolysis.
    D) Monitor serum electrolyte status in patients with significant vomiting.
    E) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with respiratory symptoms.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) One study recommended that erythrocyte protoporphyrin levels be measured in chronically exposed individuals (Kangas et al, 1984). Hydrogen sulfide and the organic sulfides may affect heme synthesizing enzymes via inhibition of cytochrome oxidase (Tenhunen et al, 1983).
    B) HEMATOLOGIC
    1) Monitor methemoglobin levels in cyanotic patients.
    2) If hemolysis is suspected, monitor hemoglobin, hematocrit, plasma free hemoglobin, urinalysis, and perhaps other tests for hemolysis.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with worsening symptoms or severe systemic symptoms should be admitted to the hospital for further evaluation.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients who are asymptomatic or with minimal symptoms after inadvertent exposure to low concentration products and are otherwise improving may be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a medical toxicologist or poison center for any patient with systemic symptoms, severe exposure, or in whom the diagnosis is unclear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with deliberate ingestions, eye exposure, or symptoms should be sent to a healthcare facility for observation until they are clearly improving and clinically stable.

Monitoring

    A) Serum methyl mercaptan concentrations are not widely available or clinically useful.
    B) Monitor vital signs, mental status, and renal function in symptomatic patients.
    C) Monitor CBC and methemoglobin concentration in patients with cyanosis. If hemolysis is suspected, monitor hemoglobin, hematocrit, plasma free hemoglobin, urinalysis, and perhaps other tests for hemolysis.
    D) Monitor serum electrolyte status in patients with significant vomiting.
    E) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with respiratory symptoms.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Prehospital gastrointestinal decontamination is generally not recommended because of the potential for CNS depression or persistent seizures and subsequent aspiration.
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment of mild to moderate toxicity consists of predominantly symptomatic and supportive care. For mild/moderate asymptomatic hypertension (no end organ damage), pharmacologic treatment is generally not necessary.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. HYPERTENSION: For severe hypertension, nitroprusside is preferred. Labetalol, nitroglycerin, and phentolamine are alternatives. METHEMOGLOBINEMIA: Symptomatic patients should be treated with methylene blue. Rarely, pediatric patients with severe methemoglobinemia not responsive to methylene blue therapy may require exchange transfusion; patients may be temporized while awaiting transfusion with hyperbaric oxygen therapy. Contraindications to treatment with methylene blue include known G-6-PD deficiency (may cause hemolysis), known hypersensitivity to methylene blue, and methemoglobin reductase deficiency. SEIZURES: Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur.
    B) MONITORING OF PATIENT
    1) Serum methyl mercaptan concentrations are not widely available or clinically useful.
    2) Monitor vital signs, mental status, and renal function in symptomatic patients.
    3) Monitor CBC and methemoglobin concentration in patients with cyanosis. If hemolysis is suspected, monitor hemoglobin, hematocrit, plasma free hemoglobin, urinalysis, and perhaps other tests for hemolysis.
    4) Monitor serum electrolyte status in patients with significant vomiting.
    5) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with respiratory symptoms.
    C) OXYGEN
    1) Administer oxygen; administer artificial respiration if required. Oxygen inhalation is recommended even after respiration has resumed (CHRIS , 1985).
    D) 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).
    E) 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).
    F) METHEMOGLOBINEMIA
    1) SUMMARY
    a) Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy.
    2) METHYLENE BLUE
    a) INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules (Prod Info PROVAYBLUE(TM) intravenous injection, 2016) and 10 mg/1 mL (1% solution) vials (Prod Info methylene blue 1% intravenous injection, 2011). REPEAT DOSES: Additional doses may be required, especially for substances with prolonged absorption, slow elimination, or those that form metabolites that produce methemoglobin. NOTE: Large doses of methylene blue may cause methemoglobinemia or hemolysis (Howland, 2006). Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection (Prod Info methylene blue 1% intravenous injection, 2011; Herman et al, 1999). NEONATES: DOSE: 0.3 to 1 mg/kg (Hjelt et al, 1995).
    b) CONTRAINDICATIONS: G-6-PD deficiency (methylene blue may cause hemolysis), known hypersensitivity to methylene blue, methemoglobin reductase deficiency (Shepherd & Keyes, 2004)
    c) FAILURE: Failure of methylene blue therapy suggests: inadequate dose of methylene blue, inadequate decontamination, NADPH dependent methemoglobin reductase deficiency, hemoglobin M disease, sulfhemoglobinemia, or G-6-PD deficiency. Methylene blue is reduced by methemoglobin reductase and nicotinamide adenosine dinucleotide phosphate (NADPH) to leukomethylene blue. This in turn reduces methemoglobin. Red blood cells of patients with G-6-PD deficiency do not produce enough NADPH to convert methylene blue to leukomethylene blue (do Nascimento et al, 2008).
    d) DRUG INTERACTION: Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome (U.S. Food and Drug Administration, 2011; Stanford et al, 2010; Prod Info methylene blue 1% IV injection, 2011).
    3) TOLUIDINE BLUE OR TOLONIUM CHLORIDE (GERMANY)
    a) DOSE: 2 to 4 mg/kg intravenously over 5 minutes. Dose may be repeated in 30 minutes (Nemec, 2011; Lindenmann et al, 2006; Kiese et al, 1972).
    b) SIDE EFFECTS: Hypotension with rapid intravenous administration. Vomiting, diarrhea, excessive sweating, hypotension, dysrhythmias, hemolysis, agranulocytosis and acute renal insufficiency after overdose (Dunipace et al, 1992; Hix & Wilson, 1987; Winek et al, 1969; Teunis et al, 1970; Marquez & Todd, 1959).
    c) CONTRAINDICATIONS: G-6-PD deficiency; may cause hemolysis.
    G) HYPERTENSIVE EPISODE
    1) Monitor vital signs regularly. For mild/moderate hypertension without evidence of end organ damage, pharmacologic intervention is generally not necessary. Sedative agents such as benzodiazepines may be helpful in treating hypertension and tachycardia in agitated patients, especially if a sympathomimetic agent is involved in the poisoning.
    2) For hypertensive emergencies (severe hypertension with evidence of end organ injury (CNS, cardiac, renal), or emergent need to lower mean arterial pressure 20% to 25% within one hour), sodium nitroprusside is preferred. Nitroglycerin and phentolamine are possible alternatives.
    3) SODIUM NITROPRUSSIDE/INDICATIONS
    a) Useful for emergent treatment of severe hypertension secondary to poisonings. Sodium nitroprusside has a rapid onset of action, a short duration of action and a half-life of about 2 minutes (Prod Info NITROPRESS(R) injection for IV infusion, 2007) that can allow accurate titration of blood pressure, as the hypertensive effects of drug overdoses are often short lived.
    4) SODIUM NITROPRUSSIDE/DOSE
    a) ADULT: Begin intravenous infusion at 0.1 microgram/kilogram/minute and titrate to desired effect; up to 10 micrograms/kilogram/minute may be required (American Heart Association, 2005). Frequent hemodynamic monitoring and administration by an infusion pump that ensures a precise flow rate is mandatory (Prod Info NITROPRESS(R) injection for IV infusion, 2007). PEDIATRIC: Initial: 0.5 to 1 microgram/kilogram/minute; titrate to effect up to 8 micrograms/kilogram/minute (Kleinman et al, 2010).
    5) SODIUM NITROPRUSSIDE/SOLUTION PREPARATION
    a) The reconstituted 50 mg solution must be further diluted in 250 to 1000 mL D5W to desired concentration (recommended 50 to 200 mcg/mL) (Prod Info NITROPRESS(R) injection, 2004). Prepare fresh every 24 hours; wrap in aluminum foil. Discard discolored solution (Prod Info NITROPRESS(R) injection for IV infusion, 2007).
    6) SODIUM NITROPRUSSIDE/MAJOR ADVERSE REACTIONS
    a) Severe hypotension; headaches, nausea, vomiting, abdominal cramps; thiocyanate or cyanide toxicity (generally from prolonged, high dose infusion); methemoglobinemia; lactic acidosis; chest pain or dysrhythmias (high doses) (Prod Info NITROPRESS(R) injection for IV infusion, 2007). The addition of 1 gram of sodium thiosulfate to each 100 milligrams of sodium nitroprusside for infusion may help to prevent cyanide toxicity in patients receiving prolonged or high dose infusions (Prod Info NITROPRESS(R) injection for IV infusion, 2007).
    7) SODIUM NITROPRUSSIDE/MONITORING PARAMETERS
    a) Monitor blood pressure every 30 to 60 seconds at onset of infusion; once stabilized, monitor every 5 minutes. Continuous blood pressure monitoring with an intra-arterial catheter is advised (Prod Info NITROPRESS(R) injection for IV infusion, 2007).
    8) PHENTOLAMINE/INDICATIONS
    a) Useful for severe hypertension, particularly if caused by agents with alpha adrenergic agonist effects usually induced by catecholamine excess (Rhoney & Peacock, 2009).
    9) PHENTOLAMINE/ADULT DOSE
    a) BOLUS DOSE: 5 to 15 mg IV bolus repeated as needed (U.S. Departement of Health and Human Services, National Institutes of Health, and National Heart, Lung, and Blood Institute, 2004). Onset of action is 1 to 2 minutes with a duration of 10 to 30 minutes (Rhoney & Peacock, 2009).
    b) CONTINUOUS INFUSION: 1 mg/hr, adjusted hourly to stabilize blood pressure. Prepared by adding 60 mg of phentolamine mesylate to 100 mL of 0.9% sodium chloride injection; continuous infusion ranging from 12 to 52 mg/hr over 4 days has been used in case reports (McMillian et al, 2011).
    10) PHENTOLAMINE/PEDIATRIC DOSE
    a) 0.05 to 0.1 mg/kg/dose (maximum of 5 mg per dose) intravenously every 5 minutes until hypertension is controlled, then every 2 to 4 hours as needed (Singh et al, 2012; Koch-Weser, 1974).
    11) PHENTOLAMINE/ADVERSE EFFECTS
    a) Adverse events can include orthostatic or prolonged hypotension, tachycardia, dysrhythmias, angina, flushing, headache, nasal congestion, nausea, vomiting, abdominal pain and diarrhea (Rhoney & Peacock, 2009; Prod Info Phentolamine Mesylate IM, IV injection Sandoz Standard, 2005).
    12) CAUTION
    a) Phentolamine should be used with caution in patients with coronary artery disease because it may induce angina or myocardial infarction (Rhoney & Peacock, 2009).
    13) NITROGLYCERIN/INDICATIONS
    a) May be used to control hypertension, and is particularly useful in patients with acute coronary syndromes or acute pulmonary edema (Rhoney & Peacock, 2009).
    14) NITROGLYCERIN/ADULT DOSE
    a) Begin infusion at 10 to 20 mcg/min and increase by 5 or 10 mcg/min every 5 to 10 minutes until the desired hemodynamic response is achieved (American Heart Association, 2005). Maximum rate 200 mcg/min (Rhoney & Peacock, 2009).
    15) NITROGLYCERIN/PEDIATRIC DOSE
    a) Usual Dose: 29 days or Older: 1 to 5 mcg/kg/min continuous IV infusion. Maximum 60 mcg/kg/min (Laitinen et al, 1997; Nam et al, 1989; Rasch & Lancaster, 1987; Ilbawi et al, 1985; Friedman & George, 1985).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) SUPPORT
    1) Refer to Oral exposure for specific treatment information.
    2) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment of mild to moderate toxicity consists of predominantly symptomatic and supportive care. For mild/moderate asymptomatic hypertension (no end organ damage), pharmacologic treatment is generally not necessary.
    3) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. HYPERTENSION: For severe hypertension, nitroprusside is preferred. Labetalol, nitroglycerin, and phentolamine are alternatives. METHEMOGLOBINEMIA: Symptomatic patients should be treated with methylene blue. Rarely, pediatric patients with severe methemoglobinemia not responsive to methylene blue therapy may require exchange transfusion; patients may be temporized while awaiting transfusion with hyperbaric oxygen therapy. Contraindications to treatment with methylene blue include known G-6-PD deficiency (may cause hemolysis), known hypersensitivity to methylene blue, and methemoglobin reductase deficiency. SEIZURES: Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur.
    B) 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) FROSTBITE
    1) PREHOSPITAL
    a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).
    2) REWARMING
    a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
    b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
    c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
    d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).
    3) WOUND CARE
    a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
    b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
    c) The injured extremities should be elevated and should not be allowed to bear weight.
    d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
    e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
    f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
    g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
    h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
    i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
    j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
    k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
    l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
    m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
    n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).
    B) 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.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) TOXICITY: Human toxicity data are insufficient to be definitive, but methyl mercaptan should be treated as dangerously toxic. Exposure to 4 ppm for several hours caused nausea and headache. Fatalities have been reported after exposure.

Minimum Lethal Exposure

    A) Human toxicity data are insufficient to be definitive, but methyl mercaptan should be treated as dangerously toxic (ACGIH, 1996; Clayton & Clayton, 1994; Hathaway et al, 1996; Lewis, 1998).

Maximum Tolerated Exposure

    A) Methyl mercaptan is a central nervous system (CNS) depressant and is extremely irritating to the eyes and the respiratory system. Signs and symptoms of exposure to methyl mercaptan include eye and mucous membrane irritation, headache, dizziness, staggering gait, nausea, and vomiting. Lower concentrations cause pulmonary edema; higher concentrations can cause hepatic and renal damage, coma, and death by respiratory paralysis (similar to hydrogen sulfide) (ACGIH, 1996; Clayton & Clayton, 1994; Hathaway et al, 1996) Raffle et al, 1994).
    1) Odor and symptoms of irritation do not provide adequate warning of exposure to high concentrations of methyl mercaptan due to olfactory fatigue (Clayton & Clayton, 1994).
    2) Exposure to 4 ppm resulted in nausea, headache and, in one of 28 cases, slight liver damage (Pickler, 1918).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CASE REPORTS
    a) An unpublished industrial report reviewed by Farr & Kirwin (1994) described a lethal methyl mercaptan exposure involving a 19-year-old male (Syntex Corporation, 1979). The reported methyl mercaptan blood level was at least 2.5 nanomoles per cubic centimeter of blood. Mishandling of the sample may have underrepresented the actual blood methyl mercaptan level (Farr & Kirwin, 1994).

Workplace Standards

    A) ACGIH TLV Values for CAS74-93-1 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Methyl mercaptan
    a) TLV:
    1) TLV-TWA: 0.5 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): Liver dam
    d) Molecular Weight: 48.11
    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 CAS74-93-1 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Methyl mercaptan
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling: 0.5 ppm (1 mg/m(3)) [15-minute]
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 150 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS74-93-1 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Methyl mercaptan
    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 ; Listed as: Methyl mercaptan
    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 CAS74-93-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Methyl mercaptan
    2) Table Z-1 for Methyl mercaptan:
    a) 8-hour TWA:
    1) ppm: 10
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 20
    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: (C) - An employee's exposure to this substance shall at no time exceed the exposure limit given.
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES

Pharmacology Toxicology

Toxicologic Mechanism

    A) CNS DEPRESSION/RESPIRATORY DEPRESSION - Methyl mercaptan causes CNS depression and depresses the respiratory center in a fashion similar to hydrogen sulfide (Farr & Kirwin, 1996).
    B) IMPAIRED OXIDATIVE PHOSPHORYLATION - Methyl mercaptan appears to have a mechanism of toxicity similar to that of hydrogen sulfide in that it reversibly impairs rat mitochondrial respiration by inhibiting cytochrome C oxidase (Vahlkamp et al, 1979). It is much less potent (in rats, about 10- fold less potent) in this respect than hydrogen sulfide (Ljunggren & Norberg, 1943) Jappinen et al, 1993).
    C) IMPAIRED HEME SYNTHESIS - One human study has suggested that exposure to methyl mercaptan and inorganic mercaptans may impair heme synthesis by interfering with the activities of enzymes involved in the biosynthetic heme pathway (Tenhunen et al, 1983). Decreased activities of omega-aminolaevulinic acid synthase and heme synthase, and decreased erythrocyte protoporphyrin levels were measured in workers exposed to methyl mercaptan, hydrogen sulfide, and dimethylsulfide.
    D) IMPAIRED IRON METABOLISM - Impairment of iron metabolism was suggested in one study in which 5 workers with high exposure to methylmercaptan, hydrogen sulfide, and dimethylsulfide had increased serum iron and transferrin levels, but decreased ferritin concentrations (Klingberg et al, 1988).
    E) IMPAIRED SODIUM-POTASSIUM ATPASE -
    1) This chemical also inhibits rat brain sodium and potassium ATPase (Foster et al, 1974; Quarfoth et al, 1976; Waller, 1977).
    2) It has been proposed that methyl mercaptan produced in vivo in persons or animals with liver disease may be linked to the development of hepatic encephalopathy or coma, possibly through effects on sodium-potassium ATPase (Quarfoth et al, 1976; Zieve et al, 1984; Zieve & Nagasawa, 1988). Others have disputed the role of methyl mercaptan in hepatic encephalopathy or coma (Al Mardini et al, 1984; Blom et al, 1990).
    F) REDUCED CATALASE ACTIVITY - Methyl mercaptan depresses catalase activity in incubated rat erythrocytes, spleen cells and hepatocytes (Finkelstein & Benevenga, 1986). Catalase is an enzyme involved in protecting the cell from oxidative damage.

Physicochemical

Physical Characteristics

    A) Methyl mercaptan is a colorless, flammable gas that liquefies at 6 degrees C and has a strong, very disagreeable, "rotten cabbage" odor. The odor is similar to hydrogen sulfide, but it can be detected at much lower concentrations (ACGIH, 1991; (Ashford, 1994; Budavari, 1996; CGA, 1990; Clayton & Clayton, 1994) Hathaway et al, 1996; (ILO, 1998; Lewis, 1996; Lewis, 1997) HSDB, 2000).

Ph

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

Molecular Weight

    A) 48.11

Other

    A) ODOR THRESHOLD
    1) 1.1 ppb (Verschueren, 1983)
    2) 2 ppb (Clayton & Clayton, 1994)

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