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NITROMETHANE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Nitromethane is a nitroparaffin compound (a nitro derivative of a saturated aliphatic hydrocarbon), prepared by interaction of sodium chloroacetate and sodium nitrite (Budavari, 1989; Grant, 1986).
    B) It is used as a solvent for cellulose compounds, polymers, waxes, and fats, in organic chemical synthesis, as a rocket fuel, as a gasoline additive, in petroleum refining, in the coating industry, and as an aircraft engine fuel (Budavari, 1989; ACGIH, 1986; Gosselin et al, 1984; Proctor et al, 1988; ITI, 1985).
    C) Nitromethane has been identified as a contaminant in technical grade 1,1,1-trichloroethane (Henschler et al, 1980).

Specific Substances

    1) Methane, nitro
    2) Nitrocarbol
    3) Nitrometan (Polish)
    4) Nitromethane
    5) CAS 75-52-5
    6) References: RTECS, 1990; Sax & Lewis, 1989
    1.2.1) MOLECULAR FORMULA
    1) CH3-NO2

Available Forms Sources

    A) FORMS
    1) Nitromethane is available in grades of 95 to 99% purity (CHRIS , 2000).
    B) SOURCES
    1) Nitromethane is produced when sodium nitrite and sodium chloroacetate interact or when methane or propane react under pressure with nitric acid. When propane is used in the production of nitromethane, nitroethane and nitropropane will also be formed. The compounds can be separated by fractional distillation (Budavari, 1996; Clayton & Clayton, 1993; Lewis, 1997; Snyder et al, 1990).
    C) USES
    1) Nitromethane is used as a fuel for rockets and racing cars, a gasoline additive, a chemical stabilizer, a chemical intermediate, a solvent, and a component in explosive mixtures (ACGIH, 1996; Hathaway et al, 1996; ITI, 1995; Lewis, 1997; Sittig, 1991).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Nitromethane is a skin, eye, and mucous membrane irritant. Anorexia, nausea, vomiting, diarrhea, cough, dizziness, headache, CNS depression and dermatitis may occur. Experimental animals have developed focal necrosis of the liver and kidney, depressed hemoglobin and hematocrit concentrations, decreased weight gain, weakness, ataxia, and seizures.
    B) Thermal decomposition may release oxides of nitrogen with the potential for serious respiratory tract irritation and pulmonary edema.
    C) Methemoglobinemia and anuria are rare effects of exposure to both nitromethane and nitrocellulose.
    0.2.6) RESPIRATORY
    A) Nitromethane vapors may cause irritation of the respiratory tract mucosa. Evolved oxides of nitrogen may cause acute bronchiolitis or pulmonary edema.
    0.2.7) NEUROLOGIC
    A) Experimental animals have had narcosis, ataxia, and seizures.
    0.2.13) HEMATOLOGIC
    A) One case of methemoglobinemia and anuria has been reported.
    0.2.14) DERMATOLOGIC
    A) Dermal irritation may occur.
    0.2.20) REPRODUCTIVE
    A) Nitromethane has been found in human breast milk (HSDB). At the time of this review, no other reproductive studies were found for nitromethane in humans or experimental animals.

Laboratory Monitoring

    A) Monitor urinalysis and liver and renal function tests. May falsely elevate serum creatinine. Patients with significant inhalation exposure or respiratory tract irritation should have arterial blood gases and chest x-ray monitored. Methemoglobin levels should be obtained in cyanotic patients.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and seizures.
    B) 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.
    C) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    0.4.3) INHALATION EXPOSURE
    A) 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) 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.
    C) METHEMOGLOBINEMIA: 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.
    D) 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.
    E) 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.
    F) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    0.4.4) 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).

Range Of Toxicity

    A) The maximum tolerated and minimum lethal human exposures have not been determined.

Clinical Effects

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) Anorexia, nausea, vomiting, and diarrhea may occur (Sax & Lewis, 1989).

Hepatic

    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATIC NECROSIS
    a) Experimental animals exposed to large doses of nitromethane have been noted to have focal hepatic necrosis at necropsy (Hathaway et al, 1996). This effect has NOT been reported in exposed humans.

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ANURIA
    1) One case of anuria associated with methemoglobinemia occurred during the handling of both nitromethane and nitrocellulose (Kaiffer et al, 1972).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NECROSIS ISCHEMIC
    a) Experimental animals exposed to large doses of nitromethane have been noted to have focal kidney necrosis at necropsy (Hathaway et al, 1996). This effect has NOT been reported in exposed humans.

Hematologic

    3.13.1) SUMMARY
    A) One case of methemoglobinemia and anuria has been reported.
    3.13.2) CLINICAL EFFECTS
    A) METHEMOGLOBINEMIA
    1) CASE REPORT - One case of methemoglobinemia with associated anuria has been reported following exposure to both nitromethane and nitrocellulose (Kaiffer et al, 1972).

Dermatologic

    3.14.1) SUMMARY
    A) Dermal irritation may occur.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Mildly irritating to the skin and mucous membranes (Henschler et al, 1980).

Endocrine

    3.16.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) THYROXINE DECREASED
    a) RABBITS - Some rabbits exposed to 745 parts per million of nitromethane for 8 weeks developed increased thyroid weight and decreased serum thyroxine levels (Lewis et al, 1979). These effects have NOT be reported in exposed humans.

Reproductive

    3.20.1) SUMMARY
    A) Nitromethane has been found in human breast milk (HSDB). At the time of this review, no other reproductive studies were found for nitromethane in humans or experimental animals.
    3.20.2) TERATOGENICITY
    A) HUMANS
    1) LACK OF INFORMATION
    a) At the time of this review, no data were available to assess the teratogenic potential of nitromethane.
    3.20.3) EFFECTS IN PREGNANCY
    A) HUMANS
    1) LACK OF INFORMATION
    a) At the time of this review, no data were available to assess the potential effects of nitromethane exposure during pregnancy and lactation.
    b) There is a concern that the fetus may have increased sensitivity to the effects of oxygen deprivation from induction of methemoglobinemia. Fetal hemoglobin is more readily oxidized to methemoglobin than the adult form, fetal hemoglobin is not reduced back to normal hemoglobin as readily as the adult form, and the fetus may be more sensitive than the adult to changes in oxygen transport.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS75-52-5 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: Nitromethane
    b) Carcinogen Rating: 2B
    1) The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential carcinogenicity of nitromethane, with the exception of one subchronic inhalation toxicity study of nitromethane and 2-nitropropane, where hepatic tumors were found in animals exposed to 2-nitropropane but not in animals with nitromethane exposure (Lewis et al, 1979). This cannot be taken as conclusive evidence that nitromethane has no carcinogenic potential.
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) Nitromethane was not carcinogenic in rats following exposure to 100 or 200 ppm for 2 years (Griffin et al, 1996).
    2) In one subchronic inhalation toxicity study of nitromethane and 2-nitropropane, hepatic tumors were found in animals exposed to 2-nitropropane but not in animals with nitromethane exposure (Lewis et al, 1979).

Summary Of Exposure

    A) Nitromethane is a skin, eye, and mucous membrane irritant. Anorexia, nausea, vomiting, diarrhea, cough, dizziness, headache, CNS depression and dermatitis may occur. Experimental animals have developed focal necrosis of the liver and kidney, depressed hemoglobin and hematocrit concentrations, decreased weight gain, weakness, ataxia, and seizures.
    B) Thermal decomposition may release oxides of nitrogen with the potential for serious respiratory tract irritation and pulmonary edema.
    C) Methemoglobinemia and anuria are rare effects of exposure to both nitromethane and nitrocellulose.

Heent

    3.4.3) EYES
    A) Conjunctival irritation may occur from exposure to vapors (Grant & Schuman, 1993).
    3.4.5) NOSE
    A) Irritation of the mucosa of the nose and throat may be seen with vapor exposure (Gosselin et al, 1984; Plunkett, 1976).
    3.4.6) THROAT
    A) Irritation of the mucosa of the nose and throat may be seen with vapor exposure (Gosselin et al, 1984; Plunkett, 1976).

Respiratory

    3.6.1) SUMMARY
    A) Nitromethane vapors may cause irritation of the respiratory tract mucosa. Evolved oxides of nitrogen may cause acute bronchiolitis or pulmonary edema.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Nitromethane vapors cause irritation of the respiratory tract mucosa (Gosselin et al, 1984; Hathaway et al, 1996).
    2) With exposure to oxides of nitrogen released from nitromethane by thermal decomposition (Sax & Lewis, 1989), the potential exists for development of an acute bronchiolitis with cough, hyperpnea, and dyspnea (Kizer, 1984).
    B) ACUTE LUNG INJURY
    1) With exposure to oxides of nitrogen evolved from nitromethane by thermal decomposition (Sax & Lewis, 1989), noncardiogenic pulmonary edema may develop with a potential for slow onset (Kizer, 1984), but no human cases have been reported from such an exposure.
    C) BRONCHOSPASM
    1) Bronchiolar spasm with wheezing and possible laryngospasm might occur following exposure to high concentrations of nitrogen oxides (Kizer, 1984) evolved from thermal decomposition of nitromethane (Sax & Lewis, 1989). No human cases have been reported from such an exposure.
    D) PNEUMONIA
    1) Late sequelae of exposure to oxides of nitrogen evolved from thermal decomposition of nitromethane (Sax & Lewis, 1989) might be bronchiolitis obliterans and chronic interstitial lung disease (Kizer, 1984). No human cases have been reported from such an exposure.

Neurologic

    3.7.1) SUMMARY
    A) Experimental animals have had narcosis, ataxia, and seizures.
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CNS DEPRESSION
    a) Experimental animals exposed to large doses of nitromethane have experienced narcosis (Hathaway et al, 1996). This effect has NOT been reported in exposed humans.
    2) ATAXIA
    a) Experimental animals exposed to large doses of nitromethane have experienced ataxia (Hathaway et al, 1996). This effect has NOT been reported in exposed humans.
    3) SEIZURES
    a) Experimental animals exposed to large doses of nitromethane have experienced seizures immediately prior to death (Hathaway et al, 1996). This effect has NOT been reported in exposed humans.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor urinalysis and liver and renal function tests. May falsely elevate serum creatinine. Patients with significant inhalation exposure or respiratory tract irritation should have arterial blood gases and chest x-ray monitored. Methemoglobin levels should be obtained in cyanotic patients.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Patients with significant exposure should have baseline liver and renal function tests repeat as indicated. Animal data have shown a potential for the development of hepatotoxicity.
    B) ENDOCRINE
    1) If the history or physical examination suggest an enlarged thyroid gland or possible hyperthyroidism, thyroid hormone levels and other thyroid testing as indicated should be performed.
    C) ACID/BASE
    1) Patients with significant inhalation exposure to oxides of nitrogen released from thermal decomposition of nitromethane (Sax & Lewis, 1989) or symptoms of respiratory tract irritation should have baseline arterial blood gases.
    D) HEMATOLOGIC
    1) If cyanosis is present following nitromethane exposure, methemoglobinemia should be suspected and methemoglobin levels obtained.
    E) LABORATORY INTERFERENCE
    1) CREATININE - Nitromethane has been shown to interfere with the Jaffe reaction in the assay for serum creatinine (Rastogi et al, 2008). De Leacy et al (1989) showed that serum creatinine concentrations were falsely elevated in the presence of nitromethane, and elevations were linearly related to the serum nitromethane concentration.
    a) CASE SERIES - Two patients developed falsely elevated serum creatinine levels of 17.9 mg/dL and 17.5 mg/dL, respectively, after exposure to nitromethane. The first patient had ingested nitromethane while the second patient had dermal exposure. The falsely elevated levels were due to nitromethane interference with the Jaffe reaction (Mullins & Hammett-Stabler, 1998).
    4.1.3) URINE
    A) URINALYSIS
    1) Patients with significant exposure should have baseline urinalysis repeat as indicated.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Patients with significant inhalation exposure to oxides of nitrogen released from thermal decomposition of nitromethane (Sax & Lewis, 1989) or symptoms of respiratory tract irritation should have baseline chest x-ray.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.1) ADMISSION CRITERIA/INHALATION
    A) Patients with signs of respiratory tract irritation following inhalation of evolved oxides of nitrogen are at risk for delayed development (up to 72 hours) of pulmonary edema and should probably be admitted.
    B) Patients with systemic symptoms following nitromethane exposure should probably be admitted for evaluation.
    6.3.3.2) HOME CRITERIA/INHALATION
    A) Patients discharged home following inhalation exposure to evolved oxides of nitrogen should be warned about the possibility for delayed onset of serious respiratory illnesses and advised to seek medical care immediately should such occur.

Monitoring

    A) Monitor urinalysis and liver and renal function tests. May falsely elevate serum creatinine. Patients with significant inhalation exposure or respiratory tract irritation should have arterial blood gases and chest x-ray monitored. Methemoglobin levels should be obtained in cyanotic patients.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and seizures.
    B) 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) EMESIS/NOT RECOMMENDED
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and seizures.
    B) 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.
    C) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) Most exposures can be expected to occur by inhalation. MORE RECOMMENDATIONS APPEAR IN THE INHALATION EXPOSURE SECTION BELOW.
    B) MONITORING OF PATIENT
    1) Obtain baseline urinalysis and liver and renal function tests. If there are symptoms suggesting hyperthyroidism or an enlarged thyroid gland on examination, thyroid hormone levels and other indicated thyroid testing should be performed.

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) Patients with respiratory tract irritation or significant vapor or evolved oxides of nitrogen exposure should be administered 100% supplemental oxygen with assisted ventilation as required.
    B) MONITORING OF PATIENT
    1) Patients with respiratory tract irritation or significant vapor or evolved oxides of nitrogen exposure should have baseline arterial blood gases and chest x-ray with follow-up as indicated.
    C) BRONCHOSPASM
    1) Patients with evolved oxides of nitrogen exposure and bronchiolar spasm may require treatment with inhaled sympathomimetic bronchodilators. Corticosteroid administration is controversial in this setting.
    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) 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.
    F) 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).
    7) PHENYTOIN/FOSPHENYTOIN
    a) Benzodiazepines and/or barbiturates are preferred to phenytoin or fosphenytoin in the treatment of drug or withdrawal induced seizures (Wallace, 2005).
    b) PHENYTOIN
    1) PHENYTOIN INTRAVENOUS PUSH VERSUS INTRAVENOUS INFUSION
    a) Administer phenytoin undiluted, by very slow intravenous push or dilute 50 mg/mL solution in 50 to 100 mL of 0.9% saline.
    b) ADULT DOSE: A loading dose of 20 mg/kg IV; may administer an additional 5 to 10 mg/kg dose 10 minutes after loading dose. Rate of administration should not exceed 50 mg/minute (Brophy et al, 2012).
    c) PEDIATRIC DOSE: A loading dose of 20 mg/kg, at a rate not exceeding 1 to 3 mg/kg/min or 50 mg/min, whichever is slower (Loddenkemper & Goodkin, 2011; Prod Info Dilantin(R) intravenous injection, intramuscular injection, 2013).
    d) CAUTIONS: Administer phenytoin while monitoring ECG. Stop or slow infusion if dysrhythmias or hypotension occur. Be careful not to extravasate. Follow each injection with injection of sterile saline through the same needle (Prod Info Dilantin(R) intravenous injection, intramuscular injection, 2013).
    e) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over next 12 to 24 hours for maintenance of therapeutic concentrations. Therapeutic concentrations of 10 to 20 mcg/mL have been reported (Prod Info Dilantin(R) intravenous injection, intramuscular injection, 2013).
    c) FOSPHENYTOIN
    1) ADULT DOSE: A loading dose of 20 mg phenytoin equivalent/kg IV, at a rate not exceeding 150 mg phenytoin equivalent/minute; may give additional dose of 5 mg/kg 10 minutes after the loading infusion (Brophy et al, 2012).
    2) CHILD DOSE: 20 mg phenytoin equivalent/kg IV, at a rate of 3 mg phenytoin equivalent/kg/minute, up to a maximum of 150 mg phenytoin equivalent/minute (Loddenkemper & Goodkin, 2011).
    3) CAUTIONS: Perform continuous monitoring of ECG, respiratory function, and blood pressure throughout the period where maximal serum phenytoin concentrations occur (about 10 to 20 minutes after the end of fosphenytoin infusion) (Prod Info CEREBYX(R) intravenous injection, 2014).
    4) SERUM CONCENTRATION MONITORING: Monitor serum phenytoin concentrations over the next 12 to 24 hours; therapeutic levels 10 to 20 mcg/mL. Do not obtain serum phenytoin concentrations until at least 2 hours after infusion is complete to allow for conversion of fosphenytoin to phenytoin (Prod Info CEREBYX(R) intravenous injection, 2014).
    G) 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).

Enhanced Elimination

    A) SUMMARY
    1) No studies have assessed the potential utility of extracorporeal elimination techniques in nitromethane poisoning.
    B) HEMODIALYSIS
    1) If anuria should occur following exposure, hemodialysis should be undertaken.

Abstracts

Case Reports

    A) Based on reports of periodic physical examinations of plant operators either manufacturing or handling nitromethane over a period of years, no systemic effects in humans have been attributed to this agent (ACGIH, 1986; Proctor et al, 1988).
    B) A 20-year-old woman chronically exposed to a solvent containing 94.05% trichlorotrifluoroethane, 5.7% methanol and 0.25% nitromethane developed severe parkinsonism and depression. Symptoms resolved upon temporary drug treatment and discontinuation of exposure. Although the authors felt that chronic methanol toxicity was possible, they concluded that nitromethane was the culprit since a) the methanol concentration in the solvent was low; b) no optic nerve damage was apparent; c) no formate was detectable in the serum; and d) since the solvent was largely trichlorotrifluoroethane, and "this agent is regarded to have low toxicity", nitromethane was the only other possibility (Sandyk & Gillman, 1984).

Range Of Toxicity

Summary

    A) The maximum tolerated and minimum lethal human exposures have not been determined.

Minimum Lethal Exposure

    A) 0.5 to 5.0 g/kg is the estimated oral lethal dose in humans (Hathaway et al, 1996).
    B) CARCINOGENICITY - According to the National Toxicology Program (NTP), inhalation studies involving rats and mice have shown clear evidence for the carcinogenicity of nitromethane (RTECS , 2000)

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) It is estimated that human exposure to 100 parts per million over 8 hours would result in uptake of about 30 milligrams per kilogram (ACGIH, 1986).
    B) ANIMAL DATA
    1) Survival was seen in 6 of 10 rats fed from 70 to 170 milligrams per kilogram per day for 15 weeks, while 7 of 10 rats fed about two-and-one-half times this dose also survived (ACGIH, 1986).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) Blood levels of nitromethane are not readily available and have not been correlated with degree of toxicity.

Workplace Standards

    A) ACGIH TLV Values for CAS75-52-5 (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) Nitromethane
    a) TLV:
    1) TLV-TWA: 20 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A3
    2) Codes: Not Listed
    3) Definitions:
    a) A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    c) TLV Basis - Critical Effect(s): Thyroid eff; URT irr; lung dam
    d) Molecular Weight: 61.04
    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 CAS75-52-5 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Nitromethane
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix D
    3) IDLH:
    a) IDLH: 750 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS75-52-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Nitromethane
    a) A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    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): 2B ; Listed as: Nitromethane
    a) 2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Nitromethane
    5) MAK (DFG, 2002): Category 3B ; Listed as: Nitromethane
    a) Category 3B : Substances for which in vitro or animal studies have yielded evidence of carcinogenic effects that is not sufficient for classification of the substance in one of the other categories. Further studies are required before a final decision can be made. A MAK value can be established provided no genotoxic effects have been detected. (Footnote: In the past, when a substance was classified as Category 3 it was given a MAK value provided that it had no detectable genotoxic effects. When all such substances have been examined for whether or not they may be classified in Category 4, this sentence may be omitted.)
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): R ; Listed as: Nitromethane
    a) R : RAHC = Reasonably anticipated to be a human carcinogen

    D) OSHA PEL Values for CAS75-52-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Nitromethane
    2) Table Z-1 for Nitromethane:
    a) 8-hour TWA:
    1) ppm: 100
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 250
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: ACGIH, 1996 Budavari, 1996 Clayton & Clayton, 1993 ITI, 1995 ) Lewis, 1996 RTECS, 2000 Snyder et al, 1990
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 110 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 950 mg/kg
    b) 1.44 g/kg
    3) LD50- (ORAL)RAT:
    a) 940 mg/kg
    b) 1.21 g/kg
    4) TCLo- (INHALATION)MOUSE:
    a) 750 ppm for 6H/2Y-I - tumorigenic
    b) 188 ppm for 6H/13W-I - deviated nasal septum; changes in bladder weight; lung, thorax, or respiration changes
    c) 1500 ppm for 6H/16D-I - somnolence; respirator stimulation; changes in liver weight
    5) TCLo- (INHALATION)RAT:
    a) 188 ppm for 6H/2Y-I - tumorigenic
    b) 100 ppm for 7H/2Y-I - changes in weight
    c) 375 ppm for 6H/16D-I - peripheral nerve and sensation changes; deviated nasal septum
    d) 1500 ppm for 6H/13W-I - normocytic anemia; changes in weight

Pharmacology Toxicology

Toxicologic Mechanism

    A) Nitromethane is a direct irritant of eyes, skin, and mucous membranes (ACGIH, 1986; Proctor et al, 1988).
    B) Reduction of the nitro group may produce limited peroxidative cellular damage (Henschler et al, 1980).
    C) Evolved oxides of nitrogen can form nitric or nitrous acid when in contact with moisture on respiratory tract mucous membranes causing direct tissue injury (Kizer, 1984).

Physicochemical

Physical Characteristics

    A) Nitromethane is a colorless, transparent, highly flammable, and oily liquid at room temperature. Its odor has been described as both 'mild and fruity' and as 'moderately strong and disagreeable' (ACGIH, 1996; Budavari, 1996; Lewis, 1996; Sittig, 1991).

Ph

    A) pH of a 0.01M solution: 6.12 (Budavari, 1996)

Molecular Weight

    A) 61.04

References

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