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SODIUM AZIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Sodium azide is a stable, neutral and highly toxic derivative of hydrazoic acid. It is a colorless liquid with explosive properties, which makes it a popular reagent used to expand air bags in the automotive industry. It is absorbed via inhalation, ingestion or dermal exposure.

Specific Substances

    1) Azide
    2) Azium
    3) CAS 26628-22-8
    4) CAS 12136-89-9
    5) Molecular Formula: Na(N3)
    6) NATRIUMMAZID (DUTCH)
    7) SODIUM, ACOTURE DE (FRENCH)
    1.2.1) MOLECULAR FORMULA
    1) N3-Na Na-N3

Available Forms Sources

    A) FORMS
    1) Sodium azide is available as the gas (hydrazoic acid) or sodium salt.
    2) Commercial isotonic buffering solutions may contain 0.1% (1 mg/mL) sodium azide as a preservative (Judge & Ward, 1989; Howard et al, 1990).
    B) SOURCES
    1) Sodium azide is manufactured in Japan and India by deriving sodium azide from hydrazine. Canada, the United States and Germany derive sodium azide from reacting ammonia with elemental sodium, forming sodium amide that in turn reacts with nitrous oxide (Rippen et al, 1996).
    C) USES
    1) Sodium azide is used in the explosive and pharmaceutical industries (as a chemical preservative). It is a common preservative used in many in vitro diagnostic products, including some automatic blood cell counters, used in hospitals and laboratories (LaLuna et al, 1979).
    2) It is used with copper or iron oxides as a gas generant in automobile safety airbags. The gas generator may contain 350 to 600 grams of sodium azide (Anon, 1983). Sodium azide use in air bags is being phased out in favor of less toxic materials (Chang & Lamm, 2003).
    a) Automotive air-bag systems are triggered when a sensor in the car's bumper sends an electrical charge to a gas generator that contains sodium azide. The electrical charge initiates a chemical reaction in the generator (sealed steel or aluminum container) that produces nitrogen gas from the azide (Anon, 1983; Pernikoff, 1989) Pers Comm, 1990).
    3) Sodium azide is used in organic syntheses; in the preparation of hydrazoic acid, lead azide, and pure sodium; in the differential selection of bacteria; in automatic blood counters; as a preservative for laboratory reagents; as a propellant for inflating automotive safety bags; as an agricultural nematocide; as a herbicide; and in fruit rot control (Budavari, 1996).
    4) It is also used industrially in the manufacturing processes of rubber, latex, wine, seed and Japanese beer (Chang & Lamm, 2003).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Sodium azide is poisonous by a variety of routes, including ingestion, skin contact, inhalation, intraperitoneal, intravenous and subcutaneous. Most industrial exposures are by inhalation. Most ingestions are either laboratory exposures or suicide attempts.
    B) Clinical effects may be nearly immediate or delayed in onset, and have required days or months to fully resolve in some cases.
    C) The most commonly reported health effect is hypotension, which can occur independent of route of exposure. Mild to moderate exposures can cause headache, mild hypotension, syncope, nausea, vomiting, diarrhea, abdominal pain, and a general feeling of apprehension and unwellness. More serious poisoning can cause central nervous system depression, coma, chest discomfort, hyperthermia or hypothermia, pulmonary edema, lactic acidosis, bradycardia or tachycardia, severe hypotension (sometimes preceded by hypertension), atrial and ventricular dysrhythmias, electrocardiographic changes, shortness of breath, diaphoresis, blurred vision, and seizures.
    D) Exposure to hydrazoic acid vapors evolved from sodium azide can cause irritation of eyes and mucous membranes of the respiratory tract with possible bronchitis or pulmonary edema as well as systemic effects such as hypotension.
    0.2.3) VITAL SIGNS
    A) Hypotension may develop, and may be preceded by hypertension. Bradycardia, tachycardia, hypo- and hyperthermia have been reported. Hyperpnea may develop at low levels of exposure.
    0.2.4) HEENT
    A) Conjunctivitis, nasal irritation, blurred vision, and mydriasis may occur.
    0.2.5) CARDIOVASCULAR
    A) Sodium azide is a potent hypotensive agent. Hypotension, transient hypertension, tachycardia and cardiac dysrhythmia may occur. Acute myocardial ischemia has been reported.
    0.2.6) RESPIRATORY
    A) Bronchial irritation may occur after inhalation of hydrazoic acid. More severe poisoning with sodium azide may cause hyperpnea, pulmonary edema, or respiratory failure.
    0.2.7) NEUROLOGIC
    A) Inhalation or ingestion may produce headache, syncope, flaccidity, muscle weakness, hand tremor, coma, and seizures.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, diarrhea and polydipsia are common after ingestions.
    0.2.11) ACID-BASE
    A) Metabolic (lactic) acidosis may develop in severe cases.
    0.2.13) HEMATOLOGIC
    A) Leukocytosis has been reported following ingestions.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no studies were found on the possible reproductive effects of sodium azide in humans.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

    A) Monitor vital signs, acid base status, ECG, ABG's and chest x-ray in symptomatic patients. Cyanide levels may be elevated but are rarely available in a clinically useful time frame.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Emesis is NOT recommended because the patient could rapidly become obtunded, comatose, or develop seizures.
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    C) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    D) 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.
    E) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    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.
    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) TOXICITY: The minimal lethal dosage is reported to be 10 mg/kg. FATALITY: 700 mg of sodium azide was fatal in a 29-year-old who ingested 700 mL of a commercial isotonic buffer solution. SURVIVAL: An adult woman survived a 1 g ingestion of sodium azide, but required intensive supportive care; no permanent sequelae was observed.

Clinical Effects

Summary Of Exposure

    A) Sodium azide is poisonous by a variety of routes, including ingestion, skin contact, inhalation, intraperitoneal, intravenous and subcutaneous. Most industrial exposures are by inhalation. Most ingestions are either laboratory exposures or suicide attempts.
    B) Clinical effects may be nearly immediate or delayed in onset, and have required days or months to fully resolve in some cases.
    C) The most commonly reported health effect is hypotension, which can occur independent of route of exposure. Mild to moderate exposures can cause headache, mild hypotension, syncope, nausea, vomiting, diarrhea, abdominal pain, and a general feeling of apprehension and unwellness. More serious poisoning can cause central nervous system depression, coma, chest discomfort, hyperthermia or hypothermia, pulmonary edema, lactic acidosis, bradycardia or tachycardia, severe hypotension (sometimes preceded by hypertension), atrial and ventricular dysrhythmias, electrocardiographic changes, shortness of breath, diaphoresis, blurred vision, and seizures.
    D) Exposure to hydrazoic acid vapors evolved from sodium azide can cause irritation of eyes and mucous membranes of the respiratory tract with possible bronchitis or pulmonary edema as well as systemic effects such as hypotension.

Vital Signs

    3.3.1) SUMMARY
    A) Hypotension may develop, and may be preceded by hypertension. Bradycardia, tachycardia, hypo- and hyperthermia have been reported. Hyperpnea may develop at low levels of exposure.
    3.3.2) RESPIRATIONS
    A) Hyperpnea may develop at low levels of exposure.
    3.3.3) TEMPERATURE
    A) Both hyper- and hypothermia have been reported (Clayton & Clayton, 1981; Edmonds & Bourne, 1982) (ACGIH, 1986) (Gosselin et al, 1984).
    3.3.4) BLOOD PRESSURE
    A) Hypotension may occur after ingestion or occupational exposure (Trout et al, 1996; Hitt, 2001; Richardson et al, 1975), and may be preceded by hypertension (Edmonds & Bourne, 1982; Albertson et al, 1986).
    B) Hypotension, with an onset of greater than one hour following sodium azide exposure, may predict an unfavorable outcome. A literature review and analysis of individuals exposed to sodium azide showed that death occurred in all cases where the onset of hypotension occurred more than one hour following exposure (Chang & Lamm, 2003).
    3.3.5) PULSE
    A) Bradycardia or tachycardia may occur (Edmonds & Bourne, 1982).

Heent

    3.4.1) SUMMARY
    A) Conjunctivitis, nasal irritation, blurred vision, and mydriasis may occur.
    3.4.3) EYES
    A) CONJUNCTIVITIS: Toxic exposures may lead to irritation of conjunctivae (Graham et al, 1948; Miljours & Braun, 2003).
    B) MYDRIASIS has been reported (ACGIH, 1986) (Clayton & Clayton, 1981; Hurst, 1942).
    C) AMBLYOPIA: Blurred vision has been reported (ACGIH, 1986) (Gosselin et al, 1984).
    3.4.5) NOSE
    A) MUCOUS MEMBRANE IRRITATION: Toxic exposures may lead to irritation of mucous membrane of the nose (Graham et al, 1948).
    B) RHINITIS: Nasal stuffiness has been reported following inhalation exposures (Haas & Marsh, 1970).

Cardiovascular

    3.5.1) SUMMARY
    A) Sodium azide is a potent hypotensive agent. Hypotension, transient hypertension, tachycardia and cardiac dysrhythmia may occur. Acute myocardial ischemia has been reported.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) Hypotension may occur after ingestion or occupational exposure (Watanabe et al, 2007; Trout et al, 1996; Hitt, 2001; Richardson et al, 1975). Symptoms of myocardial ischemia have also been reported (Edmonds & Bourne, 1982; Albertson et al, 1986; Graham et al, 1948). Rapidly progressing hypotension and metabolic acidosis may result in death within 2 to 28 hours after ingestion of greater than 13 mg/kg (Albertson et al, 1986).
    2) CASE REPORT: A 53-year-old hospitalized woman developed hypotension (systolic pressure 50 to 60 mmHg) approximately 1.5 hours after inadvertently ingesting 1 g of sodium azide. She complained of not feeling well immediately after ingestion and developed seizures requiring endotracheal intubation. Metabolic acidosis was also present and hemodialysis was started within 4 hours of exposure. The patient required intensive supportive care including an intra-aortic balloon pump (IABP) for circulatory support along with inotropic agents. The patient was weaned from the IABP on day 8. The patient was discharged from the ICU on day 11 with no long-term sequelae observed (Watanabe et al, 2007). The authors noted that this was the highest dose survived (the previously reported human lethal dose was 700 mg).
    3) In a review article evaluating 185 individual cases from 38 publications, hypotension was reported in 120 cases and was the most frequently reported health effect across all exposure routes.
    a) Early onset of hypotension (within minutes or less than one hour) produced a pharmacological response with a benign course.
    b) Hypotension, with an onset of greater than one hour following sodium azide exposure, may predict an unfavorable outcome. A literature review and analysis of individuals exposed to sodium azide showed that death occurred in all cases where the onset of hypotension occurred more than one hour following exposure (Chang & Lamm, 2003).
    4) DERMAL ABSORPTION: A 29-year-old worker was fatally injured after he was chemically burned over 45% of his body surface area following an explosion of a metal drum containing less than 1% sodium azide (actual exposure may have been more as evidenced by drum leakage). Within one hour of hospital admission, the patient became profoundly hypotensive (BP 77/50) and was treated aggressively with fluid replacement (>24 L), 9 units of PRBCs, and epinephrine (64 mg/h). Concomitantly, metabolic acidosis was also unresponsive to treatment; the patient died approximately 14 hours after admission (Gesell & Otten, 1997; Pham et al, 2001).
    5) CASE SERIES: Five patients developed nausea, vomiting, diaphoresis, headache, hypotension, syncope, lightheadedness, and a sense of impending doom shortly after drinking iced tea (sips to up to 8 ounces) that contained sodium azide at a local restaurant. Three patients had blood pressures of 84/42, 89/54, and 86/54, respectively. One patient had a blood pressure of 92/64 and the remaining patient was normotensive. Symptoms improved with IV fluids, antiemetics and supportive care. Toxicology screening was negative in all patients. Although the source of the exposure was limited to a self-service tea urn that contained sodium azide, a police investigation did not reveal how it became contaminated. Persistent symptoms were not reported in any patient (Schwarz et al, 2014).
    6) CASE SERIES: Nine patients developed hypotension 30 minutes following initiation of hemodialysis, with 2 episodes of syncope. It was later discovered that sodium azide was a probable contaminant in the water treatment system (Gordon et al, 1990).
    7) Hypotension, accompanied by an acceleration of heart rate, occurred during occupational exposure at atmospheric hydrazoic acid concentrations of 0.3 to 3.9 parts per million (Graham et al, 1948).
    8) Sodium azide administered orally (1.3 mg) to hypertensive patients resulted in a rapid fall (as early as 45 to 60 seconds) in blood pressure, particularly systolic pressure. Giving 1.3 mg sodium azide 3 times daily to normotensive patients for 10 days had no sustained effect on blood pressure (Black et al, 1954).
    B) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypertension has been reported after high doses (Edmonds & Bourne, 1982), and may precede hypotension.
    C) PALPITATIONS
    1) WITH POISONING/EXPOSURE
    a) Palpitations were reported significantly more often in workers exposed to sodium azide by inhalation, compared with unexposed workers in a sodium azide production plant (49% vs 10%) (Miljours & Braun, 2003).
    D) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: Tachycardia, cardiac dysrhythmias, and ventricular fibrillation have been reported.
    b) TACHYCARDIA preceded by an initial decrease in heart rate, may occur at high doses (Edmonds & Bourne, 1982). High pulse rate was reported following ingestion of 1.5 mL of a 10% solution (Burger & Bauer, 1964). Occupational inhalation exposures have resulted in increased heart rate (Trout et al, 1996; Graham et al, 1948).
    c) VENTRICULAR FIBRILLATION was described in a 30-year-old male who ingested 15 to 20 grams of sodium azide (Abrams et al, 1987).
    d) T-WAVE CHANGES: On ECG have been reported following accidental ingestion of sodium azide (1.5 mL of a 10% solution) (Burger & Bauer, 1964) .
    1) CASE REPORT: Approximately 40 hours after ingestion, a woman who had inadvertently ingested 1 g sodium azide developed ST-segment elevation in all leads except aVR. The patient had persistent circulatory failure and required intensive supportive care including an intra-aortic balloon pump. Although the ST-segment elevation resolved, the patient continued to have T wave inversion in leads I, II, III, aVL, aVF, and V3 to V6 up to 18 days after exposure. No dysrhythmias or organ failure were reported (Watanabe et al, 2007).
    E) CARDIOMYOPATHY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 29-year-old woman developed signs and symptoms of myocardial ischemia, left ventricular dysfunction, and ECG evidence of diffuse myocardial injury 3 days after apparent recovery following an accidental ingestion of 700 mL of a commercial buffering solution that contained 0.1% sodium azide (Judge & Ward, 1989; Howard et al, 1990). Death occurred 84 hours after ingestion.
    F) PAIN
    1) WITH POISONING/EXPOSURE
    a) Recurrent cramp-like chest pain developed in a 24-year-old man who drank an unknown quantity of sodium azide. ECG was normal (Edmond & Bourne, 1982).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HYPOTENSION
    a) Injections of hydrazoic acid into rabbits and cats produced a rapid, profound and long maintained fall in carotid blood pressure and transient increases in respiration (Graham et al, 1948).

Respiratory

    3.6.1) SUMMARY
    A) Bronchial irritation may occur after inhalation of hydrazoic acid. More severe poisoning with sodium azide may cause hyperpnea, pulmonary edema, or respiratory failure.
    3.6.2) CLINICAL EFFECTS
    A) BRONCHITIS
    1) WITH POISONING/EXPOSURE
    a) Irritation of bronchi may occur.
    B) APNEA
    1) WITH POISONING/EXPOSURE
    a) Respiratory failure may occur and may be the cause of death in lethal exposures.
    C) HYPERVENTILATION
    1) WITH POISONING/EXPOSURE
    a) Initial response at lower levels of exposure may be hyperpnea (Roberts et al, 1974). An increase in respirations occurs through stimulation of arterial chemoreceptors that is not regulated by carbon dioxide levels.
    D) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Non-cardiogenic pulmonary edema has been reported (Albertson et al, 1986).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) APNEA
    a) After several daily doses of 8 mg/kg, a monkeys developed rigidity followed by flaccidity and slow, deep and gasping breathing or fast, jerky and irregular breathing. Death was due to respiratory failure (Hurst, 1942).
    2) BRONCHOSPASM
    a) Inhalation of hydrazoic acid in rabbits and cats resulted in bronchospasm as a result of the irritant effect of the gas (Graham et al, 1948).
    3) HYPERVENTILATION
    a) Injections of hydrazoic acid in rabbits and cats produced a transient stimulation of respiration in addition to a profound drop in blood pressure (Graham et al, 1948).

Neurologic

    3.7.1) SUMMARY
    A) Inhalation or ingestion may produce headache, syncope, flaccidity, muscle weakness, hand tremor, coma, and seizures.
    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) WITH POISONING/EXPOSURE
    a) Coma has been reported (Abrams et al, 1987).
    B) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Seizures have occurred (Klein-Schwartz et al, 1989). Seizures were observed in a woman shortly after ingesting 1 gram of sodium azide; she survived following intensive supportive care (Watanabe et al, 2007).
    C) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache is common after inhalation or ingestions (Burger & Bauer, 1964; Haas & Marsh, 1970; Richardson et al, 1975; Trout et al, 1996; Miljours & Braun, 2003).
    b) CASE SERIES: Five patients developed nausea, vomiting, diaphoresis, headache, hypotension, syncope, lightheadedness, and a sense of impending doom shortly after drinking iced tea that contained sodium azide at a local restaurant. Symptoms improved with IV fluids, antiemetics and supportive care. Toxicology screening was negative in all patients. Although the source of the exposure was limited to a self-service tea urn that contained sodium azide, a police investigation did not reveal how it became contaminated. Persistent symptoms were not reported in any patient (Schwarz et al, 2014).
    D) SYNCOPE
    1) WITH POISONING/EXPOSURE
    a) Syncope has been reported after ingestion (Richardson et al, 1975).
    b) CASE SERIES: Five patients developed nausea, vomiting, diaphoresis, headache, hypotension, syncope, lightheadedness, and a sense of impending doom shortly after drinking iced tea that contained sodium azide at a local restaurant. Symptoms improved with IV fluids, antiemetics and supportive care. Toxicology screening was negative in all patients. Although the source of the exposure was limited to a self-service tea urn that contained sodium azide, a police investigation did not reveal how it became contaminated. Persistent symptoms were not reported in any patient (Schwarz et al, 2014).
    E) TREMOR
    1) WITH POISONING/EXPOSURE
    a) CHRONIC: Hand trembling was reported significantly more often in workers exposed to sodium azide by inhalation, compared with unexposed workers in a sodium azide production plant (15% vs 0%) (Miljours & Braun, 2003).
    F) VERTIGO
    1) WITH POISONING/EXPOSURE
    a) Vertigo was reported significantly more often in workers exposed to sodium azide by inhalation, compared with unexposed workers in a sodium azide production plant (39% vs 10%) (Miljours & Braun, 2003).
    G) LIGHTHEADEDNESS
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: Five patients developed nausea, vomiting, diaphoresis, headache, hypotension, syncope, lightheadedness, and a sense of impending doom shortly after drinking iced tea that contained sodium azide at a local restaurant. Symptoms improved with IV fluids, antiemetics and supportive care. Toxicology screening was negative in all patients. Although the source of the exposure was limited to a self-service tea urn that contained sodium azide, a police investigation did not reveal how it became contaminated. Persistent symptoms were not reported in any patient (Schwarz et al, 2014).
    H) FATIGUE
    1) WITH POISONING/EXPOSURE
    a) Fatigue at the end of the day was reported significantly more often in workers exposed to sodium azide by inhalation, compared with unexposed workers in a sodium azide production plant (83% vs 63%) (Miljours & Braun, 2003).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SEIZURES
    a) MONKEY: Of 11 monkeys administered IV sodium azide alone, 10 experienced seizures. Persistent ataxia was evident in several of the monkeys. Examination of the brain of one of the monkeys sacrificed 3 months later, revealed almost complete degeneration of the cerebellar cortex (Sax & Mettler, 1971).
    2) OPTIC NEURITIS
    a) Following large doses, and sometimes repeated small doses in monkeys, pathological examination revealed complete necrosis most commonly in the optic nerves (Hurst, 1942).
    3) COMA
    a) Drowsiness or coma occurred in monkeys following large doses of sodium azide (Hurst, 1942).
    4) TREMOR
    a) Coarse muscle tremor, gross twitching and shaking, and tonic cramps and rigidity occurred in monkeys following toxic doses of sodium azide (Hurst, 1942).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, diarrhea and polydipsia are common after ingestions.
    3.8.2) CLINICAL EFFECTS
    A) GASTRITIS
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting and diarrhea are common following ingestion, and may occur within 30 minutes (Burger & Bauer, 1964). Nausea was reported significantly more often in workers exposed to sodium azide by inhalation, compared with unexposed workers in a sodium azide production plant (27% vs 2%) (Miljours & Braun, 2003).
    b) CASE SERIES: Five patients developed nausea, vomiting, diaphoresis, headache, hypotension, syncope, lightheadedness, and a sense of impending doom shortly after drinking iced tea that contained sodium azide at a local restaurant. Symptoms improved with IV fluids, antiemetics and supportive care. Toxicology screening was negative in all patients. Although the source of the exposure was limited to a self-service tea urn that contained sodium azide, a police investigation did not reveal how it became contaminated. Persistent symptoms were not reported in any patient (Schwarz et al, 2014).
    B) THIRST FINDING
    1) WITH POISONING/EXPOSURE
    a) Pronounced polydipsia may occur following exposures to sodium azide (Burger & Bauer, 1964).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SALIVA INCREASED
    a) Increased salivation was noted in animals injected with sodium azide or exposed to inhalation of hydrazoic acid (Graham et al, 1948).

Acid-Base

    3.11.1) SUMMARY
    A) Metabolic (lactic) acidosis may develop in severe cases.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Metabolic (lactic) acidosis (ABGs: pH 7.343, base excess, -16.2, and HCO(3)- 7.8 mEq/L, serum lactate 76 mg/dL (normal 5 to 20 mg/dL)) occurred in a 53-year-old woman who inadvertently drank 1 g of sodium azide and immediately felt ill and developed seizures necessitating endotracheal intubation. Hemodialysis was started approximately 4 hours after exposure; continuous hemodiafiltration was continued until day 9. The patient required intensive supportive care including an intra-aortic balloon pump for circulatory support along with inotropic agents. The patient was discharged from ICU on day 11 with no long-term sequelae observed (Watanabe et al, 2007).
    b) CASE REPORT: Profound metabolic acidosis and hypotension occurred in a 29-year-old worker dermally exposed to less than 1% sodium azide from a metal drum explosion (actual amount of exposure may have been more as evidenced by drum leakage). A chemical burn was present over 45% of the body surface area. Despite aggressive therapy for the hypotension and concomitant acidosis (pH 6.89, anion gap 55 after >35 amps of sodium bicarbonate), the patient died approximately 14 hours after admission (Gesell & Otten, 1997).
    c) CASE REPORT: Persistent metabolic acidosis was reported in a patient who ingested 10 to 20 g (Albertson et al, 1986).
    B) LACTIC ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Lactic acidosis may result from toxic exposures due to inhibition of the final step of oxidative phosphorylation stopping aerobic metabolism, which changes metabolism from pyruvate to lactate production resulting in lactic acidosis (Abrams et al, 1987).

Hematologic

    3.13.1) SUMMARY
    A) Leukocytosis has been reported following ingestions.
    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) Leukocytosis, with a left shift in the differential blood count, was noted following an accidental ingestion (Burger & Bauer, 1964).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN ABSORPTION
    1) WITH POISONING/EXPOSURE
    a) SYSTEMIC EFFECTS
    1) CASE REPORT: A dermal exposure of less than 1% sodium azide from a metal drum explosion (actual amount of exposure may have been more, secondary to evidence of drum leakage) was fatal in a 29-year-old worker. Initially, a chemical burn over 45% of the body surface area was observed. Profound hypotension and metabolic acidosis followed which were unresponsive to aggressive therapy; the patient died approximately 14 hours after admission (Gesell & Otten, 1997).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE WEAKNESS
    1) WITH POISONING/EXPOSURE
    a) Muscle weakness and flaccidity may be seen (Graham, 1949). Sodium azide is reported to have a paralytic effect on isolated muscle (Graham, 1949).

Endocrine

    3.16.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HYPERGLYCEMIA
    a) A rapid rise in blood glucose levels occurred following administration of 12 mg/kg to 30 mg/kg sodium azide in rabbits (Handler, 1945).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no studies were found on the possible reproductive effects of sodium azide in humans.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) Developmental studies in hamsters and rats indicated that sodium azide was not teratogenic; however, it did produce embryotoxic effects at maternally toxic doses (Sana et al, 1990) HSDB, 1997). It has resulted in sterility in male mice (ACGIH, 1991).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS26628-22-8 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Sodium azide been determined to be tumorigenic using the equivocal tumorigenic agent by RTECS criteria. Tumors on the skin, appendages and in the endocrine system has been observed in rat studies (RTECS , 1991).
    2) Tumorigenic effects have been reported in experimental animals. Increases in pituitary adenomas and mammary tumors have been reported (Sax & Lewis, 1989; Clayton & Clayton, 1994).
    3) Tests have been completed on sodium azide in the NTP Carcinogenesis Studies (RTECS , 1991).

Genotoxicity

    A) DNA repair, DNA inhibition, mutations and chromosome aberrations have been observed in experimental animals.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs, acid base status, ECG, ABG's and chest x-ray in symptomatic patients. Cyanide levels may be elevated but are rarely available in a clinically useful time frame.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Sodium azide levels are not clinically useful or readily available.
    B) ACID/BASE
    1) Monitor acid base status in symptomatic patients.
    2) Monitor ABG's and/or pulse oximetry in patients with pulmonary symptoms.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor cardiac rhythm and vital signs.
    2) OTHER
    a) Cyanide ion concentrations of 1.6, 1.7, 0.6, and 0.1 mg/L at 0, 12, 18, and 24 hours were reported in a 52-year-old male who ingested between 1.2 and 2 grams of sodium azide in a suicide attempt (Klein-Schwartz, 1989).
    1) Elevated cyanide levels were reported in another case of fatal sodium azide poisoning. Cyanide was shown to be formed during the in vitro incubation of sodium azide with human blood (Lambert et al, 1995).

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Follow chest x-ray in patients with pulmonary symptoms.

Methods

    A) OTHER
    1) Contact of sodium azide with acids could result in evolution of toxic volatile hydrazoic acid (HN3) (Senecal et al, 1991).
    2) Emergency department personnel developed burning and watery eyes and headache during the gastric lavage of a 35-year-old female who ingested powdered sodium azide (Senecal et al, 1991).
    3) Sodium azide may be quantitated in biologic tissue by HPLC, capillary electrophoresis and GC/MS (Kikuchi et al, 2001; Hortin et al, 1999; Marquet et al, 1996).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor vital signs, acid base status, ECG, ABG's and chest x-ray in symptomatic patients. Cyanide levels may be elevated but are rarely available in a clinically useful time frame.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED
    1) Emesis is NOT recommended because the patient could rapidly become obtunded, comatose, or develop 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 is NOT recommended because of the substantial risk of sudden collapse which may result in a comatose, vomiting patient (Abrams et al, 1987). Seizures may also occur.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    C) GASTRIC LAVAGE
    1) CAUTION: Contact of sodium azide with acids could result in evolution of toxic volatile hydrazoic acid (HN3) (Senecal et al, 1991).
    2) Emergency department personnel developed burning and watery eyes and headache during the gastric lavage of a 35-year-old woman who ingested powdered sodium azide (Senecal et al, 1991).
    3) 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.
    4) 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.
    5) 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.
    6) 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).
    7) 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.
    6.5.3) TREATMENT
    A) 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).
    B) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    D) CYANIDE ANTIDOTE
    1) CYANIDE ANTIDOTE KIT
    a) Some authors have suggested the use of sodium nitrite as an antidote (Lambert et al, 1995). Evidence is lacking to support its usefulness in human case reports (Abrams et al, 1987; Emmett & Ricking, 1975; Klein-Schwartz et al, 1989). However, Lambert et al (1995) tested the hypothesis of metabolic formation of cyanide through an in vitro test, which clearly demonstrated the formation of cyanide in the presence of sodium azide. These authors recommend initiating treatment for cyanide intoxication following toxic sodium azide exposures (Lambert et al, 1995). In mice, prior administration of sodium nitrite increased the LD50 by 20% (Abbanat & Smith, 1964).
    b) In a review article, Chang and Lamm (Chang & Lamm, 2003) stated that trials of specific antidotes, including sodium nitrite, amyl nitrate and sodium thiosulfate have been unsuccessful.
    c) OBTAIN AND PREPARE for administration a CYANIDE ANTIDOTE KIT, consisting of sodium nitrite and sodium thiosulfate.
    1) Antidotes should be used only in significantly symptomatic patients (ie, impaired consciousness, convulsions, acidosis, or unstable vital signs).
    2) SODIUM NITRITE
    a) INDICATION
    1) Sodium nitrite should be given initially and administered as soon as vascular access is established.
    2) Further administration of sodium nitrite is dictated only by the clinical situation, provided no significant complications (hypotension, excessive methemoglobinemia) are present. Use with caution if carbon monoxide poisoning is also suspected.
    3) The goal of nitrite therapy is to achieve a methemoglobin level of 20% to 30%. This level is not based on clinical data, but represents the tolerated concentration without significant adverse symptoms from methemoglobin in an otherwise healthy individual. Clinical response has been reported to occur with methemoglobin levels in the range of 3.6% to 9.2% (DiNapoli et al, 1989; Johnson et al, 1989; Johnson & Mellors, 1988).
    b) ADULT DOSE
    1) 10 mL of a 3% solution (300 mg) administered intravenously at a rate of 2.5 to 5 mL/minute (Prod Info NITHIODOTE intravenous injection solution, 2011). Frequent blood pressure monitoring must accompany sodium nitrite injection and the rate slowed if hypotension occurs.
    2) If there is inadequate clinical response, an additional dose of sodium nitrite at half the amount of the initial dose may be administered 30 minutes following the first dose (Prod Info NITHIODOTE intravenous injection solution, 2011).
    c) PEDIATRIC DOSE
    1) The recommended pediatric sodium nitrite dose is 0.2 mL/kg of a 3% solution (6 mg/kg) administered intravenously at a rate of 2.5 to 5 mL/minute, not to exceed 10 mL (300 mg) (Prod Info NITHIODOTE intravenous injection solution, 2011).
    2) If there is inadequate clinical response, an additional dose of sodium nitrite at half the amount of the initial dose may be administered 30 minutes following the first dose (Prod Info NITHIODOTE intravenous injection solution, 2011; Berlin, 1970).
    3) PRESENCE OF ANEMIA: If there is a reason to suspect the presence of anemia, the following initial sodium nitrite doses should be given, depending on the child's hemoglobin (sodium nitrite should not exceed the doses listed below; fatal methemoglobinemia may result) (Berlin, 1970):
    a) Hemoglobin: 8 g/dL - Initial 3% sodium nitrite dose: 0.22 mL/kg (6.6 mg/kg)
    b) Hemoglobin: 10 g/dL - Initial 3% sodium nitrite dose: 0.27 mL/kg (8.7 mg/kg)
    c) Hemoglobin: 12 g/dL (average child) - Initial 3% sodium nitrite dose: 0.33 mL/kg (10 mg/kg)
    d) Hemoglobin: 14 g/dL - Initial 3% sodium nitrite dose: 0.39 mL/kg (11.6 mg/kg)
    d) It is highly recommended that total hemoglobin and methemoglobin concentrations be rapidly measured (30 minutes after dose), when possible, before repeating a dose of sodium nitrite to be sure that dangerous methemoglobinemia will not occur, especially in the pediatric patient.
    e) Monitor blood pressure frequently and treat hypotension by slowing infusion rate and giving crystalloids and vasopressors. Consider possible excessive methemoglobin formation if patient deteriorates during therapy.
    f) Excessive methemoglobinemia and hypotension are potential complications of nitrite therapy.
    g) In individuals with G6PD deficiency, therapy with methemoglobin-inducing agents is contraindicated because of the likelihood of serious hemolysis.
    3) SODIUM THIOSULFATE
    a) Sodium thiosulfate is the second component of the cyanide antidote kit. It is supplied as 50 mL of a 25% solution and it is administered intravenously. There are no adverse reactions to thiosulfate itself. The pediatric dose is adjusted for weight and not hemoglobin concentration.
    b) Sodium thiosulfate supplies sulfur for the rhodanese reaction, and is recommended after sodium nitrite, hydroxocobalamin, or 4-DMAP (4-dimethylaminophenol) administration (Marrs, 1988; Hall & Rumack, 1987).
    c) DOSE
    1) Follow sodium nitrite with IV sodium thiosulfate. ADULT: Administer 50 mL (12.5 g) of a 25% solution IV; PEDIATRIC: 1 mL/kg of a 25% solution (250 mg/kg), not to exceed 50 mL (12.5 g) total dose (Prod Info NITHIODOTE intravenous injection solution, 2011).
    2) A second dose, one-half of the first dose, may be administered if signs of cyanide toxicity reappear (Prod Info NITHIODOTE intravenous injection solution, 2011).
    3) Sodium thiosulfate is usually used in combination with sodium nitrite but may be used alone (Prod Info sodium thiosulfate IV injection, 2003).
    4) Sodium thiosulfate can be administered without sodium nitrite in patients at risk to develop further methemoglobinemia (ie excessive methemoglobinemia or hypotension after initial sodium nitrite administration or in the presence of methemoglobinemia or carboxyhemoglobin in patients with smoke inhalation due to fire). Sodium thiosulfate can also be used in combination with hydroxocobalamin to treat cyanide poisoning (Howland, 2011)
    5) CONTINUOUS INFUSION: It has been suggested that a continuous infusion of sodium thiosulfate be given after the initial bolus to maintain high thiosulfate levels. Low sodium intravenous fluids are required to avoid sodium overload. If large amounts of sodium thiosulfate are required, hemodialysis may be necessary to maintain a physiologic serum sodium level (Turchen et al, 1991).
    6) ADVERSE EVENTS: Sodium thiosulfate does not usually produce significant toxicity. Possible adverse events include hypotension, headache, nausea, vomiting, disorientation, and prolonged bleeding time (Prod Info NITHIODOTE intravenous injection solution, 2011).
    E) HYPERBARIC OXYGEN THERAPY
    1) Hyperbaric oxygen (HBO) therapy may be of theoretical benefit. Additional studies are needed before HBO can be recommended in the treatment of human sodium azide poisoning victims.

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.

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) CASE REPORT: A 53-year-old woman ingested 1 g sodium azide, and rapidly developed hypotension, seizures, and metabolic acidosis. Hemodialysis was initiated about 4 hours after ingestion and was continued for 3 hours. Sodium azide concentration in blood was 174 ppm predialysis and 37 ppm postdialysis; dialysis clearance was not calculated. She was also treated with plasma exchange (3200 mL fresh frozen plasma) and continuous hemodiafiltration. She survived with intensive supportive care (Watanabe et al, 2007).
    2) In a case reported by Albertson et al (1986), exchange transfusion, charcoal hemoperfusion, hemodialysis and vasopressors failed to prevent circulatory collapse and dysrhythmias (Albertson et al, 1986).

Abstracts

Case Reports

    A) ADULT
    1) A 34-year-old man ingested 10 to 20 grams of sodium azide with vodka. Initial treatment was oxygen, naloxone 0.4 mg IV, and dextrose 25 g. The patient remained stuporous.
    2) On arrival at the emergency room he was comatose, blood pressure of 158/78 mmHg, pulse 148/min, respirations 28/minute, and a rectal temperature of 36 degrees C. Pupils were dilated.
    3) The patient was lavaged and given 1 g/kg of activated charcoal. The patient subsequently developed persistent metabolic acidosis, hypotension, pulmonary edema, a wide complex dysrhythmia and died despite exchange transfusions, charcoal hemoperfusion, hemodialysis and vasopressors (Albertson et al, 1986).

Range Of Toxicity

Summary

    A) TOXICITY: The minimal lethal dosage is reported to be 10 mg/kg. FATALITY: 700 mg of sodium azide was fatal in a 29-year-old who ingested 700 mL of a commercial isotonic buffer solution. SURVIVAL: An adult woman survived a 1 g ingestion of sodium azide, but required intensive supportive care; no permanent sequelae was observed.

Minimum Lethal Exposure

    A) CASE REPORTS
    1) INGESTION
    a) A 29-year-old woman developed cardiomyopathy and died 3 days after an inadvertent ingestion of 700 mL of a commercial buffering solution that contained 0.1% sodium azide (Judge & Ward, 1989; Howard et al, 1990).
    b) A man ingested 2 tablespoons of sodium azide mixed in water, developed coma, hypotension, and ventricular arrhythmias, and died within 2 hours (Klein-Schwartz et al, 1989).
    c) A 52-year-old man ingested 1.2 to 2 g of sodium azide and developed a generalized tonic clonic seizure 3 hours postresection and tachycardia and unresponsiveness at 30 hours after admission. He continued to deteriorate, becoming more hypotensive and bradycardic, despite receiving a total of 5 treatments with the cyanide antidote kit during hospitalization. He survived for a total of 40 hours after ingestion (Klein-Schwartz et al, 1989).
    d) The minimal lethal dosage is reported to be 10 mg/kg. Severe health effects including seizures, coma, death, acute lung injury, flaccidity, metabolic acidosis, arrhythmia, bradycardia and asystole have been observed at this dosage or greater (Chang & Lamm, 2003).
    e) Ingestion of "several grams" caused collapse and death within 40 minutes in an adult (Gosselin et al, 1984).
    f) An adult male ingested an estimated 10 to 20 g of sodium azide, developed coma, acidosis, hypertension followed by hypotension, hyperthermia, pulmonary edema, and atrial and ventricular arrhythmias, and died after 28 hours (Albertson et al, 1986).
    g) Ingestion of 15 to 20 g resulted in death within 5 hours of ingestion in a 30-year-old man (Abrams et al, 1987).
    h) An adult male ingested an unknown amount and died within 8 hours (Klein-Schwartz et al, 1989).
    i) A woman ingested an unknown amount and died within 12 hours after developing pulmonary edema, lactic acidosis, hypothermia, central nervous system depression, hypotension, and shock (Emmett & Ricking, 1975).
    j) A man died 4 hours after ingesting approximately 9 g (Marquet et al, 1996).
    2) ANIMAL DATA
    a) Inhalation exposure to 1,024 ppm of hydrazoic acid vapor for 60 minutes was fatal to mice (ACGIH, 1986).

Maximum Tolerated Exposure

    A) SUMMARY
    1) The human hypotensive dose of sodium azide is between 0.2 and 4 mcg/kg (about 2 to 40 mcg for a 10 kg child, or about 14 to 280 mcg for a 70 kg adult) (Gosselin et al, 1984).
    2) In a review study, the authors (Chang & Lamm, 2003) reported the lowest dose in which adverse human health effects were seen as follows:
    1) Hypotension (0.01 mg/kg)
    2) Decreased mental status (0.04 mg/kg)
    3) Nausea, vomiting, diarrhea (0.04 mg/kg)
    4) Headache, temporary loss of vision (0.07 mg/kg)
    5) Sweating, collapse, palpitations (0.07 mg/kg)
    a) Hypotension had the largest dosage exposure range (0.004 to 786 mg/kg) followed by impaired mental status (0.04 to 786 mg/kg), collapse (0.07 to 786 mg/kg) and vomiting (0.04 to 129 mg/kg) (Chang & Lamm, 2003).
    B) CASE REPORTS
    1) Five patients developed nausea, vomiting, diaphoresis, headache, hypotension, syncope, lightheadedness, and a sense of impending doom shortly after drinking iced tea that contained sodium azide at a local restaurant. Symptoms improved with IV fluids, antiemetics and supportive care. Toxicology screening was negative in all patients. Although the source of the exposure was limited to a self-service tea urn that contained sodium azide, a police investigation did not reveal how it became contaminated. Persistent symptoms were not reported in any patient (Schwarz et al, 2014).
    2) A hospitalized woman inadvertently ingested 1 g of sodium azide and developed seizures, metabolic acidosis and hypotension requiring intensive supportive care including hemodialysis, intra-aortic balloon pumping for circulatory support and mechanical ventilation. The patient was discharged on day 11 with no long-term sequelae observed (Watanabe et al, 2007).
    3) An adult who ingested 150 mg of sodium azide in an aqueous solution developed breathlessness, tachycardia, nausea, vomiting, headache, diarrhea, polydipsia, leukocytosis, and electrocardiographic changes, but recovered over a 10 day period (Gosselin et al, 1984).
    4) An adult ingested between 50 and 60 mg and developed coma, severe headaches, hypotension, and tachycardia which lasted for an hour (Richardson et al, 1975).
    5) Ingestion of 5 to 10 mg by an adult caused only transient symptoms of indigestion, headache, sweating, and faintness (Richardson et al, 1975).
    C) LABORATORY/OCCUPATIONAL EXPOSURES
    1) Five laboratory technicians drank tea made with distilled water treated with sodium azide (concentration about 224 mg/L in the tea). Each cup of tea was estimated to contain about 40 mg of sodium azide. One technician drank a half cup (about 20 mg) and felt "vaguely unwell," while 3 individuals who each drank one cup (about 40 mg) developed palpitations and a "fuzzy head". The fifth technician drank 2 cups (about 80 mg) and developed violent cramping chest pains, numbness and tingling in the legs, and fainted. Chest discomfort and apprehension continued for up to 2 months after ingestion (Edmonds & Bourne, 1982).
    2) Sodium azide was tested in the 1950's as an antihypertensive medication (ACGIH, 1986). Daily doses of 0.65 to 3.9 mg (0.01 to 0.02 mg/kg) were administered to 30 hypertensive patients for periods up to 2.5 years (ACGIH, 1986) (Edmonds & Bourne, 1982).
    a) The only noted effects were lowering of blood pressure and transient pounding headaches (ACGIH, 1986).
    3) Normal volunteers administered 1.3 mg of sodium azide 3 times daily (3.9 mg daily dose) had transient pounding headaches but no sustained effects on blood pressure (Edmonds & Bourne, 1982).
    4) Concentrations of hydrazoic acid vapor as low as 0.5 ppm have caused irritation in laboratory workers (ACGIH, 1986).
    5) A chemist acidifying 10 mg of sodium azide in a malfunctioning hood developed symptoms of dizziness, weakness, blurred vision, shortness of breath, a faint feeling, and moderate hypotension and bradycardia which lasted for about an hour (Clayton & Clayton, 1982).
    6) Hypotension has been noted in workers with hydrazoic acid vapor exposure during the manufacture of lead azide from sodium azide and lead nitrate (Clayton & Clayton, 1982). The hypotension progressively worsened during the working day and resolved after the workers left the plant (Clayton & Clayton, 1982).
    7) Ingestion of a small amount of a Tris buffering solution containing 4% sodium azide resulted in tachycardia, hypotension, and hyperventilation in one patient. A second patient inadvertently underwent gastric lavage with the same solution for collection of gastric cytology specimens and also developed hypotension(Roberts et al, 1974).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) SURVIVAL
    a) A hospitalized 53-year-old woman inadvertently ingested 1 gram of sodium azide and developed seizures, metabolic acidosis and hypotension. The concentration of sodium azide was 174 ppm pre-hemodialysis and 37 ppm post hemodialysis. Following intensive supportive care the patient recovered without permanent sequelae (Watanabe et al, 2007).
    2) POSTMORTEM
    a) Sodium azide blood levels in a fatal ingestion of an unknown quantity were measured at 262 micrograms/milliliter. In the same case, blood cyanide levels were measured at 9 micrograms/milliliter (Lambert et al, 1995).
    b) Postmortem blood sodium azide concentrations were 7.4 to 8.3 milligrams/liter after an estimated 9-gram ingestion (Marquet et al, 1996).
    c) Postmortem blood concentration was 85 milligrams/liter in another case (Klug & Schneider, 1987).

Workplace Standards

    A) ACGIH TLV Values for CAS26628-22-8 (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) Sodium azide, as sodium azide
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling: 0.29 mg/m(3)
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: Not Listed
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    c) TLV Basis - Critical Effect(s): Card impair; lung dam
    d) Molecular Weight: 65.02
    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) Adopted Value
    1) Sodium azide, as hydrazoic acid vapor
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling: 0.11 ppm
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: Not Listed
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    c) TLV Basis - Critical Effect(s): Card impair; lung dam
    d) Molecular Weight: 65.02
    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 CAS26628-22-8 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Sodium azide
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling: 0.1 ppm (as HN3); 0.3 mg/m(3) (as NaN3)
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: [skin]
    1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.
    f) Note(s):
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS26628-22-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Sodium azide, as sodium azide
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Sodium azide, as hydrazoic acid vapor
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Sodium azide
    4) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Sodium azide
    6) MAK (DFG, 2002): Not Listed
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS26628-22-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 1992 Sax & Lewis, 1989
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 28 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 27 mg/kg
    3) LD50- (ORAL)RAT:
    a) 27 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) The exact mechanism of sodium azide toxicity remains unknown.
    B) CARDIOVASCULAR effects include induction of hypotension by relaxation of smooth muscle of blood vessels and dilation of peripheral vessels and reflex induced tachycardia. At highly toxic doses animal models have shown centrally mediated hypertension, tachycardia and cardiac arrhythmias (Kaplita et al, 1984). Graham et al (1948) reported a direct action of hydrazoic acid on heart muscle with a resultant increase in rate and force of contraction, and dilatation of the coronary arteries.
    C) PULMONARY effects include irritating effects on mucous membranes and stimulation of central nervous system with resultant increase in respiration rate. At toxic levels animal models have shown depression of respiratory center (Kaplita et al, 1984).
    D) Sodium azide toxicity may cause inhibition of cytochrome oxidase systems.
    E) Hurst et al (1948) demonstrated in monkeys lesions in the white matter with complete and sudden necrosis, most commonly in the optic nerves with resultant cortical blindness, following toxic injections of sodium azide. When compared to potassium cyanide, sodium azide produced a more frequent and severe necrosis in the caudate nucleus and putamen of the lenticular nucleus. Sax & Mettler (1971) found almost complete degeneration of the cerebellar cortex in the brain of a sacrificed primate after exposure to toxic doses of sodium azide.

Physicochemical

Physical Characteristics

    A) colorless, hexagonal crystals (Budavari, 1989)
    B) odorless (HSDB , 1992)
    C) Sodium azide hydrolyzes to form hydrazoic acid, a colorless, volatile, HIGHLY EXPLOSIVE, liquid with a characteristic odor, which has been described as sickening (Clayton & Clayton, 1981; Sax & Lewis, 1987).

Ph

    1) No information found at the time of this review.
    B) Hydrazoic acid is a weak acid (pKa = 4.72) (Clayton & Clayton, 1981).

Molecular Weight

    A) 65.02 (Budavari, 1989)

Other

    A) ODOR THRESHOLD
    1) Odorless (CHRIS , 2002)

References

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