Sodium azide is a highly toxic, odorless, white crystalline solid used in many automobile air bags; its explosive decomposition to nitrogen gas provides rapid inflation of the air bag. In addition, sodium azide is used in the production of metallic azide explosives and as a preservative in laboratories. It has no current medical uses, but because of its potent vasodilatory effects, it has been evaluated as an antihypertensive agent.

1. The mechanism of azide toxicity is unclear. Like cyanide and hydrogen sulfide, azide inhibits iron-containing respiratory enzymes such as cytochrome oxidase, resulting in inhibition of oxidative phosphorylation leading to cellular hypoxia. In the CNS, azide enhances excitatory neurotransmission. It is also a potent direct-acting vasodilator.
2. Sodium azide forms hydrazoic acid (HN₃) in aqueous and acidic solutions, particularly in the presence of solid metals (eg, drain pipes). Hydrazoic acid vapors are pungent and explosive at high concentrations. The acute toxicity of hydrazoic acid has been compared with that of hydrogen cyanide and hydrogen sulfide.

Although up to 200 grams of azide can be found in an automobile airbag, it is completely consumed during the explosive inflation process, and azide toxicity has not been reported from exposure to spent bags. However, sodium hydroxide, a by-product of the combustion reaction, can cause minor skin irritation and chemical burns. Talc or cornstarch used to lubricate the fabric may appear as white dust or smoke after air bag deployment.

1. Inhalation. Local irritation from inhalation or a pungent odor does not give adequate warning of toxicity. The recommended workplace ceiling limit (ACGIH TLV-C) is 0.29 mg/m³ for sodium azide and 0.11 ppm for hydrazoic acid. Air concentrations as low as 0.5 ppm may result in mucous membrane irritation, hypotension and headache. Workers in a lead azide plant exposed to air concentrations of 0.3-3.9 ppm experienced headache, weakness, palpitations, and mild eye and nose irritation, in addition to hypotension.
2. Dermal. Cutaneous exposure through broken skin may rarely lead to systemic toxicity. A fatal exposure was reported from the explosion of a 1% sodium azide solution, resulting in 45% body surface area burns with typical azide toxicity and a time course similar to that from oral ingestion.
3. Ingestion. Azide is well absorbed through the GI tract, with ingestions accounting for the majority of serious or fatal poisonings.
   1. Ingestion of greater than 10 mg/kg (700 mg) can be fatal.
   2. Nonfatal exposures, ranging from 0.3 to 150 mg, have been reported.
   3. Doses of 0.65-3.9 mg/d, given for up to 2.5 years, have been used experimentally as an antihypertensive. The hypotensive effect occurred within 1 minute, and headache was the only complaint noted in these patients.

1. Irritation. Exposure to azide-containing dust or gas may produce reddened conjunctivae and nasal and bronchial irritation that may progress to pulmonary edema.
2. Systemic toxicity. Both inhalation and ingestion are associated with a variety of dose-dependent symptoms affecting multiple organ systems. Early cardiovascular effects include hypotension and tachycardia, due to the direct vasodilatory effect, which may progress to bradycardia, ventricular arrhythmias, and cardiovascular collapse. Neurologic effects include headache, restlessness, loss of vision, generalized weakness, syncope, seizures, and coma. Respiratory effects include dyspnea, tachypnea, pulmonary edema, and respiratory failure. Nausea, vomiting, diarrhea, diaphoresis, and lactic acidosis are also frequently reported.

Is based on the history of exposure and clinical presentation.

1. Specific levels are not routinely available.
2. Other useful laboratory studies include electrolytes, glucose, arterial blood gases or pulse oximetry, and ECG.

Caution: Cases involving severe azide ingestion are potentially dangerous to health care providers. In the acidic environment of the stomach, azide salts are converted to hydrazoic acid, which is highly volatile. Wear appropriate respiratory protective gear, keep the patient in a well-ventilated area, and quickly isolate all vomitus or gastric washings. Azides should be disposed of with care as contact with heavy metals, such as copper or lead water pipes, may produce explosive metal azides.

1. Emergency and supportive measures
   1. Protect the airway and assist ventilation if necessary. Insert an IV line and monitor the ECG and vital signs.
   2. Treat coma, hypotension, seizures, and arrhythmias if they occur.
2. Specific drugs and antidotes. There is no specific antidote.
3. Decontamination
   1. Inhalation. Remove the victim from exposure and give supplemental oxygen if available. Rescuers should wear self-contained breathing apparatus and appropriate chemical-protective clothing.
   2. Skin. Remove and bag contaminated clothing and wash affected areas copiously with soap and water.
   3. Ingestion. Administer activated charcoal, although the affinity of charcoal for azide is not known. Consider gastric lavage if presentation is early after ingestion. See the caution statement above; isolate all vomitus or gastric washings to avoid exposure to volatile hydrazoic acid.
4. Enhanced elimination. There is no role for dialysis or hemoperfusion in acute azide poisoning.