Sodium azide is a highly toxic white crystalline solid. It has come into widespread use in automobile air bags; its explosive decomposition to nitrogen gas provides rapid inflation of the air bag (Note: some newer-generation airbags utilize ammonium nitrate as the explosive chemical). 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 vasodilator effects, it has been evaluated as an antihypertensive agent.
The mechanism of azide toxicity is unclear. Like cyanide and hydrogen sulfide, azide inhibits iron-containing respiratory enzymes such as cytochrome oxidase, resulting in cellular asphyxiation. In the CNS, enhanced excitatory transmission occurs. Azide is also a potent direct-acting vasodilator.
Although neutral solutions are stable, acidification rapidly converts the azide salt to hydrazoic acid, particularly in the presence of solid metals (eg, drain pipes). Hydrazoic acid vapors are pungent and (at high concentrations) explosive. The acute toxicity of hydrazoic acid has been compared with that of hydrogen cyanide and hydrogen sulfide.
Although several grams of azide are found in an automobile airbag, it is completely consumed and converted to nitrogen during the explosive inflation process, and toxicity has not been reported from exposure to spent air bags. However, sodium hydroxide is a by-product of the combustion reaction, and talc or cornstarch used to lubricate the fabric may appear as white dust or smoke after air bag deployment.
Inhalation. Irritation symptoms 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. A chemist who intentionally sniffed the vapor above a 1% hydrazoic acid solution became hypotensive, collapsed, and recovered 15 minutes later with residual headache. Workers in a lead azide plant exposed to air concentrations of 0.3–3.9 ppm experienced symptoms of headache, weakness, palpitations, and mild smarting of the eyes and nose, in addition to a drop in blood pressure. Laboratory workers adjacent to a sulfur analyzer that was emitting vapor concentrations of 0.5 ppm experienced symptoms of nasal stuffiness without detecting a pungent odor.
Dermal absorption. Industrial workers handling bulk sodium azide experienced headache, nausea, faintness, and hypotension, but it is unclear whether the exposure occurred via dermal absorption or inhalation. An explosion of a metal waste drum containing a 1% sodium azide solution caused burns over a 45% body surface area and led to typical azide toxicity with a time course similar to that of oral ingestion; coma and hypotension developed within 1 hour, followed by refractory metabolic acidosis, shock, and death 14 hours later.
Ingestion. Several serious or fatal poisonings occurred as a result ...