Sodium azide is an ionic solid. Two crystalline forms are known, rhombohedral and hexagonal. Both adopt layered structures. The azide anion is very similar in each form, being centrosymmetric with N–N distances of 1.18 Å. The Na+
ion has octahedral geometry. Each azide is linked to six Na+ centers, with three Na-N bonds to each terminal nitrogen center.
The common synthesis method is the "Wislicenus process," which proceeds in two steps from ammonia. In the first step, ammonia is converted to sodium amide:
2 Na + 2 NH3
→ 2 NaNH2
The sodium amide is subsequently combined with nitrous oxide:
O → NaN3
+ NaOH + NH3
These reactions are the basis of the industrial route, which produced about 250 tons/y in 2004, with production increasing owing to the popularization of airbags.
Curtius and Thiele developed another production process where a nitrite ester is converted to sodium azide using hydrazine. This method is suited for laboratory preparation of sodium azide:
+ 2 C2
→ 2 C2
ONO + Na2
+ 2 H2
ONO + N2
O + NaOH → NaN3
OH + 3 H2
Alternatively the salt can be obtained by the reaction of sodium nitrate with sodium amide.
Treatment of sodium azide with strong acids gives hydrazoic acid, which is also extremely toxic:H+
Aqueous solutions contain minute amounts of hydrogen azide, the formation of which is described by the following equilibrium:N−
(K = 10−4.6
Sodium azide can be destroyed by treatment with nitrous acid solution:
+ 2 HNO2
→ 3 N2
+ 2 NO + 2 NaOH
Older airbag formulations contained mixtures of oxidizers and sodium azide and other agents including ignitors and accelerants. An electronic controller detonates this mixture during an automobile crash:
→ 2Na + 3 N2
The same reaction occurs upon heating the salt to approximately 300 °C. The sodium that is formed is a potential hazard alone and, in automobile airbags, it is converted by reaction with other ingredients, such as potassium nitrate and silica. In the latter case, innocuous sodium silicates are generated. Sodium azide is also used in airplane escape chutes. Newer generation air bags contain nitroguanidine or similar less sensitive explosives.
Due to its explosion hazard, sodium azide is of only limited value in industrial scale organic chemistry. In the laboratory, it is used in organic synthesis to introduce the azide functional group by displacement of halides. The azide functional group can thereafter be converted to an amine by reduction with either SnCl2 in ethanol or lithium aluminium hydride or a tertiary phosphine, such as triphenylphosphine in the Staudinger reaction, with Raney nickel or with hydrogen sulfide in pyridine.
Sodium azide is a versatile precursor to other inorganic azide compounds, e.g., lead azide and silver azide, which are used in explosives.
Sodium azide is a useful probe reagent and a preservative.
In hospitals and laboratories, it is a biocide; it is especially important in bulk reagents and stock solutions which may otherwise support bacterial growth where the sodium azide acts as a bacteriostatic by inhibiting cytochrome oxidase in gram-negative bacteria; gram-positive (streptococci, pneumococci, lactobacilli) are intrinsically resistant.
It is used in agriculture for pest control of soil-borne pathogens such as Meloidogyne incognita or Helicotylenchus dihystera.
It is also used as a mutagen for crop selection of plants such as rice, barley or oats.
Sodium azide has caused deaths for decades. It is a severe poison. It may be fatal in contact with skin or if swallowed. Even minute amounts can cause symptoms. The toxicity of this compound is comparable to that of soluble alkali cyanides and the lethal dose for an adult human is about 0.7 grams. No toxicity has been reported from spent airbags.
Azide inhibits cytochrome oxidase by binding irreversibly to the heme cofactor in a process similar to the action of carbon monoxide. Sodium azide particularly affects organs that undergo high rates of respiration, such as the heart and the brain.
It produces extrapyramidal symptoms with necrosis of the cerebral cortex, cerebellum, and basal ganglia. Toxicity may also include hypotension, blindness and hepatic necrosis. Sodium azide increases cyclic GMP levels in brain and liver by activation of guanylate cyclase.