The exact mechanism of toxicity of sodium azide is not fully understood. Two mechanisms of operation are suggested.
The dissolved salt is relatively tasteless and is rapidly hydrolysed on contact with mucosa to hydrazoic acid. This has some irritant effect in the throat and, at higher concentrations, the direct effect of azide on cytochrome oxidase can cause cellular asphyxia and death in those organs with the highest need for oxygen (eg. the brain and heart). This is known as histotoxic hypoxia.
The production of nitric oxide with its effect on the central nervous system, carotid baroreceptors and potent vasodilation with associated blood pressure drop can explain the reported headache, nausea,
tachycardia, and circulatory collapse
(hypemic hypoxia). The effect of ingesting sodium azide has been likened to the simultaneous ingestion of both nitrite and cyanide. Although azide ingestion does not lead to significant blood discolouration or reduction in oxygen carrying ability.
