Highly toxic by inhalation, ingestion, or skin absorption.

The acute toxicity of sodium azide is high. Symptoms of exposure include lowered blood pressure, headache, hypothermia, and in the case of serious overexposure, convulsions and death. Ingestion of 100 to 200 mg in humans may result in headache, respiratory distress, and diarrhea. Target organs are primarily the central nervous system and brain. Sodium azide rapidly hydrolyzes in water to form hydrazoic acid, a highly toxic gas that can escape from solution, presenting a serious inhalation hazard. Symptoms of acute exposure to hydrazoic acid include eye irritation, headache, dramatic decrease in blood pressure, weakness, pulmonary edema, and collapse. Solutions of sodium azide can be absorbed through the skin.

Sodium azide has not been found to be carcinogenic in humans. Chronic, low-level exposure may cause nose irritation, episodes of falling blood pressure, dizziness, and bronchitis.

Flammability hazard is low, but violent decomposition can occur when heated to 275 °C. Decomposition products include oxides of nitrogen and sodium oxide.

Sodium azide should not be allowed to come into contact with heavy metals or their salts, because it may react to form heavy metal azides, which are notorious shock-sensitive explosives. Do not pour sodium azide solutions into a copper or lead drain. Sodium azide reacts violently with carbon disulfide, bromine, nitric acid, dimethyl sulfate, and a number of heavy metals, including copper and lead. Reaction with water and acids liberates highly toxic hydrazoic acid, which is a dangerous explosive. Sodium azide is reported to react with CH₂Cl₂ in the presence of DMSO to form explosive products.

Because of its high toxicity, sodium azide should be handled in the laboratory using the "basic prudent practices" of Chapter 5.C, supplemented by the additional precautions