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Sodium azide is the inorganic compound with the formula NaN3. This colorless salt is the gas-forming component in legacy[citation needed] car airbag systems. It is used for the preparation of other azide compounds. It is an ionic substance, is highly soluble in water and is very acutely poisonous.[5]

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Sodium azide has caused deaths for decades,[16] and even minute amounts can cause symptoms. The toxicity of this compound is comparable to that of soluble alkali cyanides,[17] although no toxicity has been reported from spent airbags.[18]

It produces extrapyramidal symptoms with necrosis of the cerebral cortex, cerebellum, and basal ganglia. Toxicity may also include hypotension,[19] blindness and hepatic necrosis. Sodium azide increases cyclic GMP levels in brain and liver by activation of guanylate cyclase.[20]

Sodium azide solutions react with metallic ions to precipitate metal azides, which can be shock sensitive and explosive. This should be considered for choosing a non-metallic transport container for sodium azide solutions in the laboratory. This can also create potentially dangerous situations if azide solutions should be directly disposed down the drain into a sanitary sewer system. Metal in the plumbing system could react, forming highly sensitive metal azide crystals which could accumulate over years. Adequate precautions are necessary for the safe and environmentally responsible disposal of azide solution residues.[21]

Acute symptoms of copper poisoning by ingestion include vomiting, hematemesis (vomiting of blood), hypotension (low blood pressure), melena (black “tarry” feces), coma, jaundice (yellowish pigmentation of the skin), and gastrointestinal distress.[1] Individuals with glucose-6-phosphate deficiency may be at increased risk of hematologic effects of copper.[1] Hemolytic anemia resulting from the treatment of burns with copper compounds is infrequent.[1]

Chronic (long-term) copper exposure can damage the liver and kidneys.[2] Mammals have efficient mechanisms to regulate copper stores such that they are generally protected from excess dietary copper levels.[2][3]

Those same protection mechanisms can cause milder symptoms, which are often misdiagnosed as psychiatric disorders. There is a lot of research on the function of the Cu/Zn ratio in neurological, endocrinological, and psychological conditions.[4][5][6] Many of the substances that protect us from excess copper perform important functions in our neurological and endocrine systems, leading to diagnostic difficulties. When they are used to bind copper in the plasma, to prevent it from being absorbed in the tissues, their own function may go unfulfilled. Such symptoms often include mood swings, irritability, depression, fatigue, excitation, difficulty focusing, and feeling out of control. To further complicate diagnosis, some symptoms of excess copper are similar to those of a copper deficit.

The U.S. Environmental Protection Agency’s Maximum Contaminant Level (MCL) in drinking water is 1.3 milligrams per liter.[1][7] The MCL for copper is based on the expectation that a lifetime of consuming copper in water at this level is without adverse effect (gastrointestinal). The US EPA lists copper as a micronutrient and a toxin.[8] Toxicity in mammals includes a wide range of animals and effects such as liver cirrhosis, necrosis in kidneys and the brain, gastrointestinal distress, lesions, low blood pressure, and fetal mortality.[9][10][11] The Occupational Safety and Health Administration (OSHA) has set a limit of 0.1 mg/m3 for copper fumes (vapor generated from heating copper) and 1 mg/m3 for copper dusts (fine metallic copper particles) and mists (aerosol of soluble copper) in workroom air during an eight-hour work shift, 40-hour work week.[12] Toxicity to other species of plants and animals is noted to varying levels.[8]