OSHA comments from the January 19, 1989 Final Rule on Air Contaminants Project extracted from 54FR2332 et. seq. This rule was remanded by the U.S. Circuit Court of Appeals and the limits are not currently in force.
CAS: 26628-22-8; Chemical Formula: NaN3
There was no former OSHA PEL for sodium azide. The proposed PELs were a ceiling of 0.1 ppm as hydrazoic acid vapor (HN(3)) and a ceiling of 0.3 mg/m3 as sodium azide (NaN(3)); NIOSH (Ex. 8-47, Table N1) concurred with the Agency’s selection. The final rule establishes this limit. In addition, a skin notation is being added to the limit in the final rule. The ACGIH (1986/Ex. 1-3) has ceiling limits for sodium azide of 0.1 ppm (as hydrazoic acid vapor) and 0.3 mg/m3 (as NaN3). Sodium azide is a colorless, crystalline solid.
Sodium azide is known to produce hypotension in laboratory animals and humans. An intravenous dose of 1 mg/kg was reported to lower blood pressure in cats (Graham 1949/Ex. 1-109). In the 1950s, the medicinal usefulness of sodium azide as a hypotensive agent was tested in 30 hypertensive patients. Their hypertension was reduced, but observed side effects included headaches; in addition, 20 of 30 patients developed increased sensitivity to sodium azide, necessitating a reduction in the dose (Black, Zweifach, and Speer 1954/Ex. 1-163). Hicks (1950, cited in ACGIH 1986/Ex. 1-3, p. 533) reported that repeated intraperitoneal injections of 5 to 10 mg/kg in rats caused demyelination of nerve fibers of the CNS. Alben and Fager (1972, cited in ACGIH 1986/Ex. 1-3, p. 533) showed that sodium azide formed strong complexes with hemoglobin and blocked oxygen transport in the blood.
Acute inhalation by humans of hydrazoic acid vapor (which forms when sodium azide contacts water) results in lowered blood pressure, eye irritation, bronchitis, headache, weakness, and collapse (Fairhall et al. 1943/Ex. 1-130; Graham 1949/Ex. 1-109). The exposure levels that produce these effects were not reported by these authors. Haas and Marsh (1970/Ex. 1-121) reported that exposure to concentrations of hydrazoic acid vapor as low as 0.5 ppm “cause[d] some discomfort to laboratory personnel.” Dr. Hecker of Abbott Laboratories (Ex. 3-678) commented that the limit for sodium azide should include a skin notation, and Sax and Lewis (Dangerous Properties of Industrial Materials, 7th ed., 1989) report the dermal LD(50) in rabbits to be 20 mg/kg, demonstrating that sodium azide readily penetrates the skin and causes systemic poisoning. Grace Ziem, an independent occupational physician, also supported a skin notation for sodium azide (Ex. 46). In the final rule, OSHA is therefore adding a skin notation for sodium azide.
Because of its hypotensive effect in humans, OSHA concludes that ceiling limits of 0.1 ppm (as HN(3)) and 0.3 mg/m3 (as NaN(3)) should be established for sodium azide to reduce the significant risk of cardiovascular and irritation effects posed to workers at the levels formerly permitted by the absence of an OSHA limit. The Agency considers the effects associated with exposure to sodium azide as material impairments of health. To reduce this significant risk substantially, OSHA is establishing these ceiling limits for sodium azide in the final rule. In addition, OSHA is adding a skin notation to the PEL to alert employers to the fact that sodium azide readily penetrates intact skin and that dermal exposure can contribute significantly to overall worker exposure.