Respiratory tract toxicity uranium

The hazard from inhaled uranium aerosols, or any noxious agent, is determined by the likelihood that the agent will reach the site of its toxic action. Two main factors that influence the degree of hazard from toxic airborne particles are the site of deposition in the respiratory tract of the particles and the fate of the particles within the lungs. The deposition site within the lungs depends mainly on the particle size of the inhaled aerosol, while the subsequent fate of the particle depends mainly on the physical and chemical properties of the inhaled particles and the physiological status of the lungs. 

In acute exposures, respiratory disease may be limited to interstitial inflammation of the alveolar epithelium, leading eventually to emphysema or pulmonary fibrosis (Cooper et al. 1982 Dungworth 1989 Stokinger 1981 Wedeen 1992). In studies of the pulmonary effects of airborne uranium dust in uranium miners and in animals, the respiratory diseases reported are probably aggravated by the inhalable dust particles (the form in which uranium is inhaled) toxicity because most of the respiratory diseases reported in these studies are consistent with the effects of inhaled dust (Dockery et al. 1993). In some of these instances, additional data from the studies show that the workers were exposed to even more potent respiratory tract irritants, such as silica and vanadium pentaoxide (Waxweiler et al. 1983). 

The pulmonary toxicity of uranium compounds varies in animals. Reports of pulmonary toxicity in animals after acute-duration exposure to uranium are limited to experiments with uranium hexafluoride. Gasping and severe irritation to the nasal passages were reported after 10 minute exposures at 637 mg U/mg in rats and mice (Spiegl 1949) and nasal hemorrhage in rats after a 5 minute exposure to 54,503 mg/m (Leach et al. 1984). Uranium hexafluoride promptly hydrolyzes on contact with water to uranyl fluoride and hydrofluoric acid. Thus, the animals were potentially exposed to hydrofluoric acid, a potent toxicant to respiratory tract epithelium, which probably contributed to pulmonary tissue destruction (Leach et al. 1984 Spiegl 1949 Stokinger et al. 1953). In addition, exposure to fluoride ions can result in hypocalcemia, hypomagnesemia, pulmonary edema, metabolic acidosis, ventricular arrhythmia, and death (Meditext 1998). 

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