Inhalation toxicity uranium

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). 

Figure 8.3 Inhalation toxicity of the fission products from a uranium-fueied LWR. 

The occupational exposure values for the inhalation of uranium have been compiled by the American Conference of Governmental Industrial Hygienists (ACGIH) [14]. These are air concentration exposure limits based on the chemical effects of uranium. In contrast, the International Commission on Radiological Protection (ICRP) has developed the annual limit on intake (ALI) for ingestion and inhalation of uranium compounds based solely on the radiation doses received by tissues and organs of the body [12,15]. Whether the primary concern is the chemical toxicity or radiation dose, the occupational limits take the solubility of the uranium compound into consideration. The occupational limits are summarized in Table 3. It must be emphasized that the air concentration exposure limits are for the typical 8-hr day (see Abbrevi-... 

Plutonium has a much shorter half-life than uranium (24.000 years for Pu-239 6,500 years for Pu-240). Plutonium is most toxic if it is inhaled. The radioactive decay that plutonium undergoes (alpha decay) is of little external consequence, since the alpha particles are blocked by human skin and travel only a few inches. If inhaled, however, the soft tissue of the lungs will suffer an internal dose of radiation. Particles may also enter the blood stream and irradiate other parts of the body. The safest way to handle plutonium is in its plutonium dioxide (PuOj) form because PuOj is virtually insoluble inside the human body, gi eatly reducing the risk of internal contamination. 

Two epidemiology studies have examined mortality among thorium workers neither found significant excess mortality. The standard mortality ratio (SMR) for all causes of death in a cohort of 3039 male workers in a thorium processing plant was 1.05 in comparison to United States white males (Polednak et al. 1983). The estimated radiation levels to the workers for inhalation intake ranged from 0.003-0.192 nCi/m (0.001-0.007 Bq/m ) for a period of 1-33 years. No evidence of overt industrial disease was found in a cohort of 84 workers at a thorium refinery exposed to <0.045-450 nCi/m (<0.002-0.02 Bq/m ) for <1-20 years (Albert et al. 1955). In both studies, the workers were exposed to other toxic compounds (uranium dust) as well as other radioactive materials (thoron, uranium daughters, thorium daughters, cerium). 

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. 

Deaths occurred after accidental releases of uranium hexafluoride at uranium-processing facilities in 1944 and 1986, but these deaths were not attributed to the uranium component of this compound (Kathren and Moore 1986 Moore and Kathren 1985 USNRC 1986). These releases resulted in the generation of concentrated aerosols of highly toxic hydrofluoric acid and uranyl fluoride. In the 1944 incident exposure time was estimated to be only 17 seconds, deaths occurred in 2 of 20 workers within an hour and were attributed to severe chemical burns of the lungs. In the 1986 incident, 1 of 23 workers died from massive pulmonary edema, indicating that inhalation of hydrofluoric acid was responsible for death. Estimated airborne concentrations were 20 mg uranium hexafluoride/m for a 1-minute exposure and 120 mg uranium hexafluoride/m for a 60-minute exposure (15.2 and 91 mg U/m, respectively). 

Table 2-1. Levels of Significant Exposure to Uranium - Chemical Toxicity - Inhalation... 

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