Recent studies have evaluated and applied the basic models. Chen et al. (2004) used the ICRP model to calculate a table of kidney burdens from inhalation and oral intakes of soluble and moderately soluble uranium. Leggett and Pellmar (2003) evaluated models for application to uranium migration from embedded DU fragments. The time-dependent rate of uptake into plasma from pellets was adjusted to match the urinary data in the DU-implanted rats from the Pellmar et al. (1999a) study. Leggett and Pellmar used data from Morris et al. (1990) on inhalation of insoluble uranium dioxide to mimic slow release from pellets. The data after the first 6 mo fit well, but the data for the first 6 mo did not, perhaps because of variable urinary excretion or some peculiarity of the biokinetics of uranium release from embedded DU metal. Leggett and Pellmar concluded that it is reasonable to apply ICRP’s updated biokinetic model for uranium to assess chemical risk to soldiers who have embedded DU fragments.
Absorption of uranium compounds is low (less than 1%) by all exposure routes, except for soluble compounds, of which 5% or more is absorbed after inhalation.
Initial distribution of uranium compounds depends on their solubility and the route of absorption. Uranium compounds complex with ions and proteins in the blood, are distributed to all tissues, and preferentially deposit in bone and kidneys. Uranium can cross the placenta and the blood-brain barrier.
The metabolism of uranium is not well understood, but oxidation of tetravalent uranium to hexavalent uranium is likely to occur.
After inhalation, elimination of soluble uranium is primarily by the kidneys, and insoluble uranium is eliminated primarily in the feces. In general, soluble compounds are cleared more rapidly than insoluble compounds.
Release of DU from embedded particles is slow and occurs over many years.
Well-established models are available to predict the toxicokinetics of uranium from inhalation exposures.