Chemical Toxicity

DOE-STD-1136-2004

Guide of Good Practices for Occupational Radiological Protection in Uranium Facilities

5.6.4 Chemical Toxicity

Inhalation is the most important route of uranium intake for industrial workers. The retention of

uranium in the lungs is influenced by the dissolution rate of the uranium compound inhaled. The major

portion of dissolved uranium is quickly absorbed into extracellular fluid (Durbin 1986). Ingestion is an

important route of uranium intake for the general public (Wrenn et al. 1985). Saliva contains digestive

enzymes and high concentrations of HCO3 - and CO32- at pH 6 to 7.4. As a result, uranyl bicarbonate

complexes would be expected to form. When no digestion is occurring, gastric juice contains high

concentrations of HCO3 - and CO32-. Under these relatively alkaline conditions, dissolved uranium available

for absorption would be expected to form uranyl bicarbonate and carbonate complexes.

When food is ingested, digestive enzymes are secreted, along with HCl to maintain the pH at about

2, which is the optimal pH for enzyme activity. Under these conditions, dissolution of less soluble

uranium compounds would increase. Uranium carbonate complexes are unstable at low pH.

Deposition of uranium in the kidney is not uniform and is located in distal tubules. Uranium

bicarbonate complexes are transported to the tubules when the complex dissociates as a result of

decreased bicarbonate concentrate and decreased pH. Uranium is excreted from the kidney as an

equilibrium between uranyl bicarbonate complex concentration and cell-bound uranyl ion becomes re-

established.

Uranyl ion transported in blood is initially deposited on endosteal bone surfaces (Neuman 1953;

Priest et al. 1982). It becomes incorporated within the bone volume so that a diffuse distribution is

achieved by 72 days after deposition (Rowland and Farnham 1969). Uranyl ion is cleared from bone

slowly by ion exchange with Ca2+ as bone remodeling progresses (Durbin, 1986).

The kidney is the primary target of the chemical toxicity of uranium. The critical level of the metal

above which damage may be expected has not been rigorously defined. The suggested guidance level of 3-

g U/g kidney is not adequately documented by experimental data; however, it provides a basis for

preventing an increased frequency of end-stage renal disease in uranium workers.

Data on human exposures and the effect of various intakes of uranium are summarized in Table 5-13.

These data indicate that a single intake of 8 mg of natural uranium would be well below the level that

could cause permanent kidney damage in most individuals, and that 4 mg intake would likely cause no

observable effects. The urine levels for situations in which chemical toxicity might be of concern are based

on interpretation of the data (McGuire 1991).

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