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Squibb, Katherine S.*; Leggett, Richard W.; McDiarmid, Melissa A.

doi: 10.1097/01.HP.0000165451.80061.7e

Mobilization of uranium (U) from embedded depleted uranium (DU) metal fragments in Gulf War veterans presents a unique exposure scenario for this radioactive and nephrotoxic metal. In a cohort of exposed veterans, urine U concentrations measured every two years since 1993 persistently range from 10 to over 500 times normal levels, indicating that embedded DU fragments give rise to chronic, systemic exposure to U. Health effects of this exposure are not fully known, but clinical surveillance of these soldiers continues in light of animal studies showing that U released from implanted DU pellets results in tissue accumulation of U. The biokinetic model for uranium recommended by the International Commission on Radiological Protection was used to predict kidney U concentrations and tissue radiation doses in veterans with DU shrapnel based on their urine U excretion. Results suggest that kidney U concentrations in some individuals reached their peak within six years after the war, while in others, concentrations continue to increase and are approaching 1 ppm after 10 y. These results are consistent with urine biomarker tests of renal proximal tubular cell function and cytotoxicity which have shown elevated mean urinary protein excretion indicative of functional effects in veterans with high urine U concentrations (≥0.10 μg g−1 creatinine). Predicted lifetime effective radiation dose from DU released to the blood for the highest exposed individual in this cohort was substantially less than the National Council on Radiation Protection (NCRP) limit for occupational exposure. These results provide further support for current health protection guidelines for DU, which are based on the metal’s chemical rather than its radiological toxicity. In light of the potential for continued accumulation of U in the kidney to concentrations approaching the traditional guidance level of 3 ppm U, these results indicate the need for continued surveillance of this population for evidence of developing renal dysfunction.

* Department of Epidemiology and Preventive Medicine, University of Maryland School of Medicine, Baltimore, MD 21201; † 1060 Commerce Park, MS6480, Oak Ridge National Laboratory, Oak Ridge, TN 37830; ‡ Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201.

For correspondence or reprints contact: Katherine S. Squibb, Department of Epidemiology and Preventive Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, or email at

(Manuscript received 14 January 2005; revised manuscript received 29 March 2005, accepted 22 May 2005)

©2005Health Physics Society