Internal contamination by actinides following wounding may occur in nuclear fuel industry workers or subsequent to terrorist activities, causing dissemination of radioactive elements. Contamination by alpha particle emitting actinides can result in pathological effects, either local or distant from the site of entry. The objective of the present study was to develop a robust experimental approach in the rat for short- and long- term actinide contamination following wounding by incision of the skin and muscles of the hind limb. Anesthetized rats were contaminated with Mixed OXide (MOX, uranium, plutonium oxides containing 7.1% plutonium) or plutonium nitrate (Pu nitrate) following wounding by deep incision of the hind leg. Actinide excretion and tissue levels were measured as well as histological changes from 2 h to 3 mo. Humid swabs were used for rapid evaluation of contamination levels and proved to be an initial guide for contamination levels. Although the activity transferred from wound to blood is higher after contamination with a moderately soluble form of plutonium (nitrate), at 7 d most of the MOX (98%) or Pu nitrate (87%) was retained at the wound site. Rapid actinide retention in liver and bone was observed within 24 h, which increased up to 3 mo. After MOX contamination, a more rapid initial urinary excretion of americium was observed compared with plutonium. At 3 mo, around 95% of activity remained at the wound site, and excretion of Pu and Am was extremely low. This experimental approach could be applied to other situations involving contamination following wounding including rupture of the dermal, vascular, and muscle barriers.

There is an important requirement following accidental actinide contamination of wounds to limit the dissemination and retention of such alpha-emitting radionuclides. To reduce wound and systemic contamination, treatment approaches include chelation therapy with or without wound excision. However, it has been hypothesized that wound excision could lead to increased contaminant release and systemic organ retention. This study in the rat addresses this question. Anesthetized rats were contaminated with plutonium nitrate following wounding by deep incision of hind leg muscle. Excision of tissue at the contaminated site was performed 7 d later with or without Diethylene Triamine Pentaacetic Acid (DTPA) treatment (30 μmol kg⁻¹ i.v.). Pu urinary excretion was then measured for a further 3 d, and animals were euthanized at 14 d after contamination. Tissue samples were evaluated for Pu activity and histology. At 7 d after contamination, around 50% of the initial activity remained at the wound site. An average of 16% of this activity was then removed by surgery. Surgery alone resulted in increased urinary excretion, suggesting release from the wound site, but no subsequent increases in organ retention (bone, liver) were observed at 14 d. Indeed, organ Pu activity was slightly reduced. The combination of surgery and DTPA or DTPA treatment alone was much more effective than excision alone as shown by the markedly increased urinary Pu excretion and decreased tissue levels. This is the first report in an experimental rodent model of resection of Pu-contaminated wound. Urinary excretion data provide evidence for the release of activity as a result of surgery, but this does not appear to lead to further Pu organ retention. However, a combination of prior DTPA treatment with wound excision is particularly effective.