A new approach to characterize very-low-level radioactive waste produced at hadron accelerators.

Radioactive waste is produced as a consequence of preventive and corrective maintenance during the operation of high-energy particle accelerators or associated dismantling campaigns. Their radiological characterization must be performed to ensure an appropriate disposal in the disposal facilities. The radiological characterization of waste includes the establishment of the list of produced radionuclides, called "radionuclide inventory", and the estimation of their activity. The present paper describes the process adopted at CERN to characterize very-low-level radioactive waste with a focus on activated metals. The characterization method consists of measuring and estimating the activity of produced radionuclides either by experimental methods or statistical and numerical approaches. We adapted the so-called Scaling Factor (SF) and Correlation Factor (CF) techniques to the needs of hadron accelerators, and applied them to very-low-level metallic waste produced at CERN. For each type of metal we calculated the radionuclide inventory and identified the radionuclides that most contribute to hazard factors. The methodology proposed is of general validity, can be extended to other activated materials and can be used for the characterization of waste produced in particle accelerators and research centres, where the activation mechanisms are comparable to the ones occurring at CERN.

Persistent oxidative stress after ionizing radiation is involved in inherited radiosensitivity.

The SW620IR1 cell line was derived from SW620 human colon cells surviving to ionizing radiations. It shows an increased radiosensitivity and a higher yield of spontaneous chromosomal aberrations. In order to check whether altered reactive oxygen intermediates (ROI) metabolism is involved in this inherited phenotype, we compared the two cell lines for their radiation-induced modifications at the level of ROI production, antioxidant activities, and chromosomal aberrations. Compared to SW620, SW620IR1 cells exhibit a higher and more persistent ROI induction after various doses of ionizing radiations and a higher yield of dicentric chromosomes. They are also characterized by lower basal activities of glutathione peroxidase and manganese-containing superoxide dismutase, and lower ability to induce these antioxidant defenses after irradiation. Resumption of cell growth after irradiation coincides with maximal induction of antioxidant activities and normalization of ROI concentration. However, at that time radiation-induced chromosomal aberrations are not completely eliminated, leading to the proliferation of genetically unstable cells. These results indicate that the inherited sensitivity of SW620IR1 cells is associated with altered antioxidant activities resulting in higher and more prolonged oxidative stress after radiation exposure. They also suggest that the normalization of ROI levels allows these p53 mutant cells to resume proliferation although high levels of DNA damages are still persisting, thereby explaining the chromosomal instability observed as a delayed effect of radiation exposure.

Correlation between antioxidant status, tumorigenicity and radiosensitivity in sister rat cell lines.

Tumorigenicity and radiosensitivity of related cell lines expressing distinct p53 mutants were analyzed in parallel with key components of the antioxidant metabolic pathway. Six sublines deriving from the same parental cell population and expressing either the mutant p53K130R or p53V270F were investigated. Both mutations abrogate the transcriptional activity of p53 as well as its ability to induce apoptosis. The cells expressing p53K130R showed a higher tumorigenicity and a higher radiosensitivity than those expressing p53V270F. An increase in tumorigenicity was associated with a decrease in manganese-containing superoxide dismutase activity, and with further decreases in the glutathione content and glutathione peroxidase (GPX) activity. A positive correlation was found between GPX activity, glutathione content and cell survival following ionizing irradiation. The fact that sister cell lines exhibit different tumorigenicity and radiosensitivity while expressing a mutant p53 further supports the notion that knowledge of p53 status is not sufficient to predict tumor outcome, especially the response to irradiation. A better understanding of antioxidant defenses might be more informative.