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Glass strategy: Hanford’s enhanced waste glass program
The mission of the Department of Energy’s Office of River Protection (ORP) is to complete the safe cleanup of waste resulting from decades of nuclear weapons development. One of the most technologically challenging responsibilities is the safe disposition of approximately 56 million gallons of radioactive waste historically stored in 177 tanks at the Hanford Site in Washington state.
ORP has a clear incentive to reduce the overall mission duration and cost. One pathway is to develop and deploy innovative technical solutions that can advance baseline flow sheets toward higher efficiency operations while reducing identified risks without compromising safety. Vitrification is the baseline process that will convert both high-level and low-level radioactive waste at Hanford into a stable glass waste form for long-term storage and disposal.
Although vitrification is a mature technology, there are key areas where technology can further reduce operational risks, advance baseline processes to maximize waste throughput, and provide the underpinning to enhance operational flexibility; all steps in reducing mission duration and cost.
Tsutomu Shimura, Yoshikazu Kuwahara, Manabu Fukumoto, Toshiyuki Umata
Fusion Science and Technology | Volume 60 | Number 3 | October 2011 | Pages 1190-1192
Biology | Proceedings of the Ninth International Conference on Tritium Science and Technology | doi.org/10.13182/FST11-A12628
Articles are hosted by Taylor and Francis Online.
Tritium is used as fuel for nuclear fusion reactions and has cancer risk for workers in nuclear fusion plant by its exposure during routine operation or accidents. Tritium exists as tritiated water (HTO) which is produced by an isotope exchange reaction from HT in normal circumstance. In this study we analyzed cellular response against HTO exposure in a human liver cancer cell line HepG2 and a cervical cancer cell line HeLa. These cells were immersed in RPMI medium containing HTO at the dose rate of 0.5 Gy/hr for 20 hrs (10 Gy). We determined whether the DNA-PK/AKT pathway is activated by chronic HTO exposure or not. As well as X-rays, exposure of HepG2 and HeLa cells to HTO activated AKT, which was shown by phosphorylated-AKT at Serine473. The activation of DNA-PK was also observed in these cells by X-ray irradiation but not by exposure to HTO. Instead of DNA-PK, epidermal growth factor receptor and ERK1/2 were activated following HTO exposure. These results suggested that certain cellular molecules are response to HTO exposure. Our study may provide molecular markers to estimate the biological effects in response to tritium exposure in human cells.