An approach to incorporate multiple forms of iodine in radiological consequence analysis.

Interest is increasing in the radiological consequences of a release of aerosol and gaseous iodine, especially after the Fukushima accident and also because of new interpretations of the results of recent severe accident experiments. This work provides a brief review of the history of iodine chemistry in containment and suggests an approach to include gaseous iodine, namely in the forms of elemental iodine and organic iodide, in consequence analyses using the MACCS code. As dry deposition is an important characteristic to distinguish each chemical form of iodine when performing a consequence analysis, the mechanisms and mathematical formulas expressing dry deposition are also investigated. The proposed approach is demonstrated by performing consequence analyses with a unit release of 131I, with the resulting trends of concentration and dose for the different chemical forms of iodine presented and discussed. For the same amount of iodine release, there is a higher surface deposition of elemental iodine (I2) because it has a higher dry deposition velocity, while the air concentration of a representative organic iodide (CH3I) is higher due to its lower dry deposition velocity, which means a lower depletion of the air concentration. Despite elemental iodine having a lower air concentration, its higher dose coefficients for the inhalation pathway compensates for this when calculating doses. Further, inhaled doses increase when considering resuspension inhalation for extended durations of exposure. The approach proposed in this study is expected to be used flexibly to perform consequence analyses incorporating both aerosol and gaseous forms of iodine.

Non-thermal atmospheric pressure plasma preferentially induces apoptosis in p53-mutated cancer cells by activating ROS stress-response pathways.

Non-thermal atmospheric pressure plasma (NTAPP) is an ionized gas at room temperature and has potential as a new apoptosis-promoting cancer therapy that acts by generating reactive oxygen species (ROS). However, it is imperative to determine its selectivity and standardize the components and composition of NTAPP. Here, we designed an NTAPP-generating apparatus combined with a He gas feeding system and demonstrated its high selectivity toward p53-mutated cancer cells. We first determined the proper conditions for NTAPP exposure to selectively induce apoptosis in cancer cells. The apoptotic effect of NTAPP was greater for p53-mutated cancer cells; artificial p53 expression in p53-negative HT29 cells decreased the pro-apoptotic effect of NTAPP. We also examined extra- and intracellular ROS levels in NTAPP-treated cells to deduce the mechanism of NTAPP action. While NTAPP-mediated increases in extracellular nitric oxide (NO) did not affect cell viability, intracellular ROS increased under NTAPP exposure and induced apoptotic cell death. This effect was dose-dependently reduced following treatment with ROS scavengers. NTAPP induced apoptosis even in doxorubicin-resistant cancer cell lines, demonstrating the feasibility of NTAPP as a potent cancer therapy. Collectively, these results strongly support the potential of NTAPP as a selective anticancer treatment, especially for p53-mutated cancer cells.