{"title":"An examination of the dose rate effect in mice assuming that the carcinogenic effect of radiation is life shortening resulting from a tissue reaction.","authors":"Nori Nakamura","doi":"10.1080/09553002.2024.2442690","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>Radiation exposures do not seem to increase the proportion of mice dying from tumors, but rather cause a shift in the appearance of spontaneous cancers, allowing them to appear earlier, and hence produce a life shortening effect. Then, it was possible to estimate the effect of the dose rate on the carcinogenic effects of radiation using life shortening effects as a measure.</p><p><strong>Conclusion: </strong>The dose response for the induction of life shortening was linear under acute exposure conditions, which indicates that the response under chronic exposure conditions is also likely to be linear, and hence the dose rate factor (DRF) would be constant throughout the dose. Furthermore, the life shortening effect decreased sharply with an increase in age at exposure. To separate the dose rate effect from the effects of age under long-term exposure conditions, a thought experiment was designed which consisted of 8 repeated exposures to an acute 1 Gy dose at intervals of 50 days with an assumption that the effect is additive, and the results were compared with those observed in a chronic continuous exposure experiment (20 mGy per day for 400 days, for a total of 8 Gy: Tanaka et al. 2003). The results showed 211 days of life shortening in the former and 120 days in the latter, which provided a DRF of 1.8 (211/120). If one assumes that a tissue reaction is the primary cause of radiation carcinogenesis, the contrasting two concepts, radiation hormesis and linear-non-threshold model at low doses, would become compatible.</p>","PeriodicalId":94057,"journal":{"name":"International journal of radiation biology","volume":" ","pages":"1-7"},"PeriodicalIF":0.0000,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of radiation biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/09553002.2024.2442690","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Purpose: Radiation exposures do not seem to increase the proportion of mice dying from tumors, but rather cause a shift in the appearance of spontaneous cancers, allowing them to appear earlier, and hence produce a life shortening effect. Then, it was possible to estimate the effect of the dose rate on the carcinogenic effects of radiation using life shortening effects as a measure.
Conclusion: The dose response for the induction of life shortening was linear under acute exposure conditions, which indicates that the response under chronic exposure conditions is also likely to be linear, and hence the dose rate factor (DRF) would be constant throughout the dose. Furthermore, the life shortening effect decreased sharply with an increase in age at exposure. To separate the dose rate effect from the effects of age under long-term exposure conditions, a thought experiment was designed which consisted of 8 repeated exposures to an acute 1 Gy dose at intervals of 50 days with an assumption that the effect is additive, and the results were compared with those observed in a chronic continuous exposure experiment (20 mGy per day for 400 days, for a total of 8 Gy: Tanaka et al. 2003). The results showed 211 days of life shortening in the former and 120 days in the latter, which provided a DRF of 1.8 (211/120). If one assumes that a tissue reaction is the primary cause of radiation carcinogenesis, the contrasting two concepts, radiation hormesis and linear-non-threshold model at low doses, would become compatible.