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Radiation Hormesis in Cancer
Published in T. D. Luckey, Radiation Hormesis, 2020
Some organs and tissues are quite susceptible to high doses of radiation. These include bone marrow, breast, thyroid, and possibly ovary. Some leukemias are the most readily induced cancers. Prolonged exposure may cause skin cancer, but it rarely metastasizes to other tissues. Organs which are moderately susceptible to radiation-induced cancer are lung, liver, gastrointestinal tract, pancreas, pharynx, and the lymphatic system.616 Not readily induced by radiation are chronic lymphatic leukemia or cancer of muscle, cervix, and prostate. These are generalizations from exposures to large doses which pinpoint the most susceptible organs. None of this implies that low doses of ionizing radiation induce cancer in these organs.
Radiation Carcinogenesis: Human Model
Published in Kedar N. Prasad, Handbook of RADIOBIOLOGY, 2020
Radiation-induced cancer is indistinguishable from cancer induced chemically or spontaneously. Therefore, the current proposed cancer prevention strategies could be adopted for radiation-induced cancer: the National Cancer Institute has recommended modification in diets and lifestyle. These recommendations include a low-fat and high-fiber diet, which is rich in fresh fruits and vegetables. In the current recommendation the total fat calories can be reduced to 20% (1 g fat = 9 calories). Excessive amounts of fat can act as tumor promoters; in addition, they produce high levels of prostaglandins, which are immunosuppressive. High fibers can bind bile acid, cholesterol, and some mutagens that are formed in the GI tract; they are eliminated through feces. The fermentation of fiber by endogenous bacteria generates millimole levels of butyric acid, a 4-carbon small fatty acid, in the lower intestinal tract. Sodium butyrate has been shown to reduce the growth of several types of cancer. Sodium butyrate may be one of the mechanisms involved in the cancer-protective effect of a high-fiber diet, and this mechanism of protection could be applicable to all cancers. In addition, the consumption of cured meat (rich in nitrite), smoked foods, and pickled foods should be reduced. The lifestyle change recommendation includes cessation of tobacco smoking and chewing, reduction in consumption of alcohol and caffeine, and adoption of habits of regular exercise and reduced stress.
Radiation Protection
Published in Eric Ford, Primer on Radiation Oncology Physics, 2020
A key reference which examines the impact of radiation exposure and presents consensus findings is the BEIR VII Report, Biological Effect of Ionizing Radiation (2006). At the highest doses the effects are deterministic, i.e. the impact can be predicted. Relevant threshold dose levels and effects are 5 Sv bone marrow depletion, 10 Sv GI syndrome, and 20 Sv CNS syndrome. At lower doses the effects are stochastic, i.e. random in nature. The main effect is a radiation-induced cancer. The model that that BEIR VII report advocates is a linear no-threshold (LNT) model for excess risk of cancer (Figure 25.1.1). Above about 100 mSv there are data on risk from the survivors of the nuclear bombing of Hiroshima and Nagasaki during World War II. Below 100 mSv, however, there are few data and so various models are possible, including even a radiation hormesis model where low levels of radiation are beneficial. The BEIR VII report concludes that there is no evidence for a low dose threshold and advocates the LNT model as a conservative estimate of risk.
Effects of oxygen on the response of mitochondria to X-irradiation and reactive oxygen species-mediated fibroblast activation
Published in International Journal of Radiation Biology, 2023
Tsutomu Shimura, Rina Totani, Hyougo Ogasawara, Keiki Inomata, Megumi Sasatani, Kenji Kamiya, Akira Ushiyama
Humans are exposed to ionizing radiation internally and externally in daily life (UNSCEAR 2018). After the Fukushima nuclear accident, mental health issues due to fear of radiation-induced cancer have become a concern in Japan (Maeda and Oe 2017). Radiation is believed to have effects on humans even when exposure levels are low. Radiation cancer risk has been intensively investigated, even at low overall radiation doses and dose rates which the public and radiation-associated workers may be exposed to (Salomaa et al. 2017; Repussard 2018; Nuclear-and-Radiation-Studies-Board 2019; Boice Jr. et al. 2022). However, sufficient data directly linked to low dose and low dose rate radiation risk assessment have yet to be obtained. Additional research may reveal the mechanism of action in radiation-induced cancer.
Adverse outcome pathways, key events, and radiation risk assessment
Published in International Journal of Radiation Biology, 2021
R. Julian Preston, Werner Rühm, Edouard I. Azzam, John D. Boice, Simon Bouffler, Kathryn D. Held, Mark P. Little, Roy E. Shore, Igor Shuryak, Michael M. Weil
For many decades, the basis for setting radiation protection guidance for exposure to low absorbed doses and low absorbed-dose rates of ionizing radiation has been the estimation of the risk of radiation-induced cancer. In addition, there is an ongoing discussion concerning risks of radiation-induced noncancer effects [for NCRP Report No. 186 (NCRP 2020), noncancer effects are specifically for circulatory disease and do not include heritable effects]. The estimates for radiation-induced cancer have been derived primarily from exposure to medium and high doses and high dose rates of ionizing radiation with assumptions on how to extrapolate to low doses and low dose rates. For the purpose of NCRP Report No. 186 (hereafter referred to as ‘NCRP 186’), for low linear-energy transfer (LET) radiation, a low absorbed dose is <100 mGy delivered acutely, and a low absorbed-dose rate is <5 mGy h−1 for any accumulated absorbed dose (NCRP 2015).
Biologically based models of cancer risk in radiation research
Published in International Journal of Radiation Biology, 2021
Jan Christian Kaiser, Maria Blettner, Georgios T. Stathopoulos
Increasing grasp of disease processes leading to cancer and concomitantly the establishment of observational data sets for the general population prompted the development of biologically based models of cancer risk (BBCR models) (Armitage and Doll 1957; Moolgavkar et al. 1980; Moolgavkar and Knudson 1981). In radiation epidemiology the first deployment of BBCR models occurred with the Life Span Study (LSS) of Japanese a-bomb survivors decades after their application to observational cancer data (Little et al. 1992; Little 1996; Heidenreich et al. 1997; Kai et al. 1997). Since the late 1990s the scope of mechanistic modeling of radiation-induced cancer risk has been extended to a growing number of epidemiological cohorts which were exposed to different radiation fields of acute and protracted exposure (Shuryak 2019). Rühm et al. (2017) have extensively reviewed the application of BBCR models to the LSS, post-Chernobyl cohorts and cohorts of uranium miners from Europe and North America.