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Radiation hormesis: Historical perspective and implications for low-dose cancer risk assessment

机译:辐射激素:低剂量癌症风险评估的历史观点和启示

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Current guidelines for limiting exposure of humans to ionizing radiation are based on the linear-no-threshold (LNT) hypothesis for radiation carcinogenesis under which cancer risk increases linearly as the radiation dose increases. With the LNT model even a very small dose could cause cancer and the model is used in establishing guidelines for limiting radiation exposure of humans. A slope change at low doses and dose rates is implemented using an empirical dose and dose rate effectiveness factor (DDREF). This imposes usually unacknowledged nonlinearity but not a threshold in the dose-response curve for cancer induction. In contrast, with the hormetic model, low doses of radiation reduce the cancer incidence while it is elevated after high doses. Based on a review of epidemiological and other data for exposure to low radiation doses and dose rates, it was found that the LNT model fails badly. Cancer risk after ordinarily encountered radiation exposure (medical X-rays, natural background radiation, etc.) is much lower than projections based on the LNT model and is often less than the risk for spontaneous cancer (a hormetic response). Understanding the mechanistic basis for hormetic responses will provide new insights about both risks and benefits from low-dose radiation exposure.
机译:当前限制人类暴露于电离辐射的指导原则基于放射致癌作用的线性无阈值(LNT)假设,在这种假设下,癌症风险随放射剂量的增加呈线性增加。使用LNT模型,即使很小的剂量也可能导致癌症,该模型用于建立限制人类辐射的准则。低剂量和剂量率下的斜率变化是通过经验剂量和剂量率有效因子(DDREF)实现的。这通常会带来未经认可的非线性,但不会在诱发癌症的剂量反应曲线中产生阈值。相比之下,对于钟表模型,低剂量的辐射降低了癌症的发生率,而高剂量的辐射则升高了癌症的发生率。根据对低辐射剂量和剂量率暴露的流行病学和其他数据的回顾,发现LNT模型严重失效。通常遇到辐射暴露(医学X射线,自然本底辐射等)后的癌症风险远低于基于LNT模型的预测,并且通常低于自发性癌症的风险(仿制药反应)。了解机械反应的机理基础将提供有关低剂量辐射暴露的风险和益处的新见解。

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