Morris M D, Jones T D, Young R W
Engineering Physics and Mathematics Division, Oak Ridge National Laboratory, TN 37831-6101.
Health Phys. 1994 Aug;67(2):183-6. doi: 10.1097/00004032-199408000-00011.
A cell-kinetics model for radiation-induced myelopoiesis has been derived for mice, rats, dogs, sheep, swine, and burros. The model was extended to humans after extensive comparisons with molecular and cellular data from biological experiments and an assortment of predictive/validation tests on animal mortality, cell survival, and cellular repopulation following irradiations. One advantage of the model is that any complex pattern of protracted irradiation can be equated to its equivalent prompt dose. Severity of biological response depends upon target-organ dose, dose rate, and dose fractionation. Epidemiological and animal data are best suited for exposures given in brief periods of time. To use those data to assess risk from protracted human exposures, it is obligatory to model molecular repair and compensatory proliferation in terms of prompt dose. Although the model is somewhat complex both mathematically and biologically, this note describes simple numerical approximations for two common exposure scenarios. Both approximations are easily evaluated on a simple pocket calculator by a health physicist or emergency management officer.
已为小鼠、大鼠、狗、绵羊、猪和驴推导了辐射诱导骨髓生成的细胞动力学模型。在与生物实验的分子和细胞数据进行广泛比较以及对辐照后动物死亡率、细胞存活和细胞再增殖进行一系列预测/验证测试后,该模型扩展到了人类。该模型的一个优点是,任何复杂的长期照射模式都可以等同于其等效的即时剂量。生物反应的严重程度取决于靶器官剂量、剂量率和剂量分割。流行病学和动物数据最适合短时间内的暴露情况。要利用这些数据评估长期人类暴露的风险,就必须根据即时剂量对分子修复和代偿性增殖进行建模。尽管该模型在数学和生物学上都有些复杂,但本说明描述了两种常见暴露场景的简单数值近似方法。健康物理学家或应急管理人员可以很容易地在简单的袖珍计算器上对这两种近似方法进行评估。