Bone marrow failure is the major cause of radiation lethality in mammals. Since bone marrow is distributed heterogeneously within trabecular spongiosa encased in a cortex of cortical bone, it is very difficult to measure the extent of the radiation damage directly. However, indirect consequences of damage to marrow, such as reductions in peripheral blood cell counts, are easily measured. In this paper, the authors investgate a mathematical model of the granulopoiesis system that provides quantitative relationships between reductions in peripheral blood cells and the bone marrow precursor cells following radiation exposure. A coarse-grained architecture of cellular replication and production as well as a mechanism for implicit regulation used in this model are discussed. The model is based on previous investigations of rodents. The authors test how well the model matches, in the principal dynamic regime of hematopoiesis, experimental data on large animals as well as empirical data on humans following radiation exposure. Due to its ability to infer, albeit indirectly, radiation damage to bone marrow, this model will provide a useful computational tool in radiation accident management, military operations involving nuclear warfare, radiation therapy, and space radiation risk assessment.