We have carried out a study of the bone marrow status in both irradiated and non-irradiated zones of 56 patients with stage I-II Hodgkin's disease in complete 9-12 (33 patients, group 1) and 18-23 (23 patients, group 2) year remission after therapeutic irradiation of the supradiaphragmatic lymphatic collectors at a dose of 40 Gy with irradiation of the spleen (33 patients) or splenectomy (23 patients). The total count of myelokaryocytes, myelogram, a relative and absolute content of lymphoid cells, immature granulocytes and elements of erythroid series were calculated in the aspirates from the exposed to radiotherapy sternum and non-irradiated upper portion of the ileum. The number of granulocyte-macrophage (CFU-GM) and stromal (CFU-F) precursor cells were defined using in vitro culture technique. There was a complete annihilation of the bone marrow in the irradiated zones, when the dose exceeded 35 Gy in 3-4 weeks. The concentration of myelokaryocytes, immature granulocytes, erythronormoblasts, CFU-GM, CFU-F in non-exposed bone marrow were significantly lower in all patients of group 2 than in normal subjects and in group 1 patients. Absolute lymphoid count in patients with 18-23 year remission was found to be normal but was considerably reduced in comparison to patients of group 1. These changes may be the result of the previous hyperactivity of the non-irradiated bone marrow which could be a cause of stem cell compartment depletion. The differential calculation of compact and diffuse subpopulations of CFU-F revealed a significant reduction of compact colony-forming CFU-F in both irradiated and unexposed bone marrow. Almost all the stromal precursor cells from irradiated zone formed diffuse colonies in cultures. These results confirm experimental data concerning greater radiosensitivity and proliferative potential of CFU-F, forming compact colonies versus diffuse colony-forming CFU-F. Aplasia of the irradiated bone marrow and hypoplasia of the non-irradiated bone marrow 18-23 years after radiotherapy completion coexisted with normal circulating CFU-GM and granulocyte blood count suggesting a compensatory mechanism involving a mitotic amplification between the progenitor cell and the final differentiated cell.