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Cell number, protein, and phorbol myristate acetate (PMA)-induced H202production were measured in cultured human peripheral blood monocytes for six days after exposure to varying doses of γ-radiation. Both the number of adherent cells and the protein per dish decreased with increasing radiation doses. The dose of radiation decreasing the number of adherent cells by 37% on days 4 and 6 postirradiation was 29 Gy. Four hours postirradiation there was a small decrease in PMA-induced H202production for doses of 7.5 Gy or greater; levels returned to normal by eight hours and increased at 24 hours postirradiation. By day 4 postirradiation significant increases in PMA-induced H202production were noted at all radiation doses (2.5 to 50 Gy). This increase was not due to a shift in the PMA dose-response curve, a change in the time course of the PMA response, or an effect of decreased cell density on the assay system. Superoxide levels were not significantly changed in cells exposed to 20 Gy. Catalase, glutathione peroxidase, and superoxide dismutase levels also were unchanged. Culturing irradiated cells with γ-interferon increased PMA-induced H202 release, which indicated that irradiated cells retained their capacity to respond to γ-interferon. These data demonstrate that irradiation affects the PMA-induced H202 production of human monocytes in a time- and dose-dependent manner. An increase in the release of reactive oxygen intermediates by the macrophage may play a role in enhancing the deleterious effects of radiation in vivo.PMA response, or an effect of decreased cell density on the assay system. Superoxide levels were not significantly changed in cells exposed to 20 Gy. Catalase, glutathione peroxidase, and superoxide dismutase levels also were unchanged. Culturing irradiated cells with γ-interferon increased PMA-induced H202release, which indicated that irradiated cells retained their capacity to respond to γ-interferon. These data demonstrate that irradiation affects the PMA-induced H202production of human monocytes in a time- and dose-dependent manner. An increase in the release of reactive oxygen intermediates by the macrophage may play a role in enhancing the deleterious effects of radiation in vivo.This is a US government work. There are no restrictions on its use. 0006-4971/87/7003-0013$0.00/0