Radiofrequency Radiation Exposure Research Articles

Radiofrequency Radiation Alters the Immune System: II. Modulation of in Vivo Lymphocyte Circulation

LIBURDY, R. P. Radiofrequency Radiation Alters the Immune System. II. Modulation of in Vivo Lymphocyte Circulation. Radiat. Res. 83, 66-73 (1980). In vivo lymphocyte circulation was significantly altered in mice exposed to whole-body radiofrequency radiation (RFR). In vivo lymphocyte circulation was followed by quantitating activity of sodium chromate-51-labeled lymphocytes in the lung, spleen, liver, and bone marrow of animals at different times after iv spleen lymphocyte injection. Immediately after cell injection, animals were exposed to 2.6-GHz RFR (CW) at 25 or 5 mW/cm2 (3.8 W/kg) for I hr. At 1, 6, and 24 hr after lymphocyte injection target organs were removed, weighed, and counted. Sham RFR, warm-air, and steroid-treated groups were included as controls. Hyperthermic RFR exposure (25 mW/cm2; 2.0oC increase in core temperature) led to a 37% reduction in lymphocytes leaving the lung to migrate into the spleen. In addition, a threefold increase in spleen lymphocytes entering the bone marrow occurred. Significantly, this pattern was also observed in the steroid-treated group; nonthermogenic RFR exposure (5 mW/cm2) and warm-air exposures did not lead to altered lymphocyte traffic. These results support the idea that steroid release associated with thermal stress and the process of thermoregulation is a significant operant factor responsible for RFR effects on the immune system.

Radiofrequency Radiation Alters the Immune System: Modulation of T- and B-Lymphocyte Levels and Cell-Mediated Immunocompetence by Hyperthermic Radiation

Acute transient lymphopenia in the mouse was induced by whole-body exposure to radiofrequency radiation (RFR) (26 MHz, 2/sup 0/C increase in core temperature over 15 min). Mice experiencing RFR-induced lymphopenia showed a relative increase in splenic T- ad B-lymphocytes; these elevated levels were further pronounced by three RFR exposures delivered at 3-hr intervals. Multiple RFR exposures also led to a significant decrease in thymic weight and thymic and splenic cell density and, moreover, to suppressed cell-mediated immune function as measured in vivo by local delayed-type hypersensitivity. Only splenic B-lymphocyte levels were elevated with no change in delayed hypersensitivity in warm air-exposed mice (2/sup 0/C increase in core temperature over 15 min). Plasma corticoid levels immediately after RFR treatment were severalfold higher than those in mice given warm air or sham exposure. Notably, administration of methyl prednisolone sodium succinate to control animals led to lymphopenia, increased splenic T- and B-lymphocyte frequency, and thymic involution that was oserved in RFR exposed animals. These results indicate that RFR hyperthermia can induce significant alterations in lymphocyte distribution and function and that RFR impact on the immune apparatus appears to be mediated at the cellular level indirectly through steroid-associated actions.