| Abstract: | The purpose of this study was to determine whether chronic, low-level exposure of mammary-tumor-prone mice to 2450 MHz radiofrequency radiation (RFR) promotes an earlier onset (decreased latency), a greater total incidence, or a faster growth rate of mammary tumors. One hundred C3H/HeJ mice were exposed in circularly polarized waveguides (CWG) for 18 months (20 h/day, 7 days/wk) to continuous-wave, 2450 MHz RFR at a whole body average specific absorption rate (SAR) of 0.3 W/kg; 100 mice were sham exposed. Before exposure, SARs were determined calorimetrically; during experimentation, SARs were monitored by differential power measurement. All animals were visually inspected twice daily and were removed from the CWG cages for a weekly inspection, palpation, and weighing. From the time of detection, tumor size was measured weekly. Animals that died spontaneously, became moribund, or were killed after 18 months of exposure were completely necropsied; tissues were fixed and subjected to histopathological evaluations. Results showed no significant difference in weight profiles between sham-irradiated and irradiated mice. Concerning mammary carcinomas, there was no significant difference between groups with respect to palpated tumor incidence (sham = 52%; irradiated = 44%), latency to tumor onset (sham = 62.3 ± 1.2 wk; irradiated = 64.0 ± 1.6 wk), and rate of tumor growth. In general, histopathological examination revealed no significant differences in numbers of malignant, metastatic, or benign neoplasms between the two groups; a significantly greater incidence of alveolar-bronchiolar adenoma in the sham-irradiated mice was the only exception. In addition, survival analysis showed no significant difference in cumulative percent survival between sham and irradiated animals. Thus, results indicate that under the conditions of this study, long-term, low-level exposure of mammary-tumor-prone mice to 2450 MHz RFR did not affect mammary tumor incidence, latency to tumor onset, tumor growth rate, or animal longevity when compared with sham-irradiated controls. Bioelectromagnetics 19:20–31, 1998. © 1998 Wiley-Liss, Inc. |
