As part of a comprehensive investigation of the potential genotoxicity of radiofrequency (RF) signals emitted by cellular telephones, in vitro studies evaluated the induction of DNA and chromosomal damage in human blood leukocytes and lymphocytes, respectively. The signals were voice modulated 837 MHz produced by an analog signal generator or by a time division multiple access (TDMA) cellular telephone, 837 MHz generated by a code division multiple access (CDMA) cellular telephone (not voice modulated), and voice modulated 1909.8 MHz generated by a global system of mobile communication (GSM)-type personal communication systems (PCS) cellular telephone. DNA damage (strand breaks/alkali labile sites) was assessed in leukocytes using the alkaline (pH>13) single cell gel electrophoresis (SCG) assay. Chromosomal damage was evaluated in lymphocytes mitogenically stimulated to divide postexposure using the cytochalasin B-binucleate cell micronucleus assay. Cells were exposed at 37+/-1 degrees C, for 3 or 24 h at average specific absorption rates (SARs) of 1.0-10.0 W/kg. Exposure for either 3 or 24 h did not induce a significant increase in DNA damage in leukocytes, nor did exposure for 3 h induce a significant increase in micronucleated cells among lymphocytes. However, exposure to each of the four RF signal technologies for 24 h at an average SAR of 5.0 or 10.0 W/kg resulted in a significant and reproducible increase in the frequency of micronucleated lymphocytes. The magnitude of the response (approximately four fold) was independent of the technology, the presence or absence of voice modulation, and the frequency (837 vs. 1909.8 MHz). This research demonstrates that, under extended exposure conditions, RF signals at an average SAR of at least 5.0 W/kg are capable of inducing chromosomal damage in human lymphocytes.

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Exposure of quail eggs 4 hr per day during the first 5 incubation days at 2450 MHz and in an exposure field of 30 mW/cm-2 and at an absorbed power of 14 mW/g does not cause any great change in body weight, observed gross malformations, rbc, wbc, hematocrit, hemoglobin, or differential wbc percentages. If small differences exist in these parameters due to microwave exposure, they are obscured by the large variability between individual quail. This variability is believed to partially result from changing blood values in the developing young quail, and the 2-day spread in ages at the time of sacrifice could account for some of the variability. The overall hatch percentages for the exposed and control eggs were approximately equal. A slight significant decrease (11%) in hemoglobin was noted in the birds irradiated on Day 2. Additional verification, however, is needed, because the observed change is less than the normal range of values observed in young quail. These data do suggest, however, that exposure of developing Japanese quail embryo to microwave radiation of the frequency and power density level used in this study does not preclude normal systemic development, hematologic differentiation, or the general hardiness of the hatched quail.

The embryofetal toxicity and teratogenicity of plane-wave 2.45 GHz continuous wave (CW) microwave radiation at different intensities were investigated in the CD-1 mouse. Mice were exposed on days 1-15 of gestation to an incident power density of 5 mW/cm2 (specific absorption rate of 6.7 mW/gm) and either on days 1-6 or 6-15 of gestation to 21 mW/cm2 (specific absorption rate of 28.14 mW/gm) or to 30 mW/cm2 (specific absorption rate of 40.2 mW/gm) for 8 hours daily. Exposure either on days 1-6 or 6-15 of gestation to a power density of 21 or 30 mW/cm2 caused an increase in colonic temperature of exposed dams of 1 degree C and 2.3 degrees C, respectively. To distinguish between "thermal" and "nonthermal" effects of 21 or 30 mW/cm2, groups of mice were also exposed to elevated ambient temperature to raise their body temperature to the level of those animals exposed to microwave. Ambient temperatures of 30 degrees C and 31 degrees C increased the deep colonic temperature to that obtained with the 21 and 30 mW/cm2 microwave exposure, respectively. The temperature-exposed mice were handled in exactly the same manner as the microwave-exposed mice. A significant reduction in maternal weight gain, either during treatment on days 1-6 or 6-15 of gestation was observed in females of all handled groups. Handling plus exposure to elevated ambient temperature (30 degrees C or 31 degrees C) during days 6-15 of gestation increased this reduction in maternal weight gain. A significant decrease in implantation sites per litter and reduction in fetal weight was noted in the group exposed to 30 mW/cm2 during days 1-6 of gestation. Exposure of mice to a power density of 30 mW/cm2 (days 6-15 of gestation) resulted in a slight, but significant increase in the percentage of malformed fetuses, predominantly with cleft palate, when compared to all other groups.