Carcinogenicity study of 217 Hz pulsed 900 MHz electromagnetic fields in Pim1 transgenic mice

In an 18-month carcinogenicity study, Pim1 transgenic mice were exposed to pulsed 900 MHz (pulse width: 0.577 ms; pulse repetition rate: 217 Hz) radiofrequency (RF) radiation at a whole-body specific absorption rate (SAR) of 0.5, 1.4 or 4.0 W/kg [uncertainty (k = 2): 2.6 dB; lifetime variation (k = 1): 1.2 dB]. A total of 500 mice, 50 per sex per group, were exposed, sham-exposed or used as cage controls. The experiment was an extension of a previously published study in female Pim1 transgenic mice conducted by Repacholi et al. (Radiat. Res. 147, 631-640, 1997) that reported a significant increase in lymphomas after exposure to the same 900 MHz RF signal. Animals were exposed for 1 h/day, 7 days/week in plastic tubes similar to those used in inhalation studies to obtain well-defined uniform exposure. The study was conducted blind. The highest exposure level (4 W/kg) used in this study resulted in organ-averaged SARs that are above the peak spatial SAR limits allowed by the ICNIRP (International Commission on Non-ionizing Radiation Protection) standard for environmental exposures. The whole-body average was about three times greater than the highest average SAR reported in the earlier study by Repacholi et al. The results of this study do not suggest any effect of 217 Hz-pulsed RF-radiation exposure (pulse width: 0.577 ms) on the incidence of tumors at any site, and thus the findings of Repacholi et al. were not confirmed. Overall, the study shows no effect of RF radiation under the conditions used on the incidence of any neoplastic or non-neoplastic lesion, and thus the study does not provide evidence that RF radiation possesses carcinogenic potential.     

Effects of exposure of newborn patched1 heterozygous mice to GSM, 900 MHz

Patched1 heterozygous knockout mice (Ptc1+/-), an animal model of multiorgan tumorigenesis in which ionizing radiation dramatically accelerates tumor development, were used to study the potential tumorigenic effects of electromagnetic fields (EMFs) on neonatal mice. Two hundred Ptc1+/- mice and their wild-type siblings were enrolled in this study. Newborn mice were exposed to 900 MHz radiofrequency radiation (average SAR: 0.4 W/kg for 5 days, 0.5 h twice a day) or were sham exposed. We found that RF EMFs simulating the Global System for Mobile Communications (GSM) did not affect the survival of the mice, because no statistically significant differences in survival were found between exposed and sham-exposed animals. Also, no effects attributable to radiofrequency radiation were observed on the incidence and histology of Ptc1-associated cerebellar tumors. Moreover, the skin phenotype was analyzed to look for proliferative effects of RF EMFs on the epidermal basal layer and for acceleration of preneoplastic lesions typical of the basal cell carcinoma phenotype of this model. We found no evidence of proliferative or promotional effects in the skin from neonatal exposure to radiofrequency radiation. Furthermore, no difference in Ptc1-associated rhabdomyosarcomas was detected between sham-exposed and exposed mice. Thus, under the experimental conditions tested, there was no evidence of life shortening or tumorigenic effects of neonatal exposure to GSM RF radiation in a highly tumor-susceptible mouse model.     

Chromosome damage and micronucleus formation in human blood lymphocytes exposed in vitro to radiofrequency radiation at a cellular telephone frequency (847.74 MHz, CDMA)

Peripheral blood samples collected from four healthy nonsmoking human volunteers were diluted with tissue culture medium and exposed in vitro for 24 h to 847.74 MHz radiofrequency (RF) radiation (continuous wave), a frequency employed for cellular telephone communications. A code division multiple access (CDMA) technology was used with a nominal net forward power of 75 W and a nominal power density of 950 W/m(2) (95 mW/cm(2)). The mean specific absorption rate (SAR) was 4.9 or 5.5 W/kg. Blood aliquots that were sham-exposed or exposed in vitro to an acute dose of 1.5 Gy of gamma radiation were included in the study as controls. The temperatures of the medium during RF-radiation and sham exposures in the Radial Transmission Line facility were controlled at 37 +/- 0.3 degrees C. Immediately after the exposures, lymphocytes were cultured at 37 +/- 1 degrees C for 48 or 72 h. The extent of genetic damage was assessed from the incidence of chromosome aberrations and micronuclei. The kinetics of cell proliferation was determined from the mitotic indices in 48-h cultures and from the incidence of binucleate cells in 72-h cultures. The data indicated no significant differences between RF-radiation-exposed and sham-exposed lymphocytes with respect to mitotic indices, frequencies of exchange aberrations, excess fragments, binucleate cells, and micronuclei. The response of gamma-irradiated lymphocytes was significantly different from that of both RF-radiation-exposed and sham-exposed cells for all of these indices. Thus there was no evidence for induction of chromosome aberrations and micronuclei in human blood lymphocytes exposed in vitro for 24 h to 847.74 MHz RF radiation (CDMA) at SARs of 4.9 or 5.5 W/kg.     

In vitro lymphocyte proliferation induced by radio-frequency electromagnetic radiation under isothermal conditions

Whole human blood was exposed or sham-exposed in vitro for 2 h to 27 or 2,450 MHz radio-frequency electromagnetic (RF) radiation under isothermal conditions (i.e., 37 +/- 0.2 degrees C). Immediately after exposure, mononuclear cells were separated from blood by Ficoll density-gradient centrifugation and cultured for 3 days at 37 degrees C with or without mitogenic stimulation by phytohemagglutinin (PHA). Lymphocyte proliferation was assayed at the end of the culture period by 6 h of pulse labeling with 3H-thymidine (3H-TdR). Exposure to radiation at either frequency at specific absorption rates (SARs) below 50 W/kg resulted in a dose-dependent, statistically significant increase of 3H-TdR uptake in PHA-activated or unstimulated lymphocytes. Exposure at 50 W/kg or higher suppressed 3H-TdR uptake relative to that of sham-exposed cells. There were no detectable effects of RF radiation on lymphocyte morphology or viability. Notwithstanding the characteristic temperature dependence of lymphocyte activation in vitro, the isothermal exposure conditions of this study warrant the conclusion that the biphasic, dose-dependent effects of the radiation on lymphocyte proliferation were not dependent on heating.     

Metabolic and vasomotor responses of rhesus monkeys exposed to 225-MHz radiofrequency energy

A previous study showed a substantial increase in the colonic temperature of rhesus monkeys (Macaca mulatta) exposed to radiofrequency (RF) fields at a frequency near whole-body resonance and specific absorption rates (SAR) of 2-3 W/kg. The present experiments were conducted to determine the metabolic and vasomotor responses during exposures to similar RF fields. We exposed five adult male rhesus monkeys to 225 MHz radiation (E orientation) in an anechoic chamber. Oxygen consumption and carbon dioxide production were measured before, during, and after RF exposure. Colonic, tail and leg skin temperatures were continuously monitored with RF-nonperturbing probes. The monkeys were irradiated at two carefully-controlled ambient temperatures, either cool (20 degrees C) or thermoneutral (26 degrees C). Power densities ranged from 0 (sham) to 10.0 mW/cm2 with an average whole-body SAR of 0.285 (W/kg)/(mW/cm2). We used two experimental protocols, each of which began with a 120-min pre-exposure equilibration period. One protocol involved repetitive 10-min RF exposures at successively higher power densities with a recovery period between exposures. In the second protocol, a 120-min RF exposure permitted the measurement of steady-state thermoregulatory responses. Metabolic and vasomotor adjustments in the rhesus monkey exposed to 225 MHz occurred during brief or sustained exposures at SARs at or above 1.4 W/kg. The SAR required to produce a given response varied with ambient temperature. Metabolic and vasomotor responses were coordinated effectively to produce a stable deep body temperature. The results show that the thermoregulatory response of the rhesus monkey to an RF exposure at a resonant frequency limits storage of heat in the body. However, substantial increases in colonic temperature were not prevented by such responses, even in a cool environment.     

Viability and phagocytosis of neutrophils exposed in vitro to 100-MHz radiofrequency radiation

Rabbit polymorphonuclear leucocytes (PMN, neutrophils) obtained from peritoneal exudate were exposed in vitro for one-half or one hour to continuous wave or amplitude-modulated (20-Hz) 100-MHz RF radiation in a temperature-controlled coaxial exposure chamber at field strengths from 2.5 to 4.1 V/cm (SARs of 120 to 341 W/kg). RF exposure at 37 +/- 0.2 degrees C had no detectable effect on PMN viability or phagocytosis compared to sham-exposed cells simultaneously subjected to the same time-temperature regime. Temperature control studies indicated that at 37 degrees C no effect on PMN viability would be expected but phagocytosis would be reduced by approximately 6%/degrees C temperature increase. The absence of an effect of RF exposure suggests that there was minimal undetected intrasample heating and that phagocytosis was not affected by 100-MHz RF radiation under the conditions of this study.     

Effects of in vivo exposure to GSM-modulated 900 MHz radiation on mouse peripheral lymphocytes

The aim of this study was to evaluate whether daily whole-body exposure to 900 MHz GSM-modulated radiation could affect spleen lymphocytes. C57BL/6 mice were exposed 2 h/day for 1, 2 or 4 weeks in a TEM cell to an SAR of 1 or 2 W/kg. Untreated and sham-exposed groups were also examined. At the end of the exposure, mice were killed humanely and spleen cells were collected. The number of spleen cells, the percentages of B and T cells, and the distribution of T-cell subpopulations (CD4 and CD8) were not altered by the exposure. T and B cells were also stimulated ex vivo using specific monoclonal antibodies or LPS to induce cell proliferation, cytokine production and expression of activation markers. The results did not show relevant differences in either T or B lymphocytes from mice exposed to an SAR of 1 or 2 W/kg and sham-exposed mice with few exceptions. After 1 week of exposure to 1 or 2 W/kg, an increase in IFN-gamma (Ifng) production was observed that was not evident when the exposure was prolonged to 2 or 4 weeks. This suggests that the immune system might have adapted to RF radiation as it does with other stressing agents. All together, our in vivo data indicate that the T- and B-cell compartments were not substantially affected by exposure to RF radiation and that a clinically relevant effect of RF radiation on the immune system is unlikely to occur.     

Non-thermal exposure to radiofrequency energy from digital wireless phones does not affect ornithine decarboxylase activity in L929 cells

L929 murine fibroblast cells were exposed to radiofrequency (RF) radiation from a time division multiple access wireless phone operating at 835 MHz frequency to determine the effect of RF-radiation energy emitted by wireless phones on ornithine decarboxylase (ODC) activity in cultured cells. Exposure was for 8 h to an average specific absorption rate (SAR) from <1 W/kg up to 15 W/kg. After exposure, cells were harvested and ODC activity was measured. No statistically significant difference in ODC activity was found between RF-radiation-exposed and sham-exposed cells at non-thermal specific absorption rates. At SARs which resulted in measurable heating of the medium, a dose-dependent decrease in enzymatic activity was observed and was shown to be consistent with a comparable decrease caused by non-RF-radiation heating. Thus we observed only the well-known enzyme inhibition due to heating, rather than the previously reported enhancement attributed to RF-radiation exposure.     

Acute radio frequency irradiation does not affect cell cycle, cellular migration, and invasion

Although in vitro studies have been previously conducted to determine the biological effects of radio frequency (RF) radiation, it has not yet been determined whether or not RF radiation poses a potential hazard. This study was conducted to determine whether RF radiation exposure exerts detectable effects on cell cycle distribution, cellular invasion, and migration. NIH3T3 mouse fibroblasts were exposed to 849 MHz of RF radiation at average SAR values of 2 or 10 W/kg for either 1 h, or for 1 h per day for 3 days. During the exposure period, the temperature in the exposure chamber was maintained isothermally by circulating water throughout the cavity. Cell cycle distribution was analyzed at 24 and 48 h after exposure, by flow cytometry. We detected no statistically significant differences between the sham-exposed and RF radiation-exposed cells. Cellular invasion and migration were assessed by in vitro Matrigel invasion and Transwell migration assays. The RF radiation-exposed groups evidenced no significant changes in motility and invasiveness compared to the sham-exposed group. However, the ionizing radiation-exposed cells, used as a positive control group, manifested dramatic alterations in their cell cycle distribution, cellular invasiveness, and migration characteristics. Our results show that 849 MHz RF radiation exposure exerts no detectable effects on cell cycle distribution, cellular migration, or invasion at average SAR values of 2 or 10 W/kg.     

Focus formation of C3H/10T1/2 cells and exposure to a 836.55 MHz modulated radiofrequency field

Disruption of communication between transformed cells and normal cells is involved in tumor promotion. We have tested the hypothesis that exposures to radiofrequency (RF) fields using a form of digital modulation (TDMA) and a chemical tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), are copromoters that enhance focus formation of transformed cells in coculture with parental C3H/10T1/2 murine fibroblasts. RF field exposures did not influence TPA's dose-dependent promotion of focus formation in coculture. Cell cultures were exposed to an 836.55 MHz TDMA-modulated field in TEM transmission line chambers, with incident energies that simulated field intensities at a user's head. Specific absorption rates (SARs) of 0.15, 1.5, and 15 μW/g were used during each digital packet, and the packet frequency was 50/s. The TEM chambers were placed in a commercial incubator at 37 °C and 95% humidity/5% CO2. The RF field exposures were in a repeating cycle, 20 min on, 20 min off, 24 h/day for 28 days. At 1.5 μW/g, TPA-induced focus formation (at 10, 30, and 50 ng/ml) was not significantly different in RF-exposed cultures compared to parallel sham-exposed cultures in ten independent experiments in terms of the number, density, and area of foci. Similarly, at 0.15 and 15.0 μW/g, in two and four experiments, respectively, RF exposure did not alter TPA-induced focus formation. The findings support a conclusion that repeated exposures to this RF field do not influence tumor promotion in vitro, based on the RF field's inability to enhance TPA-induced focus formation. Bioelectromagnetics 18:237–243, 1997 © 1997 Wiley-Liss, Inc.     

Effects of mobile phone radiation on X-ray-induced tumorigenesis in mice.

The increased use of mobile phones has raised the question of possible health effects of such devices, particularly the risk of cancer. It seems unlikely that the low-level radiofrequency (RF) radiation emitted by them would damage DNA directly, but its ability to act as a tumor promoter is less well characterized. In the current study, we evaluated the effect of low-level RF radiation on the development of cancer initiated in mice by ionizing radiation. Two hundred female CBA/S mice were randomized into four equal groups at the age of 3 to 5 weeks. The mice in all groups except the cage-control group were exposed to ionizing radiation at the beginning of the study and then to RF radiation for 1.5 h per day, 5 days a week for 78 weeks. One group was exposed to continuous NMT (Nordic Mobile Telephones)-type frequency-modulated RF radiation at a frequency of 902.5 MHz and a nominal average specific absorption rate (SAR) of 1.5 W/kg. Another group was exposed to pulsed GSM (Global System for Mobile)-type RF radiation (carrier-wave frequency 902.4 MHz, pulse frequency 217 Hz) at a nominal average SAR of 0.35 W/kg. The control animals were sham-exposed. Body weight, clinical signs, and food and water consumption were recorded regularly. Hematological examinations and histopathological analyses of all lesions and major tissues were performed on all animals. The RF-radiation exposures did not increase the incidence of any neoplastic lesion significantly. We conclude that the results do not provide evidence for cancer promotion by RF radiation emitted by mobile phones.     

The effect of 835.62 MHz FDMA or 847.74 MHz CDMA modulated radiofrequency radiation on the induction of micronuclei in C3H 10T(1/2) cells

To determine if radiofrequency (RF) radiation induces the formation of micronuclei, C3H 10T(1/2) cells were exposed to 835.62 MHz frequency division multiple access (FDMA) or 847.74 MHz code division multiple access (CDMA) modulated RF radiation. After the exposure to RF radiation, the micronucleus assay was performed by the cytokinesis block method using cytochalasin B treatment. The micronuclei appearing after mitosis were scored in binucleated cells using acridine orange staining. The frequency of micronuclei was scored both as the percentage of binucleated cells with micronuclei and as the number of micronuclei per 100 binucleated cells. Treatment of cells with cytochalasin B at a concentration of 2 microg/ml for 22 h was found to yield the maximum number of binucleated cells in C3H 10T(1/2) cells. The method used for the micronucleus assay in the present study detected a highly significant dose response for both indices of micronucleus production in the dose range of 0.1-1.2 Gy and it was sensitive enough to detect a significant (P > 0.05) increase in micronuclei after doses of 0.3 Gy in exponentially growing cells and after 0.9 Gy in plateau-phase cells. Exponentially growing cells or plateau-phase cells were exposed to CDMA (3.2 or 4.8 W/kg) or FDMA (3.2 or 5.1 W/kg) RF radiation for 3, 8, 16 or 24 h. In three repeat experiments, no exposure condition was found by analysis of variance to result in a significant increase relative to sham-exposed cells either in the percentage of binucleated cells with micronuclei or in the number of micronuclei per 100 binucleated cells. In this study, data from cells exposed to different RF signals at two SARs were compared to a common sham-exposed sample. We used the Dunnett's test, which is specifically designed for this purpose, and found no significant exposure-related differences for either plateau-phase cells or exponentially growing cells. Thus the results of this study are not consistent with the possibility that these RF radiations induce micronuclei.     

Primary DNA damage in human blood lymphocytes exposed in vitro to 2450 MHz radiofrequency radiation

Human peripheral blood samples collected from three healthy human volunteers were exposed in vitro to pulsed-wave 2450 MHz radiofrequency (RF) radiation for 2 h. The RF radiation was generated with a net forward power of 21 W and transmitted from a standard gain rectangular antenna horn in a vertically downward direction. The average power density at the position of the cells in the flask was 5 mW/cm(2). The mean specific absorption rate, calculated by finite difference time domain analysis, was 2.135 (+/-0.005 SE) W/kg. Aliquots of whole blood that were sham-exposed or exposed in vitro to 50 cGy of ionizing radiation from a (137)Cs gamma-ray source were used as controls. The lymphocytes were examined to determine the extent of primary DNA damage (single-strand breaks and alkali-labile lesions) using the alkaline comet assay with three different slide-processing schedules. The assay was performed on the cells immediately after the exposures and at 4 h after incubation of the exposed blood at 37 +/- 1 degrees C to allow time for rejoining of any strand breaks present immediately after exposure, i.e. to assess the capacity of the lymphocytes to repair this type of DNA damage. At either time, the data indicated no significant differences between RF-radiation- and sham-exposed lymphocytes with respect to the comet tail length, fluorescence intensity of the migrated DNA in the tail, and tail moment. The conclusions were similar for each of the three different comet assay slide-processing schedules examined. In contrast, the response of lymphocytes exposed to ionizing radiation was significantly different from RF-radiation- and sham-exposed cells. Thus, under the experimental conditions tested, there is no evidence for induction of DNA single-strand breaks and alkali-labile lesions in human blood lymphocytes exposed in vitro to pulsed-wave 2450 MHz radiofrequency radiation, either immediately or at 4 h after exposure.     

The effect of chronic exposure to 835.62 MHz FDMA or 847.74 MHz CDMA radiofrequency radiation on the incidence of spontaneous tumors in rats

This study was designed to determine whether chronic exposure to radiofrequency (RF) radiation from cellular phones increased the incidence of spontaneous tumors in F344 rats. Eighty male and 80 female rats were randomly placed in each of three irradiation groups. The sham group received no irradiation; the Frequency Division Multiple Access (FDMA) group was exposed to 835.62 MHz FDMA RF radiation; and the Code Division Multiple Access (CDMA) group was exposed to 847.74 MHz CDMA RF radiation. Rats were irradiated 4 h per day, 5 days per week over 2 years. The nominal time-averaged specific absorption rate (SAR) in the brain for the irradiated animals was 0.85 +/- 0.34 W/kg (mean +/- SD) per time-averaged watt of antenna power. Antennas were driven with a time-averaged power of 1.50 +/- 0.25 W (range). That is, the nominal time-averaged brain SAR was 1.3 +/- 0.5 W/kg (mean +/- SD). This number was an average from several measurement locations inside the brain, and it takes into account changes in animal weight and head position during irradiation. All major organs were evaluated grossly and histologically. The number of tumors, tumor types and incidence of hyperplasia for each organ were recorded. There were no significant differences among final body weights or survival days for either males or females in any group. No significant differences were found between treated and sham-exposed animals for any tumor in any organ. We conclude that chronic exposure to 835.62 MHz FDMA or 847.74 MHz CDMA RF radiation had no significant effect on the incidence of spontaneous tumors in F344 rats.     

Low-level exposure to pulsed 900 MHz microwave radiation does not cause deficits in the performance of a spatial learning task in mice

There is some concern that short-term memory loss or other cognitive effects may be associated with the use of mobile cellular telephones. In this experiment, the effect of repeated, acute exposure to a low intensity 900 MHz radiofrequency (RF) field pulsed at 217 Hz was explored using an appetitively-motivated spatial learning and working memory task. Adult male C57BL/6J mice were exposed under far field conditions in a GTEM cell for 45 min each day for 10 days at an average whole-body specific energy absorption rate (SAR) of 0.05 W/kg. Their performance in an 8-arm radial maze was compared to that of sham-exposed control animals. All behavioral assessments were performed without handlers having knowledge of the exposure status of the animals. Animals were tested in the maze immediately following exposure or after a delay of 15 or 30 min. No significant field-dependent effects on performance were observed in choice accuracy or in total times to complete the task across the experiment. These results suggest that exposure to RF radiation simulating a digital wireless telephone (GSM) signal under the conditions of this experiment does not affect the acquisition of the learned response. Further studies are planned to explore the effects of other SARs on learned behavior. Bioelectromagnetics 21:151-158, 2000. Published 2000 Wiley-Liss, Inc.     

Effects of continuous and pulsed 2450-MHz radiation on spontaneous lymphoblastoid transformation of human lymphocytes in vitro.

Normal human lymphocytes were isolated from the peripheral blood of healthy donors. One-ml samples containing (10(6)) cells in chromosome medium 1A were exposed for 5 days to conventional heating or to continuous wave (CW) or pulsed wave (PW) 2450-MHz radiation at non-heating (37 degrees C) and various heating levels (temperature increases of 0.5, 1.0, 1.5, and 2 degrees C). The pulsed exposures involved 1-microsecond pulses at pulse repetition frequencies from 100 to 1,000 pulses per second at the same average SAR levels as the CW exposures. Actual average SARs ranged to 12.3 W/kg. Following termination of the incubation period, spontaneous lymphoblastoid transformation was determined with an image analysis system. The results were compared among each of the experimental conditions and with sham-exposed cultures. At non-heating levels, CW exposure did not affect transformation. At heating levels both conventional and CW heating enhanced transformation to the same extent and correlate with the increases in incubation temperature. PW exposure enhanced transformation at non-heating levels. This finding is significant (P less than .002). At heating levels PW exposure enhanced transformation to a greater extent than did conventional or CW heating. This finding is significant at the .02 level. We conclude that PW 2450-MHz radiation acts differently on the process of lymphoblastoid transformation in vitro compared with CW 2450-MHz radiation at the same average SARs.     

Effect of high-frequency electromagnetic fields with a wide range of SARs on chromosomal aberrations in murine m5S cells

To investigate the induction of chromosomal aberrations in mouse m5S cells after exposure to high-frequency electromagnetic fields (HFEMFs) at 2.45 GHz, cells were exposed for 2 h at average specific absorption rates (SARs) of 5, 10, 20, 50 and 100 W/kg with continuous wave-form (CW), or at a mean SAR of 100 W/kg (with a maximum of 900 W/kg) with pulse wave-form (PW). The effects of HFEMF exposure were compared with those in sham-exposed controls and with mitomycin C (MMC) or X-ray treatment as positive controls. We examined all structural, chromatid-type and chromosome-type changes after HFEMF exposures and treatments with MMC and X-rays. No significant differences were observed following exposure to HFEMFs at SARs from 5 to 100 W/kg CW and at a mean SAR of 100 W/kg PW (a maximum SAR of 900 W/kg) compared with sham-exposed controls, whereas treatments with MMC and X-rays increased the frequency of chromatid-type and chromosome-type aberrations. In summary, HFEMF exposures at 2.45 GHz for 2 h with up to 100 W/kg SAR CW and an average 100 W/kg PW (a maximum SAR of 900 W/kg) do not induce chromosomal aberrations in m5S cells. Furthermore, there was no difference between exposures to CW and PW HFEMFs.     

Effects of GSM-modulated radiofrequency electromagnetic fields on B-cell peripheral differentiation and antibody production

We examined the effects of in vivo exposure to a GSM-modulated 900 MHz RF field on B-cell peripheral differentiation and antibody production in mice. Our results show that exposure to a whole-body average specific absorption rate (SAR) of 2 W/kg, 2 h/day for 4 consecutive weeks does not affect the frequencies of differentiating transitional 1 (T1) and T2 B cells or those of mature follicular B and marginal zone B cells in the spleen. IgM and IgG serum levels are also not significantly different among exposed, sham-exposed and control mice. B cells from these mice, challenged in vitro with LPS, produce comparable amounts of IgM and IgG. Moreover, exposure of immunized mice to RF fields does not change the antigen-specific antibody serum level. Interestingly, not only the production of antigen-specific IgM but also that of IgG (which requires T-B-cell interaction) is not affected by RF-field exposure. This indicates that the exposure does not alter an ongoing in vivo antigen-specific immune response. In conclusion, our results do not indicate any effects of GSM-modulated RF radiation on the B-cell peripheral compartment and antibody production and thus provide no support for health-threatening effects.     

Chronic exposure of cancer-prone mice to low-level 2450 MHz radiofrequency radiation

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.     

Effect of cell phone radiofrequency radiation on body temperature in rodents: Pilot studies of the National Toxicology Program's reverberation chamber exposure system

Radiofrequency radiation (RFR) causes heating, which can lead to detrimental biological effects. To characterize the effects of RFR exposure on body temperature in relation to animal size and pregnancy, a series of short‐term toxicity studies was conducted in a unique RFR exposure system. Young and old B6C3F1 mice and young, old, and pregnant Harlan Sprague‐Dawley rats were exposed to Global System for Mobile Communication (GSM) or Code Division Multiple Access (CDMA) RFR (rats = 900 MHz, mice = 1,900 MHz) at specific absorption rates (SARs) up to 12 W/kg for approximately 9 h a day for 5 days. In general, fewer and less severe increases in body temperature were observed in young than in older rats. SAR‐dependent increases in subcutaneous body temperatures were observed at exposures ≥6 W/kg in both modulations. Exposures of ≥10 W/kg GSM or CDMA RFR induced excessive increases in body temperature, leading to mortality. There was also a significant increase in the number of resorptions in pregnant rats at 12 W/kg GSM RFR. In mice, only sporadic increases in body temperature were observed regardless of sex or age when exposed to GSM or CDMA RFR up to 12 W/kg. These results identified SARs at which measurable RFR‐mediated thermal effects occur, and were used in the selection of exposures for subsequent toxicology and carcinogenicity studies. Bioelectromagnetics. 39:190–199, 2018. © 2018 The Authors. Bioelectromagnetics Published by Wiley Periodicals, Inc.