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.     

In vitro fertilization of mouse ova by spermatozoa exposed isothermally to radio-frequency radiation

Mouse spermatozoa were exposed in vitro for 1 h to 27- or 2,450-MHz CW RF radiation at SARs of 0 to 90 W/kg under isothermal (37 +/- 0.2 degrees C) conditions. Exposure at either frequency to RF radiation at SARs of 50 W/kg or greater resulted in a statistically significant reduction in the ability of irradiated sperm to fertilize mouse ova in vitro (P less than .05). Over the range of SARs there was no apparent difference in the effects of 27- vs. 2,450-MHz RF radiation. There were no readily detectable exposure effects on spermatozoan morphology, ultrastructure, or capacitation. The reduction of in vitro fertilization is attributed to a direct effect of RF radiation on spermatozoa rather than to heating.     

Effects of continuous and intermittent exposure to RF fields with a wide range of SARs on cell growth, survival, and cell cycle distribution

To examine the biological effects of radio frequency (RF) electromagnetic fields in vitro, we have examined the fundamental cellular responses, such as cell growth, survival, and cell cycle distribution, following exposure to a wide range of specific absorption rates (SAR). Furthermore, we compared the effects of continuous and intermittent exposure at high SARs. An RF electromagnetic field exposure unit operating at a frequency of 2.45 GHz was used to expose cells to SARs from 0.05 to 1500 W/kg. When cells were exposed to a continuous RF field at SARs from 0.05 to 100 W/kg for 2 h, cellular growth rate, survival, and cell cycle distribution were not affected. At 200 W/kg, the cell growth rate was suppressed and cell survival decreased. When the cells were exposed to an intermittent RF field at 300 W/kg(pk), 900 W/kg(pk) and 1500 W/kg(pk) (100 W/kg(mean)), no significant differences were observed between these conditions and intermittent wave exposure at 100 W/kg. When cells were exposed to a SAR of 50 W/kg for 2 h, the temperature of the medium around cells rose to 39.1 degrees C, 100 W/kg exposure increased the temperature to 41.0 degrees C, and 200 W/kg exposure increased the temperature to 44.1 degrees C. Exposure to RF radiation results in heating of the medium, and the thermal effect depends on the mean SAR. Hence, these results suggest that the proliferation disorder is caused by the thermal effect.     

Teratogenicity of 27.12-MHz radiation in rats is related to duration of hyperthermic exposure

Five groups of pregnant Sprague-Dawley rats were either sham exposed or were irradiated in a 27.12-MHz radiofrequency (RF) field at 55 A/m and 300 V/m on gestation day 9. The absorbed power (approximately 11 W/kg) caused a relatively rapid increase in the rat's colonic temperature. Rats in group I were sham irradiated for 2.5 h at 0 A/m, 0 V/m. In group II RF irradiation was terminated after the rat's colonic temperature reached 41.0 degrees C. In group III the 41.0- degrees C temperature was maintained an additional 2 h by manually varying the incident field strength. In group IV irradiation was terminated after the rat's colonic temperature reached 42.0 degrees C. In group V the 42.0- degrees C temperature was maintained an additional 15 min by varying the field strength. At both temperatures the teratogenic and embryotoxic effects of the RF-induced hyperthermia increased as the exposure duration increased, but the increase was especially noticeable at 42.0 degrees C. The results indicate that the teratogenic and embryotoxic effects of RF-induced hyperthermia are related to both the temperature of the dam during exposure and the length of time the dam's temperature remains elevated.     

Immunological effects of amplitude-modulated radio frequency radiation: B lymphocyte capping

B lymphocytes collected from normal ICR Swiss mouse spleens were exposed in vitro in a Crawford cell to 147-MHz radiofrequency (RF) radiation, amplitude modulated by a 9-, 16-, or 60-Hz sine wave. The power densities ranged between 0.11 and 48 mW/cm2. The irradiated samples and the controls were maintained at 37 degrees C or 42 degrees C, with temperature variations less than 0.1 degrees C. Immediately after a 30-minute exposure, the distribution of antigen-antibody (Ag-Ab) complexes on the cell surface was evaluated at 37 degrees C by immunofluorescence. Under normal conditions (37 degrees C, no RF), Ag-Ab complexes are regrouped into a polar cap by an energy-dependent process. Our results demonstrate that the irradiated cells and the nonirradiated controls capped Ag-Ab complexes equally well after exposure at 37 degrees C. Capping was equally inhibited at 42 degrees C in both the controls and irradiated cells. No statistically significant differences in capping were observed between the RF-exposed and control samples at any of the modulation frequencies and power densities employed as long as both preparations were maintained at the same temperature.     

Multiple power-density windows and their possible origin

We have previously reported that in vitro exposure of chick forebrain tissue to 50-MHz radiofrequency (RF) electromagnetic radiation, amplitude modulated (AM) at 16 Hz, would enhance the efflux of calcium ions within only two power-density ranges: one from 1.44 to 1.67 mW/cm2, and the other including 3.64 mW/cm2. No effect on efflux occurred at 0.37, 0.72, 2.17, and 4.32 mW/cm2. We confirmed and extended these results by testing at another set of power densities, which included the range of the previous study. Forebrain tissue from 1-7-day-old chickens was labeled in vitro with radioactive calcium ions (30 min, at 37 degrees C), rinsed, placed in a physiological salt solution, and then exposed for 20 min to 50-MHz radiation, AM at 16 Hz, in a transverse electric and magnetic field (TEM) cell maintained at 37 degrees C. The solution was then assayed for radioactive calcium activity. A power-density series was tested. An enhanced efflux of calcium ions was found at 1.75, 3.85, 5.57, 6.82, 7.65, 7.77, and 8.82 mW/cm2; no change was observed at 0.75, 2.30, 4.50, 5.85, 7.08, 8.19, 8.66, 10.6, and 14.7 mW/cm2. Power density is converted to specific absorption rate (SAR) by 0.36 mW/kg per mW/cm2. Even the highest SAR tested (0.005 W/kg) is much too low to result in generalized heating of the sample and thus to be the underlying cause of the enhanced response. A hypothetical mechanism is proposed involving dynamic systems that may account for the power-density dependency as well as for part of the frequency dependency observed with both modulated RF radiation and extremely-low-frequency (ELF) fields.     

Radiofrequency radiation does not induce stress response in human T-lymphocytes and rat primary astrocytes

Heat shock proteins (HSPs) are rapidly induced by a variety of stressors, including heat shock, ethanol, heavy metals, UV, and gamma-radiation. Mitogen-activated protein kinases (MAPKs) are also involved in the stress transduction pathways in all eukaryotes. In this study, we attempted to determine whether radiofrequency (RF) radiation is able to induce a non-thermal stress response. Human T-lymphocyte Jurkat cells and rat primary astrocytes were exposed to 1763 MHz of RF radiation at an average specific absorption rate (SAR) of either 2 W/kg or 20 W/kg, for 30 min or 1 h. Temperature was completely controlled at 37 +/- 0.2 degrees C throughout the exposure period. The sham exposures were performed under exactly identical experimental conditions without exposure to RF radiation. We assessed alterations in the expression of HSPs and the activation of MAPKs in the RF-exposed cells. No detectable difference was observed in the expression levels of HSP90, HSP70, and HSP27. The phosphorylation status of MAPKs, extracellular signal-regulated kinases (ERK1/2), c-Jun N-terminal protein kinases (JNK1/2), or p38, did not change significantly. In order to determine whether RF radiation can promote the effects of 12-O-tetradecanoylphorbol 13-acetate (TPA) on stress response, cells were exposed to RF radiation coupled with TPA treatment. When TPA alone was applied, the MAPKs were found to be phosphorylated in a dose-dependent manner. However, RF radiation did not result in any enhancement of TPA-induced MAPK phosphorylation. Neither TPA nor RF radiation exerted any detectable effect on the induction of HSPs. These results indicate that 1763 MHz RF radiation alone did not elicit any stress response, nor did it have any effect on TPA-induced MAPK phosphorylation, under our experimental conditions.     

Measurement of DNA damage and apoptosis in Molt-4 cells after in vitro exposure to radiofrequency radiation

To determine whether exposure to radiofrequency (RF) radiation can induce DNA damage or apoptosis, Molt-4 T lymphoblastoid cells were exposed with RF fields at frequencies and modulations of the type used by wireless communication devices. Four types of frequency/modulation forms were studied: 847.74 MHz code-division multiple-access (CDMA), 835.62 MHz frequency-division multiple-access (FDMA), 813.56 MHz iDEN(R) (iDEN), and 836.55 MHz time-division multiple-access (TDMA). Exponentially growing cells were exposed to RF radiation for periods up to 24 h using a radial transmission line (RTL) exposure system. The specific absorption rates used were 3.2 W/kg for CDMA and FDMA, 2.4 or 24 mW/kg for iDEN, and 2.6 or 26 mW/kg for TDMA. The temperature in the RTLs was maintained at 37 degrees C +/- 0.3 degrees C. DNA damage was measured using the single-cell gel electrophoresis assay. The annexin V affinity assay was used to detect apoptosis. No statistically significant difference in the level of DNA damage or apoptosis was observed between sham-treated cells and cells exposed to RF radiation for any frequency, modulation or exposure time. Our results show that exposure of Molt-4 cells to CDMA, FDMA, iDEN or TDMA modulated RF radiation does not induce alterations in level of DNA damage or induce apoptosis.     

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.     

Radiofrequency radiation at 2.856 GHz does not affect key cellular endpoints in neuron-like PC12 cells

To investigate the potential cytotoxicity of radiofrequency (RF) radiation on central nervous system, rat pheochromocytoma (PC12) cells were exposed to 2.856 GHz RF radiation at a specific absorption rate (SAR) of 4 W/kg for 8 h a day for 2 days in 35 mm Petri dishes. During exposure, the real-time variation of the culture medium temperature was monitored in the first hour. Reactive oxygen species (ROS) production, intracellular Ca²⁺ concentration, and cell apoptosis rate were assessed immediately after exposure by flow cytometry. The results showed that the medium temperature raised about 0.93 °C, but no significant changes were observed in apoptosis, ROS levels or intracellular Ca²⁺ concentration after treatment. Although several studies suggested that RF radiation does indeed cause neurological effects, this study presented inconsistent results, indicating that 2.856 GHz RF radiation exposure at a SAR of 4 W/kg does not have a dramatic impact on PC12 cells, and suggests the need for further investigation on the key cellular endpoints of other nerve cells after exposure to RF radiation.     

Reduction in metabolic heat production during exposure to radio-frequency radiation in the rat

The purpose of this study was to assess the ability of the rat to reduce metabolic rate when exposed to deep-penetrating radio-frequency (RF) radiation. Male Sprague-Dawley rats were maintained at an ambient temperature (Ta) of 10 degrees C and exposed to 600-MHz radiation while metabolic rate (MR) was measured by indirect calorimetry. RF radiation exposures were made in a waveguide-type system that permitted the continuous control of specific absorption rate (SAR). SAR's of 2-5 W/kg led to significant reductions in MR when averaged from 30 to 60 min after the initiation of RF radiation exposure. The total decrease in MR during RF radiation exposure accounted for approximately 37% of the total RF heat load. Exposure of another group of rats to the same SAR's at a Ta of 10 degrees C resulted in a significant elevation in colonic temperature. Thus, despite the decrease in MR, heat gain still exceeded heat loss during RF radiation exposure, with a resultant elevation in deep body temperature. In conclusion, in a cold environment the rat exposed to RF radiation decreases its MR. However, the response time and efficiency of the response is not adequate to prevent an increase in body temperature.     

Temperature-specific inhibition of human red cell Na+/K+ ATPase by 2,450-MHz microwave radiation

The ATPase activity in human red blood cell membranes was investigated in vitro as a function of temperature and exposure to 2,450-MHz continuous wave microwave radiation to confirm and extend a report of Na+ transport inhibition under certain conditions of temperature and exposure. Assays were conducted spectrophotometrically during microwave exposure with a custom-made spectrophotometer-waveguide apparatus. Temperature profiles of total ATPase and Ca+2 ATPase (ouabain-inhibited) activity between 17 and 31 degrees C were graphed as an Arrhenius plot. Each data set was fitted to two straight lines which intersect between 23 and 24 degrees C. The difference between the total and Ca+2 ATPase activities, which represented the Na+/K+ ATPase activity, was also plotted and treated similarly to yield an intersection near 25 degrees C. Exposure of membrane suspensions to electromagnetic radiation, at a dose rate of 6 W/kg and at five temperatures between 23 and 27 degrees C, resulted in an activity change only for the Na+/K+ ATPase at 25 degrees C. The activity decreased by approximately 35% compared to sham-irradiated samples. A possible explanation for the unusual temperature/microwave interaction is proposed.     

Phosphorylation and gene expression of p53 are not affected in human cells exposed to 2.1425 GHz band CW or W-CDMA modulated radiation allocated to mobile radio base stations

A large-scale in vitro study focusing on low-level radiofrequency (RF) fields from mobile radio base stations employing the International Mobile Telecommunication 2000 (IMT-2000) cellular system was conducted to test the hypothesis that modulated RF fields induce apoptosis or other cellular stress response that activate p53 or the p53-signaling pathway. First, we evaluated the response of human cells to microwave exposure at a specific absorption rate (SAR) of 80 mW/kg, which corresponds to the limit of the average whole-body SAR for general public exposure defined as a basic restriction by the International Commission on Non-Ionizing Radiation Protection (ICNIRP) guidelines. Second, we investigated whether continuous wave (CW) and wideband code division multiple access (W-CDMA) modulated signal RF fields at 2.1425 GHz induced apoptosis or any signs of stress. Human glioblastoma A172 cells were exposed to W-CDMA radiation at SARs of 80, 250, and 800 mW/kg, and CW radiation at 80 mW/kg for 24 or 48 h. Human IMR-90 fibroblasts from fetal lungs were exposed to both W-CDMA and CW radiation at a SAR of 80 mW/kg for 28 h. Under the RF field exposure conditions described above, no significant differences in the percentage of apoptotic cells were observed between the test groups exposed to RF signals and the sham-exposed negative controls, as evaluated by the Annexin V affinity assay. No significant differences in expression levels of phosphorylated p53 at serine 15 or total p53 were observed between the test groups and the negative controls by the bead-based multiplex assay. Moreover, microarray hybridization and real-time RT-PCR analysis showed no noticeable differences in gene expression of the subsequent downstream targets of p53 signaling involved in apoptosis between the test groups and the negative controls. Our results confirm that exposure to low-level RF signals up to 800 mW/kg does not induce p53-dependent apoptosis, DNA damage, or other stress response in human cells.     

Behavioral effects of chronic exposure to 0.5 mW/cm2 of 2,450-MHz microwaves

Adult male, Long-Evans rats were exposed 7 h a day for 90 days to continuous wave (CW) 2,450-MHz microwaves at an average power density of 0.5 mW/cm2. Exposures were in a monopole-above-ground radiation chamber with rats in Plexiglas cages. The resulting specific absorption rate (SAR) was 0.14 W/kg (+/- 0.01 SEM). Additional rats served as sham-exposed and home-caged controls. All were evaluated daily for body mass and food and water intakes. Once each 30 days, throughout baseline and exposure phases of the experiment, rats in the sham- and microwave-exposed groups were tested for their sensitivity to footshock. After 90-days of exposure, the rats were evaluated an open field, an active avoidance task and an operant task for food reinforcement. Performance of sham- and microwave-irradiated rats was reliably different on only one measure, the lever-pressing task. The general conclusion reached was that exposure to CW 2,450-MHz microwave radiation at 0.5 mW/cm2 was below the threshold for behavioral effects over a wide range of variables, but did have an effect on a time-related operant task, although the direction of the effect was unpredictable.     

Radiofrequency (microwave) radiation exposure of mammalian cells during UV-induced DNA repair synthesis

The effect of continuous-wave (CW) and pulsed-wave (PW) radiofrequency radiation (RFR) in the microwave range on UV-induced DNA repair has been investigated in MRC-5 normal human diploid fibroblasts. RFR exposure at power densities of 1 (or 5) and 10 mW/cm2 gave a maximum specific absorption rate (SAR) (at 10 mW/cm2) of 0.39 +/- 0.15 W/kg for 350 MHz RFR, 4.5 +/- 3.0 W/kg for 850 MHz RFR, and 2.7 +/- 1.6 W/kg for 1.2 GHz RFR. RFR exposures for 1 to 3 h at 37 degrees C, in either continuous-wave or pulsed-wave modes, had no effect on the rate of repair replication label incorporated into preexisting UV-damaged DNA. RFR exposures (PW), with a constant medium temperature of 39 degrees C at 350 and 850 MHz during the repair period after UV damage, also had no effect. Assay for induction of repair synthesis by RFR exposure alone in non-UV irradiated cells was negative for the 350-, 850-, and 1200-MHz CW and PW RFR at 37 degrees C and the 350- and 850-MHz PW RFR at 39 degrees C. RFR does not induce DNA repair under these exposure conditions. In preliminary experiments--with the tissue culture medium maintained at 39 degrees C and RFR exposures (PW) at the frequencies of 350, 850, and 1200 MHz--no effect on incorporation of [3H]thymidine into DNA undergoing semiconservative synthesis was observed.     

In vitro study of the stress response of human skin cells to GSM-1800 mobile phone signals compared to UVB radiation and heat shock

The evolution of mobile phone technology is toward an increase of the carrier frequency up to 2.45 GHz. Absorption of radiofrequency (RF) radiation becomes more superficial as the frequency increases. This increasingly superficial absorption of RF radiation by the skin, which is the first organ exposed to RF radiation, may lead to stress responses in skin cells. We thus investigated the expression of three heat-shock proteins (HSP70, HSC70, HSP27) using immunohistochemistry and induction of apoptosis by flow cytometry on human primary keratinocytes and fibroblasts. A well-characterized exposure system, SXC 1800, built by the IT'IS foundation was used at 1800 MHz, with a 217 Hz modulation. We tested a 48-h exposure at an SAR of 2 W/kg (ICNIRP local exposure limit). Skin cells were also irradiated with a 600 mJ/cm2 single dose of UVB radiation and subjected to heat shock (45 degrees C, 20 min) as positive controls for apoptosis and HSP expression, respectively. The results showed no effect of a 48-h GSM-1800 exposure at 2 W/kg on either keratinocytes or fibroblasts, in contrast to UVB-radiation or heat-shock treatments, which injured cells. We thus conclude that the GSM-1800 signal does not act as a stress factor on human primary skin cells in vitro.     

Glioma proliferation modulated in vitro by isothermal radiofrequency radiation exposure

Isothermal (37 +/- 0.2 degrees C) exposure of glioma cells (LN71) for 2 h to 27 or 2450 MHz continuous-wave radiofrequency (RF) radiation in vitro modulated the rates of DNA and RNA synthesis 1, 3, and 5 days after exposure. The alterations indicate effects on cell proliferation and were not caused by RF-induced cell heating. The dose response for either frequency of the radiation was biphasic. Exposure to specific absorption rates (SARs) of 50 W/kg or less stimulated incorporation rates of tritiated thymidine (3H-TdR) and tritiated uridine (3H-UdR), whereas higher SARs suppressed DNA and RNA synthesis. Statistically significant time-dependent alterations were detected for up to 5 days postexposure, suggesting a kinetic cellular response to RF radiation and the possibility of cumulative effects on cell proliferation. General mechanisms of effects are discussed.     

Apoptosis induced by ultraviolet radiation is enhanced by amplitude modulated radiofrequency radiation in mutant yeast cells

The aim of this study was to investigate whether radiofrequency (RF) electromagnetic field (EMF) exposure affects cell death processes of yeast cells. Saccharomyces cerevisiae yeast cells of the strains KFy417 (wild-type) and KFy437 (cdc48-mutant) were exposed to 900 or 872 MHz RF fields, with or without exposure to ultraviolet (UV) radiation, and incubated simultaneously with elevated temperature (+37 degrees C) to induce apoptosis in the cdc48-mutated strain. The RF exposure was carried out in a special waveguide exposure chamber where the temperature of the cell cultures can be precisely controlled. Apoptosis was analyzed using the annexin V-FITC method utilizing flow cytometry. Amplitude modulated (217 pulses per second) RF exposure significantly enhanced UV induced apoptosis in cdc48-mutated cells, but no effect was observed in cells exposed to unmodulated fields at identical time-average specfic absorption rates (SAR, 0.4 or 3.0 W/kg). The findings suggest that amplitude modulated RF fields, together with known damaging agents, can affect the cell death process in mutated yeast cells. Bioelectromagnetics 25:127-133, 2004.     

Nonthermal 60 Hz sinusoidal magnetic-field exposure enhances 45Ca2+ uptake in rat thymocytes: dependence on mitogen activation

The effect of a 60 Hz sinusoidal magnetic field of nonthermal intensity on Ca2+ metabolism in rat thymic lymphocytes (thymocytes) was assessed in resting cells and in cells activated with the mitogen Concanavalin A (Con A). A 60 min exposure at 37 degrees C to an induced electric field of 1.0 mV/cm produced an average 2.7-fold increase in Con A-dependent 45Ca2(+)-uptake compared to non-exposed, isothermal control cells. In contrast, 45Ca2+ uptake remained unaltered during exposure of resting thymocytes. It was also found that thymocytes with a diminished ability to mobilize Ca2+ in response to Con A were most sensitive to the 60 Hz magnetic field. Although the precise mechanism of field interaction is at present unknown, modulation of Ca2+ metabolism during cell activation may represent a common pathway for field coupling to cellular systems.     

1950 MHz IMT‐2000 field does not activate microglial cells in vitro

Given the widespread use of the cellular phone today, investigation of potential biological effects of radiofrequency (RF) fields has become increasingly important. In particular, much research has been conducted on RF effects on brain function. To examine any biological effects on the central nervous system (CNS) induced by 1950 MHz modulation signals, which are controlled by the International Mobile Telecommunication‐2000 (IMT‐2000) cellular system, we investigated the effect of RF fields on microglial cells in the brain. We assessed functional changes in microglial cells by examining changes in immune reaction‐related molecule expression and cytokine production after exposure to a 1950 MHz Wideband Code Division Multiple Access (W‐CDMA) RF field, at specific absorption rates (SARs) of 0.2, 0.8, and 2.0 W/kg. Primary microglial cell cultures prepared from neonatal rats were subjected to an RF or sham field for 2 h. Assay samples obtained 24 and 72 h after exposure were processed in a blind manner. Results showed that the percentage of cells positive for major histocompatibility complex (MHC) class II, which is the most common marker for activated microglial cells, was similar between cells exposed to W‐CDMA radiation and sham‐exposed controls. No statistically significant differences were observed between any of the RF field exposure groups and the sham‐exposed controls in percentage of MHC class II positive cells. Further, no remarkable differences in the production of tumor necrosis factor‐α (TNF‐α), interleukin‐1β (IL‐1β), and interleukin‐6 (IL‐6) were observed between the test groups exposed to W‐CDMA signal and the sham‐exposed negative controls. These findings suggest that exposure to RF fields up to 2 W/kg does not activate microglial cells in vitro. Bioelectromagnetics 31:104–112, 2010. © 2009 Wiley‐Liss, Inc.