Temperature regulation in the unrestrained rabbit during exposure to 600 MHz radiofrequency radiation

Six male New Zealand white rabbits were individually exposed to 600 MHz radiofrequency (RF) radiation for 90 min in a waveguide exposure system at an ambient temperature (Ta) of 20 or 30 degrees C. Immediately after exposure, the rabbit was removed from the exposure chamber and its colonic and ear skin temperatures were quickly measured. The whole-body specific absorption rate (SAR) required to increase colonic and ear skin temperature was determined. At a Ta of 20 degrees C the threshold SAR for elevating colonic and ear skin temperature was 0.64 and 0.26 W/kg, respectively. At a Ta of 30 degrees C the threshold SARs were slightly less than at 20 degrees C, with values of 0.26 W/kg for elevating colonic temperature and 0.19 W/kg for elevating ear skin temperature. The relationship between heat load and elevation in deep body temperature shown in this study at 600 MHz is similar to past studies which employed much higher frequencies of RF radiation (2450-2884 MHz). On the other hand, comparison of these data with studies on exercise-induced heat production and thermoregulation in the rabbit suggest that the relationship between heat gain and elevation in body temperature in exercise and from exposure to RF radiation may differ considerably. When combined with other studies, it was shown that the logarithm of the SAR required for a 1.0 degree C elevation in deep body temperature of the rabbit, rat, hamster, and mouse was inversely related to the logarithm of body mass. The results of this study are consistent with the conclusion that body mass strongly influences thermoregulatory sensitivity of the aforementioned laboratory mammals during 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.     

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.     

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.     

Thermoregulatory adjustments in squirrel monkeys exposed to microwaves at high power densities

The present study was undertaken to investigate the thermal adjustments of squirrel monkeys exposed in a cold environment to relatively high energy levels of microwave fields. The animals (Saimiri sciureus) were equilibrated for 90 min to a cool environment (Ta = 20 degrees C) to elevate metabolic heat production (M). They were then exposed for brief (10-min) or long (30-min) periods to 2,450-MHz continuous-wave microwaves. Power densities (MPD) were 10, 14, 19, and 25 mW/cm2 during brief exposures and 30, 35, 40, and 45 mW/cm2 during long exposures (rate of energy absorption: SAR = 0.15 [W/kg]/[mW/cm2]). Individual exposures were separated by enough time to allow physiological variables to return to baseline levels. The results confirm that each microwave exposure induced a rapid decrease in M. In a 20 degree C environment, the power density of a 10-min exposure required to lower M to approximate the resting level was 35 mW/cm2 (SAR = 5.3 W/kg). During the long exposures, 20 min was needed to decrease M to its lowest level. Cessation of irradiation was associated with persistence of low levels of M for periods that depended on the power density of the preceding microwave exposure. Vasodilation, as indexed by changes in local skin temperature, occurred at a high rate of energy absorption (SAR = 4.5 W/kg) and was sufficient to prevent a dramatic increase in storage of thermal energy by the body; vasoconstriction was reinstated after termination of irradiation. Patterns of thermophysiological responses confirm the influence both of peripheral and of internal inputs to thermoregulation in squirrel monkeys exposed to microwaves in a cool environment.     

Body temperature in the mouse,hamster, and rat exposed to radiofrequency radiation: An interspecies comparison

• 1.1.|Colonic temperatures of BALB/c and CBA/J mice, golden hamsters, and Sprague-Dawley rats were taken immediately after exposure for 90 min to radiofrequency (RF) radiation.
• 2.2.|Exposures were made in 2450 MHz (mouse and hamster) or 600 MHz (rat) waveguide exposure systems while the dose rate, specific absorption rate (SAR), was continuously recorded. Experiments were performed on naive, unrestrained animals at ambient temperatures (T_a) of 20 and 30°C.
• 3.3.|Body mass and T_a) were found to be significant factors in influencing the threshold SAR for the elevation of colonic temperature. The threshold SARs at T_a's of 20 and 30°C were respectively: 27.5 and 12.1 W/kg for the BALB/c mouse; 40.7 and 8.5 W/kg for the CBA/J mouse; 8.7 and 0.61 W/kg for the golden hamster; and 1.58 and 0.4 W/kg for the Sprague-Dawley rat.
• 4.4.|The relationship between threshold SAR or SAR for a 1.0°C elevation in colonic temperature vs body mass were linearly and inversely related on a double logarithmic plot. The results of this study suggest that the thermoregulatory sensitivity to RF radiation in these rodent species is heavily dependent on body mass and T_a.

     

DNA damage and micronucleus induction in human leukocytes after acute in vitro exposure to a 1.9 GHz continuous-wave radiofrequency field

Human blood cultures were exposed to a 1.9 GHz continuous-wave (CW) radiofrequency (RF) field for 2 h using a series of six circularly polarized, cylindrical waveguides. Mean specific absorption rates (SARs) of 0.0, 0.1, 0.26, 0.92, 2.4 and 10 W/kg were achieved, and the temperature within the cultures during a 2-h exposure was maintained at 37.0 +/- 0.5 degrees C. Concurrent negative (incubator) and positive (1.5 Gy (137)Cs gamma radiation) control cultures were run for each experiment. DNA damage was quantified immediately after RF-field exposure using the alkaline comet assay, and four parameters (tail ratio, tail moment, comet length and tail length) were used to assess DNA damage for each comet. No evidence of increased primary DNA damage was detected by any parameter for RF-field-exposed cultures at any SAR tested. The formation of micronuclei in the RF-field-exposed blood cell cultures was assessed using the cytokinesis-block micronucleus assay. There was no significant difference in the binucleated cell frequency, incidence of micronucleated binucleated cells, or total incidence of micronuclei between any of the RF-field-exposed cultures and the sham-exposed controls at any SAR tested. These results do not support the hypothesis that acute, nonthermalizing 1.9 GHz CW RF-field exposure causes DNA damage in cultured human leukocytes.     

The effect of ambient temperature on beta-adrenergic responsiveness in rats.

The responses of tail skin and colonic temperatures of female rats to ambient temperatures of 20, 22, 24, 26, 28, and 30 degrees C were measured. Within this range, colonic temperature was stable while tail skin temperature increased linearly with increasing ambient temperature. Administration of the beta-adrenergic agonist, d,l-isoproterenol, at 10.0, 25.0, and 62.5 micrograms/kg, sc, at each ambient temperature was accompanied by increases in tail skin and colonic temperatures that were dependent on both the dose of isoproterenol administered and the ambient temperature. The integrated responses of tail skin temperature following administration of the three doses of isoproterenol were maximal at an ambient temperature of 26 degrees C while the integrated responses of colonic temperature were maximal at 30 degrees C. The results suggest that tests of beta-adrenergic responsiveness using this technique should be performed at an ambient temperature of 26 degrees C for maximal sensitivity.     

Mechanism of vasoconstriction in the rat's tail when warmed locally.

The vascular response of the tail to local warming was investigated in urethan-anesthetized rats whose colonic temperature was maintained at 39.5 degrees C with an intravenous thermode at an ambient temperature of 23 degrees C. The tail, covered with thin latex tubing, was immersed in temperature-controlled water initially kept at 35 degrees C. The tail was warmed by raising the water bath temperature from 35 to 44 degrees C at a constant rate. Tail blood flow (BF), mean arterial blood pressure (BP), and tail skin temperature (Tsk) were measured before and during the local warming. Tail vascular conductance (VC) was computed as 100 x tail BF/BP. When Tsk exceeded 37 degrees C, tail BF and VC significantly decreased from the levels at Tsk of 35 degrees C, and significant reductions in tail BF and VC occurred until Tsk reached 42 degrees C. Surgical deafferentation of the tail, chemical sympathectomy with 6-hydroxydopamine (100 mg/kg), and alpha-blockade with phentolamine (7 or 40.1-45.5 mg/kg) or phenoxybenzamine (5 mg/kg) failed to stop the decrease in tail BF and VC during the local warming. These results suggest that a reflex via the central nervous system and the alpha-adrenergic sympathetic nervous system is not indispensable for heat-induced vasoconstriction (HIVC). It is therefore assumed that, at least in the rat's tail, HIVC predominantly originates from a local vascular response to high temperature.     

Thermoregulatory responses of the immature rat following repeated postnatal exposures to 2,450-MHz microwaves

This study was designed to determine the changes that occur in the thermoregulatory ability of the immature rat repeatedly exposed to low-level microwave radiation. Beginning at 6-7 days of age, previously untreated rats were exposed to 2,450-MHz continuous-wave microwaves at a power density of 5 mW/cm2 for 10 days (4 h/day). Microwave and sham (control) exposures were conducted at ambient temperatures (Ta) which represent different levels of cold stress for the immature rat (ie, "exposure" Ta = 20 and 30 degrees C). Physiological tests were conducted at 5-6 and 16-17 days of age, in the absence of microwaves, to determine pre- and postexposure responses, respectively. Measurements of metabolic rate, colonic temperature, and tail skin temperature were made at "test" Ta = 25.0, 30.0, 32.5, and 35.0 degrees C. Mean growth rates were lower for rats exposed to Ta = 20 degrees C than for those exposed to Ta = 30 degrees C, but microwave exposure exerted no effect at either exposure Ta. Metabolic rates and body temperatures of all exposure groups were similar to values for untreated animals at test Ta of 32.5 degrees C and 35.0 degrees C. Colonic temperatures of rats repeatedly exposed to sham or microwave conditions at exposure Ta = 20 degrees C or to sham conditions at exposure Ta = 30 degrees C were approximately 1 degrees C below the level for untreated animals at test Ta of 25.0 degrees C and 30.0 degrees C. However, when the exposure Ta was warmer, rats exhibited a higher colonic temperature at these cold test Ta, indicating that the effectiveness of low-level microwave treatment to alter thermoregulatory responses depends on the magnitude of the cold stress.     

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.     

Human exposure to 2450 MHz CW energy at levels outside the IEEE C95.1 standard does not increase core temperature

Permission was received from the Brooks AFB Institutional Review Board and the AF Surgeon General's Office to exceed the peak power density (PD = 35 mW/cm(2)) we had previously studied during partial body exposure of human volunteers at 2450 MHz. Two additional peak PD were tested (50 and 70 mW/cm(2)). The higher of these PD (normalized peak local SAR = 15.4 W/kg) is well outside the IEEE C95.1 guidelines for partial body exposure, as is the estimated whole body SAR approximately 1.0 W/kg. Seven volunteers (four males, three females) were tested at each PD in three ambient temperatures (T(a) = 24, 28, and 31 degrees C) under our standard protocol (30 min baseline, 45 min RF exposure, 10 min baseline). The thermophysiological data (esophageal and six skin temperatures, metabolic heat production, local sweat rate, and local skin blood flow) were combined with comparable data at PD = 0, 27, and 35 mW/cm(2) from our 1999 study to generate response functions across PD. No change in esophageal temperature or metabolic heat production was recorded at any PD in any T(a). At PD = 70 mW/cm(2), skin temperature on the upper back (irradiated directly) increased 4.0 degrees C in T(a) = 24 degrees C, 2.6 degrees C in T(a) = 28 degrees C, and 1.8 degrees C in T(a) = 31 degrees C. These differences were primarily due to the increase in local sweat rate, which was greatest in T(a) = 31 degrees C. Also at PD = 70 mW/cm(2), local skin blood flow on the back increased 65% over baseline levels in T(a) = 31 degrees C, but only 40% in T(a) = 24 degrees C. Although T(a) becomes an important variable when RF exposure exceeds the C95.1 partial body exposure limits, vigorous heat loss responses of blood flow and sweating maintain thermal homeostasis efficiently. It is also clear that strong sensations of heat and thermal discomfort will motivate a timely retreat from a strong RF field, long before these physiological responses are exhausted. Published 2001 Wiley-Liss, Inc.     

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.     

Effect of Exposure to a Radiofrequency Electromagnetic Field on Body Temperature in Anesthetized and Non-Anesthetized Rats

Exposure to a radiofrequency (RF) signal at a specific absorption rate (SAR) of 4 W/kg can increase the body temperature by more than 1 °C. In this study, we investigated the effect of anesthesia on the body temperature of rats after exposure to an RF electromagnetic field at 4 W/kg SAR. We also evaluated the influence of body mass on rats’ body temperature. Rats weighing 225 and 339 g were divided into sham- and RF-exposure groups. Each of the resulting four groups was subdivided into anesthetized and non-anesthetized groups. The free-moving rats in the four RF-exposure groups were subjected to a 915 MHz RF identification signal at 4 W/kg whole-body SAR for 8 h. The rectal temperature was measured at 1-h intervals during RF exposure using a small-animal temperature probe. The body temperatures of non-anesthetized, mobile 225 and 339 g rats were not significantly affected by exposure to an RF signal. However, the body temperatures of anesthetized 225 and 339 g rats increased by 1.9 °C and 3.3 °C from baseline at 5 and 6 h of RF exposure, respectively. Three of the five 339 g anesthetized and exposed rats died after 6 h of RF exposure. Thus, anesthesia and body mass influenced RF exposure-induced changes in the body temperature of rats. Bioelectromagnetics. 2020;41:104–112. © 2019 Bioelectromagnetics Society.     

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.     

Exposure of human peripheral blood lymphocytes to electromagnetic fields associated with cellular phones leads to chromosomal instability

Whether exposure to radiation emitted from cellular phones poses a health hazard is at the focus of current debate. We have examined whether in vitro exposure of human peripheral blood lymphocytes (PBL) to continuous 830 MHz electromagnetic fields causes losses and gains of chromosomes (aneuploidy), a major "somatic mutation" leading to genomic instability and thereby to cancer. PBL were irradiated at different average absorption rates (SAR) in the range of 1.6-8.8 W/kg for 72 hr in an exposure system based on a parallel plate resonator at temperatures ranging from 34.5-37.5 degrees C. The averaged SAR and its distribution in the exposed tissue culture flask were determined by combining measurements and numerical analysis based on a finite element simulation code. A linear increase in chromosome 17 aneuploidy was observed as a function of the SAR value, demonstrating that this radiation has a genotoxic effect. The SAR dependent aneuploidy was accompanied by an abnormal mode of replication of the chromosome 17 region engaged in segregation (repetitive DNA arrays associated with the centromere), suggesting that epigenetic alterations are involved in the SAR dependent genetic toxicity. Control experiments (i.e., without any RF radiation) carried out in the temperature range of 34.5-38.5 degrees C showed that elevated temperature is not associated with either the genetic or epigenetic alterations observed following RF radiation-the increased levels of aneuploidy and the modification in replication of the centromeric DNA arrays. These findings indicate that the genotoxic effect of the electromagnetic radiation is elicited via a non-thermal pathway. Moreover, the fact that aneuploidy is a phenomenon known to increase the risk for cancer, should be taken into consideration in future evaluation of exposure guidelines.     

Temperature regulation following nickel intoxication in the mouse: effect of ambient temperature

1. The purpose of this study was to examine the interaction between ambient temperature (Ta) and the effects of nickel chloride on the thermoregulatory system of the mouse. 2. Male mice of the BALB/c strain were injected with nickel chloride at dosages of 0, 0.1, 1.0, 2.5, 5.0 and 10.0 mg/kg intraperitoneally and placed in an environmental chamber set at a Ta of either 10, 20, 30 or 35 degrees C for 60 min. Colonic temperature was then measured after one hour of exposure at a given Ta. 3. The thermoregulatory effects of nickel chloride were highly dependent on Ta. Nickel chloride had no effect on body temperature at Ta's of 30 and 35 degrees C. 4. 10 mg/kg dosage of nickel chloride caused a significant reduction in colonic temperature at a Ta of 20 degrees C. At a Ta of 10 degrees C the 5 and 10 mg/kg dosages of nickel chloride caused a significant lowering of body temperature. 5. Using segmented linear regression techniques it was shown that the threshold dose of nickel chloride for causing hypothermia was 9.6 and 3.3 mg/kg at Ta's of 20 and 10 degrees C, respectively. 6. This study has shown that two stressors, low Ta and nickel chloride intoxication, when applied independently have no effect on body temperature; however, when applied simultaneously, they have a significant toxic effect on thermoregulation.     

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.     

Effects of field orientation during 700-MHz radiofrequency irradiation of rats

Ketamine-anesthetized Sprague-Dawley rats were exposed to far-field 700-MHz continuous-wave radiofrequency radiation (RFR) in both E and H orientations. Irradiation was conducted at whole-body average specific absorption rates (SARs) of 9.2 and 13.0 W/kg (E and H, respectively) that resulted in approximately equivalent colonic specific heating rates (SHRs). Exposures were performed to repeatedly increase colonic temperature by 1 degree C (38.5 to 39.5 degrees C). Tympanic, tail, left and right subcutaneous (toward and away from RFR source), and colonic temperatures, arterial blood pressure, and respiratory rate were continuously recorded. In spite of equivalent colonic SHRs and the reduced E-orientation average SAR, the right subcutaneous, tympanic, and tail SARs, SHRs and absolute temperature increases were significantly greater in E than in H orientation. The cooling rate at all monitoring sites was also significantly greater in E than in H orientation. Heart rate and mean arterial blood pressure significantly increased during irradiation; however, changes between orientations were not different. Respiratory rate significantly increased during irradiation in H, but not in E orientation. These results indicate that during resonant frequency irradiation, differences occur in the pattern of heat deposition between E- and H-orientation exposure. When compared with previous investigations performed at supraresonant frequencies, the lower level of cardiovascular change in this study was probably related to the lower periphery-to-core thermal gradient.     

Thermophysiological consequences of whole body resonant RF exposure (100 MHz) in human volunteers

Thermophysiological responses of heat production and heat loss were measured in seven adult volunteers (six males and one female, aged 31-74 years) during 45 min dorsal exposures of the whole body to 100 MHz continuous wave (CW) radio frequency (RF) energy. Three power densities (PD) (average PD = 4, 6, and 8 mW/cm(2); whole body specific absorption rate [SAR] = 0.068 [W/kg]/[mW/cm(2)]) were tested in each of three ambient temperatures (T(a) = 24, 28, and 31 degrees C), as well as in T(a) controls (no RF). A standardized protocol (30 min baseline, 45 min RF or sham exposure, 10 min baseline) was used. Measured responses included esophageal and seven skin temperatures, metabolic heat production, local sweat rate, and local skin blood flow. No changes in metabolic heat production occurred under any test condition. Unlike published results of similar exposures at 450 and 2450 MHz, local skin temperatures, even those on the back that were irradiated directly, changed little or not at all during 100 MHz exposures. The sole exception was the temperature of the ankle skin, which increased by 3-4 degrees C in some subjects at PD = 8 mW/cm(2). During the 45 min RF exposure, esophageal temperature showed modest changes (range = -0.15 to 0.13 degrees C) and never exceeded 37.2 degrees C. Thermoregulation was principally controlled by appropriate increases in evaporative heat loss (sweating) and, to a lesser extent, by changes in skin blood flow. Because of the deep penetration of RF energy at this frequency, effectively bypassing the skin, these changes must have been stimulated by thermal receptors deep in the body rather than those located in the skin.