Increased serum enzyme activity in microwave-exposed rats

Heat stable serum enzymes were studied in rats exposed to microwaves (2.45 GHz, 120 Hz amplitude modulated) 24 hr after a single 4-hr exposure or immediately after 3 and 10 exposures to 0.1 to 55 mW/cm2. In addition, stable colonic temperature at 41.5 degrees C for 30 min was maintained by microwave exposure in a group of five rats under barbiturate anesthesia. Alkaline phosphatase and lactic dehydrogenase did not increase as a result of microwave exposure. Increased serum glutamic pyruvic transaminase (GPT) and glutamic oxaloacetic transaminase (GOT) were noted in the 41.5 degrees C group 24 hr after exposure. A threshold body temperature for acute cellular injury after microwave exposure was demonstrated. The acute cellular injury could be in the liver. These mild elevations in the serum enzyme levels (mean +/- SE, GOT = 167 +/- 40 U/liter: GPT = 74 +/- 26 U/liter) indicated that the injuries were not accompanied by any significant sequelae in the rat. From this threshold and colonic temperature (41.5 degrees C for 30 min) in barbiturate-anesthetized, microwave-exposed rats, we derived a tentative threshold for the whole-body average absorption rate at 14 W/kg (70 mW/cm2 at 2.45 GHz for adult rats) for 4 hr. This tentative threshold is subject to changes by duration of exposure and by compounding variables influencing maintenance of body temperature.     

Effects of microwaves on the adrenal cortex

Six-hundred-and-one male Long-Evans rats were used to study the effect of microwaves on adrenocortical secretion. Power density ranged from 0.1 to 55 mW/cm2 (SAR 0.02 to 11 W/kg). The microwave signal was 2.45 GHz amplitude modulated at 120 Hz. Serum corticosterone (CS) concentration was used as an index of adrenocortical function. Ten different exposure protocols were used to identify confounding factors influencing the sensitivity of adrenal cortex to microwave exposure. Increases in CS concentration were proportional to power density or colonic temperature and inversely proportional to the baseline CS. Increased CS concentration was never observed without increased colonic temperature and was not persistent 24 h after exposure. Acclimation (reduction in magnitude of response) could be noted after the tenth exposure. Facilitated heat loss attenuated the magnitude of CS increases by limiting the degree of hyperthermia. Ethanol enhanced the hyperthermic response and desensitized the adrenal response to microwave hyperthermia by increased baseline CS. Ether stimulated adrenal secretion irrespective of previous microwave exposure or adrenal stimulation induced by microwaves. Minor inhibition was also noted occasionally as decreased CS concentration at lower intensity (less than 20 mW/cm2) and decreased postexposure urinary CS excretion at 40 mW/cm2. Adrenal stimulation required minimally a 20 mW/cm2 (4 W/kg) or 0.7 degrees C increase in colonic temperature. An SAR lower than 4 W/kg may stimulate adrenal secretion by potentiating the hyperthermic effect if the ambient temperature is well above 24 degrees C.     

Serum-thyroxine levels in microwave-exposed rats

The nature of the response of the thyroid gland in animals exposed to microwave irradiation is controversial. An enlarged thyroid and an increase of radioiodine uptake in microwave workers have been reported. Absence of thyroid disorders has also been reported in other exposed populations. Animal experimentation has contributed to the controversy because both increased and decreased thyroid functions have been reported. The thyroxine concentration in rats as representative of thyroid function in animals exposed to 2.45-GHz, 120-Hz amplitude-modulated microwaves has been studied. Comparison was made between thyroxine concentrations in microwave- and sham-exposed rats by Student's t test. After a 1-hr exposure, an increased thyroxine concentration was found in rats exposed at 40 and 70 mW/cm2, but not at 1, 5, 10, 20, 50, or 60 mW/cm2. After a 2-hr exposure, increased thyroxine concentration was noted in rats exposed at 25, 30, and 40 mW/cm2, but not at 1, 5, 10, and 20 mW/cm2. After a 4-hr exposure, thyroxine concentration increased in rats exposed at 1 mW/cm2 and decreased in rats exposed at 20 mW/cm2; but changes were not noted at 5 or 10 mW/cm2. Other experiments included animals that were exposed once for 4 hr (0.1, 1, 10, 25, and 40 mW/cm2), sampled 24 hr after a 4-hr exposure (0.1, 1, 10, 25, and 40 mW/cm2), or exposed for 4 hr 3 times (1, 10, 20, 30, 40, and 55 mW/cm2) and 10 times (1, 10, 20, 25, 30, and 40 mW/cm2), to evaluate the consistency of the thyroxine response. None of the rats in these experiments displayed any alteration of thyroxine concentration, except that decreased thyroxine was noted in rats exposed at 40 mW/cm2 for the third time. These studies covered a long time span; rats from two commercial sources (BS and CR) were used and subjected to different numbers of exposures, and therefore these data were evaluated for their stability. Two factors could influence the result significantly, i.e., source of animal and number of sham exposures. Rats used in the 2-hr exposures were from two different commercial sources; rats from CR had a higher (but normal) thyroxine concentration than did rats from BS. Therefore the data of these animals were separated by commercial source for reevaluation. Instead of increased thyroxine concentration in rats exposed at 25, 30, and 40 mW/cm2, changes were not noted in any microwave-exposed rats. The influence of sham exposure revealed that appropriate concurrent control and specification of animal source are needed in longitudinal studies.(ABSTRACT TRUNCATED AT 400 WORDS)     

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.     

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.     

Glutathione concentration and peptidase activity in the lens after exposure to microwaves

This study was undertaken for observation of early changes in glutathione concentration and the activity of carboxypeptidase A and aminopeptidase in the cortex and core of the lens as well as for determination of the cumulating effect of microwave energy after repeated exposures to microwaves. Experiments were carried out on New Zealand rabbits. The control group was compared to experimental groups exposed every day for 5 minutes to microwave irradiation of the eyeballs at power densities of 5 X 10(-3) W/cm2 and 10 X 10(-3) W/cm2 during 10, 20 and 30 days. Differences were found between the control group and the groups of animals exposed to microwaves in which the glutathione concentration in the cortex and core of the lens was decreasing with time in proportion to the number of exposures. Parallelly to the number of days of exposure to microwaves the enzymatic activity of carboxypeptidase A and aminopeptidase increased in the cortex of the lens. The observed changes demonstrate cumulation of the absorbed microwave energy leading to changes in the permeability of the capsule and membranes of lenticular fibres which lead to secondary metabolic disturbances in the lens of the eye.     

Thermal and metabolic responsiveness of Japanese quail embryos following periodic exposure to 2,450 MHz microwaves

Two studies were performed to determine if repeated exposure of the avian egg to microwaves can alter metabolism, temperature, and growth rate of embryos. Another aim was to supplement conventional heating with microwave heating and provide an optimal temperature for growth. Japanese quail (Coturnix coturnix japonica) eggs were exposed from day 1 through 15 of incubation (8 h/day) to sham or microwave (2,450 MHz) irradiation. Microwave exposures were at two power densities, 5 or 20 mW/cm2, and at three ambient temperatures (Tas), 30.0, 33.1, or 35.4 degrees C. Specific absorption rates for unincubated and 15-day-old incubated eggs were, respectively, 0.76 and 0.66 W kg-1 mW-1 cm-2 (i.e., 3.8 and 3.3 W/kg at 5 mW/cm2 and 15.2 and 13.2 W/kg at 20 mW/cm2). Eggs were concurrently sham exposed at each of five Tas, ranging from 27.9 to 37.5 degrees C. Tests were conducted during the 16th day of incubation (i.e., 1 day post-treatment), in the absence of microwaves, to determine metabolic rate of embryos and internal and external egg temperatures at different Tas. Repeated exposures to microwaves at 5 and 20 mW/cm2 at the same Ta (30 degrees C) increased wet-embryo mass on the 16th day by an average, respectively, of 9% and 61% when compared with predicted masses for embryos exposed at the same Ta in the absence of microwave radiation. There was no reliable indication, from post-treatment tests and comparisons with control embryos of similar mass, that repeated exposure to microwave radiation resulted in abnormal physiological development. Microwave radiation can be used to increase egg temperature and embryonic growth rate at Tas below normal incubation level without altering basic metabolic and thermal characteristics of the developing bird.     

Effects of microwaves on three different strains of rats

Confounding factors influencing the sensitivity of biological indicators of microwave exposure--lethality, colonic temperature (Tco), decreased body mass (dW), corticosterone (CS), thyrotropin (TSH), thyroxine (T4), free thyroxine (FT4), and prolactin (PRL) concentration--were studied in Long-Evans (LE), Wistar-Kyoto (WKY), and spontaneous hypertensive (SHR) rats. The microwave signal was 2.45 GHz amplitude modulated at 120 Hz. Test power density ranged from 1 to 50 mW/cm2 for 2 h. In contrast to the LE and WKY rats, the SHR rats were characterized by intolerance (death) between 40 and 50 mW/cm2 (9.2 to 11.5 W/kg). The lowest lethal Tco was 41.1 degrees C. Survivors including all the LE and WKY rats were capable of maintaining Tco lower than 41.0 degrees C. In general, strain of rat seemed to influence other bioindicators and to interact with power density on these bioindicators. Except for Tco and PRL, baseline for the various bioindicators varied among the different strains of rats. Responses of T4 and FT4 were limited in magnitude and inconsistent among strains of rats. In general, the magnitude of Tco increase was more pronounced in SHR than in WKY. Differences between SHR and LE, however, could be noted only at 1, 10, and 50 mW/cm2. Increased Tco, increased magnitude of Dw, increased CS, decreased TSH, and increased PRL (stress reactions) could be noted in rats exposed to 30 mW/cm2 (approximately 6 W/kg) or higher, irrespective of strain. At least two of three strains of rats (WKY and SHR) exposed to 20 mW/cm2 (approximately 4 W/kg) showed changes in Tco, CS, TSH, and PRL. At 10 mW/cm2 (2 W/kg), increased Tco could be found in all three strains of rats accompanied by changes in dW and TSH in LE, TSH in WKY, and dW and CS in SHR. At 1 mW/cm2 (0.2 W/kg), increased Tco could be noted in two of three strains (LE and SHR) and increased PRL in LE only. The smallest Tco increases for a consistent response (increased magnitude of response with power density) were 1.59 degrees C for dW, 0.70 degrees C for CS, 0.24 degrees C for TSH, and 0.97 degrees C for PRL. Tentatively, the threshold intensity for response to microwave exposure for rats could be considered as 2 W/kg or a 0.24 degrees C increase at 24 degrees C ambient temperature.     

The effect of pulsed cyclical microware radiation on the conditioned behavior of rats

Research has been carried out to investigate the effects of pulsed cyclical microware exposure (7 GHz, 400 pps, 100 mcs, 10-20 mW/cm2, 10 or 20 cycles of "5 min exposure--4 min pause") on avoidance learning of rats. It was shown that reductions in conditioned behavior after cyclical pulsed microware exposure occurred at an SAR of 2.1 W/kg (10 mW/cm2). It was found the cumulation of the effects of the cycles at prolonged cyclical microwave exposures.     

Microwave effects on energy metabolism of rat brain

Rat brain was exposed to 591-MHz, continuous-wave (CW) microwaves at 13.8 or 5.0 mW/cm² to determine the effect on nicotinamide adenine dinucleotide, reduced (NADH), adenosine triphosphate (ATP) and creatine phosphate (CP) levels. On initiation of the in vivo microwave exposures, fluorimetrically determined NADH rapidly increased to a maximum of 4.0%–12.5% above pre-exposure control levels at one-half minute, then decreased slowly to 2% above control at three minutes, finally increasing slowly to 5% above control level at five minutes. ATP and CP assays were performed on sham- and microwave-exposed brain at each exposure time. At 13.8 mW/cm², brain CP level was decreased an average of 39.4%, 41.1%, 18.2%, 13.1%, and 36.4% of control at exposure points one-half, one, two three, and five minutes, respectively, and brain ATP concentration was decreased an average of 25.2%, 15.2%, 17.8%, 7.4%, and 11.2% of control at the corresponding exposure periods. ATP and CP levels of rat brain exposed to 591-MHz cw microwaves at 5 mW/cm² for one-half and one minute were decreased significantly below control levels at these exposure times, but were not significantly different from the 13.8 mW/cm² exposures. For all exposures, rectal temperature remained constant. Heat loss through the skull aperture caused brain temperature to decrease during the five-minute exposures. This decrease was the same in magnitude for experimental and control subjects. Changes in NADH, ATP, and CP levels during microwave exposure cannot be attributed to general tissue hyperthermia. The data support the hypothesis that microwave exposure inhibits mitochondrial electron transport chain function, which results in decreased ATP and CP levels in brain.     

Physiological changes in rats after exposure to low levels of microwaves

The effects of exposure to sublethal levels of microwaves were studied. Young albino rats of both sexes were exposed for 60 days to 7.5-GHz microwaves (1.0-KHz square wave modulation, average power 0.6 mW/cm2) for 3 h daily. During and after microwave exposure several physiological parameters were measured in both control and exposed animals. It was found that the animals exposed to microwaves tended to eat and drink less and thus showed a smaller gain in body weight. Some of the hematological parameters and organ weights were also significantly different. It is proposed that a nonspecific stress response due to microwave exposure and mediated through the central nervous system is responsible for the observed physiological changes.     

Hematologic and immunologic effects of pulsed microwaves in mice

Mice were exposed in the far field in an anechoic chamber to 2,880-MHz pulsed microwaves 3 to 7.5 h daily, 5 days/week for 60 to 360 h. Three experiments were performed at average power densities of 5 mW/cm2 and six at 10 mW/cm2, corresponding to averaged specific absorption rates (SARs) of 2.25 and 4.50 mW/g, respectively. Each experiment consisted of eight mice, with a concurrently sham-exposed group of eight. In two of three studies at 5 mW/cm2, there was a significant increase in bone marrow cellularity in the microwave-exposed groups compared to the sham-exposed groups. Significant differences were occasionally seen in erythrocyte, leukocyte, and platelet values from microwave-exposed groups, but were not consistently observed. In one of six groups exposed at 10 mW/cm2, mean bone marrow cellularity was reduced significantly in the microwave-exposed mice; in another group, the lymphocyte count was increased. In only one exposure (10 mW/cm2 for 360 h) was any significant effect noted on serum proteins: a reduction to 5.1 +/- 0.3 g/dl in the exposed versus 5.6 +/- 0.4 g/dl in the sham-exposed mice. This was due to a decrease in alpha and beta globulins, with no effect on albumin or gamma globulin concentrations. No effect on bone marrow granulocyte/macrophage colony-forming units (CFU) was revealed following exposure of mice to pulsed microwaves at 5 mW/cm2. In one of four exposures at 10 mW/cm2, there was a significant increase in CFU-agar colonies. No significant effects of exposures at 10 mW/cm2 were observed on in vivo and in vitro assays of cell-mediated immune functions. No exposure-related histopathologic lesions were found from examination of several tissues and organs. Results of these series of exposures of mice at SARs of 2.25 and 4.50 mW/g indicated no consistent effects on the hematologic, immunologic, or histopathologic variables examined.     

Naltrexone pretreatment blocks microwave-induced changes in central cholinergic receptors

Repeated exposure of rats to pulsed, circularly polarized microwaves (2,450-MHz, 2-microseconds pulses at 500 pps, power density 1 mW/cm2, at an averaged, whole-body SAR of 0.6 W/kg) induced biphasic changes in the concentration of muscarinic cholinergic receptors in the central nervous system. An increase in receptor concentration occurred in the hippocampus of rats subjected to ten 45-min sessions of microwave exposure, whereas a decrease in concentration was observed in the frontal cortex and hippocampus of rats exposed to ten 20-min sessions. These findings, which confirm earlier work in the authors' laboratory, were extended to include pretreatment of rats with the narcotic antagonist naltrexone (1 mg/kg, IP) before each session of exposure. The drug treatment blocked the microwave-induced changes in cholinergic receptors in the brain. These data further support the authors' hypothesis that endogenous opioids play a role in the effects of microwaves on central cholinergic systems.     

Low intensity microwave radiation effects on the ultrastructure of Chang liver cells

Chang liver cells (CCL-13 ATCC) exposed to 2450 MHz microwaves of field intensities ranging from 5 to 20 mW/cm2 for different periods up to 2 h show distinct alterations in the cytomembrane ultrastructure. A 30-min exposure of 10 mW/cm2 produces well-defined cytoplasmic lesions which appear as clear areas of degenerated rough endoplasmic reticulum (RER). Extensive degeneration of RER along with fragmentation and vacuolation, disorganization of mitochondrial membranes and matrix, increased lysosomal activity, and in some cases disruptions of nuclear membrane are seen in longer exposures. Radiation at 20 mW/cm2 produces significant damage to cell membranes in short exposures and treatments of 30 min and longer exposures lead to total disruption of organized cell ultrastructure. The identity of many organelles is lost as the cells become highly heteropycnotic with numerous cytoplasmic projections. Short exposures of 5 mW/cm2 produce very few noticeable differences in ultrastructure. These results confirm earlier observations that membranes may be the primary targets of microwave radiation in cells.     

Thermoregulatory consequences of long-term microwave exposure at controlled ambient temperatures

This study was designed to identify and measure changes in thermoregulatory responses, both behavioral and physiological, that may occur when squirrel monkeys are exposed to 2450-MHz continuous wave microwaves 40 hr/week for 15 weeks. Power densities of 1 or 5 mW/cm2 (specific absorption rate = 0.16 W/kg per mW/cm2) were presented at controlled environmental temperatures of 25, 30, or 35 degrees C. Standardized tests, conducted periodically, before, during, and after treatment, assessed changes in thermoregulatory responses. Dependent variables that were measured included body mass, certain blood properties, metabolic heat production, sweating, skin temperatures, deep body temperature, and behavioral responses by which the monkeys selected a preferred environmental temperature. Results showed no reliable alteration of metabolic rate, internal body temperature, blood indices, or thermoregulatory behavior by microwave exposure, although the ambient temperature prevailing during chronic exposure could exert an effect. An increase in sweating rate occurred in the 35 degrees C environment, but sweating was not reliably enhanced by microwave exposure. Skin temperature, reflecting vasomotor state, was reliably influenced by both ambient temperature and microwaves. The most robust consequence of microwave exposure was a reduction in body mass, which appeared to be a function of microwave power density.     

Hyperthermia in radiofrequency-exposed rhesus monkeys: a comparison of frequency and orientation effects

To compare the effects of exposure to a near-resonant frequency of microwaves at two orientations with a higher frequency exposure, five rhesus monkeys were exposed for 4 hr to 225 MHz, electric field oriented parallel to the long axis of the body (225 MHz-E), and to 225 MHz, magnetic field orientation (225 MHz-H), or to 1290 MHz, electric field orientation. On a separate occasion, the monkeys were exposed at night to 225 MHz-E. Exposures were conducted with the animal chair restrained in an anechoic chamber with rectal temperature continuously monitored. Blood samples were taken hourly during the 225-MHz-E exposures for cortisol analysis. The power densities used were 0, 1.2, 2.5, 5.0, 7.5, 10.0, and 15.0 mW/cm2 for 225 MHz-E (day), 0 and 5 mW/cm2 (225 MHz-E night and 225 MHz-H), and 0, 20, 28, and 38 mW/cm2 (1290 MHz). The monkeys were unable to tolerate exposure at power densities equal to or greater than 7.5 mW/cm2 (5.1 W/kg) at 225 MHz-E for longer than 90 min. The criterion for tolerance was that the rectal temperature would not exceed 41.5 degrees C. Average rectal temperature increases for day exposure to 225 MHz-E were 0.4 and 1.7 degrees C for 4-hr exposures to 2.5 and 5.0 mW/cm2 (1.7 and 3.4 W/kg). No changes in circulating cortisol levels occurred during any exposures to 5 mW/cm2 or less. Night exposures to 5 mW/cm2 (3.4 W/kg) at 225 MHz-E raised mean rectal temperature 2.1 degrees C. Exposure to 5 mW/cm2 (1.2 W/kg) at 225 MHz-H for 4 hr resulted in a 0.2 degree rise in mean rectal temperature. For 4 hr of 1290-MHz exposure to 20, 28, or 38 mW/cm2 (2.9, 4.0, and 5.4 W/kg), the mean body temperature increases were 0.4, 0.7, and 1.3 degrees C, respectively. The degree of hyperthermia caused by radiofrequency (rf) exposure was shown to be frequency and orientation dependent for equivalent power densities of exposure.     

Teratogenic, biochemical, and histological studies with mice prenatally exposed to 2.45-GHz microwave radiation

Pregnant CD-1 mice were exposed to 2.45-GHz continuous wave microwave radiation at an incident power density of 30 mW/cm2. The local specific absorption rate near the uterine area (deep colonic location), as determined from time-temperature profiles measured with a Vitek thermistor probe, was 40.2 mW/g. Groups of mice were exposed 8 hr per day through Days 1-6 or 6-15 of pregnancy. Other groups of animals were exposed to an elevated ambient temperature of 31 degrees C which increased the colonic temperature 2.3 degrees C, the same as that produced by the microwaves. Sham-irradiated groups of animals were treated exactly the same as the microwave-exposed animals. For the two conditions, temperature exposed and sham exposed, two groups of animals were used. One group was handled in the same manner as the microwave-irradiated group and the other group was not handled so as to evaluate the effects of stressing the animals by handling. Eleven groups of animals were used in the complete study: five groups for gestational Days 1-6, five groups for gestational Days 6-15, and one group of cage control animals. On Day 18 of gestation the dams of all experimental groups were sacrificed and their reproductive status was determined. The fetuses were examined for visceral and skeletal alterations. Brain cholinesterase activity and histology were evaluated in the groups exposed on Days 6-15. The results show that microwave radiation increases embryo lethality at the early stages of gestation (exposure Days 1-6). Fetal toxicity and teratogenicity were not significantly increased by exposure to microwaves on either Days 1-6 or 6-15 of gestation. Cholinesterase activity and histology of the brain of 18-day-old fetuses were not adversely affected.     

Effects of acute low-level microwaves on pentobarbital-induced hypothermia depend on exposure orientation

Two series of experiments were performed to study the effects of acute exposure (45 min) to 2,450-MHz circularly polarized, pulsed microwaves [1 mW/cm², 2-μs pulses, 500 pps, specific absorption rate (SAR) 0.6 W/kg] on the actions of pentobarbital in the rat. In the first experiment, rats were irradiated with microwaves and then immediately injected with pentobarbital. Microwave exposure did not significantly affect the extent of the pentobarbital-induced fall in colonic temperature. However, the rate of recovery from the hypothermia was significantly slower in the microwave-irradiated rats and they also took a significantly longer time to regain their righting reflex. In a second experiment, rats were first anesthetized with pentobarbital and then exposed to microwaves with their heads either pointing toward the source of microwaves (anterior exposure) or pointing away (posterior exposure). Microwave radiation significantly retarded the pentobarbital-induced fall in colonic temperature regardless of the orientation of exposure. However, the recovery from hypothermia was significantly faster in posterior-exposed animals compared to those of the anterior-exposed and sham-irradiated animals. Furthermore, the posterior-exposed rats took a significantly shorter time to regain their righting reflex than both the anterior-exposed and sham-irradiated animals.     

Effects of continuous-wave, pulsed, and sinusoidal-amplitude-modulated microwaves on brain energy metabolism

A comparison of the effects of continuous-wave, sinusoidal-amplitude-modulated, and pulsed square-wave-modulated 591-MHz microwave exposures on brain energy metabolism was made in male Sprague-Dawley rats (175-225 g). Brain NADH fluorescence, adenosine triphosphate (ATP) concentration, and creatine phosphate (CP) concentration were determined as a function of modulation frequency. Brain temperatures of animals were maintained between -0.1 and -0.4 degrees C from the preexposure temperature when subjected to as much as 20 mW/cm2 (average power) CW, pulsed, or sinusoidal-amplitude modulated 591-MHz radiation for 5 min. Sinusoidal-amplitude-modulated exposures at 16-24 Hz showed a trend toward preferential modulation frequency response in inducing an increase in brain NADH fluorescence. The pulse-modulated and sinusoidal-amplitude-modulated (16 Hz) microwaves were not significantly different from CW exposures in inducing increased brain NADH fluorescence and decreased ATP and CP concentrations. When the pulse-modulation frequency was decreased from 500 to 250 pulses per second the average incident power density threshold for inducing an increase in brain NADH fluorescence increased by a factor of 4--ie, from about 0.45 to about 1.85 mW/cm2. Since brain temperature did not increase, the microwave-induced increase in brain NADH and decrease in ATP and CP concentrations was not due to hyperthermia. This suggests a direct interaction mechanism and is consistent with the hypothesis of microwave inhibition of mitochondrial electron transport chain function of ATP production.     

Thermal effects of 2.45 GHz microwaves on survival and viability of Chinese hamster V-79 cells

The possible existence of thermal effects specific to microwaves at 2.45 GHz and not found with classical heating in a waterbath was studied by measuring cell survival (colony-forming ability) and cell viability (the ability to exclude trypan blue) in Chinese hamster V79 cells. The microwaves were employed at high power densities (125 to 175 mW/cm2) corresponding to specific absorption rates ranging between 62 and 87 mW/g. When matching the rises in temperature, the effects of microwave-induced hyperthermia at 125 mW/cm2 on cell survival were comparable to those of classical heating. However, they were statistically significantly different when using power densities of 150 and 175 mW/cm2. The response obtained in terms of cell viability appeared to be comparable. The conclusions are also valid when taking into account a correction factor for energy losses during microwave treatment. The apparent specific effect of microwaves appears to be associated with exposures at high power densities involving short treatment times and rapid rises in temperature.