Growth and development of mice offspring after irradiation in utero with 2,450-MHz microwaves

Mice offspring irradiated in utero with 2,450-MHz radio-frequency (RF) radiation at 0 or 28 mW/cm2 (whole-body averaged specific absorption rate = 0 or 16.5 W/kg) for 100 minutes daily on days 6 through 17 of gestation were evaluated for maturation and development on days 1, 5, 10, 12, 15, and 17 of age. The tests used to determine differences in developmental age in the two treatment groups were body weight, urine concentrating ability, brain weight, tolerance to ouabain, and bone lengths. Fifteen sham-irradiated and 26 RF-irradiated litters, normalized to eight pups/litter, were used in this study. Mean body weight of the microwave-irradiated offspring were significantly (p = .0003) decreased only on day 1 of age. Brain weight on days 10, 12, and 17 were significantly lower in microwave-irradiated pups (p = .01). There were no significant differences in the two groups in urine concentrating ability on day 5, ouabain tolerance on day 15, or bone length on days 5, 10, 12, and 17. It is concluded that there is a persistent delay in postnatal development of the brain after RF irradiation with 16.5 W/kg during gestation.     

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.     

Interaction of ethanol and microwaves on the blood-brain barrier of rats

The combined effects of ethanol and microwaves on the permeation of Evans blue dye through the mammalian blood-brain barrier was studied in male Wistar rats. Anesthetized rats were infused through a cannula in the left femoral vein with 0.1, 0.3, 0.5 or 0.7 grams of absolute ethanol per kilogram of body mass. A control group was given 0.7 g/kg of isotonic saline. The left hemisphere of the brain was irradiated by 3.15-GHz microwave energy at 3.0 W/cm2 rms for 15 min. The rat's rectal temperature was maintained at 37.0 degrees C. Immediately after irradiation, 2% Evans blue dye in saline (2.0 ml/kg body mass) was injected through the cannula. The results show that as the quantity of alcohol was increased, the degree of staining was decreased or eliminated. The temperature of the irradiated area of the brain increased for the first 4 to 5 minutes of irradiation and then stabilized for the remainder of the irradiation period. The steady-state temperature was highest in animals receiving saline or the smallest dose of alcohol. As the quantity of alcohol was increased, the steady-state temperature was reduced. These results indicate that ethanol inhibits microwave-induced permeation of the blood-brain barrier through reduced heating of the brain.     

Absorption of microwave radiation by the anesthetized rat: electromagnetic and thermal hotspots in body and tail

Anatomic variability in the deposition of radiofrequency electromagnetic energy in mammals has been well documented. A recent study [D'Andrea et al., 1985] reported specific absorption rate (SAR) hotspots in the brain, rectum and tail of rat carcasses exposed to 360- and to 2,450-MHz microwave radiation. Regions of intense energy absorption are generally thought to be of little consequence when predicting thermal effects of microwave irradiation because it is presumed that heat transfer via the circulatory system promptly redistributes localized heat to equilibrate tissue temperature within the body. Experiments on anesthetized, male Long-Evans rats (200-260 g) irradiated for 10 or 16 min with 2,450, 700, or 360 MHz radiation at SARs of 2 W/kg, 6 W/kg, or 10 W/kg indicated that postirradiation localized temperatures in regions previously shown to exhibit high SARs were appreciably above temperatures at body sites with lower SARs. The postirradiation temperatures in the rectum and tail were significantly higher in rats irradiated at 360 MHz and higher in the tail at 2,450 MHz than temperatures resulting from exposure to 700 MHz. This effect was found for whole-body-averaged SARs as low as 6 W/kg at 360 MHz and 10 W/kg at 2,450 MHz. In contrast, brain temperatures in the anesthetized rats were not different from those measured in the rest of the body following microwave exposure.     

Inhibition of Brain Glutamate Decarboxylase Activity Is Related to Febrile Seizures in Rat Pups

Because previous work showed that in the newborn brain, but not in the adult brain, glutamate decarboxylase (GAD) is notably susceptible to heat, we have studied the possible involvement of GAD inhibition in febrile convulsions and the related changes in gamma-aminobutyric acid (GABA) content. Rats of different ages were subjected to hyperthermia, and GAD activity was determined in brain homogenates by measuring the release of 14CO2 from labeled glutamate and by measuring the formation of GABA. The latter method gave considerably lower values than the former in the youngest rats, and was considered more reliable. With this method, we found a 37-48% inhibition of GAD activity in rat pups 2-5 days old, which showed febrile seizures at progressively higher body temperatures, whereas in 10- and 15-day-old animals, which did not show convulsions, GAD activity was not affected by hyperthermia. Whole-brain GABA levels, however, did not change at any age. In contrast to GAD, choline acetyltransferase and lactic dehydrogenase activities were not altered by hyperthermia at any of the ages studied. These results suggest that a decreased efficiency of the inhibitory neurotransmission mediated by GABA, consequent to the inhibition of GAD activity, may be a factor related to febrile convulsions.     

1439 MHz pulsed TDMA fields affect performance of rats in a T-maze task only when body temperature is elevated

This study sought to clarify the effects of exposure to electromagnetic waves (EMW) used in cellular phones on learning and memory processes. Sprague-Dawley rats were exposed for either 1 h daily for 4 days or for 4 weeks to a pulsed 1439 MHz time division multiple access (TDMA) field in a carousel type exposure system. At the brain, average specific absorption rate (SAR) was 7.5 W/kg, and the whole body average SAR was 1.7 W/kg. Other subjects were exposed at the brain average SAR of 25 W/kg and the whole body average SAR of 5.7 W/kg for 45 min daily for 4 days. Learning and memory were evaluated by reversal learning in a food rewarded T-maze, in which rats learned the location of food (right or left) by using environmental cues. The animals exposed to EMW with the brain average SAR of 25 W/kg for 4 days showed statistically significant decreases in the transition in number of correct choices in the reversal task, compared to sham exposed or cage control animals. However, rats exposed to the brain average SAR of 7.5 W/kg for either 4 days or for 4 weeks showed no T-maze performance impairments. Intraperitoneal temperatures, as measured by a fiber optic thermometer, increased in the rats exposed to the brain average SAR of 25 W/kg but remained the same for the brain average SAR of 7.5 W/kg. The SAR of a standard cellular phone is restricted to a maximum of 2 W/kg averaged over 10 g tissue. These results suggest that the exposure to a TDMA field at levels about four times stronger than emitted by cellular phones does not affect the learning and memory processes when there are no thermal effects.     

Monosodium L-glutamate-induced convulsions: temporary alteration in blood-brain barrier permeability to plasma proteins.

Monosodium L-glutamate (MSG), a commonly used food additive, induces convulsive disorders in rats. A reversible change in the cerebrovascular permeability of plasma proteins occurs during convulsions induced by the intraperitoneal administration of 4.0 g/kg of MSG to the neonatal rat. During MSG-induced seizures, but not before or after, trypan blue dye enters into the brain tissues, whereas no dye penetration occurs in control rats receiving saline. The frequency of the incidence of MSG-induced convulsions is inversely proportional to the age of the animal. It decreases with the age of the rat. By 42 days of age no substantial seizure activity of dye penetration into the brain tissue occurs in MSG-treated rats. Histological examination indicates that seizure activity is not correlated with characteristic periventricular-arcuate area lesions known to be induced in neonates by parenteral MSG administration. No hypothalamic damage was observed in MSG-treated rats older than 10 days of age.     

Regional brain heating during microwave exposure (2.06 GHz), warm-water immersion,environmental heating and exercise

Nonuniform heating may result from microwave (MW) irradiation of tissues and is therefore important to investigate in terms of health and safety issues. Hypothalamic (T_hyp), cortical (T_ctx), tympanic (T_ty), and rectal (T_re) temperatures were measured in rats exposed in the far field, k-polarization (i.e., head pointed toward the transmitter horn and E-field in vertical direction) to two power densities of 2.06 GHz irradiation. The high-power density (HPM) was 1700 mW/cm² [specific absorption rate (SAR): hypothalamus 1224 W/kg; cortex 493 W/kg]; the low-power density (LPM) was 170 mW/cm² (SAR: hypothalamus 122.4 W/kg; cortex 49.3 W/kg). The increase (rate-of-rise, in °C/s) in T_hyp was significantly greater than those in T_ctx or T_re when rats were exposed to HPM. LPM produced more homogeneous heating. Quantitatively similar results were observed whether rats were implanted with probes in two brain sites or a single probe in one or the other of the two sites. The qualitative difference between regional brain heating was maintained during unrestrained exposure to HPM in the h-polarization (i.e., body parallel to magnetic field). To compare the temperature changes during MW irradiation with those produced by other modalities of heating, rats were immersed in warm water (44 °C, WWI); exposed to a warm ambient environment (50 °C, WSED); or exercised on a treadmill (17 m/min 8% grade) in a warm ambient environment (35 °C, WEX). WWI produced uniform heating in the regions measured. Similar rates-of-rise occurred among regions following WSED or WEX, thus maintaining the pre-existing gradient between T_hyp and T_ctx. These data indicate that HPM produced a 2–2.5-fold difference in the rate-of-heating within brain regions that were separated by only a few millimeters. In contrast, more homogeneous heating was recorded during LPM or nonmicrowave modalities of heating. Bioelectromagnetics 19:341–353, 1998. © 1998 Wiley-Liss, Inc.     

Failure of phenobarbitone to prevent febrile convulsions.

One-hundred-sixty-five children without known neurological disorder who presented with their first febrile convulsion between the ages of six months and three years were assigned to daily phenobarbitone treatment or to a control group and followed up at a special clinic for six months. One-hundred-and-sixty-one-one children completed the trial, and of the 88 children assigned to phenobarbitone treatment 10 had further convulsions during this period compared with 14 of the 73 control children. Only 49 of those assigned to phenobarbitone took the drug regularly throughout the trial, and four of these had further febrile convulsions, a proportion not significantly different from that in the controls. All four had mean plasma phenobarbitone concentrations over 69 mumol/l (16 mug/ml) during the trial and in three the plasma concentration was at or over this figure within eight hours over 69 mumol/l (16 mug/ml) during the trial and in three the plasma concentration was at or over this figure within eight hours of the repeat convulsion. Regular phenobarbitone does not seem to prevent febrile convulsions. Attention should instead be directed to organising emergency services to allow early termination of fevrile convulsions, whether first or subsequent, to prevent irreversible brain damage.     

The effects of 860 MHz radiofrequency radiation on the induction or promotion of brain tumors and other neoplasms in rats

Sprague-Dawley rats were irradiated with a continuous- wave (CW) or a pulsed-wave (P) radiofrequency (RF) for 6 h/day, 5 days/week from 2 up to 24 months of age. The RFs emanated from dipole antennas (1 W average output) 2.0 +/- 0.5 cm from the tip of each rat's nose. The RFs had an 860 MHz frequency, and the specific absorption rate was 1.0 W/ kg averaged over the brain. Fifteen groups of 60 rats (900 total) were formed from offspring of females injected i.v. with 0 (groups 1, 2, 9, 10, 13), 2.5 (groups 5, 6, 7, 8, 11, 12, 14) or 10 mg/kg (groups 3, 4, 15) ethylnitrosourea (ENU) to induce brain tumors. Groups 1, 3, 5 and 7 received the PRF, and groups 9 and 11 the CWRF; groups 2, 4, 6, 8, 10 and 12 were sham-irradiated, and groups 13-15 were cage controls. All rats but 2, totaling 898, were necropsied, and major tissues were studied histopathologically. There was no statistically significant evidence that the PRF or CWRF induced neoplasia in any tissues. Additionally, there was no significant evidence of promotion of cranial or spinal nerve or spinal cord tumors. The PRF or CWRF had no statistically significant effect on the number, volume, location, multiplicity, histological type, malignancy or fatality of brain tumors. There was a trend for the group that received a high dose of ENU and was exposed to the PRF to develop fatal brain tumors at a higher rate than its sham group; however, the result was not significant using the log-rank test (P = 0.14, 2-tailed). No statistically significant differences were related to the PRF or CWRF compared to controls in the low- or zero-dose groups regarding tumors of any kind.     

Genotoxic potential of 1.6 GHz wireless communication signal: in vivo two-year bioassay

Timed-pregnant Fischer 344 rats (from nineteenth day of gestation) and their nursing offspring (until weaning) were exposed to a far-field 1.6 GHz Iridium wireless communication signal for 2 h/day, 7 days/week. Far-field whole-body exposures were conducted with a field intensity of 0.43 mW/cm(2) and whole-body average specific absorption rate (SAR) of 0.036 to 0.077 W/kg (0.10 to 0.22 W/kg in the brain). This was followed by chronic, head-only exposures of male and female offspring to a near-field 1.6 GHz signal for 2 h/day, 5 days/week, over 2 years. Near-field exposures were conducted at an SAR of 0.16 or 1.6 W/kg in the brain. Concurrent sham-exposed and cage control rats were also included in the study. At the end of 2 years, all rats were necropsied. Bone marrow smears were examined for the extent of genotoxicity, assessed from the presence of micronuclei in polychromatic erythrocytes. The results indicated that the incidence of micronuclei/2000 polychromatic erythrocytes were not significantly different between 1.6 GHz-exposed, sham-exposed and cage control rats. The group mean frequencies were 5.6 +/- 1.8 (130 rats exposed to 1.6 GHz at 0.16 W/kg SAR), 5.4 +/- 1.5 (135 rats exposed to 1.6 GHz at 1.6 W/kg SAR), 5.6 +/- 1.7 (119 sham-exposed rats), and 5.8 +/- 1.8 (100 cage control rats). In contrast, positive control rats treated with mitomycin C exhibited significantly elevated incidence of micronuclei/2000 polychromatic erythrocytes in bone marrow cells; the mean frequency was 38.2 +/- 7.0 (five rats). Thus there was no evidence for excess genotoxicity in rats that were chronically exposed to 1.6 GHz compared to sham-exposed and cage controls.     

Systems for exposing mice to 2,450-MHz electromagnetic fields

Two systems for exposing mice to 2,450-MHz electromagnetic fields are described. In a waveguide system, four mice were placed in a Styrofoam cage and exposed dorsally to circularly polarized electromagnetic fields. The temperature and humidity in the mouse holder were kept constant by forced-air ventilation. For 1-W input power to the waveguide, the average specific absorption rate (SAR) was determined by twin-well calorimetry to be 3.60 ± 0.11 (SE) W/kg in 27-g mice. The maximum SAR at the skin surface determined thermographically was 8.36 W/kg in the head of the mouse. The second system was a miniature anechoic chamber. Six mice were irradiated dorsally to far field plane waves. Copper shielding and high-temperature absorbing material were lined inside the chamber to accommodate the high input power. The air ventilation at the location of the mice was separately controlled so that any heating in the absorber would not affect the animals. For 1-W input power, the average SAR was 0.17 ± 0.01 W/kg and the maximum SAR at the skin surface was 0.41 W/kg in the animal when irradiated with body axis parallel to the E field; the SARs were 0.11 ± 0.01 W/kg and 0.64 W/kg, respectively, when irradiated perpendicular to the E field.     

Evidence that Alterations in γ-Aminobutyric Acid and Acetylcholine in Rat Striata and Cerebella Are Not Related to Soman-Induced Convulsions

Many reports have suggested that gamma-aminobutyric acid (GABA) may play a role in organophosphate-induced convulsions. The balance between GABA and acetylcholine (ACh) in the brain also has been suggested by some investigators to be related to brain excitability. We examined these questions by studying the levels of GABA and ACh and the ratios of GABA to ACh in rat striata and cerebella (two major motor control areas in the CNS) after the administration of soman, an organophosphate acetylcholinesterase inhibitor also known as nerve gas. Male Sprague-Dawley rats weighing 250-300 g were injected subcutaneously with three different doses of soman: a subconvulsive dose of 40 micrograms/kg (approximately 30% of the ED50 for convulsions in rats), a convulsive dose of 120 micrograms/kg (approximately one ED50 for convulsions), and a higher convulsive dose of 150 micrograms/kg (approximately 120% of the ED50 for convulsions). The incidence and severity of convulsions were monitored in individual rats until they were sacrificed by focused microwave irradiation of the head at the following time points after soman administration: 4 min, a time prior to the onset of convulsions; 10 min, the time of onset of convulsions; 1 h, the time of peak convulsive activity; and 6 h, a time at which rats were recovering from convulsions. Results showed that in rat striata and cerebella, neither changes in levels of GABA and ACh nor changes in ratios of GABA to ACh were related to soman-induced convulsions, i.e., none of the changes in either levels or ratios of these two neurotransmitters were related to the initiation of, maintenance of, or recovery from soman-induced convulsions.     

Increased neural damage to global hemispheric hypoxic ischemia (GHHI) in febrile but not nonfebrile lipopolysaccharide Escherichia coli injected rats

Experiments were conducted to compare the impact of febrile versus nonfebrile lipopolysaccharide (LPS) induced bacterial infection at the time of global hemispheric hypoxic ischemia (GHHI) on the neural damage evoked by the GHHI insult. In the first study acute intraperitoneal (i.p.) sterile saline (SS) or LPS Escherichia coli (60 microg/kg) was given to groups of male, conscious Long Evans rats, and core (colonic, Tc) temperatures were monitored over 6 h postinjection. Peak febrile response occurred approximately 5 h after the LPS E. coli was injected. Upon sacrifice 7 days later, no hemispheric or regional brain damage occurred in the saline or LPS-injected groups of this first study. In the second study, GHHI was applied (ligation of right common carotid artery + 35 min of 12% O2) in groups of anesthetized, male Long Evans rats previously given an acute i.p. injection of sterile saline or 60 microg/kg LPS E. coli 5 h earlier. Temperatures (Tc) were monitored before, during, and 1.5 and 24 h following GHHI. The LPS-injected group was subdivided into a febrile (Tc > 38 degrees C before and (or) after GHHI) and nonfebrile (Tc < 38 degrees C before and after GHHI) subgroups. A significant correlation was found between the peak temperature rise from preinjection control values following drug administration of either saline or LPS E. coli and the resultant hemispheric damage caused by GHHI. Moreover, upon sacrifice 7 days later ipsilateral hemispheric and regional (i.e., hippocampal, thalamic) damage to GHHI of the febrile LPS E. coli group was significantly increased from respective hemispheric, hippocampal, and thalamic damage of the saline and nonfebrile, LPS groups given the same ischemic insult. Results suggest that the heightened Tc of a LPS infection at the time of global ischemia exacerbated the neural damage of GHHI, a finding similar to that reported with heightened core temperatures induced by external heating.     

Two-year chronic bioassay study of rats exposed to a 1.6 GHz radiofrequency signal

The purpose of this study was to determine whether long-term exposure to a 1.6 GHz radiofrequency (RF) field would affect the incidence of cancer in Fischer 344 rats. Thirty-six timed-pregnant rats were randomly assigned to each of three treatment groups: two groups exposed to a far-field RF Iridium signal and a third group that was sham exposed. Exposures were chosen such that the brain SAR in the fetuses was 0.16 W/kg. Whole-body far-field exposures were initiated at 19 days of gestation and continued at 2 h/day, 7 days/week for dams and pups after parturition until weaning (approximately 23 days old). The offspring (700) of these dams were selected, 90 males and 90 females for each near-field treatment group, with SAR levels in the brain calculated to be as follows: (1) 1.6 W/kg, (2) 0.16 W/kg and (3) near-field sham controls, with an additional 80 males and 80 females as shelf controls. Confining, head-first, near-field exposures of 2 h/day, 5 days/week were initiated when the offspring were 36 +/- 1 days old and continued until the rats were 2 years old. No statistically significant differences were observed among treatment groups for number of live pups/litter, survival index, and weaning weights, nor were there differences in clinical signs or neoplastic lesions among the treatment groups. The percentages of animals surviving at the end of the near-field exposure were not different among the male groups. In females a significant decrease in survival time was observed for the cage control group.     

Effect of electromagnetic radiofrequency radiation on the rats' brain, liver and kidney cells measured by comet assay

The goal of study was to evaluate DNA damage in rat's renal, liver and brain cells after in vivo exposure to radiofrequency/microwave (Rf/Mw) radiation of cellular phone frequencies range. To determine DNA damage, a single cell gel electrophoresis/comet assay was used. Wistar rats (male, 12 week old, approximate body weight 350 g) (N = 9) were exposed to the carrier frequency of 915 MHz with Global System Mobile signal modulation (GSM), power density of 2.4 W/m2, whole body average specific absorption rate SAR of 0.6 W/kg. The animals were irradiated for one hour/day, seven days/week during two weeks period. The exposure set-up was Gigahertz Transversal Electromagnetic Mode Cell (GTEM--cell). Sham irradiated controls (N = 9) were apart of the study. The body temperature was measured before and after exposure. There were no differences in temperature in between control and treated animals. Comet assay parameters such as the tail length and tail intensity were evaluated. In comparison with tail length in controls (13.5 +/- 0.7 microm), the tail was slightly elongated in brain cells of irradiated animals (14.0 +/- 0.3 microm). The tail length obtained for liver (14.5 +/- 0.3 microm) and kidney (13.9 +/- 0.5 microm) homogenates notably differs in comparison with matched sham controls (13.6 +/- 0.3 microm) and (12.9 +/- 0.9 microm). Differences in tail intensity between control and exposed animals were not significant. The results of this study suggest that, under the experimental conditions applied, repeated 915 MHz irradiation could be a cause of DNA breaks in renal and liver cells, but not affect the cell genome at the higher extent compared to the basal damage.     

Primary immunisation and febrile convulsions in Oxford 1972-5.

A three-year study of febrile convulsions in Oxford with comprehensive notification from general practice and hospitals showed a 3% risk for all children of suffering at least one febrile convulsion by the age of 5 years. Children were most at risk between 6 and 27 months, and febrile convulsions were most likely to be prolonged in children aged 9-15 months. The association between febrile convulsions and primary immunisations in the preceding 28 days was compared in case and control children, matched for age and sex. Results suggested that such association was a chance relationship with age. If association was direct, the febrile convulsion rates per 1000 immunisation doses were estimated as follows: diphtheria, pertussis, tetanus--0-09 per 1000; poliomyelitis--0-6 per 1000; and measles--0-9 per 1000. Hence if any of these vaccines had a secific causal relationship with febrile convulsions, these rates would probably have been much higher.     

Complex segregation analysis of febrile convulsions.

Complex segregation analysis was performed on 467 nuclear families ascertained through febrile-convulsion probands. The probands were identified as having their first febrile convulsion while residents of Rochester, MN, during the years 1935-64. Parents and first- and second-degree relatives of probands were identified through the Olmsted County, MN, record-linkage system. Diagnoses of convulsive activity were made from review of medical records. The genetic models investigated included both single-major-locus and polygenic models, with likelihoods computed jointly on children and parents as well as being conditioned on parental phenotype. Possible heterogeneity was investigated by means of analyses of frequency of febrile convulsions in the proband. Analyses of the entire data set indicated that the single-major-locus models could be rejected. The most parsimonious model for these data was the pure polygenic (or common familial environment) model with a large heritable component (68% +/- 7%). However, when families were partitioned on the basis of frequency of febrile convulsions in the proband, significant heterogeneity was present. Our results indicated that the polygenic model was strongly corroborated in families of probands with a single febrile convulsion. In families of probands with multiple febrile convulsions, evidence was consistent with a single-major-locus model with nearly dominant seizure susceptibility.     

Febrile convulsions in a national cohort followed up from birth. II--Medical history and intellectual ability at 5 years of age.

Three hundred and three children with febrile convulsions were identified in a national birth cohort of 13 135 children followed up from birth to the age of 5 years. Breech delivery (p less than 0.05) was the only significantly associated prenatal or perinatal factor. There were no associations with socioeconomic factors. Excluding the 13 known to be neurologically abnormal before their first febrile convulsion, children who had had a febrile convulsion did not differ at age 5 from their peers who had not had febrile convulsions in their behaviour, height, head circumference, or performance in simple intellectual tests.     

Effect of amplitude modulated RF radiation on calcium ion efflux and ODC activity in chronically exposed rat brain

The effect of exposing rats to amplitude modulated radiofrequency radiation (112 MHz modulated to 16 Hz) during development and growth has been examined. Wistar rats (35 days old) when exposed at above frequency at the power level 1.0 mW/cm2 (SAR, 0.75 W/kg) for 35 days showed enhanced ornithine decarboxylase activity and Ca2+ efflux in brain indicating potential health hazards due to exposure.