CSIRO - June 1994 BIOLOGICAL EFFECTS AND SAFETY OF EMR |
3.0 ANIMAL STUDIESAnimal studies allow assessment of the potentially hazardous effects of physical or chemical agents on different body systems. The potential for adverse effects on reproduction and prenatal and postnatal development can be tested. The induction of mutagenic changes is important in the assessment of possible hereditary effects. Carefully controlled animal studies are an essential step in the extrapolation of biological effects to human health and safety. 3.1 OCULAR EFFECTSSUMMARYThe absorption of radiofrequency electromagnetic energy, particularly in the GHz frequency range, has been shown to result in damage to ocular tissues in experimental animal studies. The site of damage depends on the radiation frequency (related to depth of penetration) whereas the magnitude of effect primarily depends on the power density of the field, the quantity of absorbed energy and on the duration of exposure. The lens of the eye is susceptible to microwave and RF heating because of its lack of a blood supply and hence limited heat dissipating capability. Its constituent fibres have a limited capacity for repair and tend to accumulate the effects of minor insults. Microwave induced temperature increase has been shown to produce cataracts in the lenses of anaesthetised rabbits. Microwave frequencies between 1 and 10 GHz are most effective in inducing lens cataracts. The threshold temperature for cataract induction from prolonged exposure (>100 mins) is 41 - 43°C, with a corresponding SAR of 100-140 W/kg resulting from exposure to power densities greater than 1.5 kW/m2. Most experimental work on microwave induction of lens opacities (cataracts) has been carried out using near-field exposures at 2.45 GHz. The intense exposures used were generally far above perception threshold and the animals were normally anaesthetised. Cataracts produced in rabbits eyes are either caused by intense exposures sufficient to damage other ocular structures and rapidly produce opaque lenses or less severe exposures that result in posterior cortical opacities several days or weeks after exposure. The mechanism for cataract formation is considered to be thermal in origin. Lens opacities have not been produced in the eyes of rhesus monkeys after acute exposures to 5 kW/m2 (anaesthetised) or after chronic exposures of conscious monkeys to 1.5 kW/m2. The difference in acute response may be due to structural anatomical differences in the eyes and skull of rabbits and monkeys. Recent studies on monkeys have shown that other structures including the cornea and iris are susceptible to microwave radiations in combination with ophthalmologic drugs where the exposure levels are too low to involve a thermal mechanism. Well-conducted studies by a single research group (Kues et al 1992, 1994) have shown degenerative changes in the retina, iris and corneal endothelium of primates to be caused by low level microwave irradiation, particularly when pulsed. Localised threshold SARs were found to be as low as 0.26 W/kg when irradiated together with the glaucoma drug, timolol maleate. It is clearly important that these results are independently verified. The apparent sensitisation of ocular tissues to microwave radiation by the application of a drug used in the treatment of glaucoma may provide evidence of a non-thermal effect. Timolol maleate normally offers protection to the eye against heat induced disruption of the blood aqueous barrier and the ocular temperature was said to have increased by less than 0.8°C at a SAR of 0.26 W/kg during the irradiation (Kues et al 1992). The extrapolation of results of animal experimentation to human exposures is complicated by anatomical/structural differences in the head and eyes that result in different in vivo exposure conditions. Frequency and orientation dependent factors may have a significant impact on EM field distributions in the eyes of different species. Experimental Evidence3.1.1 CataractsPosterior cortical cataracts have been reported to form within 1 week of exposure to 2.45 GHz radiation at approximately 4.2 kW/m2 for 5 min or 1.5 kW/m2 for 60 min (Carpenter 1979). The reaction varied from narrow translucent or milky bands in the posterior cortex that disappeared within a few days to permanent lesions. The extent of cataract formation varied with the power and duration of the exposure from a few fibrous “streaks” at the posterior suture to diffuse opacities. The threshold power density for cataract formation in the rabbit eye by a single exposure of up to 100 min was calculated to be 1.5 kW/m2 (Guy et al 1975). Based on temperature measurements in a dead animal it was estimated that the peak level of SAR occurred in the vitreous humour immediately behind the lens, with a threshold for 100 min exposure determined to be 138 W/kg. Calculation of the heat flow within the rabbit eye predicted threshold temperatures at the back of the lens of 41 - 43°C, similar to the experimental data on temperature induced cataract formation in dogs. Induction of cataracts in the lens was shown to be heat-dependent when cataractogenic RF exposures applied to hypothermic rabbits failed to produce lesions (Kramar et al 1975). The existence of a thermal mechanism was given further support in a study that produced cataracts in rabbit eyes by heating the lenses above 43°C with circulating heated water. Different results were reported in rhesus monkeys where 2.45 GHz radiation did not produce cataracts, even after exposure to power densities up to 5 kW/m2 for 60 min (Kramar et al 1978). This is far above the threshold for cataract formation in the rabbit and sufficient to cause severe facial burns in the monkey. Peak temperatures occurred behind the lens in the monkey eye but were lower for a given exposure than those in the rabbit. Power densities of 2 and 5 kW/m2 raised the retrolental temperature to 39 and 42°C, respectively. The different anatomical structure and size demonstrate important species differences. The extrapolation of results of animal experimentation to human exposures is complicated by anatomical/structural differences in the head and eyes that result in different in vivo exposure conditions. Frequency and orientation dependent factors may have a significant impact on EM field distributions in the eyes of different species. It is well known that absorption of EMR by a lossy dielectric scatterer such as the mammalian head alters as a function of its shape and the applied frequency (NCRP 1986). It has been shown that (at 2.45 GHz) the measured field intensity at the position of the head of a rabbit was reduced by 40% by the presence of the animal in the field, and by a further 40% when its ears were fastened against its body (Carpenter et al 1974). In a comparison of the effects of 2.45 GHz radiation (Kramar et al 1978) cataracts were induced in rabbits but not in monkeys (table 3.1.1). These differences have been interpreted as being due to differences in field concentrations and heating of the lens. The efficacy with which microwave or radiofrequency radiation can induce cataracts depends on the depth of penetration and hence on frequency. It has been reported that below 1.5 GHz the dimensions of the orbit-eye combination are too small to result in local field concentration (NCRP 1986). Table 3.1.1 Summary of Studies on Cataractogenic Effects of Microwave Radiation TO BE ADDED LATER
At frequencies above 10 GHz, penetration decreases and power absorption is increasingly restricted to the superficial tissue. At 915 MHz the estimated distribution of SAR (Guy et al 1974) in the eyes of rabbits gave the peak SAR as 25% lower than that resulting from exposure at 2.45 GHz. The maximal SAR was found to occur in the rabbit brain, being 36% higher than in the eye. It is likely that other biological endpoints will become limiting factors before exposure is sufficient to induce cataracts. At higher frequencies of 35 and 107 GHz effects of acute exposure were limited to the cornea of rabbit eyes (Rosenthal et al 1976). Whole-body exposure to far-field radiation, which is relevant to many occupational situations, has not been reliably associated with experimental cataract induction. The lenses of anaesthetised rabbits exposed in the far-field to 3 GHz for 15-30 min at 5 kW/m2 were unchanged. Cataracts were not found in macaque monkeys trained to expose their faces to 9.3 GHz radiation at 1.5 kW/m2 for a total exposure period of up to about 10 h over 3 months (McAfee et al 1979). In a study of the cumulative effects (table 3.1.1) of repeated sub-threshold exposure of anaesthetised rabbits to 2.45 GHz radiation, the lowest power density capable of producing cataracts was 1.2 kW/m2 for 1 h, repeated 20-24 times (Carpenter 1979). 3.1.2 Corneal LesionsIn addition to lens opacity, corneal endothelial lesions were produced in the eyes of anaesthetised monkeys exposed to continuous or pulsed wave (10 µs pulses repeated at 100 pulses per second) 2.45 GHz radiation (Kues et al 1985) (Table 3.1.2). Pulsed radiation produced endothelial lesions after a single 4 h exposure to 100 W/m2 where the average SAR in the anterior chamber of the eye was estimated in vivo as 2.6 W/kg. Body temperatures dropped during exposure by about 2.5°C in both sham-exposed and exposed monkeys due to the anaesthesia. When the exposure was increased to 4 h on three consecutive days, there was increased vascular leakage from the iris blood vessels into the aqueous humour (Kues et al 1988). When the eyes were pretreated with the ophthalmic drug timolol maleate used in the treatment of glaucoma, the leakage was increased at power densities as low as 10 W/m2 where the local SAR was estimated at 0.26 W/kg (Monahan et al 1988).
Table 3.1.2 Summary of Ocular Effects from Low Level Microwave Radiation
TO BE ADDED LATER
Damage to the retina has since been reported (Kues et al 1990) following exposure to pulsed 2.45 GHz radiation at 50 W/m2 for 10 weeks. When exposure to 100 W/m2 followed timolol maleate treatment extensive vacuolation of the outer retinal layers was observed together with focal retinal detachment. The effects were produced when microwave radiation immediately followed the application of a single drop of the ophthalmic drug timolol maleate (0.5%) or pilocarpine (2%). When combined with either drug the power density threshold was reduced by an order of magnitude (from 10 to 1 mW/cm2 ) for the induction of corneal endothelial lesions and increased vascular permeability of the iris (Kues et al 1992). Sodium fluorescein iris angiography was used to diagnose vascular integrity. Positive results were also obtained using the glycoprotein horseradish peroxidise showing that microwave exposure resulted in diffusion of large molecules (40,000 molecular weight, and 100 times larger than sodium fluorescein) out of the iris blood vessels. In the latest addition to this work on ocular lesions from low SARs, Kues et al (1994) reported cytological damage in retinal neuroepithelium under various exposure conditions, when monkeys were chair-restrained. The effect is considered to be permanent as it is still apparent at one year post-irradiation. Using frequencies of 1.25, 2.45 and 2.85 GHz, they reported effects at 4 W/kg SAR that were related to the shape of the pulse and the ratio of peak power to pulse length rather than to the SAR value. When applied using rapid rise-time square pulses, the effects were demonstrated by histology and depressed electro-retinogram. The cellular changes reported include cytoplasmic vacuolation and disrupted plasma membrane. The mechanism is uncertain. At a frequency of 2.45 GHz, and 10 µs pulses repeated at 100 Hz, the effects were observed at a SAR of 2.6 W/kg (average value in the eye, i.e., not whole-body average). It has been proposed that the action of free radicals may be involved in the breakdown of the ocular membranes leading to extravasation. Oxygen radicals are known to increase vascular permeability (Hull 1985) in the rabbit iris. As both timolol and pilocarpine are known to bind to ocular melanin, and microwave interaction with melanin generates free radicals, a potential mechanism exists. It needs to be established if free radicals can be released by the low energy levels causing vascular leakage in these animal experiments.
3.2 HAEMATOLOGY AND IMMUNOLOGYSUMMARYThe literature contains reports of a large number of studies on the effects of microwave and RF radiation on the haematopoietic system and on immune responses. These have been well reviewed (Roberts 1983; Smialowicz 1984; NCRP 1986; Szmigielski et al 1988; NRPB 1992; WHO 1993). The conflicting nature of many early reports makes interpretation difficult and although later studies have been improved with more rigorous experimental design and improvement in dosimetry, the overall effects of microwave and RF exposure are still not well understood. There is good evidence that receptor sites on cell membranes are sensitive to EMR and, therefore, some effects on the sensitive immunological system may be expected. Many of the effects are transient. Contradictory effects have been reported in rodents. Various components of the immune system have been affected by microwave exposures. Interpretation may be confounded by the complex nature of immune responses, which can involve changes in the numbers of circulating lymphocytes and leucocytes, and the sensitivity of the system to minor changes in temperature. Consistent effects on the haematopoietic and immune systems are mostly associated with thermal stress, although the occasional report appears at SAR levels too low to induce significant amounts of heating. A recent report of stimulated immune response in male rats exposed to low level (0.14 W/kg) microwave radiation is contrary to expectations. Difficulties in interpretation are exacerbated by the experimental constraints of making isolated observations within a complicated sequence of changes. This problem is common to much of the research carried out on cellular RF responses. Separate research groups generally study a small part of a chain of events. Species difference is a further variable that complicates these issues. IntroductionThe lymphocyte population consists of B-lymphocytes, the precursors of plasma cells or antibody secreting cells, and T-lymphocytes required to express cellular immune responses including delayed hypersensitivity, cell-mediated cytotoxicity and helper cell function. Experiments have been studied on the mitogen responses of B- and T- lymphocytes, the number of B- lymphocytes bearing complement receptors, natural killer cell (a T-lymphocyte sub-group) activity and the antibody response of B-lymphocytes. Lymphocytes from exposed animals have been studied by way of their in vitro response to mitogens (agents that stimulate transformation to lymphoblasts and mitotic division). Thus, the functional integrity of the cell and the relative frequencies of B- and T- cells can be evaluated by using B- and T- specific mitogens. Experimental Evidence3.2.1 Haematopoietic SystemEarly studies measured peripheral blood cell concentrations and reported an increase in erythrocyte and neutrophil counts but a reduction in total leucocyte and lymphocyte counts in rats exposed to pulsed 24 GHz microwave radiation at 100 W/m2 for 18 h or 200 W/m2 for 7.5 h. The SARs were estimated to be 1.5 and 3 W/kg, respectively (Smialowicz 1984). These experiments are typical of many early studies that are complicated by the lack of appropriate sham-exposed controls and absence of interpretation of the biological significance of the effect. Heating is often involved in haematological responses to microwave and RF radiation. A reported decrease in peripheral lymphocyte count and increase in neutrophil count (Liburdy 1977) was observed in mice exposed to 26 MHz at a SAR of 13 W/kg, which raised the rectal temperature by 2 - 4°C (Table 3.2.1). The response was greatest after 3 h exposure. In contrast, exposures that were not accompanied by a detectable increase in body temperature have reported absence of effects. A lack of effect on peripheral blood count in mice exposed to 2.45 GHz was reported where the SAR was estimated at 22 W/kg (Smialowicz et al 1979 a). Peripheral blood cell count was unchanged in rats, in the absence of a measurable rise in whole body temperature, following exposure for; (a) 1 h per day for 90 days to 2.4 GHz at 50 W/m2 (SAR estimated at 1 W/kg) (Djordjevic et al 1977), (b) 22 h per day for 70 consecutive days to 970 MHz at a SAR of 2.5 W/kg (Smialowicz et al 1981a), or (c) for 8 h to 2.45 GHz at SAR 0.44 to 2.2 W/kg (Galvin et al 1982). See table 3.2.1.
Table 3.2.1 Summary of Reported Effects of Electromagnetic Radiation on the Haematopoietic System TO BE ADDED LATER Table 3.2.1 Summary of Reported Effects of Electromagnetic Radiation on the Haematopoietic System
TO BE ADDED LATER
Substantial abnormalities in haematopoietic development in bone marrow cells have been reported in guinea pigs following a single exposure to 3 to 4°C hyperthermia for 60 min (Edwards & Penny 1985). Similar significant changes in nuclear development were observed following a temperature increase of only 2.5°C for 6 mins when produced by localised absorption of pulsed ultrasound (Barnett et al 1991) in a single acute exposure. A review of early studies (Smialowicz 1984) reported a lack of consistent effect of microwave or RF exposure on peripheral blood cells in developing rats. Studies by the same author (Table 3.2.1) also reported no consistent changes in erythrocyte, leucocyte or differential leucocyte cell count in rats exposed prenatally and postnatally (for up to 41 days) over a range of frequencies; 100 MHz radiation at SAR 2-3 W/kg (Smialowicz et al 1981 b); 425 MHz radiation at 3-7 W/kg (Smialowicz et al 1982); and 2.45 GHz radiation at 1-5 W/kg (Smialowicz et al 1979 b). The apparent trend of a temperature-related effect has doubtlessly contributed to the notions, commonly expressed, that if the energy deposition from EMR does not heat it cannot hurt. This rather simplistic approach is only acceptable for gross effects. The subtleties of cell membrane responses requires an understanding and development of other non-thermal mechanisms. Studies on the effects of microwave exposure on haemopoietic tissue in bone marrow revealed abnormalities in nuclear structure and depressed mitosis (Baranski 1971) in guinea-pigs and rabbits exposed to pulsed or continuous wave 3 GHz microwave radiation at 35 W/m2 for 3 h per day over a period of 3 months. The SAR was estimated to be 0.5 W/kg and rectal temperatures were unchanged. Studies to evaluate the effects of low level exposure on the haemopoietic stem cells using in vitro colony forming assays have been inconsistent. Huang and Mold (1980) exposed mice to 2.45 GHz radiation at 150 W/m2 (SAR 11 W/kg ) for 30 min per day for 9 days and reported a reduction in the ability of bone marrow cells to form myeloid and erythroid colonies. Rectal temperature was variable, but not significantly increased. An inconsistent lack of effect on cloning efficiency of myeloid stem cells from mice exposed for up to 360 h to 2.88 GHz pulsed microwaves at SARs up to 4.5 W/kg was reported (Ragan et al 1983). In a review Smialowicz (1984) suggested that there is a marked difference in the kinetic response of the haematopoietic system to heat stress from microwave- induced heating and conventional heating. Radiation at 2.45 GHz frequency is quite penetrating (in small animals) and is likely to have set up temperature gradients within the mouse different to those set up by external heating, even though rectal temperatures were similar.
3.2.2 Immune SystemA single study on rhesus monkeys reported enhanced mitogen response in lymphocytes after 30 min exposure to 10.5, 19.27 or 26.6 MHz radiation at SARs between 0.4 and 2.0 W/kg (Prince et al 1972). Rectal temperatures were reported to be increased by 2.5°C at the higher level of exposure. Contradictory results have been reported using the appearance of a surface marker (complement-receptor) specific to a stage in the maturation of B-lymphocytes, following microwave radiation. One group of workers (Wiktor-Jedrzejczak et al 1977, 1980) reported an increase in the number of complement-receptor positive lymphocytes and an increase in B- cell mitogen response following exposure to 2.45 GHz radiation at 15 W/kg for 30 min. The effect was thought to be due to stimulation of B- cells into early maturation. Independent duplication of the study found a similar result only when the exposure level was raised to 28 W/kg resulting in a level of thermal stress that killed some mice (Smialowicz et al 1981 c) (See Table 3.2.2). There is a suggestion that differences in results may be due to differences in mice strain specificity as Schlagel et al (1980, 1982) reported a negative effect in Balb/C mice and an increase in complement-receptor lymphocytes in CBA/J mice. It has been suggested that the difference in response between the two strains may be due to the presence of a single gene (Schlagel et al 1982; WHO 1993). An important experimental variable that has not been adequately investigated is that of the environmental conditions associated with each of the exposures. Differences in air flow, humidity and ambient temperature may significantly alter the levels of thermal stress for a given level of microwave exposure. Liburdy (1980, 1987) has examined the central role of thermal stress in the effect of microwaves on the immune system. Mice were exposed or sham-exposed for 15 min (single or repeated exposures) to 26 MHz radiation at 5.6 W/kg or to warm air to induce an increase in core temperature of 2-3°C. A number of effects were observed when the RF-treated mice were compared with either the sham-exposed or the heat-treated animals.
Table 3.2.2 Summary of Reported Effects of Microwave Irradiation on the Immune System TO BE ADDED LATER
Table 3.2.2 Summary of Reported Effects of Microwave Irradiation on the Immune System TO BE ADDED LATER
Table 3.2.2 Summary of Reported Effects of Microwave Irradiation on the Immune System TO BE ADDED LATER
A transient reduction in peripheral lymphocytes and an increase in numbers of neutrophils occurred, which could be sustained by multiple exposures. RF exposure also resulted in an increase in T- and B-lymphocytes in the spleen and elevated plasma corticosteroid levels. In addition, the ability of mice to develop a delayed hypersensitivity (to sheep red blood cells) was suppressed by the RF exposure. The effect of RF exposure and elevated temperature was also determined on lymphocyte migration (Liburdy 1980). This was measured by the activity of radio-labelled splenic lymphocytes in mice exposed for 1 h to 2.6 GHz radiation at 3.8 W/kg. This was compared with exposure to 19 W/kg or to warm air, both of which were sufficient to raise rectal temperatures by 2°C. Exposure at 19 W/kg caused a significant alteration in the distribution of lymphocytes between the lung, spleen and bone marrow, whereas exposures to 3.8 W/kg or warm air did not produce these changes. Liburdy suggested that whole-body RF or microwave exposure induces heat stress which activates the hypothalamic-hypophyseal-adrenal complex to release adrenal steroids into the blood, leading to the transient changes in blood cell counts and other haematopoietic and immunologic changes associated with RF or microwave exposure. The difference in response to exposures with warm air and microwave radiation is probably due to differences in energy deposition. Microwave-induced heating works by a different mechanism by being more rapid, and will have acted as a thermal stress for longer than warm air in a given exposure. Exposure to thermogenic levels of microwave radiation has also been shown to cause changes in macrophage and natural killer cell (NK) activity, implicated for example in tumour cell cytolysis (Table 3.2.2). Activation of macrophages and some transient decrease in the NK activity of T- lymphocytes was reported after exposure to 2.45 GHz radiation (Table 3.2.2). Since colonic temperature (and plasma corticosteroids) was appreciably elevated at the higher level of exposure, the decreased activity is probably due to heat stress. The latest reported effects from a group in Hungary (Elekes et al 1994) adds a further degree of uncertainty to the subject. The data was presented at the BEMS conference and, therefore, has not yet been peer-reviewed, but a paper has been submitted for publication (for this reason the data is not included in the table 3.2.2). In their study Balb/C mice were exposed to 2.45 GHz, cw or 50 Hz amplitude modulated, at SAR 0.14 W/kg. Exposures of different durations were applied for six consecutive days and mice were injected with sheep red blood cells on the second day of exposure. The number of antibody producing cells in the spleen of male mice was significantly increased with daily 3 h exposures. Exposures for longer durations had less of an effect. Female mice were unaffected. No logical explanation was given for the observed result. The authors have experience in ionizing radiation biology and have recently turned their attention to EMR.
3.3 TERATOGENIC EFFECTSSUMMARYIt is well understood that a moderate elevation of body temperature during embryonic/fetal development is teratogenic in many animal species (Warkany 1986) and in humans (WFUMB 1992; Edwards 1986, 1993). Data from whole-body heating of pregnant animals in environmental chambers, indicates a threshold of 2.5°C above basal physiological temperature for the development of major abnormalities in the central nervous system (Germaine et al 1985 ). The type and magnitude of effect depends on the gestation stage and extent of the thermal insult. Thus, exposures to microwave or RF radiation that will induce significant rises (>1.5°C) in maternal body temperature would be expected to result in teratogenic effects. Most of the literature reports effects of exposure to substantial levels of SAR and the associated adverse developmental effects are consistent with RF-induced hyperthermia. These are gross effects that are easily detected. More sensitive, and potentially important, disturbance of CNS function has not been adequately investigated, particularly where where offspring may appear normal. Research in this area is recommended. Most of the work has been clearly focused on the safety issues relating to microwave ovens at 2.45 GHz frequency. It is tempting to assume that teratogenesis will only be produced when the RF radiation is sufficient to significantly raise the embryonic or fetal temperature. However, recent reports from a single laboratory have claimed delayed development in chick embryos exposed to 428 MHz at 5.5 mW/cm2 which they consider to be a non-thermal effect. Similarly, a report by an apparently respectable research group (Tofani et al 1986) of significant effects on postimplantation survival and cranial ossification in rat fetuses following chronic exposure to very low level RF radiation cannot be explained by the accepted thermal mechanism (Table 3.3.1). Data that is relevant to exposures at telecommunications frequencies, particularly for cellular telephones, is urgently needed.
IntroductionCells are most sensitive to damage by physical agents, such as heat, during the process of cell division. If mitosis in neurons is arrested by a transient temperature increase during embryonic development the resulting neural deficit may not be restored, although the fetus may continue to develop and appear morphologically normal (Edwards et al 1974). There are critical periods during gestation when the embryo is more susceptible to teratogenic effects. At the time of formation of the neural plate and closure of the neural tube interactions can result in severe neural tube defects, retarded brain development, exencephaly, and microphthalmia. Other effects have been reported following a single brief exposure to an increase in temperature of 3.5°C (Cuff et al 1993). These gross effects are readily detected. However, low level interference that delays development of the cerebral cortex or impairs neural migration at later stages (around 22 weeks human gestation) is far more difficult to detect. The resulting impairment of neurological function may create learning difficulties. Non-deforming retardation of brain growth with reduced learning performance is the most common abnormality found in offspring from heat-exposed guinea pigs (Edwards 1968). The literature on teratogenic effects of electromagnetic radiation does not address this more sensitive issue.
3.3.1 Experimental EvidenceExposure to high levels of RF will induce significent rises in the temperature of the mother and embryo. The resulting hyperthermia will bring about abnormal development both by direct interaction on the embryo and fetus and indirectly through compromised maternal physiology. Such an effect has been demonstrated where absorbed ultrasonic energy produced maternal hyperthermia (Barnett & Williams 1990). The teratogenic nature of hyperthermia is now widely accepted (Edwards 1993). Although many of the studies on RF- induced teratogenicity applied repeated exposures this would add little value to the results if the effect was due entirely to a thermal mechanism. For the type of abnormalities reported, there is no reason to assume that repeated exposures at subthreshold levels would be any more effective than a single exposure to heat. In fact, the bioeffects data base on hyperthermia consists primarily of results from a single exposure to heat usually at a predetermined critical stage of neural development.
Table 3.3.1 Summary of Teratogenic Effects of RadioFrequency Radiation TO BE ADDED LATER Table 3.3.1 Summary of Teratogenic Effects of RadioFrequency Radiation TO BE ADDED LATER Table 3.3.1 Summary of Teratogenic Effects of RadioFrequency Radiation TO BE ADDED LATER
In reviews of the teratogenic effects of RF exposure (O'Connor 1980, 1990) the effects commonly described for rodents (CNS abnormalities including exencephaly, reduced fetal weight, and increased fetal resorptions) are typical of those induced by a single exposure to whole body hyperthermia. The reported abnormalities and deaths (Lary et al 1982) in rats exposed to 11 W/kg at 27.12 MHz were associated with elevated rectal temperature to 43°C in the dam (Table 3.3.1.). This represents an increase of 4.5°C above the basal temperature for rats and exceeds the threshold temperature level for such abnormalities (Walsh et al 1985; Germaine et al 1985; NCRP 1992; WFUMB 1992). However, later experiments by the same author found the threshold temperature for a 40 min. exposure to be 41.5°C ( DđT 3 ° |