CSIRO - June 1994





The majority of studies show that exposure to RF radiation does not result in an increase in chromosome aberration frequency when temperatures are maintained within physiological limits. It is well known that hyperthermia induces profound alteration in gene expression as demonstrated by the heat-shock response in early post-implantation rodent embryos (Walsh et al 1985). The so-called heat-shock response is elicited by a wide range of irritants and stresses apart from heat. There is evidence of a synergistic effect when embryos are exposed to pulsed ultrasonic energy combined with a modest increase in bulk heating (Angles et al 1990). Potentiating effects of non-ionizing radiation by environmental factors require investigation.

Reported increased frequency of cytogenetic effects after in vivo exposure to 2.45 GHz at SAR up to 20 W/kg was not successfully replicated in a study using a different strain of mouse. Reported increases in the frequency of sister chromatid exchanges following in vitro exposure have not been verified.

The literature contains disagreement on the effect of microwave radiation on chromosome aberration frequency in male germ cells.

An indicator of altered chromosome aberrations, increased dominant lethality (assessed as impaired survival of implanted embryos), was reported after acute exposure to high power levels where hyperthermic effects were dominant. There is no evidence of induced dominant lethals in rodents exposed to SAR up to 5 W/kg in chronic exposures over periods up to 8 weeks. While this is interesting, its use in establishing health risk is somewhat limited. To be meaningful for human health implications, it is essential that these studies are conducted in a manner that is relevant to environmental exposures of EMR. Humans are exposed to low level EMR from prenatal existence throughout life and it is appropriate that animal models should at least be exposed to similar conditions if the scientific data base is to be improved.


The potential interference by EMR on the structure of DNA or chromosomes is an important consideration in somatic cells where a non-lethal change could be associated with the development of cancers. If such effects occur in the male or female germ cells, surviving mutations might be passed on to subsequent generations. These effects are conveniently studied in cell culture and small animal exposures where relatively sensitive tests can assess the rate of change in single and multiple generations.

The possibility of adverse effects of RF radiation on male germ cells has received media attention recently in the USA where claims that RF emissions from public radar guns may be responsible for an increase in the incidence of testicular tumours. It is not certain whether effects on sperm cell integrity were also considered.

6.1 Experimental Evidence

Studies on the possible hereditary interference by RF exposure are summarised in table 6.1. No confirmed adverse effects assessed by structural aberrations and sister chromatid exchanges were reported following in vivo exposures (Huang et al 1977; McRee et al 1981).

The literature contains disagreement on the effect of microwave radiation on chromosome aberration frequency in male germ cells. Original experiments exposing germ cells in male mice to microwave radiation (Manikowska et al 1979, 1985) reported an SAR dependant increase in the frequency of chromosome aberrations that has not been confirmed in subsequent studies when the rectal temperature increased by up to 3°C above the normal basal value (Beechey et al 1986). A further study exposed the spermatogonial stem cells (greatest risk of accumulating genetic damage) and found no evidence of altered frequency of chromosome translocations or fragments after in vivo exposures to 5 W/kg for a total of 120 h over a period of 8 weeks (Saunders et al 1988). There was no change in rectal temperature in exposed and sham-exposed mice. Temperature in the germ cells was not reported.

A number of studies has assessed the ability of microwave radiation to induce dominant lethal mutations which result in pre-implantation death or subsequent embryonic or fetal mortality. Contradictory results have been reported (table 6.1). Whilst one study (Varma & Traboulay 1977) reported an increase in induction of dominant lethal mutations after exposure to 1.7 GHz at 500 W/m2 (SAR estimated as 25-45 W/kg), this was not replicated in two subsequent studies. The first of which exposed mice to 2.4 GHz at either 600 W/m2 for 12 min or 8,000 W/m2 for 21 s (Ramaiaya et al 1980) without observing an effect, although up to 10% of the mice died from the severity of the exposure.


Table 6.1 Summary of studies on Genetic Bioeffects of EMR

Table 6.1 Summary of studies on Genetic Bioeffects of EMR

Table 6.1 Summary of studies on Genetic Bioeffects of EMR

The second study found no evidence of increased dominant lethality in mice exposed to SAR 43 W/kg (Saunders et al 1983). However, significant reductions in pregnancy rate were observed which was subsequently attributed to impaired male fertility resulting from decreased sperm counts and an increase in the proportion of abnormally shaped sperm (Kowalezuk et al 1983). This is hardly surprising when one considers the likelihood of substantial heating of the testes from the absorbed dose.

It is interesting that previous studies apparently did not consider the possibility of impaired sperm cell function which is known to be sensitive to elevated temperature. Beechey et al (1986) reported an increase in rectal temperature of 3°C in mice exposed to 20 W/kg, while Saunders et al (1988) reported no change in temperature at 5 W/kg in mice exposed at the same 2.45 GHz frequency.

Chronic, low level exposures are more relevant to public health risk of electromagnetic radiations. There is no evidence to date of the induction of dominant lethal mutations in mice (Saunders et al 1988) or rats (Berman et al 1980). However, the longest term of these experimental exposures was 8 weeks which is rather short, even in relation to the life span of rodents.

Studies have been carried out using standardised techniques for clastogenic and cytogenic effects following in vitro radiation with microwaves. Effects on cell cycle kinetics and cell proliferation rates are endpoints that would be expected to show a response to cellular perturbation. Elevated temperature is a common cause of altered rates of mitotic division.

Although the generally-held opinion is that the energy levels available in non-ionizing radiation are insufficient to cause chromosome breaks a recent study reported a statistically significant increase in the frequency of chromosome aberrations and micronuclei (Maes et al 1993) in human peripheral blood lymphocytes. A temperature controlled “normothermal" exposure system exposed lymphocytes in vitro in a tube containing a thermistor to regulate the microwave output and maintain a constant temperature of 36.1°C. It is not certain that the thermistor did not perturb the field or create localised "hot spots" of energy deposition. The 2450 MHz microwave exposure was pulsed (50 Hz, duty cycle 1:3) with a nominal SAR of 75 W/kg. While the paper reports an increase in percentage of chromosome aberrations and of micronuclei there is no effect on the rate of sister chromatid exchanges. Cell cycle kinetics was unchanged as would be expected if temperature was unchanged.

In a recent presentation by this group (Verschaeye et al 1994) at the BEMS conference, they reported effects from mobile telephones in 32 subjects exposed to 450 or 954 MHz. Chromosome aberrations were assayed by changes in DNA electrophoresis. In addition, rats exposed to 954 MHz showed a statistically significant increase (_25%) in the SCE frequency when microwave radiation accompanied application of the mutagen, mitomycin C. Evidence of a synergistic association is presented. However, the details of this work were very sketchy, with very small populations and little useful information on dosimetry, (no SAR values given on exposure duration). The data appeared to be sparse and the authors reported it as "preliminary". The obvious question then is; how does the acceptance of such material at an international conference assist the development of scientific knowledge? Previous studies using SCE as an endpoint have failed to demonstrate an effect of microwave radiation or a synergistic effect when applied together with known mutagens (Meltz et al 1989, Meltz 1991).

Concerns about this paper relate to the dosimetry and the population size and relevance of the statistical analysis. A result is published on the basis of two blood samples from two donors. Groups of different sizes are compared. In fact the data is weighted in one experiment where a control group of 500 was compared with exposed groups of 200 and the aberrations expressed as a percentage. The fact that only 100 cells could be examined in the third group suggests a problem in the culture protocol. The data is rather weak, and the authors state that; “This work must be considered as a preliminary pilot experiment ... ...”. As far as implications to human health are concerned, there is little that can be inferred from this study.

Although it was not the intent to criticise individual scientific publications this may be taken as representative of some of the peer-reviewed literature. There were almost 100 papers published in the Bioelectromagnetics journal in 1993. One has to wonder about the peer-review process that allows publication of preliminary work-in-progress standard of manuscript as scientific papers. Perhaps a more restrictive policy would limit the otherwise vast number of publications in the EMR field, many of which contribute little other than adding to the confusion and fuelling the desire for more independent reviews. The situation is further exacerbated by the apparently unconditional acceptance of every abstract submitted to the BEMS annual conferences. As a result the 1994 conference yields 198 abstracts and 222 posters.

Another study has addressed the issue of possible long-term effects of RF exposure on lymphocyte chromosome integrity in an occupationally exposed group (Garson et al 1991). The endpoint involved chromosome breakages and compared a high risk group of radio-linemen with a control group from office workers in the telecommunications industry. The exposed group received radiation over the range 400 kHz to 20 GHz at or below the safety standard for occupational exposure. An assay for chromatid gaps and breaks, chromosome breaks and “other” aberrations found no statistically significant difference between the exposed and control groups. A requirement of the study was that all subjects had worked for at least 5 out of the previous 6 years as radio-linesmen, and the last exposure was no more than 12 months before the study. The lymphocytes were obtained from the peripheral blood circulation. Although this is an acceptable protocol for chromosome breaks, it might have been more desirable to have used an exposed group comprised entirely of people who were exposed to RF radiation at the time of the assay rather than up to 12 months before.

The information from this paper supports the commonly accepted view that there is no evidence that chronic exposure to low level RF radiation has clastogenic effects.

Recent reports contrary to that opinion were presented at the 16th conference of the BEMS (June 1994). In one report on the health effects of radar exposures on workers an increased incidence in aberrations and micronuclei was reported (Garaj-Vrhovac & Fucic 1994). The study group comprised 40 workers employed in antenna maintenance occupations for a mean of 12.5 years (range from 0.5 to 26 years). Peripheral blood lymphocytes were reported to have significantly higher incidence of structural aberrations and micronuclei in the exposed group (8.2 - 26 GHz, SAR mostly 5 mW/cm2 up to a maximum value of 26 mW/cm2).

These authors have previously published findings that microwave exposure is clastogenic and that it produces an increase in the number of micronuclei in human lymphocytes following in vivo exposure (Fucic et al 1992) in the workplace to pulsed microwave radiation in the range 1.25 to 1.35 GHz at power densities 0.01 to 20 mW/cm2. They also reported an increase in aberrations including chromosome and chromatid breaks, acentrics and dicentrics following in vitro (Garaj-Vrhovac et al 1992) exposure at 7.7 GHz. Increased rates of aberrations were reported for power densities from 0.5 to 30 mW/cm2 for 10 to 60 min. It is uncertain why these studies should contain such a high degree of sensitivity.


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