mini review genetic, carcinogenic and teratogenic effects of...

Ž .Mutation Research 410 1998 141–165

Mini review

Genetic, carcinogenic and teratogenic effects of radiofrequencyfields 1

L. Verschaeve ), A. MaesVITO, EnÕironmental Toxicology Unit, Boeretang 200, B-2400 Mol, Belgium

Received 9 November 1996; accepted 15 August 1997

Abstract

Ž .This paper reviews the literature data on the genetic toxicology of radiofrequency RF radiation. Whereas in the pastmost studies were devoted to microwave ovens and radar equipment, it is now mobile telecommunication that attracts mostattention. Therefore we focus on mobile telephone frequencies where possible. According to a great majority of the papers,radiofrequency fields, and mobile telephone frequencies in particular, are not genotoxic: they do not induce genetic effects invitro and in vivo, at least under non-thermal exposure conditions, and do not seem to be teratogenic or to induce cancer. Yet,some investigations gave rather alarming results that should be confirmed and completed by further experiments. Amongthem the investigation of synergistic effects and of possible mechanisms of action should be emphasised. q 1998 ElsevierScience B.V.

Keywords: Radiofrequency radiation; Carcinogenicity; Teratogenicity; Genetic toxicology

1. Introduction

Radiofrequency fields, and especially microwavesŽ .300 MHz–300 GHz are a very important part ofthe electromagnetic spectrum with respect to theirapplications and possible health consequences. Thesenon ionising radiations have relatively short wave-lengths and high frequencies compared to, e.g., ex-treme low frequency fields, and therefore also agreater amount of energy which is sufficient to cause

Ž .heating in conductive materials Fig. 1 . Close to thetransmitter, these high-frequency fields may thus be

) Corresponding author. Tel.: q32 14 335217; Fax: q32 14320372; E-mail: [email protected]

1 This is the second in a series of four papers, the first of whichŽ .was published in Mutation Res. 387 1997 pp. 165–171.

harmful to human beings by producing thermal ef-fects that may sometimes, when thermoregulationprocesses are insufficient, produce irreversible dam-

Ž w x.age e.g. cataract; 1,2 . This kind of effect is wellknown from animal experiments and for that reasondoes not constitute a particular health problem, asmeasures can be taken to prevent excessive expo-sure. But also low-level exposures leading to non-thermal effects are, at least according to certaininvestigators, possible. Non-thermal effects havebeen reported in cell cultures and animals, in re-sponse to exposure to low-level fields. They are notwell established and therefore highly controversial.

While in the past decade people were especiallyŽconcerned about the safety of microwave ovens 2450

.MHz and even before radar equipment, it is wirelessŽ .communications e.g. mobile telephones that is par-

1383-5742r98r$19.00 q 1998 Elsevier Science B.V. All rights reserved.Ž .PII S1383-5742 97 00037-9

( )L. VerschaeÕe, A. MaesrMutation Research 410 1998 141–165142

Fig. 1. The electromagnetic spectrum.

ticularly considered at present. It is now indeedgenerally accepted that modern microwave ovens are

Žharmless leakage of microwaves from ovens is in-.significant at least when properly used, whereas a

number of investigations on radar operators has iden-tified some ‘‘thermal’’ effects that lead to safetyprecautions minimising the hazards. But little isknown about the health hazards of cellular tele-phones that are rapidly gaining popularity. There areseveral systems in use which allow many users tocommunicate via the system simultaneously. Thedominant access technique in Europe is the so-called

Ž .TDMA technique Time Division Multiple AccessŽwhich is used in GSM Global System for Mobile

. Žcommunication , DECT Digital European Cordless. ŽTelecommunications , DCS 1800 Digital personal

. ŽCommunication System and in TETRA Trans Eu-.ropean Trunked RAdio systems. The carrier fre-

quency bands allocated for these services are setmainly in the spectrum regions of 800–900 MHz and

Ž1.8–2.2 GHz. With regard to these and other mobile.phone systems, one has to distinguish the possible

effects emanating from transmission antennas andmobile base station antennas from the mobile phonehandset itself. People may be exposed to all these

sources, but it is the handset that is most oftensuspected of having deleterious effects. There is aconcern that, as the antenna of the handset is broughtclose to the head when calls are made or received,there may be a thermal insult at the molecular orcellular level. According to some scientists part ofthe microwave-energy is absorbed by the head andmay eventually produce so-called ‘hot-spots’ in the

Ž w x.brain e.g. 3,4 . Also, non-thermal effects are oftenanticipated. Most often headache, eye injury andcancer are mentioned as potential biological effectsw x5 . However, the only established possible danger-ous effect of mobile phones is the interference insome circumstances with pacemakers and other ap-paratus prompting a warning to users from health

Ž w x.authorities e.g. 6 . With regard to headache, canceror other serious illnesses, little is known for sure.Therefore there is an urgent need for the updating ofour knowledge. Indeed, not only the general public,but also some of the scientists involved in researchon microwave or radiofrequency bioeffects are suffi-ciently worried about the possible adverse healtheffects of present-day mobile telephones to recom-mend restricted use of mobile phone handsets. A feweven advise not to use them at all. Although most

( )L. VerschaeÕe, A. MaesrMutation Research 410 1998 141–165 143

scientists claim that no research to date suggestsserious cause for concern, they all agree that the

Žexplosive growth in use of mobile telephones In1995 there were over 85 million mobile telephone

.subscribers world-wide justifies further research.In this paper we review the investigations that

have been performed on the genotoxic effects ofradiofrequency fields, including investigations oncancer and teratogenic effects.

2. Quantities and units

Non ionising radiations are those electromagneticradiations with a wavelength equal or higher than10y7 m. The different non-ionising radiations aregiven in Fig. 1 where it can be seen that wavelength,frequency and photon energy are inter-related. Non-ionising radiations have photon energies lower thanapproximately 12 eV, which is considered theboundary with ionising radiations. This energy is toolow to induce ionisations of molecules and too lowto break even the weakest chemical bond. Quantitiesand units differ greatly between the different kindsof electromagnetic radiations as the physical, butalso the biological properties differ greatly. There-fore there is no such thing as an absorbed dose ordose-equivalent that we know from ionising radia-tions and that is common to all non-ionising electro-magnetic fields or waves. High-frequency electro-magnetic fields are quantified in terms of electric

Ž .field strength E, expressed as volts per meter Vrm ,and magnetic field strengths H, expressed as am-

Ž .peres per meter Arm . A ‘dose’ to which the bodyor tissue or cells are exposed is expressed as the

Ž .specific absorption ratio SAR . It gives an evalua-tion of the energy transfer to the body, tissue or cellsper unit of time and per mass. It is expressed as

Ž .watts per kilogram Wrkg . In biological materialsonly the electric field contributes to energy absorp-tion. The specific absorption rate is given by thefollowing formula:

< < 2SARs E srr

where s is the electrical conductivity of the medium

Ž .in Siemens per meter and r the density of theŽ 3.medium in kgrm . The SAR can thus be calcu-

Žlated by above equation or measured by measure-ments of temperature increases in the exposed sub-

.ject or object . However, the ‘dosimetry’ remains avery complicated task, among others because of the

w xdifferent electrical properties of different tissues 4,7 .The SAR is, e.g., dependent on the radiation source,

Ž .the exposed body or object and its configuration. Itshould be noted that, whereas biological media donot have absorption mechanisms with regard to mag-netic fields, rapidly varying magnetic fields mightyet induce absorption through secondary inducedelectric currents.

Exposure to fields can be in the near field, whichis the region close to the source antenna, or in the farfield. In the far field the high-frequency electromag-netic field is often quantified in terms of power fluxdensity, expressed in units of watts per squared

Ž 2 .meter Wrm .

3. Epidemiological investigations

Epidemiological studies, unlike most laboratorystudies, tend to take several years and can only giveinformation on exposures that have already occurredin people. Therefore, as mobile telephone bio-effectsare only a very recent concern, there are until nowno published epidemiological investigations oncause-specific morbidity or mortality in relation tomobile telephone use. Up to now only limited pre-liminary notes were published on, e.g., the methodol-ogy of epidemiological research with respect to the

w xuse of wireless communication 8–10 . However,some epidemiological investigations were conductedin the past with regard to other radiofrequency fieldsand applications. These studies were, among others,related to occupational exposures to radar, popula-tions living near military installations and nearbroadcasting towers, amateur radio operators and

Žusers of hand-held traffic radar devices for review,w x.see 5,10,11 . Most studies were rather small and

criticised, e.g. on grounds of wrong or insufficientdata collection, the absence of any, or adequatedosimetry and the omission to investigate potential

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Table 1Overview of investigations on in vitro RF-induced genetic effects

Exposure conditions Biological model Biological endpoint Results Comments Reference

RF-effects alonew x2.45 GHz, CW, 94 Commercialised calf thy- Analysis of thermal de- No difference with unex- Control and exposed 59

2mWrcm mus DNA naturation curves posed DNA DNA solutions weremaintained at the sametemperature

w x2.45 GHz, 15.2 Wrkg Rat kangaroo cells Chromosomal aberrations Increased incidence of The observed aberrations 60unstable chromosome are more commonly asso-aberrations ciated with ionising radi-

ationsw x2.45 G H z, 0 – 200 Chinese hamster cell lines Cytological effects C y to log ica l e ffec ts Effects observed under 21

2 ŽmWrcm nuclear vacuoles, pycnic elevated temperature con-and decondensed chro- ditionsmosomes, chromosome

.breakagew x2.45 GHz, 15 Wrkg, Rat kangaroo cells Chromosome aberrations Increased chromosome A change in cell popula- 61

Žlong-term exposure dur- aberration frequency tion by repeated passage.ing 320 days of the cells and senes-

cence may have influ-enced the resultsw x2.45 GHz, CW, 20 min Human lymphocytes Chromosomal aberrations No evidence of cytoge- 62,63

exposure, SAR from 104 and sister chromatid ex- netic damage, even underŽup to 200 Wrkg mild changes mild hyperthemia

.hyperthermia3w x w x7.7 GHz, 2 W max. power V79 Chinese hamster Cytogenetic effects Increased H thymidine Thermal effect probable 64

output, SAR not reported cells incorporation and chro-mosome aberrations

w x7.7 GHz, 2 W max. power V79 Chinese hamster Cytogenetic effects Effect on colony forming Thermal effect probable 23output, SAR not reported cells ability, chromosome

aberrations and micronu-clei

w x7.7 GHz, 2 W max. power Human lymphocytes Cytogenetic effects Chromosome aberrations Thermal effect probable 65output, SAR not reported and micronuclei

w x2.45 GHz, 50 Hz modu- Human lymphocytes Chromosome aberrations, Increased frequency of Temperature computer- 22lated, 30 and 120 min micronuclei and sister chromosome aberrations controlled at 36.18C dur-exposure, 75 Wrkg chromatid exchanges and micronuclei. No mi- ing the complete expo-

crowave induced sister sure time. Yet a heatingchromatid exchange fre- effect cannot be ruled outquency or influence onthe cell proliferation

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w xIn situ exposure near var- Tradescantia Micronuclei Increased micronucleus The effect occurred at 24ious broadcasting antenna frequency field levels of 27.5 VrmŽ10 – 21 M Hz short and 0.073 Arm which

.waves should not cause any sig-nificant heating of thesamples

w x96 GHz, 50 Hz amplitude Human lymphocytes Micronuclei Increased micronucleus Thermal increase of 58C 20modulated, 10 min expo- frequencysure, 100 Wrkg

w x0.954 GHz from a GSM Human lymphocytes Chromosome aberrations Slight increase in chro- No increased DNA dam- 66base-station, continuous, mosome aberration fre- age according to the alka-

Ž60–120 min exposure quency after exposure line comet assay unpub-.lished results

w xTEM or GTEM-cells; Human lymphocytes Chromosome aberrations, No indications of any 67440, 900 and 1800 MHz, sister chromatid ex- RF-induced cytogeneticexposure at 378C during changes, micronuclei, cell damage39 to 70 h proliferation, HGPRT-

mutationsw x415 MHz, 10–30 min, 15 Human lymphocytes Micronuclei Increased micro nucleus Increase in micronucleus 68

W frequency frequency was related tothe exposure time

w x935.2 MHz, CW, 2 h Human lymphocytes Chromosome aberrations No indication of direct 27exposure, SAR s 0.4 and DNA single strand DNA or chromosome ef-

ŽWrkg breaks single cell gel fect.electrophoresis assay

Synergismsw x2450 MHz pulsed, CHO cells SCEs No increased SCE fre- 69

249mWrcm , SARs34 quency in cells exposedWrkg. Cells are simulta- to RFs alone or withneously irradiated and MMC compared to MMCMMC exposed alone

w x350 and 850 MHz and Human diploid fibrob- DNA repair RF alone, either continu- 701.2 GHz, pulsed 1 to 10 lasts ous or pulsed, has no

2mWrcm , SARs0.39– effect on the DNA repair.4.5 Wrkg. RF irradiation RF exposure after UVof the cells followed UV damage also had no ef-irradiation fect

w x2450 MHz, pulsed, 48.8 L5178Y mouse leukae- Forward mutation assay RF exposure alone is not 712 Ž .mWrcm SAR s 30 mia cells thymidine kinase locus mutagenic. RF does not

Wrkg. Cells are simulta- affect either the inhibi-neously irradiated and tion of cell growth or theMMC exposed extent of mutagenesis re-

sulting from treatmentwith MMC alone

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Ž .Table 1 continued

Exposure conditions Biological model Biological endpoint Results Comments Reference

w x2450 MHz, pulsed CHO cells Cell cycle progression RF does not affect 72249 mWrcm , SAR s and SCEs changes in cell progres-

33.8 Wrkg. Cells are si- sion caused by adri-multaneously irradiated amycin. RF does notand adriamycin exposed change the number of

SCEs that were inducedby adriamycin

w x2450 M Hz, pulsed CHO cells Chromosome aberrations RF alone does not en- 73249 mWrcm , SAR s hance the chromosome

33.8 Wrkg. Cells are si- aberration frequency. Nomultaneously irradiated alteration in the extent ofand exposed to MMC and chromosome aberrationsadriamycin for the combined treat-

ment compared to thechemicals alone

w x2450 MH , pulsed, SAR L5178Y mouse Forward mutations at the RF alone is not muta- 742

;40 Wrkg. Cells are leukaemic cells TK-locus genic. No increased mu-simultaneously exposed tation frequency for theto Proflavin combined treatment com-

pared to proflavin alone.No difference in colonysize distribution of themutant colonies

w x954 MHz, continuous, 15 Human lymphocytes SCE RF alone did not increase 26W, 49 Vrm, SARs1.56 the SCE frequency. TheWrkg. Cells exposed to SCE frequency for themitomycin C following combined treatment was

ŽRF-irradiation during always higher than for.lymphocyte cultivation MMC alone. There was

no change in cell prolifer-ation compared to controlcultures

w x935.2 MHz, CW, 2 h Human lymphocytes SCE The combined exposure 27Ž .exposure, SAR s 0.4 RFqMMC revealed a

Wrkg. Cells exposed to weak effect compared tomitomycin C following cells exposed to MMC

ŽRF-irradiation during alone.lymphocyte cultivation


confounders. This is for example illustrated in aw xrecent review paper 5 where five studies relevant to

adult cancer and RF-exposure were extensively dis-cussed. In a study on RF-exposed US Embassypersonnel in Moscow no deleterious effects werefound, but the limited number of cancer cases makesthis study rather non-informative in comparison with

w x w xother studies 12 . Milham 13 found an increasedŽ .standard mortality ratio SMR for certain cancer

sites in radio amateurs, but there was no adjustmentfor confounders and most subjects were also profes-

Ž .sionally exposed to other electric and magneticw xfields. Armstrong et al. 14 investigated electric

Ž .utility workers in France and Quebec Canada whowere exposed to different non-ionising radiation fre-quencies, including radiofrequencies. They espe-cially found a relationship with lung cancer in one of

Ž .the utilities Quebec whereas a less indicative rela-tionship was found with stomach cancer in another

Ž .utility France . These differences from one utility toanother detract somewhat from the credibility ofthese findings regarding the connection betweenelectromagnetic fields and cancer. An associationbetween lung or respiratory system cancer and RF-

w xexposure was also found by Robinette et al. 15 , butthese authors did not adjust for the possible influence

w xof smoking. Finally, Szmigielski 16 examined thecancer morbidity in Polish career military personnel.He found an excess occurrence of cancers at severalcancer sites but no individual assessment was madeof exposure levels or duration and, apart from age,adjustments for other factors, e.g. possible carcino-gen exposures, were not made. These, and otherepidemiological investigations concerned many dif-ferent modes of exposure and different frequencies.For several studies, the link between the subject’soccupation and actual exposure was questionable andvery often exposure was also to extreme low-frequency fields and different chemicals. Therefore,taking the limited epidemiological evidence togetherit must presently be concluded that no definite con-clusion can be drawn so far, either about the mobile

Ž .telephone no adequate data so far , or about otherradiofrequency fields. A number of investigations arenow being conducted with regard to cancer and otherdisorders, especially in the USA and Scandinaviancountries, but the results of most of these studies areseveral years away.

4. Genetic toxicology: in vitro laboratory investi-gations

Possible effects on DNA or chromosome structurein somatic cells are considered to be very importantas these changes could be associated with cell deathor, possibly, with the development of cancer. Fur-thermore, such effects in male or female germ cellsare important, as surviving mutations might be passedon to the next generation. Many investigations ofRF-induced genetic effects in somatic- as well as ingerm cells, therefore, have already been conducted inmany different cell and animal systems. Again, dif-ferent frequencies were investigated with emphasison the 2450 MHz frequency of microwave ovens. Anumber of frequencies used in mobile telecommuni-cation were recently also investigated, but most ofthese studies are still going on.

In the 1970s and 1980s, several investigationswere performed on RF-induced genetic changes inmicrobial test systems, essentially including Es-cherichia coli, Salmonella typhimurium and Saccha-romyces cereÕisiae. They gave invariably negativeresults and will therefore not be further discussedŽ w x.for a review, see e.g. 17–19 .

In vitro investigations using different eukaryoticcell systems are described in Table 1. It can be seenthat both positive and negative results were obtained.Most often, when some evidence for a genetic effectwas reported, this could be ascribed to hyperthermia,as the exposure conditions were clearly or mostprobably thermal in nature. This was, for example,clearly the case in an investigation by d’Ambrosio et

w xal. 20 who found an increased incidence of mi-cronuclei in microwave exposed human lympho-cytes. However, the exposure was accompanied by athermal increase of 58C. Cytological effects werealso found in Chinese hamster cells that were ex-posed to 2.45 GHz fields, but again these effectswere observed under elevated temperature conditionsw x21 . Investigating the same microwave frequency,we exposed human whole blood cells in such a waythat the temperature of the blood remained constantat 36.18C. The SAR was calculated as 75.5 Wrkg,which again clearly suggests that the observed chro-mosomal abnormalities in the lymphocytes were ob-

w xtained under thermal exposure conditions 22 . Insome instances a thermal effect might be anticipated


even if the exposure was described as ‘‘being com-parable to everyday environmental conditions’’. SARvalues or temperature measurements were missingbut the data were so much resembling, e.g. thermalkilling curves, that a thermal effect is more than

Ž w x.probable e.g. 23 . Some non-thermal positive re-Ž w x.sponses were also reported e.g. 24 , but they could

possibly be due to so called sporadic positive re-sponses. Reviews of assays used to detect DNAalterations have shown that such sporadic positive

w xresponses are indeed obtained from time to time 25 .Yet, a number of positive results remain puzzlingand should be further investigated.

ŽBecause of the many negative findings especiallyin bacteria and algae but also in mammalian or

.human cells and as positive findings were almostinvariably connected with thermal exposure condi-tions or with RF-independent situations, it may beconcluded that in vitro RF-exposure appears not toinduce any genetic damage under non-thermal condi-tions. Therefore we believe that synergistic investiga-tions deserves special attention. Indeed, people areexposed to many different influences, and theoreti-cally it may well be that a RF-exposure alone isineffective whereas this exposure might enhance themutagenicity, carcinogenicity or teratogenicity ofchemical or physical factors. As shown in Table 1,most often no synergistic effect was found betweenthe applied field and a number of known mutagensŽ .e.g. mitomycin C, adriamycin, proflavin when theexposures were simultaneous. However, when theRF-exposure precedes the mutagen, a synergisticeffect is sometimes found. This was the case withmitomycin C in a recent investigation of 954-MHzwaves emitted by the antenna of a GSM base stationŽ . w x15 W power output, SARs1.5 Wrkg 26 . How-ever, when cells were exposed waves to 935.2 MHzŽ .4.5 W followed by mitomycin C, synergism was

w xmuch less evident 27 . We are presently investigat-Žing the possible synergistic effects of 450 MHz 15

. Ž .W , and 900 MHz 2–50 W fields with mitomycinC and X-rays, but so far the results are not very clearand predominantly negative. According to anotherinvestigation microwave radiation also increases themutagenic properties of ethyl methanesulfonateŽ . w xEMS in CHO cells 28 . The above investigationsreporting a synergistic action of RF-fields withchemical or physical agents corroborates the earlier

finding that microwaves enhance, in human cancers,w xthe effects of some cytotoxic agents 29 . It should

be stressed that, so far, no mechanistic studies havebeen conducted in order to explain the reportedsynergisms. As long as this is not done, the resultsare only of limited value.

5. Genetic toxicology: in vivo laboratory investi-gations

Several studies were conducted over the past 20years using Drosophila melanogaster as the testorganism. As for the experiments with micro-organisms, they all yielded negative results. There-fore we will also refer to the earlier mentionedreview papers. As seen in Tables 2 and 3, experi-ments in mammals gave more conflicting results.This was true as well for investigations on germ cellsas for investigations on somatic cells.

5.1. Testicular function and male infertility

Most of the studies on reproduction and develop-ment of small mammals exposed to radiofrequency-and microwave radiation have shown effects that canbe related to an increase in temperature. Severalstudies have shown, for example, that acute mi-crowave exposure can affect spermatogenic epithe-lium and thus male fertility through a raising of the

Ž w x.testicular temperature e.g. 30,31 . The primaryspermatocytes were often identified as a particularlysensitive stage and the response identified as identi-cal to conventional heating. Some of the investiga-tions were conducted in anaesthetised rats and miceŽ w x.e.g. 30–32 and are therefore of little value withrespect to the determination of acceptable limits ofhuman exposure. Anaesthetised animals indeed showan altered temperature regulation. The exposure ofconscious animals is thus of greater relevance toexposure standards. Here, experiments have shownthat acute and chronic exposure of conscious miceand rats very often do not alter the testicular function

Ž w x.or fertility e.g. 33 . Effects were only found inŽextreme conditions e.g. extreme high increase in

rectal andror testicular temperature.

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Table 2Overview of investigations on in vivo RF-induced genetic effects in somatic cells

Exposure Animal Biological Main Comments Referencesconditions species endpoint results

w x2.45 GHz, SAR up to 21 Chinese hamsters Chromosomal aberrations No RF-effect found Rectal temperature in- 75Wrkg in blood lymphocytes crease of 1.68C in the

high exposure group.Long cell cultivation timefollowing exposure maydisadvantage cells withcytogenetic damage

w x9.4 GHz, pulse-mod- Male Balbrc mice Chromosome aberrations SAR dependent increase 762ulated, 1–100 Wrm , 1 in male germ cells ex- in the frequency of chro-

hrday over 2 weeks posed as spermatocytes mosome exchanges andother cytogenetic effects

w x2.4 GHz, SAR s 21 Mouse Sister chromatid ex- No RF-effect found 77Wrkg, chronic exposure changes in bone marrow8 hrday for 28 days cells

w x2.45 GHz, CW, 2 hrday, Male Swiss albino mice DNA analysis with syn- Altered band patterns of 3812, 150 and 200 days, 0.1 thetic oligo probes brain and testes DNA

2W rm , SA R s 1.2 from exposed miceWrkg

w x2.45 GHz, pulsed, 2 ms Male Sprague-Dawley DNA damage in brain Increased DNA damage 39,40puls width, 500 pps, or rats cells by the single cell for both continuous andCW, SARs1.2 Wrkg, 2 gel electrophoresis assay pulsed fieldsh exposure

Ž w x2.45 GHz 2 ms pulses, Male Sprague-Dawley DNA double-strand Increased DNA double- 41.500 pps , 2 h exposure at rats breaks in brain cells with strand breaks following

22 mWrcm , SARs1.2 the single cell gel elec- RF-exposure. The effectWrkg Naltrexone injec- trophoresis assay was partially blocked by

Ž .tions 1 mgrkg before treatment with naltrexoneand after RF-exposure

w x2.45 GHz; 20 hrday, 7 C3HrHeJ mice; prone to Micronuclei in peripheral No significant difference Also no difference in mi- 125daysrweek during 18 mammary tumours blood and bone marrow in exposed and sham-ex- cronuclei between bothm onths; SAR s 1.0 posed animals groups when the animalsWrkg with mammary tumours

were considered sepa-rately

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Overview of investigations on in vivo RF-induced genetic effects with regard to reproduction and teratogenesis

Exposure Animal Biological Main Comments Referenceconditions species endpoint results

w xAcute microwave expo- Anaesthetised rats and Effects on male reproduc- Elevated testicular tem- 30sure of testes mice tive system perature and depletion of

the spermatogonic epithe-lium

w x9.4 GHz, pulse-modula- Mice Effects on male reproduc- Chromosome aberrations SAR-dependent increase 762ted, 1–100 Wrm , 1 hrd tive system in male germ cells ex- in the frequency of chro-

over 2 weeks posed as spermatocytes mosome exchanges andother cytogenetic effects

w x2.45 GHz, 30 min expo- Anaesthetised Mice Effects on male reproduc- Temperature dependent Response identical to that 32sure, half-body SARs30 tive system depletion of primary of conventional heatingWrkg spermatocytes. Threshold

at 398Cw x2.45 GHz, SAR s 44 Anaesthetised Mice Effects on male reproduc- Decreased sperm count Maximal effect at sper- 31

Wrkg tive system and increase in abnormal matocyte and spermatidsperm exposure

w x1.3 GHz, pulse modu- Rats Effects on male reproduc- No statistical significant Body temperature raised 78Žlated 1 ms pulses at 600 tive system effect on daily sperm pro- by 1.58C

.pps , whole body SARs duction, number of epi-6.3 Wrkg; exposure 6 didymal sperm, spermhrd for 9 days morphology and mass of

testes and epididymesw x1.3 GHz, CW, exposure 8 Conscious rats Effects on male reproduc- No significant differences Rectal temperature raised 79

h at SARs9 Wrkg tive system in testicular function by 4.58Cw x2.45 GHz, SAR s 5.6 Conscious rats Effects on male reproduc- Transient reduction in Rectal temperature esti- 80

Wrkg, exposure for 80 h tive system fertility mated to have raised toover a 4 w period 418C and testicular tem-

Žperature to 378C prob-ably no loss in fertility at

.lower temperatures2 w x2.45 GHz, 100 mWrcm Mice Dominant lethality No dominant lethality, in- Males mated 6–7 weeks 812for 10 min; 50 mWrcm crease in mutagenicity in after exposure. Effects on

Ž .3= over 1 day or 4= some instances mutagenicity thought toover 2 weeks be due to a temperature

increasew x2.45 GHz, CW, 1.7 Mice Dominant lethality Increased dominant May be due to tempera- 82

2kWrm for 70 s lethality, abnormal sperm ture changesmorphology and reducedmale fertility

w x1.7 GHz, 50 Wrkg dur- Mice Dominant lethality Induction of dominant 83ing 30 min lethals

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w x2.45 GHz, CW, 43 Wrkg Mice Dominant lethality Reduced pregnancy rate Effects probably the re- 84during 30 min and pre-implantation sur- sult of a heating effect

vival. No dominantlethality

w x2.45 GHz, exposure dur- Conscious mice Dominant lethality No effect on pregnancy 85ing 120 h over an 8-week rates, pre-implantationperiod, SARs5 Wrkg; survival or testes weight.mated after the exposureperiod over the following8 weeks

w x2.45 GHz, CW, 0.05–20 Mice Sperm abnormalities Increased frequency of 86Wrkg, 6 h over 2 weeks sperm abnormalities

w x2.45 GHz, exposure 16 Conscious mice Sperm abnormalities No significant effect on Testes temperature unaf- 87hrday for up to 30 days; sperm count and number fectedSARF20 Wrkg of abnormal sperm

w x2.45 GHz, exposure at Mice Embryogenesisrteratoge- Mainly exencephaly Effects increased with in- 88SARsF112 Wrkg for nesis creasing exposureup to 5 min

w x2.45 GHz, exposure 100 Mice Embryogenesisrteratoge- Significant decreased No abnormal raise in 89minrday throughout ges- nesis mean mass of live foe- body temperaturetation at SARs2, 8 or tuses in the high expo-22 Wrkg sure group

w x2.7.12 GHz, exposure Rats Embryogenesisrteratoge- Abnormal development, Rectal temperature raised 90–92during 20–40 minrday at nesis embryorfoetal deaths at to 438C. TeratogenicitySARs11 Wrkg all stages of development directly related to the

temperature of the damduring exposure and tothe duration of exposure

w x6 GHz, SARs7 Wrkg, Rats Embryogenesisrteratoge- Slight growth retardation Here the SAR was re- 93,94exposure 8 hrday nesis no evidence of increased ported to be insufficientthroughout pregnancy embryo or foetal deaths to raise the body temper-

or of developmental ab- ature significantlynormalities subtle be-havioural effects werenoticed post-natally

w x2.45 GHz, 100 minrday Rats Embryogenesisrteratoge- Significant mean body Maternal temperatures 95,96Žfrom day 6 to day 15 of nesis weight of the foetuses at raised to about 408C both.gestation at 6 or 4 Wrkg 6 Wrkg exposure conditions

w x2.45 GHz, 6 hrday Rats Embryogenesisrteratoge- No effect No increased rectal tem- 97,98throughout gestation; es- nesis peraturetimated SAR s 2 – 4Wrkg

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Exposure Animal Biological Main Comments Referenceconditions species endpoint results

w x915 MHz, 6 hrday Rats Embryogenesisrteratoge- No effect Maternal temperature un- 99,100throughout pregnancy, es- nesis affectedtim ated SA R s 3.5Wrkg

w x100 MHz, 0.4 Wrkg, 6 h Rats Embryogenesisrteratoge- No effect 10140 minrday on day 6–11 nesisof gestation

2 w x27.12 MHz at 1 Wrm Rats Embryogenesisrteratoge- Significant decrease in Normal rectal tempera- 102from day 0 up to day 20 nesis post-implantation sur- ture results difficult toof gestation, SARs10–4 vival and reduced cranial reconcile with other in-Wrkg ossification vestigations

w x2.45 GHz, SARs7, 28 Mice Embryogenesisrteratoge- Significant reduction in Colonic temperature rose 103,104or 40 Wrkg, 8 hrday for nesis implantation sites per lit- by 1 or 2.38C in the 2various times of gestation ter and in foetal weight at highest exposure groups;

40 Wrkg and exposure respective exposure lev-during day 1–6; signifi- els assumed to be atcant increase in % of thresholdm alform ed foetusesŽ .mainly cleft palate forexposures at day 6–15Ž .same SAR ; not con-firmed at later experi-ment

w x2.45 GHz, CW, 100 Mice Embryogenesisrteratoge- Lowered foetal weight 105,106minrday during 6–17 nesis and delayed skeletal mat-days of gestation, SARs uration persistent delay of16 Wrkg brain maturation

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w x2.45 GHz, 100 minrday Syrian hamster Embryogenesisrteratoge- Increased foetal deaths, Mean maternal rectal 107from day 6–14 of gesta- nesis decreased foetal weight temperature raised 0.4tion, SAR s 16 – 18 and decreased skeletal and 1.68C resp.Wrkg maturity observed at the

highest SAR-valuesw x2.45 GHz, 2 hrday, 7 Mice Embryogenesisrteratoge- Significant reduction in Rectal temperature in- 108

daysrweek on day 1–7, nesis post-implantation sur- creased by 1.5–2.08C8–18 or 1–18 of gesta- vival; increased intra- during each exposuretion, SARs6 or 9 Wrkg cranial and intra-abdomi-

nal bleeding; post-natallymarkedly decreased resis-tance to viral and bacte-rial infection

w x2.45 GHz et 10, 100 or Mice Embryogenesisrteratoge- Enhanced effect of the 28C increased rectal tem- 1092400 Wrm , SARs0.5, nesis chemical teratogen cyto- perature in highest expo-

Ž4–5 and 16–18 Wrkg, 2 sine arabinoside 10 sure group.hrday from day 1 to 18 mgrkg on day 9 ; mi-

of gestation crowaves alone resultedin reduced foetal body

ŽŽ .mass 4–5 Wrkg ; in-creased post-implantation

Ž .deaths 16–18 Wrkgw x10 MHz, continuous wa- Rats Embryogenesisrteratoge- Combined exposures en- 110

ves, SAR s6.6 Wrkg nesis hance the foetal malfor-Ž2-methoxyethanol oral mation frequency as well

.intake administration 5 as the severity of malfor-min before RF irradiation mations

w x2.45 GHz Mice Sex-linked recessive No difference between Rectal temperature in the 33lethals sham-exposed and RF- highest exposed group

exposed animals rose by up to 38C

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Table 4Overview of investigations on RF-induced genetic effects in human subjects

Exposed subjects Cells investigated Genetic endpoint Main results Comments Referencew xProfessionally exposed sub Human lymphocytes Chromosome aberrations No increase in chromo- Exposure to RF-fields is 44

Žjects; frequencies ranging some damage found in relatively pure no knownŽ .from 400 kHz to 20 GHz radio-lineman who work other professionally ex-

with radiofrequencies at posuresor below occupational ex-posure limits

w xProfessionally exposed sub- Human lymphocytes Micronuclei Increased micronucleus Workers exposed to other 432Ž .jects 10 mWrcm , fre- frequency in exposed environmental influ -

quencies ranging from 1250 subjects compared to ences?to 1350 MHz controls

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Table 5A few in vitro cancer related studies

Exposure Biological Biological Main Comments Referenceconditions model endpoint results

w xCells in test-tubes ex- Human lymphocytes According to control ex- 111Lymphoblastoıd transfor- Induction of lymphoblas-¨posed for 3–5 days in periments the effect wasmation toıd transformation by the¨anechoic chamber to not due to a heating ef-microwave radiationpulsed 10 cm mi- fectcrowaves from a box hornantenna

w xAmplitude modulated 45 Reuber H35 hepatoma ODC activity Increased ODC activity 48O MHz waves, 10 cells, CHO cells and 294

2Wrm , eventually after T human melanoma cellsTPA application

w xAmplitude modulated mi- Mouse fibroblasts ODC activity Increased ODC activity Increase is at much lower 49,112crowaves, SAR s 3 level than treatment withWrkg a chemical promoter

w xAmplitude modulated mi- C3H10T1r2 cells in vitro cell transforma- Enhanced cell transfor- Some inconsistency was 113–115crowaves, SAR s 0.1– tion mation found between the differ-4.4 Wrkg, eventually ent studies. Furthermore,combined with X-rays, C3H10T1r2 cells arefollowed by treatment chromosomally abnormalwith TPA and their response to pro-

liferative stimuli may beatypical

q q q q w x2.45 GHz Human red blood cells Na ,K -ATPase activity Inhibition of Na ,K - 45ATPase activity

w x2.45 GHz, CW, SARs Glioma cells or human RNA precursor Elevated transcription and 46,473w x5–20 Wrkg lymphocytes H uridine or DNA pre- proliferation at SARs25

3w xcursor H thymidine in- Wrkg but unchanged atcorporation higher SARs

w x27 MHz or 2.45 GHz, CHO cells Cell cycle alterations Cell cycle alterations Exposure under ‘‘isother- 116ŽCW, SAR s 5 or 25 found at both frequen- mal’’ conditions 37"

.Wrkg cies, 2.45 GHz being 0.28Cmore effective in induc-ing alterations

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Table 6Review of some cancer studies in RF or microwave exposed laboratory animals

Exposure conditions Biological model Biological endpoint Results Comments References

w x9.27 GHz, 2 ms pulses at Swiss mice Post-mortem analysis Microwave-induced leu- The investigation was 1172500 pps, 1000 Wrm , cosis severely criticised for

4 .5 m in r d a y , 5 several reasonsdaysrweek for 59 weeks

w x800 MHz, 2 hrday; 5 RFM adult mice Effect on longevity Non-significant increase 118daysrweek over a period in the life-span of theof 25 weeks. SAR up to exposed mice compared1.5 Wrkg to the controls. No signif-

icant changes in mean redand white blood cells

w x5 Hz pulses of 447 kVrm AKRrJ male mice Leukaemia 21% of exposed mice had Absence of complete 119peak electric field leukaemia at the end of analysis of leukaemia in-strength; 5 daysrweek for the exposure compared to cidence precludes any33 weeks 46% in the sham-exposed definite conclusion

groupw x2.54 GHz pulsed at 800 Sprague-Dawley rats General health and Significant raise in over- The biological signifi- 120

Hz; SAR s 015 – 0.4 longevity all incidence of malig- cance of the results wasWrkg nancies questioned by the authors

because the higher inci-dence level of specificmalignancies was similarto what was previouslyreported as being normalfor untreated rats

w x2.45 GHz, 35 Wrkg; 20 CFW mice exposed in Tumour incidence Significantly lower tu- 121minrday during days utero. Mice injected with mour incidence in mice11–14 of gestation lymphoreticular sarcoma irradiated in utero and ir-

cells at day 16 of age and radiated or sham-irradia-further irradiated or not ted post-natally. Mice ir-

radiated in utero and fol-lowed for 36 months hadinitially a lower tumourdevelopment rate, butthen the rate increased tobecome similar

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2 w x2.45 GHz, 500 Wrm , BALBrc mice s.c. in- Tumour growth and lung Temporary tumour re- 122SARs25 Wrkg; 2 hr jected prior to irradiation metastases gression followed by re-day for 7 days with mouse sarcoma cells newed growth 12 days

later. More lung metas-tases in the exposed groupcompared to controls butmean survival timegreater in exposed ani-

Žmals 53 days vs. 38.days

2 w x2.45 GHz, 500 Wrm , Idem but irradiation prior Tumour growth and lung Significantly accelerated 122SARs25 Wrkg; 2 hr to injection of sarcoma metastases tumour growth and in-day for 7 days cells crease in the number of

lung metastases. Meansurvival time shortened inirradiated mice

Ž w x2.45 GHz, 50 or 150 C3HrHe mice irradiated Effect of microwaves on SAR-dependent accelera- C3HrHeA mice are ge- 542Wrm , SAR up to 3 and at age 6 weeks to 12 tumour growth and lung tion of both mammary netically predisposed to

.8 Wrkg resp.; 2 hrday, months or BALBrC cancer colony assay tumours in C3HrHeA m am m ary tum ours.6 daysrweek mice irradiated 1 or 3 mice and skin tumours in BABLrc mice exposed

months prior to or simul- BALBrc mice. Mi- to 3,4-benzopyrene byŽtaneously with exposure crowave exposure re- skin painting 5 months

w x .to benzo a pyrene sulted in an increase in treatment 2–3 Wrkgthe number of L1- gave results similar to thesarcoma cell colonies in effect of overcrowding

Ž .the lungs of irradiated chronic stressmice

w x2.45 GHz, CW or PW C57BLr6 J mice, irradia- Effect of microwaves on No effect on the rate of 52Ž10 ms pulses for 10 ms tion 15 days exposure tumour progression development of melano-

.repeated at 25 Hz ; SAR prior to s.c. injection of ma or on the mean sur-6 Ž .s1.2 Wrkg 3=10 B16 melanoma vival time 25 days

cells and during subse-quent tumour develop-ment

w xLow level pulsed 2.45 Sprague-Dawley rats Life time study including No clear evidence of an Data should eventually be 123,124GHz waves, SAR up to determination of cause of increase in tumour inci- re-analysed0.4 Wrkg; exposure from death, frequency and site dence as a result of expo-2 to 27 months of age of neoplastic and non- sure to microwaves

neoplastic lesions

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Exposure conditions Biological model Biological endpoint Results Comments References

w x915 MHz, CW, 1 W and Fisher 344 rats, injected Histopathological brain No significant difference 53modulated with 4,8,16 with rat glioma cells examination in tumour size betweenand 200 Hz in 0.5 ms experimental and controlpulses, and 50 Hz in 6 ms animals

Ž .pulses 2 W per pulse , 7hrday, 5 daysrweek dur-ing 3 weeks

2 w x2.45 GHz, 10 mWrcm BALBrc mice, 4 weeks Colon tumour incidence The 2.45 GHz microwave 512in anechoic chamber, 3 old. Animals injected radiation at 10 mWrm

hrday, 6 daysrweek over with dimethylhydrazine did not promote DMH-in-Ž .a 5-month period. SAR DMH once per week duced colon cancers in

s10–12 Wrkg during the course of the young micemicrowave treatment. Agroup DMH-treated ani-mals were also exposedto TPA once per weekfor 10 weeks from thethird week on after initialtreatment

w x900 MHz pulsed at 217 Em-Pim1 transgenic mice Lymphoma Lymphoma risk was This study does not indi- 55Hz and pulse width of 0.6 found to be significantly cate that RF-field expo-ms. Two half-hour expo- higher in the exposed sure would be specifi-sure periods per day for mice than in the controls cally lymphomagenic in18 months. SARs0.13– normal mice. So far the0.4 Wrkg significance of the find-

ing for mobile phone-lin-ked human health is notclear


5.2. Teratogenicity

Several studies have shown that sufficiently ele-vated body temperatures are teratogenic to a number

Ž wof mammalian species, including primates e.g. 34–x.36 .

Ž .As microwave or RF -induced teratogenic effectswere usually accompanied by a significant rise inmaternal body temperature, they hence could be

Ž w x .ascribed to this thermal effect see 37 for a review .Yet, the results of studies on microwave inducedfoetal loss and developmental malformations weresometimes inconsistent with others. This is mostprobably due to species differences with regard totheir thermo-susceptibility; rats appear more likely tolose heat-damaged embryos than to give birth to

w xmalformed young 34 , whereas in other mammals awider range is observed between a teratogenic expo-sure and a lethal exposure.

Overall, the conclusion should be that the evi-dence suggests that only exposures that have anappreciable heating effect are likely to affect theembryo adversely.

5.3. Somatic cell genetic effects

Most studies that were published so far did notdemonstrate convincingly any direct DNA damageafter acute or chronic exposure of biological systems

Ž w x.to RF-fields e.g. 17,19 , in particular when temper-atures were maintained within normal physiologicallimits. However, especially two recent investigationshave suggested that RF-fields yet can affect DNAŽ . w xsee Table 2 . In the first, Sarkar et al. 38 foundevidence of an alteration in the length of a DNAmicrosatellite sequence in cells from brain and testisof mice exposed to 2.45-GHz fields. In another

w xseries of experiments, Lai and Singh 39,40 demon-strated that acute exposure to low-intensity radiofre-quency radiation increased DNA strand breaks inbrain cells of the rat. Furthermore, DNA double-strand breaks were lower in animals to which theopioid antagonist naltrexone was injected immedi-

w xately before and after the RF-exposure 41 . Thesedata support the hypothesis that radiofrequency radi-ation activates endogenous opioids in the brain which

w xin turn cause biological effects 42 . Before speculat-ing about the possible consequences of these find-

ings, especially with regard to the use of cellularŽ .phones which was abundantly done in the media , it

should be realised that the data were obtained formore than a worst-case exposure situation and for2450-MHz fields that do not correspond to mobilephone frequencies. The significance of these data,therefore, remain unclear to date. These experimentsshould also be replicated before the results can beused in any health risk assessment, especially giventhe weight of evidence suggesting that RF fields arenot genotoxic.

In humans only few studies have been performedŽ .Table 4 . An increased incidence in micronucleatedwhite blood cells from professionally exposed sub-

w xjects was found in one investigation 43 , but it is notclear to what extent the subjects were also exposedto other environmental influences. A previous cyto-genetic investigation of radio-linemen that were al-most solely exposed to RF-fields gave negative re-

w xsults 44 . We are presently performing another studyon maintenance workers being professionally ex-posed to microwaves of different frequencies, and sofar we have not found a cytogenetic effect in thesesubjects as compared to non-exposed control sub-jects. However, the study is not yet completed and in

Ž .particular some in vitro synergy experiments shouldbe repeated.

Ž .According to above and other cytogenetic inves-tigations, it must be clear that caution must beexercised in making any general conclusion on theclastogenicity, genotoxicity and heritable effects ofradiofrequency fields and microwaves.

6. Cancer-related in vitro investigations

As stated above, the evidence for a clastogenic orgenetic effect of microwaves is rather contradictory,although overall it may be concluded that RF-fieldsrmicrowaves are not genotoxic under non-ther-mal conditions. Therefore it may also be concludedthat RF-fields or microwaves are not tumour initia-tors and that, if they are somehow related to carcino-genicity, this should be by some other mechanismŽe.g. by influencing tumour promotion or by increas-

.ing the uptake of carcinogens in cells . Table 5summarises most relevant investigations on in vitrocancer related RF-effects. It shows that RF-fields


Žmay affect ion fluxes through cell membranes im-.portant signalling mechanisms via effects on ion

q q w xpumps such as Na ,K -ATPase 45 in human redblood cells exposed to RF and microwave radiation.Non-thermal effects were also reported on grosstranscription as measured by incorporation of spe-

w3 xcific RNA or DNA precursor H uridine orw3 x w xH thymidine 46,47 . Cell transformation was

Žshown to be induced in a dose-dependent way in-.crease with increasing SAR value and according to

a series of papers, low-level Hz-modulated mi-crowave radiation may affect intracellular activitiesof enzymes involved in neoplastic promotion withoutmeasurable influence on the overall DNA synthesis.For example, a number of investigations broughtsome evidence of an effect on intracellular levels of

Ž .ornithine decarboxylase ODC which is an enzymew xusually implicated in tumour promotion 48,49 . Tu-

mour promoters do increase the ODC synthesis. Thiswas also found for microwaves although the mi-crowave effect was much weaker and occurred onlyfor certain modulations of the carrier wave.

To date it is not very clear what these resultsmean in terms of in vivo carcinogenesis.

7. Cancer-related in vivo investigations

A relatively large number of in vivo investiga-tions, mainly on 2450-MHz waves but also on other

Žfrequencies, have already been performed Table 6w x.and 50 . Results of many cancer investigations

Žespecially when ongoing and so far unpublished.investigations are included do not support the sug-

gestion that even an extensive daily exposure toEMF causes tumour growth or tumour promotionŽ w x.e.g. 51–53 . Overall, the evidence for a co-carcinogenic effect or a RF-induced influence ontumour progression is not substantive. Yet, therewere a few positive results that are sufficiently in-dicative to merit further investigation. This is the

w xcase for the investigation of Szmigielski et al. 54w h o o b serv ed faste r d ev e lo p m en t o f

w xbenzo a pyrene-induced skin tumours in mice thatwere exposed for some months to sub-thermal 2450-MHz microwaves. Also, a very recent investigationon transgenic mice expressing an activated Pim1oncogene in their lymphoid cells furthermore turned

up to be probably the most significant finding yet ofw xadverse effects 55 . The mice were exposed to

Ž .pulsed digital GSM-type phone radiation at a powerdensity roughly equal to a cell-phone transmitting fortwo half-hour periods each day. A significant in-crease in B-cell lymphoma was evident early in theexperiment, but the incidence continued to rise overthe 18-month exposure period. The experiment wasconducted in the ‘‘far field’’ at distances greaterfrom the mice than the cell phone is normally heldfrom the head. It is not yet clear what these resultsmean in terms of public health, but it seems clearthat they should be taken seriously and prompt fur-ther research.

8. Other cancer-related studies

The above-mentioned investigations may be con-sidered more or less directly related to cancer. Otherinvestigations on other physiological processes mayof course also be related to cancer. This is especiallytrue for effects on the immune system. It is indeedwell known that the immune system plays an impor-tant role in controlling the proliferation of cancercells. Therefore, numerous studies have also beenperformed at various power levels and frequencies.However, these investigations are well beyond thescope of this report and will therefore not be dis-cussed in detail. The interested reader can find some

Žexcellent review papers on this subject e.g. thisw x.issue and 18,56–58 .

9. Conclusion

Today, it is still not very clear whether proper useof radiofrequency fields and microwave-emitting de-vices may be harmful to human beings. Many inves-tigations have been performed in the past and manydifferent end-points have been studied. Investigationson genetic- or cancer-related effects are among them.It was almost invariably found that biological effectsof acute exposure to these fields were consistent withresponses to induced heating, resulting in frank risesin cellular, tissue or body temperature of 18C ormore. This is consistent with a SAR-value above

Ž .1–2 Wrkg. Most often, experimental thermal con-


ditions are not encountered in normal life situationsor correspond to a worst-case situation that mayoccur for short periods of time. However, in the caseof low-level exposures, the site of energy depositionmight be such that micro-heating could occur. Somedata are rather puzzling, and effects obtained undernon-thermal conditions should require further inves-tigations. There is a need for better understanding ofthis type of interaction. In particular, synergisticeffects and mechanistic investigations should behighlighted. With regard to potential health effects ofmobile phones, especially long term effects, theavailable data are at present too scarce. Furtherstudies are needed before any valid conclusion canbe drawn.

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