Ecolog2000

Mobile Telecommunications and Health

Review of the current scientific research
in view of precautionary health protection

April 2000
ECOLOG-Institut

Translated by
Andrea Klein


Review of the Current Scientific Research
in view of Precautionary Health Protection

Commissioned by
T‐Mobil
DeTeMobil Deutsche Telekom MobilNet GmbH

Authors
Dr Kerstin Hennies
Dr H.‐Peter Neitzke
Dr Hartmut Voigt

With the support of
Dr Gisa‐Kahle Anders

ECOLOG‐Institut
für sozial‐ökologische Forschung und Bildung gGmbH
Nieschlagstrasse 26
30449 Hannover
Tel. 0511‐92456‐46
Fax 0511‐92456‐48
Email mailbox@ecolog‐institut.de
Hannover, April 2000

Contents
1

1

1.1
1.2
2

Introduction

1
3

New Technologies and Precautionary Health Protection
Terms of Reference and Structure of the Review

5

2.1
2.2
3

Collating and Interpreting the Scientific Data (Methodology)

5
5

Primary Reciprocal Effects between High Frequency Electromagnetic Fields
and Biological Systems (Biophysical and Biochemical Processes)
3.1

3.2

3.3
3.4
3.5
4

Thermal Effects
3.1.1
Effects of Homogenous Warming
3.1.2
Microthermal Effects
Direct Field Effects
3.2.1
Effects from the Electrical Component of the Electromagnetic Field
3.2.2
Effects from the Magnetic Component of the Electromagnetic Field
Quantum Effects
Other Effects
Particular Properties of Pulsed Electromagnetic Fields

Biological Primary Effects of High Frequency Electromagnetic Fields Effects
on Cellular Level
4.1
4.2

4.3

5

Criteria for the Selection of Papers
Assessment Criteria

Gene Toxicity
Cellular Processes
4.2.1
Gene‐Transcription and Gene‐Translation
4.2.2
Membrane Function
4.2.3
Signal Transduction
4.2.4
Cell Cycle
Cell Transformation and Cell Proliferation
4.3.1
Cell Transformation
4.3.2
Cell Communication
4.3.3
Cell Proliferation

8
8
8
8
9
9
10
10
10
11
12
12
13
13
14
14
16
16
17
17
17

Patho‐Physiological Effects

19

5.1
5.2

19
19
19
20
20
22
23
23
24

5.3

Immune System
Central Nervous System
5.2.1
Blood Brain Barrier
5.2.2
Neurotransmitters
5.2.3
Electroencephalogram (EEG)
5.2.4
Cognitive Functions
Hormone Systems
5.3.1
Stress Hormones
5.3.2
Melatonin
iii

Pathological Effects

26

6.1

6

26
26
27
28

6.2
7
8

Results of Experimental Studies
6.1.1
Cancer
6.1.2
Infertility and Teratogenic Effects
Results of Epidemiological Studies

Health Risks to Humans Resulting from Exposure to the Electromagnetic
Fields of Mobile Telecommunications

33

Recommendations

37

8.1
8.2

Precautionary Health Protection in Relation to Exposures to
Electromagnetic Fields of Mobile Telecommunications
Scientific Studies Regarding the Health Risk of Mobile
Telecommunications

37
38

Literature

40

Appendix A

56

Studies of the effects of high frequency electromagnetic fields on the cellular level 56
Table A.1 Genotoxic Effects of High Frequency Electromagnetic Fields
Table A.2 Effects of High Frequency Electromagnetic Fields on Cellular Processes
Table A.3 Effects of High Frequency Electromagnetic Fields on Cell
Transformation and Cell Proliferation
Appendix B

66

Studies of the effects of high frequency electromagnetic fields on the central
nervous system (Blood‐Brain‐Barrier)
Table B.1 Effects of High Frequency Electromagnetic Fields on the Blood‐Brain‐
Barrier
Appendix C

66

68

Studies of the Carcenogenic Effects of High Frequency Electromagnetic Fields in
Animal Experiments
Table C.1 Animal Experiments Regarding the Carcinogenic Effects of High
Frequency Electromagnetic Fields
Appendix D

68

71

Epidemiological Studies of the health Risks of HF EMFs
Table D.1 Overview of the results of epidemiological studies regarding
exposures in the high frequency spectrum and health risks
Appendix E (only available in German)

71

82

Extracts of our database (EMFbase)
Important research papers relevant to the assessment of health risks resulting from
exposure to the electromagnetic fields of mobile telecommunications under the aspect of
precautionary health protection

iv

1 Introduction
1.1 New Technologies and Precautionary Health Protection
No technology covering virtually entire countries with its emissions has ever been rolled
out as quickly as mobile telecommunications. At the same time, there are only few direct
studies of the potential health risks of typical mobile telecommunications frequencies and
modulations for the exposed population. Also, many of the existing studies worked with
high intensities, which will only be found in rare cases in the real environment. High
intensities of high frequency electromagnetic fields can heat the absorbing tissue and
trigger stress reactions in the body and thus with rising temperatures lead to thermal
damage. Effects from high intensity high frequency EMFs, also know as thermal effects,
on the central nervous system, the immune system, the cardio‐vascular system and the
reproductive system including teratogenic effects, have been proven for mammals with a
multitude of experiments.
The results of studies of the thermal effects of high frequency EMFs form the basis of the
recommendations of the International Commission on Non‐Ionizing Radiation Protection
(ICNIRP), which, in the past, were the basis for the guidelines set by the government in
Germany and many other countries. The base guideline was an upper limit on the Specific
Absorption Rate (SAR), i.e. the amount of energy absorbed by the body from the field
within a given unit of time.
According to ICNIRP, thermal damage will not occur at SAR values of under 4 W/kg and
exposure levels of 0.4 W/kg for professional exposures and 0.08W/kg for the general
population are considered safe.
Parallel to the experiments examining thermal effects, there have been a growing number
of studies examining the effects on the body of HF EMFs at sub‐thermal intensities. We
now have a plethora of experimental studies examining a variety of effects on all levels of
the organism, ranging from effects on single cells to effects which manifest themselves as
reactions of the entire body. In addition to the experimental studies, there have been a
number of epidemiological studies in order to establish the possible causal correlations
between higher exposures to HF EMFs, for example as found near base stations, and
health damage amongst the population groups with higher exposures.
The mobile telecommunications situation reflects, once again, the dilemma already known
from chemical toxicology: The study of potential health effects cannot generally compete
with the speed of technical development and the roll out of the product. The extremely
fast roll out of the mobile telecommunications technology and the accompanying public
fear of the potential danger of this technology have stimulated research insofar that now
we have more studies examining the effects of frequencies and modulations as used in
mobile telecommunications on biological systems. There are also a growing number of
experiments using lower intensities, reflecting the real conditions of exposure in the
vicinity of base stations and equipment, so that effects found in the studies can be
extrapolated into real life conditions. The number of studies which examine the


1

physiological effects of real mobile exposures is still very low, compared to the degree of
penetration achieved by the technology and the number of (potentially) exposed persons.
The WHO amongst others, have only recently begun to develop targeted strategies to
examine the potential health risk from mobile telecommunications and results can earliest
be expected within several years.
In the meantime, it is only possible to assess the potential dangers of mobile
telecommunications using the results generated by uncoordinated research, which is still
mainly orientated towards topics and criteria of relevant to science only, rather than
addressing the requirements of society as a whole.
Faced with a state of incomplete scientific research it is necessary to chose between two
fundamentally different assessment theories when planning to assess the potential health
risks of new technologies:
The first theory is based on the (without doubt correct) scholarly understanding that is
practically impossible to prove the ‘non‐harmfulness’ to human health or the environment
of a technology, a material or a product. This understanding is interpreted in such a way
that a presupposition of ‘not guilty’ is adopted and any risks have to be unequivocally
proven.
‘Unequivocal proof’ in this context means the consistent evidence for a biological‐
physiological or an ecological chain of effects, from the biophysical or biochemical
primary effect through to the physiological effects and the resulting illness or, if
applicable, the ecological damage.
This theory, which is firmly based in scientific conservatism, has the advantage that it will
stand up in court and will not hinder the introduction of new technologies. It is
methodologically simple, since it is sufficient to examine studies which are presented as
‘proof’ with regards to their methodological correctness and their validity and then to put
all these reviewed pieces of evidence together like a jigsaw to produce a whole picture.
The complete whole picture finally constitutes the scientific proof required by the
legislators and courts.
The disadvantage of this theory is obviously the length of time necessary to obtain
enough knowledge for a completed chain of proof, during which many facts will be
created, which may later prove irreversible or only reversible with very high costs
attached, such as investments and irreversible damage to health and the environment.
The second theory solves the dilemma of the time delay. It is based on the assessment of
the potential risks of a technology on the basis of existing knowledge. If there are
sufficient indications that there may be damaging effects, the precautionary principle for
the protection of health and the environment will apply and avoidable exposures will be
avoided until such time when there is enough knowledge for a wider introduction of the
technology in question. This theory draws its justification not least from the experiences
with the introduction of technologies and products (such as asbestos, DDT, CFCs,
formaldehyde, wood preservatives, mass X‐ray screenings etc.), which were widely used,
even many years after the first clear indications of health and ecological damage had
appeared. When finally sufficient scientific proof for the health and ecological damage

2


was provided, it took many more years until the further use was finally reduced and
banned through the courts and international negotiations.
The advantage of the precautionary principle is of course primarily medical and
ecological, since exposures are initially limited to a level recognised as safe under the
precautionary principle. But it can also offer economical advantages, because firstly, it
may prevent potentially highly risky investments, but also secondly, because the
commitment to and observance of the precautionary principle will create trust within the
general population and thus increase acceptance for the placing of emitting equipment.
On the other hand, it will be the industry – as the owner of emitting equipment – who has
to bear the disadvantage of this principle, when it becomes clear that, for precautionary
reasons, an economically and technically perfectly‐suited site can’t be approved, or maybe
even an entire technology has to be abandoned.
Furthermore, the methodological difficulties of this theory must not be underestimated,
since it is not enough to prove the reliability of single scientific studies, which is just as
essential under this premise as under the first theory. The ultimate goal however is – to
remain with the jigsaw analogy – to put the existing jigsaw pieces together and recognise
early on which pictures might appear once the work is completed.

1.2 Terms of Reference and Structure of the Review
The aim of this study was the assessment of the potential risks of electromagnetic fields as
they are used for mobile telecommunications with respect to precautionary health
protection. To this aim, the scientific literature was reviewed with regards to study results
which might be of importance to the assessment of potential health risks from mobile
telecommunications.
To create a base for later scientific discussion, a list of studies which are particularly
important in this respect should be created. On the basis of these papers, the health risk
from exposure to electromagnetic fields from mobile telecommunications should be
assessed. Finally, recommendations for future scientific studies should be formulated.
The methodological aspects of this examination are presented in Chapter 2. This is
followed by a review of the current scientific knowledge of the effects of high frequency
electromagnetic fields. This review is structured according to the different levels of effects:
■ biophysical and biochemical primary effects of HF fields on organic matter as a whole
or at the level of cells and membranes (Chapter 3)
■ primary biological effects on the cellular level, i.e. on the genetic substance and on
intracellular processes as well as cell transformation and cell proliferation (Chapter 4)
■ patho‐physiological effects, i.e. physiological effects with possible but not certain
negative health implications (Chapter 5)
■ pathological effects, which means manifested illness and other effects such as the
damage of cognitive functions, which have been found in epidemiological or
experimental studies (Chapter 6).


3

The conclusions of all findings are drawn in Chapter 7. In Chapter 8, we make
recommendations for precautionary health protection with regards to exposures to the
electromagnetic fields of mobile telecommunications and for focal points for further
research.

4


2 Collating and Interpreting the Scientific Data
(Methodology)
2.1 Criteria for the Selection of Papers
In order to include a maximum of relevant literature, we analysed the literature we have
catalogued in our own database, EMFbase, as well as exploring the three following paths:
■ research in other relevant scientific databases
■ complete sifting of at least the last two full years’ issues of all relevant scientific
journals available in the Central Library of Medicine in Cologne, the Technical
Information Library in Hanover, and the Library of the Medical University of Hanover
■ evaluation of all existing monographs, reviews and conference reports related to the
subject matter
The basic literature research was finished in February 2000.
Literature databases are a convenient research tool, but their value in assessing the
current scientific knowledge in a subject matter is limited by the number of registered
publications, inconsistent use of keywords, the changing understanding of certain
procedures, effects etc. and last but not least, due to long time delays between the time of
publication and availability in the database. Furthermore, databases usually only keep
abstracts of papers, and those differ often from the full text with regards to the
presentation and interpretation of the results. Our research for this review confirmed this
observation, reflecting the results of a study of Pitkin et al. (1999) according to which
almost 40% of all papers published in the six largest medical journals contained
inaccuracies and mistakes in the abstracts. To be at the cutting edge of scientific
knowledge, it is necessary to research current scientific journals and find older papers via
monographs and reviews. Reviews are only useful to gain an overview over a subject
matter and as a source for literature leads. It is inappropriate to use assessments or
interpretations of a review study since some authors of reviews will have based their
conclusion on abstracts rather than the full texts of the papers they discuss.

2.2 Assessment Criteria
One sub‐goal of the present paper was to identify those scientific papers which are
particularly interesting for the assessment of potential health risks caused by the
electromagnetic emissions of mobile telecommunications. (Extracts from our database
EMFbase with a summary of the results of these papers can be found in Annex E. In the
source references, these papers carry an asterisk*). Only peer reviewed papers published
in scientific journals were included in our review. We also accorded weight to the ‘Impact
Factor’, which is calculated by the Institute for Scientific Information in Philadelphia. This
factor is a rough measure for the amount of importance and reputation attributed to a
scientific journal in its subject matter.

5

The papers able to pass this first filter were subsequently interpreted according to the
following criteria:
■ carrier frequency or frequency range
■ manner of modulation
■ modulation frequency or frequency range
■ power flux density
■ specific Absorption Rate
■ electric filed strength
■ duration of exposure
■ other parameters of exposure (such as other fields [incl. ELF], ambient and if applicable
body temperature, particular forms of modulation)
■ source of exposure or environment of the exposure (such as antenna emitting freely,
anechoic chamber, transmission line)
■ object of experiments (human, animal, cell system)
■ examined pathological results (manifested illness and other effects on the whole body)
■ examined patho‐physiological effects (physiological effects with a potential for health
damage)
■ examined biological effects (mostly on the cellular level)
■ examined biophysical and biochemical processes (primary effects on the level of
molecules, membranes etc.)
■ methodology of the experiments (procedures used)
■ results (including a mention if our own interpretations differ from those of the author)
■ statistical significance of the results
■ appropriateness of the model (with regards to the statements made about effects on
humans)
■ appropriateness of the methodology (methodical weakness analysis)
■ documentation of the conditions of the experiments (completeness, reproducibility)
■ context of other experiments (mention of experiments with the same or contradicting
results)
■ meaning (Main conclusions drawn from the results, importance for the assessment of
health risks for humans)
Because of the delay of science with regards to the electromagnetic frequencies emitted by
mobile telecommunications, a risk analysis cannot be limited to the frequencies and
6


modulations actually used by this technology. Therefore, we have included all papers
examining carrier frequencies from 100MHz to 10GHz. In the experiments at cellular
level, but also in animal experiments, effects have been found that only appear at certain
modulations or are a lot stronger at these modulations (chapter 3 and 4). At this point in
time it is not possible to determine whether the majority of the found effects are caused by
the HF carrier wave or the modulation. This is why we have included all forms of
modulation into this review. Because of the nature and the importance of the so‐called
‘thermal effects’ (chapter 3.1) we have not set an exclusion limit for power flux density
and Specific Absorption Rate. However, we did not include papers, in which the EMF
exposure led to a considerable rise in body temperature (>1ºC) of the animals or human
subjects.
When evaluating the papers, we kept making the following observations:
■ important single results are ‘masked’ for example when data are ‘pooled’
■ certain observations are dismissed by the authors as ‘blips’ if they don’t fit the
(expected/otherwise observed) general trend, without sufficient explanation being
offered for this dismissal
■ single results are not taken into account for statistical reasons, but a common trend is
not recognised or not sufficiently acknowledged.
In such cases, whenever this was possible based on the existing data, we proceeded to
make our own interpretations. Where our evaluation differed from the main statements of
the authors, it will be noted.


7

3 Primary Reciprocal Effects between High
Frequency Electromagnetic Fields and Biological
Systems (Biophysical and Biochemical Processes)
3.1 Thermal Effects
3.1.1 Effects of Homogenous Warming
HF electromagnetic fields are absorbed depending on the frequency and polarisation of
the fields on the one hand and the dimensions and material characteristics of the
biological system on the other hand. They cause electric currents (dominant in the range
under 1 MHz), polarisation effects and potential differences on cell membranes (in the
range between 1 MHz and 100 MHz) or trigger rotational oscillations of polar molecules
(mainly within the GHz range). All these processes can lead to a warming of the biological
material if the intensity is sufficient (Ohmic losses in the low frequency range and
dielectrical losses in the GHz range). The avoidance of health‐damaging warming is the
base of the concept of SAR, expressed by limiting the specific absorption rate, measured
as the energy absorption per unit, to a rate which will exclude overheating based on the
body’s own thermo‐regulative processes. For humans, a whole body exposure of 0.4 W/kg
corresponds approximately to half the metabolic base rate. In absence of heat conduction
or other thermal dissipation, a SAR of 0.4 W/kg will lead to a temperature rise of 10‐4K/sek
(Foster 1996) in soft tissue like muscles or the brain.

3.1.2 Microthermal Effects
The warming through microwaves is fundamentally different from the warming through
a water bath for example. In the latter case the energy is transmitted by stochastic
collisions. In microwave heating it is in the simplest case the electrical component which
puts polar molecules within the medium collectively in vibration (3.2.1). Because of
‘friction’ with the dense ambient medium, the energy is quickly transmitted to this
medium and further dissipated by collisions. When corresponding inner molecular
degrees of freedom exist, the microwave energy can also be absorbed as a quantum and,
in a large molecule, stored (3.3.). Compared to conventional warming, the absorption of a
microwave quantum is a singular process, which can lead to localised warming if the
absorbing molecules are suitably distributed. Liu & Cleary (1995) show in a theoretical
model that at the cellular level, membrane‐bound water can lead to frequency dependent
spatial discrepancies in dissipation of the SAR and the induced HF fields.
Microthermal effects can also be caused by the non‐uniformity of thermal conductivity of
tissue at microscopic level, especially when the warming is short, strong and local. This is
of importance mainly for the evaluation of pulsed fields, because in such fields, even at a
low average power flux density, the energy absorbed during a pulse can be very high.
Radiation in the form of short pulses can lead to a very high rate of temperature rise,
which can itself trigger thermoelastic waves, a phenomenon, which is inked to the
8


acoustic perception of microwaves. A high peak‐SAR can also trigger thermally‐induced
membrane phenomena (Foster 1996).

3.2 Direct Field Effects
3.2.1 Effects from the Electrical Component of the Electromagnetic
Field
The electric component of the electromagnetic field exerts a force on electrical charges,
permanent dipole moments, induced dipole moments and higher multipole moments.
The forces on charges create currents, however these only play a role in the lower HF
range, causing changes in membrane potentials (stimulation) or thermal effects (see
above).
Permanent charge distributions in biomolecules and cells lead to permanent dipole (or
higher multipole) moments. The electrical field exerts a torque on dipoles, which tries to
align the dipole moment parallel to the field. In alternating fields with not too high
frequencies, the interactions lead to oscillations of the dipoles. In dense media, these
oscillations are hindered by interactions with the surrounding particles, which lead to
heating (see above). If the particles are too large or the surrounding particle density is too
high or if the frequency of the field is too high, the oscillations cannot develop.
The threshold field strengths for the orientation of dipolar cells and other objects of
similar size (radius of approx. 1 μm) are at 100 V/m, the cut‐off frequencies in water
(temperature 300K) are at circa 0.05Hz, hence far outside the HF range. DNA molecules and
other bio‐polymers can be put into oscillation by fields with frequencies in the kHz range.
Spherical protein molecules (radius approx. 5nm) can still follow fields with frequencies
up to 400 kHz, however this requires field strengths of 106V/m (Foster 1996). Such field
strengths are not usually reached in the environment.
The interaction between a field and a particle with an induced dipole moment depends on
the field strength to the power of 2, that means, a continuous electrical alternating field
influences the particle via a constant torque, however the torque of a modulated field
follows the modulation. There is no limitation through a cut‐off frequency for the
interaction between a field and an induced dipole moment, however for frequencies over
1 MHz, the forces exerted on the cells are very small unless field strengths of several
thousand V/m are used. With such field strengths however, strong dielectrophoretic
forces appear, which can lead to cell deformations, to the orientation of non‐spherical cells
and to the so‐called coin roll effect, a stringing together of cells. Since the induced dipole
moment depends on the polarizability of the particle and the latter on the size of the
particle, even higher field strengths are needed for smaller bodies than cells
(biopolymers).
Electric fields can induce electrical potentials on cell membranes. The size of these
potentials depends on the electric field strength, the dimensions of the cell, the frequency
of the field, the electrical conductivity within and outside of the cell as well as the
capacitance of the cell membrane.


9

With frequencies above 1 MHz the membrane is practically short‐circuited and the
induced membrane potentials become very small. However, theoretical rectification
processes and non‐linear phenomena at the cell membrane have been discussed, and
these could lead to an intensification of the effect and to membrane potentials that have
an effect on cell physiology.

3.2.2 Effects from the Magnetic Component of the Electromagnetic
Field
With some exceptions, biological tissue is not magnetic and the mutual effects between
the magnetic component of an electromagnetic field and tissue are generally small.
However, the presence of magnetite crystals, which have a strong capacity to absorb the
frequency range of 0.5 to 10 GHz which is relevant for mobile telecommunications, has
been found in the human brain as well as in the tissue of many animals (*Kirschvink
1996). Under exposure to amplitude modulated or pulse modulated microwaves, the
frequency of the crystal vibrations varies according to the modulation frequency, and thus
transmits it, for example in the form of an acoustic wave onto the ambient medium and
the cell membrane, which possibly leads to changes of the permeability of the membrane
(*Kirschvink 1996). Theoretical calculations show that magnetite transmitted effects can
only occur at high densities of superparamagnetic particles (*Dobson & St. Pierre 1998).

3.3 Quantum Effects
The quantum energy from radio and microwaves in the frequency range between 100
MHz to 10 GHz is far too low to break ionic, covalent or hydrogen bonds. Bohr et al.
(*1997) have however shown theoretically, that wring resonances can be triggered in
chain molecules. The frequencies of these resonances are in the range from 1 to 10 GHz for
proteins and 10 MHz to 10 GHz for DNA molecules. The wring modes of molecules
manifest themselves as ‘torsions’ in the molecule chain, which can lead to structural
changes.
The influences of microwaves on structural changes in molecules have been found in
experiments using the protein ß‐Lactoglobuline (*Bohr & Bohr 2000). The triggering of
resonant wring modes can even lead to chain breaks, since due to White’s Theory, the
added energy can be concentrated in a very limited part of the molecule during structural
changes (*Bohr et al.). In this part, the chain can break.

3.4 Other Effects
Resonance Phenomena
When the frequency of the electromagnetic wave meets the natural vibrations in the cell
structures or in tissue, it can lead to resonances. Rhythmical fluctuations of signal
substances, matter‐exchange‐processes and Ion‐conductivity can be found in many
neurones, receptors and cell types. These oscillations can influence the membrane
potentials and switch certain stimuli on and off. An external field – according to theory –
can imprint an external oscillation frequency onto these structures. Neurones which have

10


been modified in this way can even synchronise the following neurones in the same way.
This external synchronisation would even remain after the disappearance of the external
stimulus.
Indirect Effects
In addition to the previously described triggering of wring resonances, microwaves can
possibly damage the genetic substance via the formation of hydroxyl radicals. The input
energy of microwaves is sufficient to raise the ratio of oxidants to anti‐oxidants, a self‐
accelerating chain reaction of free radicals can lead to damage of the DNA (Scott 1992, see
also Maes et al. 1995).

3.5 Particular Properties of Pulsed Electromagnetic Fields
In an evaluation of circa 40 studies, in which the biological effects of pulsed high
frequency fields were directly compared to those of continuous fields of the same median
power density, Postow & Swicord (1996) concluded that in half of the studies, the
biological effectiveness of pulsed fields was significantly higher. Only in a few studies
were the continuous fields more effective and in the remainder of the studies the
effectiveness of both was practically the same. The studies which are mainly discussed in
chapter 4 and 5 convey a similar picture.
At first glance, the higher biological effectiveness of pulsed electromagnetic fields in
comparison to continuous fields at the same median power flux densities could have an
almost trivial cause:
The individual pulses of pulse modulated fields have a higher amplitude than the
continuous fields; the possible threshold for the triggering of biological reactions could
therefore be passed in these fields during the duration of the pulse.
However, numerous experiments found that the biological response depends in a
complicated manner on the duration of the pulse and its frequency. Given that some
effects have only been observed at certain pulse frequencies, we presume that in addition
to the described effect, there are others which can be originally attributed to the low
frequency modulation (see also chapter 4).


11

4 Biological Primary Effects of High Frequency
Electromagnetic Fields Effects on Cellular Level
At the cellular level, it is possible that there may be direct effects of the EM field on the
genetic material, which we have collated under the heading Gene Toxicity and which will
manifest as mutations if the cell’s own repair mechanisms fail. On the other hand, it is also
possible that the fields influence cellular processes such as gene‐transcription and gene‐
translation. Furthermore it is possible that the fields can impact on the cell membranes,
the intracellular processes of signal transmission and not least the cell cycle. Just like
direct damage of the genetic substance, a disruption of these processes can lead to a
transformation of the cell, to disruptions of inter‐cellular communication and to a changed
rate of cell division, which can lead to a slower – or very importantly with respect to a
potential carcinogenic effect – faster growth.

4.1 Gene Toxicity
A basic question for the evaluation of the potential dangers of mobile telecommunication
is whether the electromagnetic fields used are genotoxic. If the fields had the potential to
damage genetic substance directly, they would not only amplify the effects of other
carcinogenic teratogenic or mutagenic substances, but they would induce these effects
themselves. A direct genotoxic effect of electromagnetic fields with frequencies as they are
used for mobile telecommunications has been thought to be not likely in the past (Brusick
et al. 1998, Moulder et al. 1999, Repacholi 1997, Repacholi 1998, Saunders et al.1991,
Verschaeve 1995, Verschaeve & Maes 1998). The reasons for this assumption were on the
one hand that the quantum energy contained in EM field in the radio and microwave
range was not sufficient to break molecular bonds. This assumption is no longer tenable
after the experiments of Bohr et al. (*1997) and Bohr & Bohr (*2000) (see also chapter 3.3).
On the other hand, it was argued that there was a large number of experiments showing
no genotoxic effects. Our list of papers in Annex A, Table A.1 shows however, that the
much debated findings of the work of Lai & Singh (*1995), in which the direct damage of
DNA (single strand and double strand breaks) has been proven, have been confirmed by
a whole range of other studies, some by the same laboratory, but also by other groups
(*Lai & Singh 1996, 1997, *Phillips 1998, *Sarkar 1994). A study by Varma & Traboulay
(1977) on the effect of HF fields on pure DNA had already resulted in hints of direct
genotoxic effects, however, this experiment used a relatively high power flux density and
therefore significant warming may have occurred, at least locally. Lai and Singh (*1997)
found that the dispensation of melatonin and N‐Tert‐Butylalpha‐Phenylnitron (PBN)
before the EMF exposure prevented the occurrence of DNA breaks. Melatonin captures
free radicals and for PBN it has been proven that it protects cells from cell death induced
by free radicals.
In Appendix Table A.1 we also list the experiment of Meltz et al. (*1987) and Stagg et al.
(*1997) which examined the influences of EMF fields on the DNA repair mechanisms and
the DNA synthesis.

12


The term chromosome aberration sums up all anomalies of the DNA double strand level
with respect to chromatids and chromosomes. Examples for structural chromosome
aberrations are: chromatid and chromosome breaks, chromatid gaps, acentric fragments
as well as di‐ and tetracentric chromosomes.
Chromosome aberrations have been observed in a multitude of experimental conditions,
in vivo as well as in vitro (Table A.1). Maes et al.(*1997) found a rise of chromosome
aberrations in human lymphocytes in workers who were professionally exposed to
radiation from mobile equipment, but also in experiments with human blood under
controlled exposure conditions (GSM base station, 15 W/m², exposure time of 2 hours).
However, this was the only study so far which used the actual fields of a real base station.
The incidence of micronuclei indicates whether the distribution of chromosomes into the
daughter nuclei after a cell division has been normal and complete. A number of studies
have proven a higher incidence of micronuclei under the influence of HF EMF fields,
which is interpreted as an indication for chromosome damage (Table A.1). With one
exception, the frequencies were all over 1 GHz and in most cases the intensities were
relatively high.
For the incidence of sister chromatid exchange as a measure for damage at DNA single
strand level, only very few studies using typical mobile frequencies and intensities have
been done so far (Table A.1). Maes et al.(*1996) found that the radiation of a GSM base
station (954 MHz, 217 Hz, duration of exposure: 2 hours) raises the genotoxic effects of
Mitomycin C significantly, demonstrated via the sister chromatid exchange.
Genetic damage can lead to cell mutation with possibly damaging effects for the living
organism. Mutations which promote faster cell division will be discussed in chapter 4.3.
Table A.1 shows in its last block some studies which focussed on the evidence of changes
in the genetic materials which manifest themselves as changed properties within the
organism.

4.2 Cellular Processes
4.2.1 Gene-Transcription and Gene-Translation
The code of the DNA controls protein synthesis in the ribosomes via the RNA. The
creation of RNA, i.e. the imprinting of genetic information happens in the cell nucleus
(transcription). The encoded information is transported via messenger‐RNA (M‐RNA) to
the ribosomes and is read there with the help of Transfer RNA (t‐RNA). According to the
transmitted code, proteins are subsequently synthesized. This process of synthesis is
called translation. Since one m‐RNA chain can be used by several ribosomes, the rate of
synthesis of the corresponding protein can be a lot higher than that of the m‐RNA.
Mistakes made during the genetic transcription can thus be ‘raised to a higher power’ at
the protein level.
In the first block of Appendix Table A.2, we list several recent studies which
demonstrated changes of gene transcription and translation under the influence of
electromagnetic fields of mobile telecommunications. Fritze et al. (*1997) observed


13

changed gene transcription in certain areas of the brains of rats which had been exposed
to the field of a GSM phone for four hours.
In an in vitro experiment, Ivaschuk et al. (*1997) exposed cells to a pulse modulated HF
field (836.55 MHz, TDMA 50Hz) and afterwards extracted and analysed the entire cellular
RNA.
This showed statistically significant changes with regards to the transcription of the
response gene c‐jun (90W/m², duration of exposure: 20 minutes), however no changes
with regards to c‐fos. The results of the experiments by Goswami et al. (*1999) found a
evidence for an influence on the transcription of the response gene c‐fos by a similar field,
whilst for c‐jun and c‐myc, no statistically significant effect was observed. The intensities
at which effects on gene translation had been observed were well below the values at
which thermal effects would occur in mammals.

4.2.2 Membrane Function
There is a large number of experimental evidence that high frequency fields, non‐pulsed
and pulsed can affect different properties of the ion channels in cell membranes, for
example in the form of a lowering of the rate of channel formation or the reduction of
frequency of the opening of individual channels (Repacholi 1998). The frequency of
openings of ion channels which are activated by acetylcholine was significantly lowered
by a microwave field (10.75 GHz) with a power flux density of a few μW/cm². (*D’Inzeo et
al.1988). Changes of the membranes as a whole have also been observed under the
influence of weak fields. Thus, Phelan et al. (*1992) observed that a 2.45 GHz field, with a
pulse modulation of 100 Hz could trigger a phase transition from liquid to solid in
melatonin containing cells after an exposure of 1 hour at a SAR of 0.2 W/kg.

4.2.3 Signal Transduction
Ca2+
The divalent Calcium cation Ca2+ plays an important role in the cell‐signal‐transduction:
regulating the energy output, the cellular metabolism and the phenotypical expression of
cell characteristics.
The signal function of the Ca2+ is based on a complicated network of cellular channels and
transport mechanisms, which maintains the Ca2+ concentration within the cell at a lower
level than outside, but which is also linked to dynamic reservoirs. This allows the
transduction of extracellular signals (hormones, growth factors) as Ca2+ peaks in the
cytosol, transmitting information encoded in their intensity and frequency. It is known
that this signal process can be disrupted by a variety of toxic chemicals in the
environment, which can lead to cell damage and even cell death (Kass & Orrenius 1999).
Studies by Bawin et al. (*1975) and Blackman et al. (*1979) showed very early on in vitro
experiments that the Ca2+ balance of nerve cells and brain tissue can be disrupted by HF
fields with low frequency amplitude modulations.

14


Both studies worked with amplitude modulated 147 MHz fields (with intensities ranging
from 5 to 20 W/m2). The maximum effect occurred at a modulation frequency of 16 Hz.
Experiments conducted by Dutta et al. (*1984 *1989) and Lin‐Liu & Adey (*1982) also
showed significant dependence on the modulation frequencies, in some cases at Specific
Absorption Rates of as low as 0.5 W/kg. Equally, Somosy et al. (*1993) found that an effect
on the distribution of Ca in intestinal cells is only possible within a field modulated with a
low frequency. Wolke et al. (*1996) observed in their experiment on myocytes that
exposure to fields with mobile‐like carrier frequencies of 900 MHz and 1800 MHz resulted
in lower intracellular concentrations of Ca2+ for all modulation frequencies (16 Hz, 50 Hz,
217 Hz, 30 KHz) compared to exposures to a continuous 900 MHz field or no exposure at
all. A statistically significant effect was only found with the combination of a carrier wave
of 900MHz and a modulation frequency of 50 Hz. The Specific Absorption Rate for this
experiment was between 0.01 and 0.034 W/kg, far below the range which might be
relevant for ‘thermal’ effects.
Enzymes
Protein kinases are enzymes with the property to phosphorylate other enzymes or
proteins. Phosphorylation, a covalent modification by addition of a phosphate group,
changes the activity or function of a protein. The protein kinases play an important role in
the transmission of information from the membrane receptors for hormones and
cytokines into the interior of the cell, and thus in the regulation of many intracellular
processes such as glucose and lipid metabolisms, protein synthesis, membrane
permeability, enzyme intake and transformation by viruses.
An amplitude modulated 450 MHz field is capable of decreasing the activity of protein
kinases which are not activated by cyclical Adenosine monophosphate. Byus et al. (*1984)
showed that the degree of inactivity depended on the exposure time as well as the
modulation frequency. Maximum effects occurred at exposure times of 15 to 30 minutes
with a modulation frequency of 16 Hz.
The enzyme ornithine decarboxylase (ODC) determines the speed of the biosynthesis of
polyamines. Polyamines are needed for DNA synthesis and cell growth. ODC is also
activated in relation to carcinogenesis. The control of OCD activity from the exterior is
facilitated via processes on the cell membrane. Byus et al. (*1988) exposed three different
cell types (rat hepatoma cells, egg cells of the Chinese hamster, human melanoma cells)
for one hour to a 450 MHz field with a 16 Hz amplitude modulation and a power flux
density of 10W/m2. The exposure raised ODC activity by a little more than 50%. The
heightened ODC activity remained for several hours after the exposure. Similar fields
with a 60 Hz and a 100 Hz modulation had no effects. Another study (*Penafiel et al. 1997)
observed heightened ODC activity after the radiation of L929‐cells of mice with a 835
MHz field which had been amplitude modulated at 60Hz or pulse modulated at 50Hz. No
effects whatsoever were observed with an analogue mobile phone, a frequency
modulation at 60 Hz and a speech amplitude modulation. This last finding confirms other
results by the same group, according to which a minimum coherence time of 10 seconds
of the field needs to be present for an effect on ODC activity to manifest (*Litovitz et
al.1993, 1997, see also Glaser 1998 and Litovitz 1998). The coherence time of speech
modulated fields however is shorter than a second.


15

Further important proof that low frequency modulation has a determining influence on
the effects of electromagnetic fields on enzyme activity was found by Dutta et al. (*1994):
They compared the effects of a low frequency modulated 147 Hz field (0.05 W/kg) and a
combined low frequency electric and magnetic field (ELF EM, 21.2V/97nT). A continuous
high frequency field only had a small effect (3.6 per cent) on the activity of enolase in
Escheria Coli, a 16 Hz modulated field led to an increase in activity of nearly 62 per cent, a
60 Hz modulated field led to a decrease of activity of 28.5 per cent. At ELF‐EM a similar
response could be observed: increase of enzyme activity by more than 59 per cent at a
frequency of 16 Hz and decrease of 24 per cent at 60 Hz. The results of the experiments by
Behari et al.(*1998) point in the same direction. They found that a 30 to 35 day long
exposure of rats to amplitude modulated fields (6.11 – 9.65 W/kg) led to a significant
increase in Na+‐K+‐ATPase activity, which was independent from the carrier frequency,
but characteristically dependent on the modulation frequency, because the effect was
always stronger at a 16 Hz modulation than at a 76 Hz modulation.

4.2.4 Cell Cycle
An undisrupted signal transduction or efficient cell cycle control mechanisms which are
capable of correcting false information or facilitating repairs are the prerequisite for cell
cycle progression if the genomic integrity of the cell is to be maintained (Shackelford et al.
1999). Disturbances of the DNA replication can lead to detrimental mutations and as a
consequence to cell death or in multicellular organisms to cancer. The causes for
irregularities in the course of the cell cycle are almost always to be found in mistakes
during signal transduction and/or the failure of control mechanisms.
In Appendix Table A.2. we list studies which examined disruption of the cell cycle. The
only in vivo experiment is the one by Mankowska et al. (*1979) which also used intensities
as they are found in the environment of real emitting equipment. Statistically significant
increases of disrupted metaphases with uni‐, quadri‐ and hexavalencies were
demonstrated in this study from a power flux density of 5 W/m2.
Cleary et al. (81996) found in their experiment that 2.45 GHz fields are roughly twice as
effective as 27 MHz fields when it comes to the triggering of cell cycle disturbances.
Whilst the 27 MHz fields had no influence on the G2/M phase of egg cells of the Chinese
hamster, disturbances of all phases were observed in a 2.45 GHz field.

4.3 Cell Transformation and Cell Proliferation
In vitro experiments of the effects of high frequency fields on the rate or division or the
rate of proliferation of cells, expressed in the proliferation rate and the (neoplastic)
transformation of cells can offer important findings with regards to possible carcinogenic
effects of the fields. The adverse influences of the fields which could not be prevented by
the cell’s own repair mechanisms manifest themselves in disrupted cell proliferation and
cell transformation rates.
Table A.3 gives an overview of the studies, in which the effects of high frequency fields on
cell transformation and cell proliferation rates were the focus of the examinations.

16


4.3.1 Cell Transformation
Balzer‐Kubiczek & Harrison (*1985, *1989, *1991) found an increase in neoplastic
transformations in cells which had been exposed in vitro to a high frequency field with a
low frequency pulse. The effect depended on intensity, but was only observable, if a
tumour promoter (TPA) was added after the exposure.
Czerska et al. (*1992) found that low frequency pulsed microwave radiation (2.45 GHz)
increased the rate of transformation of small inactive lymphocytes into large activated
lymphoblasts. Continuous radiation could trigger this effect only at power flux densities
that also led to measurable warming.
However, the experiments with pulsed radiation which triggered the cell transformation
at power flux densities, for which a homogenous warming can be ruled out, showed that
homogenous warming cannot be responsible for this effect.

4.3.2 Cell Communication
Disrupted communication between transformed cells and normal cells plays an important
role in tumor promotion. Cain et al. (*1997) co‐cultivated transformed cells with normal
cells. The co‐culture was exposed for 28 days to a TDMA (50Hz) modulated 836.55 MHz
field as well as to the tumor promoter TPA in various concentrations. At power flux
densities of 3 and 30 W/m2, which corresponded to Specific Absorption Rates of 1.5 and 15
mW/kg, they did not find a statistically significant difference of focus formation between
the exposed and the control cultures for any of the TPA concentrations. The data for the
lowest intensity (0.3 W/m2/0.15 mW/kg) show for two of the three TPA concentrations that
there was a small but statistically significant difference in the number of foci, and for the
lowest TPA concentration also for the surface and density of the foci.

4.3.3 Cell Proliferation
Anderstam et al. (*1983) found in their experiments with bacteria that some strains
reacted to the exposure with an amplitude modulated 2.45 GHz field (500Hz, 35 to 100
W/kg) with an increased proliferation. Also for some species, the number of mutations
and the frequency of mutations were increased. These results were confirmed by
Hamnerius et al. (*1985) amongst others. Grospietsch et al. (1995) found similar results for
150 MHz fields with several amplitude modulations.
Cleary et al. (*1990 a,b) demonstrated on human lymphocytes and on Glioma cells that the
rate of cell division was increased after exposure with a continuous 2.45 GHz field. In a
newer experiment, the same effect could be observed for exposures with a pulse
modulated field of the same carrier frequency (*Cleary et al. 1996).
In the first of the two experiments which were conducted with fields displaying all the
characteristics of real pulsed mobile emissions (see also Table A.3), an increased DNA
synthesis rate was observed, but no faster proliferation of the examined cells was found.
(*Stagg et al. 1997). In the second experiment, at similarly low intensities (0.0021 W/kg)
however, transmitted by a GSM modulated 960 MHz wave, an increase of the cell


17

proliferation rate was found (*Velizarov et al. 1999). The EMF exposure in this experiment
was conducted at two different temperatures, which also applied to the relating control
cultures. The increase of the proliferation rate only happened in the exposed cell cultures.
Similar experiments to prove that microwaves and ‘conventional’ heat have different
effects, were conducted by La Cara et al. (*1999) on a thermophile bacterium, in which the
radiation with a 10.4 GHz field led to an irreversible inactivation of the thermostable
enzyme ß‐galactosidase, whilst heating in a water bath had no effect. This result
confirmed the results of Saffer & Profenno (*1992) which had worked with frequencies in
the lower GHz range.

18


5 Patho-Physiological Effects
5.1 Immune System
The immune system plays a central role in the protection against infectious micro‐
organisms in the environment and, also, against several kinds of cancer cells. Experiments
on hamsters, mice and rats found, amongst other things, that there was a reduction in the
activity of natural killer cells and an increase in macrophage activity (see e.g. Yang et al.
1983; Ramo Rao et al. 1983; Smialowicz et al. 1983). However, the majority of experiments
on living animals were carried out at power flux density levels that produced an increase
in body temperature of more than 1oC. On the other hand, it was observed in parallel in
vitro experiments, that in vitro heating of macrophages did indeed lead to increased
activity; the effect was, however, weaker than that of the in vivo radiation which produced
the same temperature (Ramo Rao et al. 1983).
Elekes et al. (*1996) observed that, after exposing mice for a period of 3 hours per day over
several days using microwaves (2.45 GHz) with a power flux density of 1W/m2 (SAR =
0.14 W/kg), there was an increase in antibody‐producing cells in the spleen of about 37%
with continuous radiation and around 55% with amplitude‐modulated radiation.
In contrast to the in vivo experiments, numerous in vitro experiments were carried out
with intensities at which an effect due to warming can be excluded. Thus, Lyle et al.
(*1983) observed an inhibition of cytotoxicity of T‐Lymphocytes in the mouse with a 450
MHz field that was amplitude modulated with various frequencies in the range between
3Hz to 100 Hz. The effect that was demonstrated with a relatively low power flux density
of 15 W/m2 was greatest at the 60 Hz modulation. The inhibition of cytotoxic effectiveness
of the irradiated lymphocytes declined continually for both the lower and higher
modulation frequencies.
The tables in Appendix A list further experiments with (human) leucocytes in which
damaging effects were proven at non‐thermal power flux density levels, especially also
with low frequency amplitude modulated fields.
The work of Maes et al.(*1995) deserves special consideration. In an in vitro experiment
with human leucocytes at a GSM base station and also in the examination of the
lymphocytes in the blood of workers who were exposed to the fields of the mobile phone
base stations during maintenance work, they found that there was an increase in
chromosome damage (chromatid breakage, acentric fragments and some chromosome
breaks).

5.2 Central Nervous System
5.2.1 Blood Brain Barrier
The brain of mammals is protected from potentially dangerous materials in the blood by
the blood brain barrier, a specialized neurovascular complex. The blood brain barrier

19

functions as a selective hydrophobic filter that can only be easily passed through by small
fat‐soluble molecules. Other non fat‐soluble molecules, e.g. glucose, can pass through the
filter with the help of carrier proteins that have a high affinity for specific molecules.
It is known that a large number of disorders of the central nervous system are caused by
disturbances of the barrier function of the blood brain barrier (*Salford et al. 1994).
Severe warming of the brain can lead to an increased permeability of the blood‐brain
barrier for those materials whose passage should actually be prevented. The results of
first experiments with high frequency fields of high intensity, which led to a higher
permeability of the blood brain barrier, were then interpreted as a consequence of
warming by the HF radiation.
However, Appendix Table B.1 lists a whole series of studies in which a greatly increased
permeability of the blood brain barrier was produced through pulsed high frequency
fields of very low intensity (*Oscar & Hawkins 1977, *Neubauer et al. 1990, *Salford et
al.1994, *Fritze et al.1997) amongst others with carrier frequencies and modulation
frequencies which corresponded to those of mobile telephony (GSM).

5.2.2 Neurotransmitters
Pulsed and continuous high frequency fields of low intensity may lead to chemical
changes in the brain. Inaba et al. (*1992) exposed rats to a continuous 2.45 GHz field with
a power flux density of between 50 to 100 W/m2 and found a significant reduction in the
Noradrenalin content of the Hypothalamus, whilst the two other neurotransmitters
Dihydroxyphenylacetic acid and 5‐Hydroxyindolacetic acid were found in the pons and
medulla oblongata in significantly increased concentrations. The radiation did not
produce significant changes in the dopamine or serotonin concentrations.
Lai et al. (*1987, 1989 a, b, see above Lai et al. 1988) found also in experiments using rats
that a 2.45 GHz field modulated with 500 Hz pulse‐modulation influences brain activity,
especially in the frontal cortex and the hippocampus, via the most important
parasympathetic neurotransmitter acetylcholine. It could be demonstrated that the effect
was related to the exposure duration. A 45 minute exposure duration led to significant
reductions in choline‐uptake, the reduction to 20 minutes exposure produced a significant
increase. A similar behaviour was found in animals also as a reaction to stress through the
reduction of the freedom of movement and through acoustic white noise.

5.2.3 Electroencephalogram (EEG)
In contrast to the neuroendocrine effects, which can barely be measured directly in the
brain of humans, EEG studies can be carried out relatively easily. Several valid studies of
that kind do now exist.
Most animal experiments have limited validity, since they were carried out with relatively
high power flux density values (see e.g. Chizhenkova 1988: 2.397 MHz, cw, 400 W/m2,
Chizhenkova & Safroshkina 1996: 799 MHz, cw, 400 W/m2, Thuroczy et al. 1994; 2.45 GHz,
AM 16 Hz, 100 W/m2).

20


One of the few exceptions are the studies by Vorobyov et al. (*1997), who observed an
increase on the left‐right symmetry in the EEG in rats that were exposed to a 945 MHz
field (AM, 4Hz, 1 to 2 W/m2, within the first 20 seconds after the start of the exposure.
Early experiments by von Klitzing (1995) with EEG recording during the exposure of
subjects to pulsed high frequency fields, that were similar to those of mobile telephone
fields (150 MHz, 217 Hz, power flux density in the pulse in the brain at a 6 cm depth
below 10‐2 W/m2), found changes in the awake EEG, these were called into question
because of insufficient documentation.
In later experiments however, a clear effect was demonstrated in the awake and sleeping
EEGs.
Reiser et al. (*1995) observed, both with exposures to a 150 MHz field (modulated
frequency 9.6 Hz, peak power 0.5 mW, 4 cm distance, near‐field conditions) and also in
the field of a mobile telephone (902 MHz, modulation frequency 217 Hz, peak power 8W,
40 cm distance), a significant increase in the energy in the EEG frequency bands ‐ Alpha,
Beta 1 and Beta 2.
Experiments by Röschke & Mann (*1997) resulted in no significant difference in the EEGs
for exposed and sham‐exposed subjects under short exposure conditions (3.5 minutes, 900
MHz, GSM, 0.5 W/m2). However, the peak of approx. 9Hz in the presented averaged
power density spectra of exposed subjects was clearly lower and narrower than for non‐
exposed subjects. The same authors (*Mann & Röschke 1996) demonstrated again in the
field of a GSM mobile telephone (8W, distance 40 cm power flux density 0.5 W/m2), a
reduction of the time taken to fall asleep and a statistically significant reduction of the
duration and the proportion of the REM sleep. Furthermore, the spectral analysis revealed
an increased power density of the EEG signal during REM sleep above all in the ‘Alpha’
frequency band. The REM suppressive effect and the reduction of the time taken to fall
asleep were also confirmed by the same research team (*Mann et al.1997, *Wagner et al.
1998). The study carried out in 1997 also found a significant increase in the cortisol
concentration in the blood of humans exposed to a 900 MHz/217 Hz field with a power
flux density value of 0.2 W/m2. Systematic deviations were also observed for the Growth
Hormone and Melatonin levels, but these did not reach significance level.
Whilst in the previously cited studies, changes in the sleep EEG could be demonstrated
only as a consequence of the influence of mobile telecommunications fields for several
hours, Borbély et al. (1999) were able to demonstrate that changes in sleep were already
occurring after 15 to 30 minutes exposure. This research team used also a 900 MHz field,
which could be selectively pulse‐modulated with either 2, 8, 217 or 1736 Hz. As in the
other experiments, a statistically significant reduction in the proportion of REM sleep was
found at a Specific Absorption Rate of less than 1W/kg. In addition, the waking‐up phase
was noticeably reduced.
Freude et al. (*1998, see also Henschel et al. 1999) examined the effect of the radiation
from mobile telephones on slow brain potentials.
Slow brain potentials are event‐correlated brain potentials that arise during the
preparation for motor action and/or information processing. Changes in the slow brain


21

potentials give an indication about the influences on specific aspects of human
information processing. Freude et al. found that the fields of a mobile telephone (916.2
MHz, 217 Hz, SAR 0.882‐1.42 W/kg, exposure time 3 to 5 minutes) led to a statistically
significant decrease of the slow readiness potentials for specific tasks, in specific brain
areas.

5.2.4 Cognitive Functions
Impairments of the brain, e.g. by modification of the choline‐uptake, can be expected to
cause learning deficits. These were demonstrated in many learning experiments, in which
rats were previously exposed to pulsed microwave fields (*Lai et al. 1989, 1994; *Wong &
Lai 2000, see above D’Andrea 1999 for older studies). In the study by Lai et al. (*1994), rats
were exposed for 45 minutes to a 500 Hz pulsed 2.45 GHz field with a power flux density
of 10 W/m2. This intensity resulted in a mean whole body SAR of 0.6 W/kg. Following the
exposure, the starved rats were placed in a labyrinth with several arms in which food was
placed. The researchers measured how effectively the ‘exposed rats’ and the ‘sham‐
exposed rats’ searched the labyrinth for food. For the ‘exposed’ group, significantly more
failed attempts were observed, i.e. searching already emptied labyrinth arms. The authors
attributed the low performance of the ‘exposed’ rats to deficits in spatial memory. The
‘handicap’ of the EMF exposure could be levelled out in a follow‐up experiment, in which
the rats were given either the acetylcholine agonist Physostigmin or the opiate antagonist
Naltrexone before their exposure. According to the authors, these findings are
confirmation of their results from previous studies (see above), in which they had found
that high frequency electromagnetic fields influence cholinergic and endogenous opioid
neurotransmitter systems in the brain and that this effect can lead to memory deficits. In
the meantime, the effect has been confirmed by other experiments (Mickley & Cobb 1998).
In a further experiment (*Wang & Lai 2000), rats were trained over several sessions to find
a platform situated just under the water surface inside a round water basin. Subsequently,
they were exposed to pulsed microwave radiation for an hour (2.45 GHz, 500 pulses per
second, mean power flux density 2W/m2, mean whole‐body SAR 1.2 W/kg). Testing was
then carried out to determine how long the ‘exposed rats’ needed to find the platform
from different starting positions, compared to the ‘non‐exposed rats’ or ‘sham‐exposed
rats’. The ‘exposed rats’ clearly required longer for this, as they spent significantly less
time in the correct quadrant of the water basin. Finally, the recorded traces of the
swimming lanes used by the ‘exposed animals’ differed from those of the control groups,
this suggests that different strategies were used when searching for the platform. This
result confirms the findings from other studies that pulsed high frequency fields can
influence specific aspects of memory performance.
The effects of a 600 MHz field on the memory of rats were also demonstrated by Mickley
et al. (*1994). In this experiment, the capacity of the animals to recognize familiar objects
was measured in relation to the radiation they received. Whilst the ‘non‐exposed control
animals and also the animals who were exposed to a SAR of 0.1 W/kg occupied
themselves for longer with a novel object compared to a familiar object, the higher
exposed animals spent just as much time examining an actually familiar object as with a

22


novel object. The limit for this exposure dependent change in behaviour was between 0.1
and 1.0 W/kg
The lowest SAR so far which has been shown to have an effect on cognitive functioning in
rats was 0.072 W/kg. However, in this experiment, pulses with a peak of more than 700
MW (megawatts) were used (Raslear et al. 1993). The low SAR in this case resulted only
from averaging over time with a very low pulse repetition rate of 0.125 pulses per second
and a pulse width of only 80 nsec.
It has been shown in experiments by Preece et al. (*1999) that fields like those used in
mobile telephony can influence cognitive functions of the brain. In this study, 36 subjects
were subjected to a 915 MHz field of a simulated mobile telephone. The field was overlaid
either with a 217 Hz sinusoidal modulation or a 217 Hz pulse modulation. In the analogue
simulation the net forward power was about one Watt, and in the digital simulation it
was 0.125 Watt. Under the conditions ‘Exposure to analogue field’, ‘Exposure to digital
field’ or ‘Sham exposure without any field’, each of the test persons had to carry out
several tests to measure ability to react and various tests of memory performance. In both
exposed groups there was a slight but statistically significant decrease in reaction time,
which was more marked for ‘Analogue exposure’ than for ‘Digital exposure’.

5.3 Hormone Systems
5.3.1 Stress Hormones
Environmental pollution can act as a stressor on the body, like physical and mental
stressors, and cause ‘alarm reactions’. Such reactions are associated with hormonal
changes. The presence of a stress‐situation can be proved by the presence of hormones
like adrenocorticotropin [the adrenocorticotrophic hormone] (ACTH), cortisol and
corticosterone in the blood, and also to a lesser extent by changes in the concentration of
prolactin and growth hormone.
Electromagnetic fields can clearly cause stress reactions in animals used for experiments.
Thus, the experiment by Imaida et al. (*1998a) on rats that were exposed for a duration of
90 minutes daily over a period of 6 weeks to a field with a carrier frequency of 929.9MHz
and a 50 Hz pulse modulation, showed a statistically significant increase in the ACTH and
corticosterone levels. The whole‐body SAR value in this experiment was between 0.58 and
0.8 W/kg. The exposure in the 1.439 GHz field, equally with a 50 Hz pulse modulation and
a SAR value between 0.453 and 0.680 W/kg had the same effect (*Imaida et al. 1998b).
Chou et al.(*1992) exposed rats in a long‐term experiment (25 months) to 800 MHz pulse‐
modulated 2.45 GHz field that led to a Specific Absorption Rate of 0.15 to 0.4 W/kg.
Alongside other physiological parameters the corticosterone profile was regularly
measured for the first half year of the experiment. Whilst the hormone profile of the
exposed animals and the non‐exposed animals were practically identical in the later
stages of the experiment, with the exception of a slight increase in the sham‐exposed
group of animals in the third phase of the experiment, the first examination after 6 week’s
exposure showed a statistically significant increase in the corticosterone profile in the
blood of the exposed animals.

23

The authors report that their attempt to replicate this effect produced no statistically
significant results, however, only 20 animals were tested in this second experiment whilst
the actual series of experiments contained 200 animals.
A similarly extensive experiment on rats like that of Chou et al. However, with an
unmodulated 435 MHz field showed no difference in the concentration of the hormones
ACTH, corticosterone and prolactin between the exposed animals and the non‐exposed
animals (Toler et al. 1988).
The few experiments previously carried out on humans do not yet produce a clear
picture. Mann et al. (*1998) exposed 24 volunteer subjects whilst asleep to the field of a
mobile telephone that was transmitted from a separate antenna (900 MHz, 217 Hz, 0.2 W/
m2). Blood samples were withdrawn via a catheter whilst the subjects were asleep and
they were analysed for, amongst other things, cortisol and growth hormone
concentrations. There were systematic differences between the ‘exposed subjects’ and the
‘sham‐exposed subjects’ during the course of the night for both hormones, which only
reached statistical significance levels for cortisol.
De Seze et al. (*1998) examined the effect of a GSM mobile telephone (900MHz, 217 Hz) on
subjects who were exposed to the field for 2 hours per day, 5 days per week for over a
month. Based on nine blood sample withdrawals per week; amongst other things, the
change in the concentrations of ACTH, growth hormone and prolactin were determined
over time.
The authors’ evaluation of their studies was that at one month, intermittent exposure in
the radio‐frequent field from the mobile telephone had no lasting or accumulative effects
on the hormone secretions from the anterior lobe of the pituitary gland. In their data, it is
however noticeable that that ACTH and prolactin follow a quite similar profile over time:
the concentrations started at high initial values at the start of the exposure and then
decreased in the following 3 weeks, and they then rose slightly again. The growth
hormone concentrations are very high for the first measurements during the exposure
period, they then fall to the pre‐exposure concentration levels and maintain these levels
until the end of the experiment. Possibly, these measurements show a temporary stress
reaction, which reduced in the following weeks.

5.3.2 Melatonin
The hormone melatonin, which is produced in the pineal gland, functions as a regulating
hormonal signal that synchronizes the endocrine rhythms of all the hormone glands. It
regulates, amongst other things, the daily cycles of ACTH and the cortisol‐release and
thereby regulates the daily rhythms of many metabolic processes.
Melatonin also exerts influences (inhibitory) on sex hormones and it has a stimulatory
effect on the immune system. Melatonin also influences specific cancer illnesses via the
regulation of the release of the sex hormones. In addition, melatonin is a free radical
scavenger, inactivating radicals such as OH, which amongst other things can be
dangerous for the genetic material. Furthermore, during in vivo experiments, it was
demonstrated that melatonin hinders changes in DNA produced by chemical carcinogens

24


and it protects lymphocytes from chromosome damage in high frequency electromagnetic
fields (*Lai & Singh 1997).
In the previously described experiments carried out by Imaida et al.(*1998 a, b), it was
found that the experimental animals that were exposed to a pulse‐modulated high
frequency field had a reduced melatonin concentrations in the blood. This finding could
not be confirmed by Heikkinen et al. (1999), who exposed mice for 17 months to a 900
MHz field with a 217 Hz GSM pulse modulation (SAR: 0.35 to 1.5 W/kg). Studies by
Vollrath et al. (1997) using rats and hamsters with a 900 MHz field (217 Hz GSM, SAR:
0.04 to 0.36 W/kg) could not contribute much to the clarification of the problem, since in
several sub‐sets of the experiment statistically significant differences between ‘exposed
animals’ and ‘non‐exposed animals’ had been found, but according to the authors these
resulted from mistakes in the experimental order.
In experiments by Mann et al. (*1997 see above), the stress hormones were measured as
well as the serum melatonin profile. This showed, in the case of the exposed humans, that
for a period of between 3 to 4 hours in the middle of the night there was an increase
compared to the control values, but these were not statistically significant according to the
evaluation of the authors.


25

6 Pathological Effects
6.1 Results of Experimental Studies
6.1.1 Cancer
Carcinogenesis
Carcinogenesis is a multi‐layered process, at the beginning of which is a certain impact on
the level of the genetic material. This can be a direct impact (for example ionising
radiation) or an indirect action via the product of a reaction (for example OH radicals). A
direct or indirect interaction with DNA can lead to damage of the DNA or the chromatin
structures (see also Chapter 3). If those damages are not repaired by endogenous
processes, the damage will be permanent. Thus, the initiated cell can, if the
immunological control fails, under the influence of hormones and promoters develop into
a pre‐neoplastic focus, which can then lead to a malignant tumor. The different steps of
carcinogenesis are summarised in three phases:
■ Initiation: Triggering of damage on the DNA and mutations on critical genes
■ Promotion: Increased rate of DNA synthesis and proliferation of transformed cells
■ Progression: Transition of a pre‐neoplastic focus to a malignant tumor
A physical or chemical pollutant can in principle be effective in all three phases of
carcinogenesis.
■ Initiation: Triggering of direct DNA damage or of a substance which causes DNA
damage, disruption of repair processes of the DNA
■ Promotion: Promotion of the proliferation of transformed cells
■ Progression: Suppression of immune‐reactions and promotion of tumor growth
Results from Animal Experiments
In vivo experiments using animals with an inbred genetic predisposition for certain tumor
illnesses or in which animals were injected with cancer cells, yielded very different results
(see Appendix C, Table C.1). In the majority of the studies, no cancer promoting effect of
high frequency electromagnetic fields could be found, or effects were only observed under
certain conditions of exposure (marked in the Table with ‘partly’), and even in those cases
they were often not statistically significant. However, it needs to be noted that many studies
with negative results had very short exposure times and durations of the study itself (for
example Chagnaud et al. 1999: 2 weeks, Salford et al. 1993: 2 to 3 weeks) and hence they do
not have much relevance to answer the question whether high frequency electromagnetic
fields have carcinogenic potential.
Some long‐term studies have yielded results which indicate a carcinogenic or co‐
carcinogenic effect of electromagnetic fields with mobile telecommunications frequencies
26


if the animals are exposed over a long period of time. (*Repacholi et al. 1997, *Szmigielski
et al. 1982 and *Szudinski et al. 1983). Important in this context is also the study of Chou
et al. (*1992). This study did not find a statistically significant rise in tumors in a particular
organ. However, the exposed group developed not only a higher number of tumors in
total, but also the number of primary malignant and metastatic malignant neoplasms was
significantly higher in the exposed animals. In their discussion of the results, the authors
point to the fact that the number of the primary malignant neoplasms in the exposed
group compared to the control group is four times higher and that this finding is
statistically significant, but then go on to undermine their finding by quoting literature,
according to which the tumor incidence of the exposed group should still be within the
normal range.
The experiment of Toler et al. (*1997) using animals with a predisposition for chest tumors
did not result in a higher incidence of these, but the number of ovarian tumors was
significantly higher in the exposed group compared to the controls.
The intensities at which an increase in tumors was found in animals were one to two
powers of ten below the values at which one would expect a triggering of ‘thermal’
effects. According to the presenting results, low frequency modulation does not seem to
be responsible for the carcinogenic effect.

6.1.2 Infertility and Teratogenic Effects
Teratogenesis
Teratogenic effects of a pollutant can – as with the carcinogenic effect – either be caused by
the triggering of a genetic defect or a harmful impact on the foetal development. The
formation of a genetic malformation during its initiation phase is analogous to carcino‐
genesis, i.e. teratogenic effects are also caused by direct or indirect impact on the DNA and
disruptions of the endogenous repair mechanisms. Later damages of the foetus can either
be caused by direct effects of the pollutant on the foetus or by reactions to the pollutant
within the mother’s organism, which would then be passed on to the foetus.
Results from Animal Experiments
A multitude of studies have demonstrated that high body temperatures in mammals lead
to a spermatotoxic and teratogenic effect. Since many studies examining such effects from
high frequency electromagnetic fields worked with intensities that were capable of
significantly raising body temperature, it cannot be excluded that the observed
spermatotoxic and teratogenic effects were caused by a thermal effect, (see for example
Berman et al. 1982, 1983, Berman & Carter 1984, Jensh et al. 1983a,b, Kowalczuk et al.
1983, Lary et al. 1983, Nawrat et al. 1985, Saunders et al. 1981, 1983, for the results of older
studies, see O’Connor 1980). The results of these studies do not always appear consistent,
however, this can possibly be explained by a different thermal susceptibility of the
different animal species used. In rats for example, a loss of thermally damaged embryos is
often observed, whilst the birth of malformed animals is rare. Other mammals show a
wider bandwidth between teratogenic and lethal exposures. (Verschaeve & Maes 1998).


27

However, there are some indications in the literature for teratogenic effects at intensities
that cause no (or, if at all very small) rises in temperature. Magras & Xenos (1997) exposed
mice during six months to a real transmitter. The mice had offspring five times during this
period and a continuous decrease in offspring was found down to irreversible infertility.
The exposure consisted of several radio and TV transmitters in the VHF and UHF bands
and measured between 0.00168 and 0.01053 W/m2. A repetition of this study would be
desirable in order to exclude that the effect was due to problems with the maintenance of
the animals or the screening of the control group.
Khillare and Behari (*1998) found that male rats that had been exposed to a 200 MHz field
(power flux density:14.7W/m2, SAR:1.65 to 2.0W/kg) during a period of 35 days for six
days per week and two hours per exposure day and which were afterwards mated with
unexposed females, produced significantly less offspring that the males in the unexposed
control group.
In an experiment by Akdag et al. (1999) male rats were exposed one hour every day to a
9.45 GHz field (power flux density:2.5W/m2, SAR:1.8 W/kg) during different periods of 13,
26, 39 or 52 days corresponding to one, two, three and four cycles of the seminal
epithelium.
At the end of each exposure period the following data were measured and compared to
an unexposed control group: number of sperm in the epididymides, morphology of the
sperm and weight of the testicles, epididymides, seminal vesicles and prostate.
They found amongst other effects a decrease in the number of sperm (statistically
significant in the group exposed for 53 days) and an increase of abnormal sperm
(statistically significant in the groups exposed for 26, 39 and 52 days).
A co‐teratogenic effect under non‐thermal exposures with power flux densities of 10 to
100 W/m2 in combination with cytosine arabinoside (CA) was found in a study by
Marcickiewicz et al. (*1986). In the experiment, mice were exposed in utero for two hours
a day to 2.45 GHz from the first to the 18th day of the pregnancy. The field, which alone
was not teratogenic, significantly increased the teratogenic effect of CA. A direct
teratogenic effect of microwave radiation with a frequency of 2.45 GHz on the brains of
newborn rats was found by Inalösz et al. (*1997). However the authors declared that the
SAR of 2.3W/kg led to a rise of rectal temperature of 1.0ºC.

6.2 Results of Epidemiological Studies
Methodological Requirements
In principle, epidemiological studies are an effective instrument to prove potential health
risks of a pollutant under real environmental and exposure conditions. Usually, they are
carried out by comparing statistical data about the incidence of an illness in an exposed
population as opposed to the incidence of this illness in an unexposed population. The
exact classification of exposure would require the metrological recording of the pollutant
for all participants (exposed and unexposed) during the entire latency period of the
illness. This is often not practicable and for long latency periods, which can usually only
be addressed via retrospective studies, inherently impossible. Under such circumstances it
28


has to suffice that surrogates are used, for example having a profession which is linked to
a certain exposure or the proximity of the home to an emitting installation. In some cases,
if the emitting installations have been used for a long time in the same mode, it is possible
to extrapolate past exposures from current measurements.
The quality of the exposure classification determines the validity of an epidemiological
study. Possible weaknesses, which can lead to wrong results, are:
■ People are classified as ‘exposed’ or ‘strongly exposed’ although in fact there is no or
only little exposure. An example with regards to high frequency fields is the often‐used
exposure classification on the basis of professional categories, such as radar operators
or telecommunications engineers, for whom it cannot be excluded that the main
occupation is a desk job without exposure.
■ It is assumed that the control group is completely unexposed, although the pollutant is
actually ubiquitous, which will lead to smaller but still potentially significant
exposures in the control group. One known example are mains frequency magnetic
fields, which affect the immediate neighbours of power supply equipment, but still
exist at non‐negligible strengths in houses which are further away from such
equipment.
Both effects lead to a levelling out between the exposed and unexposed group and hence
to an underestimation of the real health risk posed by the pollutant in question.
Another weakness of epidemiological studies can be the presence of unrecognized
confounders, i.e. other influences, which also affect the groups studied and influence the
development of the illness. This can be environmental factors, such as exposures to other
pollutants, but also socio‐economic and behavioural factors. If not all potentially relevant
confounders are factored in, the results can be distorted, either towards an overestimation
or an underestimation of the real risk.
The fast development of mobile technology has lead to a double dilemma with regards to
the study of potential risks through epidemiological studies:
■ For illnesses like cancer with latency periods of many years it is still too early to expect
valid results. If mobile telecommunications are indeed linked to a higher incidence of
cancer, the illness will only have manifested in a few people so far. This should at least
be valid for the part of the population whose exposures are from base stations only.
Potentially it could be different for direct mobile phone users, since these are generally
exposed to significantly higher intensities. But also for this group, at this moment in
time, we would expect results from epidemiological studies to underestimate the real
risk.
■ In some years epidemiological studies will hit a different obstacle: once base stations
cover the entire country and a large proportion of the population use a mobile phone,
it will become difficult to find the necessary unexposed control groups.
Given this dilemma, epidemiological studies carried out in the past have a certain
validity, even if the exposures are not exactly the same as they would be today and the
studies do not always correspond to today’s quality standards.


29

The Selection of Studies
At the time of finishing this present report there were only two epidemiological studies of
health risks in relation to actual existing mobile telecommunications exposures (*Rothman
at al. 1996, *Hardell et al. 1999). However there are a much larger number of studies
available, in which the health effects of high frequency electromagnetic fields in humans
were examined (see also Appendix D, Table D.1). Just under a quarter of all results relate
to exposures with low frequency pulse or amplitude modulated high frequency fields,
such as they are used for mobile telecommunications, even if the carrier and modulation
frequencies are in most cases not identical with those of mobile telecommunications.
In Appendix Table D.1, the examined illnesses are listed with their evaluated end point
(incidence or mortality), data describing the exposure situation is given and the quality of
the exposure classification is assessed. Finally, the result of the study is evaluated as
‘Relative Risk’ (RR) which includes the relevant risk factors in the form of standardised
mortality rates, standardised morbidity rates and odds ratios, and the statistical
significance is assessed. For each study we list the value for the highest exposure class or
if there was a further differentiation of the examined groups, for example according to
occupational groups, the highest found value.
Values are considered statistically significant (s.s.) if the value RR=1 outside of the 95%
confidence interval or if p<0.05.
A statistical evaluation of the results presented in Table D.1 can be found in Table 6.1.
Here, we list for every illness how many studies or separate results are available, how
many of these show a relative risk RR >1 and how many are statistically significant.
Almost all the studies, in which the total cancer risk without any differentiation according
to tumor form were examined, showed a risk factor of RR>1. Half of the studies resulted
in statistically significant risk factors with a maximum value of 2.1, which corresponds to
a doubling of the statistical risk to develop cancer from exposure to high frequency
electromagnetic fields.
A similar picture was found in relation to tumors of the nervous system, especially brain
tumors. Here, the maximum value for relative risk found was 3.4. Eleven of the total of 15
studies yielded a positive result, more than half of which were statistically significant.
The incidence of breast cancer in relation to high frequency fields must be examined
separately for men and women. All three studies relating to the breast cancer incidence in
women yielded risk factors greater than 1, the statistically significant values were 1.15 and
1.5. For men, risk factors of up to 2.9 were found; however, not all were statistically
significant.
Of the total of 16 results for leukaemia without further differentiation of the illness, 13
were positive (RR>1), more than half of these results were statistically significant. The
highest statistically significant value for the relative risk was 2.85. Amongst the results of
the differentiated studies, the following are notable: lymphatic leukaemia (7 results, 5
positive, 4 statistically significant, RR maximum value: 2.74) and acute myeloic leukaemia
(4 different studies, 3 positive results, 2 statistically significant, maximum RR value: 2.89).

30


With regards to the correlation of high frequency electromagnetic fields from radar and
other sources and testicular cancer, three studies have been conducted. All lead to
statistically significant risk factors with a maximum value of 6.9.
The studies regarding cardio‐vascular diseases did not result in a clear picture, not least
because of the multitude of the symptoms examined.
All four studies of fertility problems in relation to the exposure of men to microwaves
indicate increased risk. In two studies statistically significant risk factors of up to 2.7 were
found.
With regards to irregular courses of pregnancies and malformations in children of
mothers which had been exposed to high frequency fields, there are a large number of
studies with positive results, of which only two fit into the frequency range relevant to
our report. Both of these studies found statistically significant positive results with risk
factors of up to 2.36.
Of the studies of cancer risk of children whose fathers had been exposed to electro‐
magnetic fields, only two correspond to the quality criteria required for inclusion into this
report. Both indicate an increased risk, but only one result is statistically significant at a
value of RR=2.3. (With regards to the cancer risk of children in correlation to the exposure
of their parents, see also Colt & Blair 1998).
Regarding the disruption of motor functions as well as psychological functions and well‐
being, there is only one valid study for the frequency bands relevant to this report, which
yielded a slightly increased risk factor. However since other studies of transmitters with
frequencies below 100 MHz resulted in serious indications of increased risk, indicating
that this problem should be given more attention in the future, we also included the study
of Zhao et al. (1994), although it didn’t meet our quality standards with regards to the
statistical evaluation.
Unfortunately, the majority of the studies do not state the actual strength of the
exposures. Measurements are only available for the radio and television transmitter used
for the studies of Hocking et al. (1996) and McKenzie et al. (1998). The mean power flux
densities for all 16 municipalities affected by this transmitter were 3.3 10‐3W/m2 within the
range from 2.6 10‐4 to 1.46 10‐2W/m2 (McKenzie et al. 1998). The ICNIRP guidelines for the
general population recommend a maximum value of 2 to 2.51 W/m2 for the range of
frequencies emitted by this transmitter (64.25 to 527.25MHz). This means that the
exposures in these studies were below the German guidelines by a factor of 10‐4.


31

Table 6.1
Overview over the results of epidemiological studies with regards to the health risks of high
frequency electromagnetic exposures (see also Appendix D, Table D.1)
Illness

Number of
studies (results)

Studies (results)
with RR>1

Statistically
significant
results

All illnesses

2

0

0

Cancer, unspecified

6 (7)

5 (6)

3

Brain tumours unspecified and tumours of the
nervous system unspecified

14 (21)

10 (15)

6 (7)

Cancer (eyes)

1

1

1

Cancer of the respiratory organs, lung cancer

5

2

1

Chest cancer, men

2

2

0

Breast Cancer, women

3

3

2

Cancer of the lymphatic and blood forming
system unspecified

4

4

1

Leukaemia unspecified

12 (16)

9 (13)

5 (7)

Acute leukaemia unspecified

4

4

0

Lymphatic leukaemia unspecified

4 (7)

2 (5)

1 (4)

Acute lymphatic leukaemia

2

2

0

Chronic lymphatic leukaemia

4

4

1

Leukaemia, non lymph. non-myelo

1 (4)

1 (4)

1 (2)

Lymphoma, Hodgkin-Syndrome

5 (7)

3 (4)

1

Testicular cancer

3 (5)

3 (5)

3 (4)

Uterine cancer

1

1

1

Skin cancer

4

3

1

Cardio-vascular diseases

4 (5)

3 (4)

1

Infertility, reduced fertility, men

4 (7)

4 (7)

2 (4)

Infertility, reduced fertility, women

1

1

0

Miscarriages, stillbirths, malformations and
other birth defects

2 (3)

2 (3)

2

Cancer, offspring (parental exposure)

2

2

1

Neurodegenerative diseases, Alzheimer’s

1

1

0

Disruptions of motor and psychological
functions and well-being

2 (9)

2 (9)

1 (7)

32


7 Health Risks to Humans Resulting from Exposure
to the Electromagnetic Fields of Mobile
Telecommunications
The triggering of an illness caused by an (environmental) pollutant and the development
of this illness are a multi‐phased process, which begins with a biological, biochemical or
biophysical primary interaction of the pollutant with the biological system and ends with
the manifestation of the illness. During the different phases of the process, the body’s own
repair mechanisms can intervene and impede the further development of the illness. An
assessment of the potential health risks of electromagnetic fields as they are used for
mobile telecommunications should therefore be mainly based on studies conducted
directly on humans, because extrapolations from animal studies or even in vitro studies on
cell cultures only have limited validity for effects in humans, due to the difference in
susceptibilities and the lack of organic interactions in cell cultures. However, due to the
ethical limits to the research on humans, it is unavoidable to use results from experiments
with animals, single organs or cells in order to discover the biological and physiological
mechanisms.
Cancer
Given the results of the present epidemiological studies, it can be concluded that
electromagnetic fields with frequencies in the mobile telecommunications range do play a
role in the development of cancer. This is particularly notable for tumours of the central
nervous system, for which there is only the one epidemiological study so far, examining
the actual use of mobile phones. The most striking result of this study was an obvious
correlation between the side at which the phone was used and the side at which the
tumour occurred. The brain tumour incidence however was only slightly increased. A
(hypothetical) explanation of such a finding could for example be that mobile fields have
a promoting effect on previously initiated (multiple) tumours, triggering a defence
mechanism in the body which is capable of suppressing unpromoted tumours.
Higher risks were also demonstrated for several forms of leukaemia.
Although the studies in relation to testicular cancer were examining particular exposure
conditions (emitting equipment worn partly on the body at hip level), given the high risk
factor found, a possible risk cannot be excluded, especially not for mobile users wearing
the devices in standby mode on their belts. The epidemiological findings for testicular
cancer also need to be interpreted in conjunction with the results of the studies of fertility
problems occurring in relation to high frequency electromagnetic fields.
The risk factors for cancers other than testicular cancer are only moderately increased, but
not negligible, considering this technology will potentially reach full coverage of the
entire population.


33

Reliable conclusions about a possible dose‐response‐relationship cannot be made on the
basis of the present results of epidemiological studies, but an increase of cancer risk
cannot be excluded even at power flux densities as low as 0.1 W/m2.
In long‐term animal experiments, the carcinogenic effect of pulse modulated high
frequency fields was demonstrated for power flux densities of circa 3W/m2 (mouse,
exposure duration 18 months, 30 minutes per day, SAR (mouse) circa 0.01 W/kg).
On the cellular level, a multitude of studies found the type of damage from high
frequency electromagnetic fields which is important for cancer initiation and cancer
promotion:
Direct damage on DNA as well as influences on DNA synthesis and DNA repair
mechanisms were demonstrated in in vivo and in vitro experiments for continuous and
pulsed fields at power flux densities from 10W/m2 and 9W/m2 respectively.
Chromosome aberrations and micronuclei occurred at power flux densities from 5 W/m2.
Neoplastic cell transformation and an enhanced cell proliferation were demonstrated for
Specific Absorption Rates of below 0.5W/kg, and individual studies demonstrated that the
obvious disturbance of the communication between cells, which is a prerequisite for the
uninhibited proliferation of cells that is characteristic for cancer development, occurs at
just a few W/m2.
Conclusion:
The results of the studies for all stages of cancer development from the damage of the
genetic material via the uninhibited proliferation of cells and debilitation of the immune
system (see below) up to the manifestation of the illness prove effects at power flux
densities of less than 1 W/m2. For some stages of cancer development, intensities of 0.1
W/m2 or even less may suffice to trigger effects.
Debilitation of the Immune System
Damaging effects on the immune system which can aid the development of illnesses were
demonstrated in animal experiments at power flux densities of 1 W/m2 (mouse, exposure
duration 6 days, 3 hours per day, SAR (mouse) 0.14W/kg). In in vitro experiments on
lymphocytes, defects of the genetic material were demonstrated at power flux densities of
circa 10 W/m2. The presence of stress hormones, which when permanent can debilitate the
immune system, was found to be increased in human experiments from power flux
densities of 0.2W/m2. In animal experiments (rat) a similar effect was observed at a
Specific Absorption Rate of circa 0.2 W/kg.
Conclusion:
Experiments on animals prove harmful effects on the immune system from circa 1 W/m2;
at power flux densities of 0.2 W/m2 higher secretions of stress hormones in humans have
been demonstrated.

34


Influences on the Central Nervous System and Cognitive Function
The effects of pulsed and continuous high frequency fields on the blood‐brain‐barrier and
the activity of neurotransmitters were demonstrated in animal experiments for power flux
densities of 3 and 10 W/m2 respectively.
In humans, influences on the slow brain potentials were found at SAR values of 0.882 to
1.42W/kg, i.e. well below the current guidelines for partial body exposure of 2 W/kg.
Changes in the sleep EEG of humans, which showed a shortening of the REM sleep phase
occurred at intensities as low as 0.5 W/m2.
In animal experiments, changes in the EEG were demonstrated at power flux densities of
1 to 2W/m2.
Impairment of cognitive functions was found in animal experiments at power flux
densities of 2W/m2. In humans, there are indications that brain functions are influenced by
fields such as they occur when using a mobile telephone.
An epidemiological study of children who had been exposed to pulsed high frequency
fields, found a decrease in the capability to concentrate and an increase in reaction times.
Conclusion:
Effects of high frequency electromagnetic fields on the central nervous system are proven
for intensities well below the current guidelines. Measurable physiological changes have
been demonstrated for intensities from 0.5 W/m2. Impairments of cognitive functions are
proven for animals from 2W/m2.
Electrosensitivity or Electromagnetic Hypersensitivity
The terms ‘electrosensitivity’ or ‘electromagnetic hypersensitivity’ describe disturbances
of well‐being and impairments of health, such as they are suffered by certain sensitive
people when working with or being in the presence of devices and equipment emitting
electrical, magnetic or electromagnetic fields. The sensitivity manifests in a variety of
symptoms including:
■ nervous symptoms such as sleep disturbances, headaches, exhaustion, lack of
concentration, irritability, anxiety, stress
■ cardio‐vascular complaints
■ disruptions of hormones and metabolism
■ skin complaints
The composition and strength of the complaints varies enormously in different
individuals. The correlation of the complaints with electromagnetic exposures and other
environmental influences seems to vary strongly not only between affected persons but
also in time, a fact that has so far impeded the conclusive scientific proof of a cause‐effect‐
relationship in provocation studies. The present results of scientific studies are often not
conclusive and partly contradictory. On the other hand, however, there is a wealth of data


35

collected by the self‐help organisations of affected people, which has not yet been
explored.
Conclusion:
On the basis of current knowledge it is impossible to estimate the risk of electrosensitive
reactions or to make recommendations for guidelines designed to avoid such a risk for the
general population, which is composed of sensitive and non‐sensitive persons.

36


8 Recommendations
8.1 Precautionary Health Protection in Relation to Exposures
to Electromagnetic Fields of Mobile Telecommunications
With mobile telecommunications we have to differentiate to exposure situations:
■ exposure of residents near base stations
■ exposure of mobile users when using the devices
To limit exposure to an acceptable degree, if this is possible at all, there need to be
different strategies for the two different exposure groups.
Exposures from Base Stations
In humans, harmful organic effects of high frequency electromagnetic fields as used by
mobile telecommunications have been demonstrated for power flux densities from
0.2W/m2 (see Chapter 7). Already at values of 0.1 W/m2 such effects cannot be excluded. If
a security factor of 10 is applied to this value, as it is applied by ICNIRP and appears
appropriate given the current knowledge, the precautionary limit should be 0.01W/m2.
This should be rigorously adhered to by all base stations near sensitive places such as
residential areas, schools, nurseries, playgrounds, hospitals and all other places at which
humans are present for longer than 4 hours.
We recommend the precautionary limit of 0.01 W/m2 independent of the carrier
frequency. The rough dependency on frequency with higher limits outside of the
resonance range, as it is applied in the concept of SAR, is not justifiable given the results
of the scientific studies which conclusively prove non‐thermal effects of high frequency
fields. Also, the current allowed higher exposures for parts of the body, as long as they
refer to the head or thorax are not justifiable.
Exposures of Mobile Phone Users
Given the state of technology now and in the foreseeable future, it is currently technically
impossible to apply the recommended maximum value for mobile base stations also to
the use of mobile phones. However, a lowering of the guidelines to a maximum of 0.5
W/m2 should urgently be considered.
A particular problem in this exposure group is posed by children and adolescents, not
only because their organism is still developing and therefore particularly susceptible, but
also because many adolescents have come to be the most regular users of mobile phones.
Advertising towards this population group should be banned. Furthermore, particular
efforts should be made to lower the exposures during calls. It would be recommendable
to conduct (covert) advertising campaigns propagating the use of headsets. It would also
be important to develop communications and advertising aiming at minimising the
exposures created by carrying mobile phones in standby mode on the body.


37

8.2 Scientific Studies Regarding the Health Risk of Mobile
Telecommunications
The precautionary limits recommended in Chapter 8.1 are based on the current scientific
knowledge. This is, however, still incomplete and in the case of this technology, which is
exposing the entire population to its emissions, further research efforts are needed to
create a base for the setting of truly reliable guidelines. Based on the scientific knowledge
presented in this report, the further research requirements are mainly for studies on living
organisms (humans or animals):
Epidemiological studies
■ studies that metrologically record the exposure on existing radio transmitters (USW),
TV transmitters and longer‐established radio communications and paging networks.
(The emissions of this type of equipment with regards to the modulation frequencies
may not be directly comparable to those of mobile telecommunications, but such
studies could nevertheless offer important indications for the assessment of the
exposure risks of high frequency electromagnetic fields; the studies should focus on
cancer and illnesses of the central nervous system including neurodegenerative
diseases as well as cardio‐vascular diseases and any diseases caused by a disruption of
the immune system; such studies should also address potential clusters of unspecified
symptoms and impairments of well‐being (electrosensitivity)).
■ a meta‐study with retrospective dosimetry for the studies which examined the
residents near emitting base stations (see Appendix D) with the help of measured data
from comparable sites
■ a cohort study examining the health (see above) of mobile users and residents near
mobile base stations
■ epidemiological animal studies on pets
Experimental long‐term studies
Studies of the chronic effects of the fields emitted by mobile telecommunications
■ on the central nervous system (preferably on humans)
■ on the immune and endocrine system (preferably on humans, but further animal
experiments at low intensities would also be helpful for example with regards to EMF‐
induced stress)
■ on the cardio‐vascular system (variability of heartbeat rates, blood pressure, etc., on
humans and on animals)
Experimental short‐term studies
Studies of the acute effects of the fields emitted by mobile telecommunications
■ on the brain in various rest and stress situations (preferably making use of EEG and
similar methods)

38


Beyond these suggestions, it would be important to develop a strategy for the research of
the ‘electrosensitivity’ phenomenon and its incidence, which would acknowledge the
failure of traditional scientific methods to address the problem and allow the inclusion of
the data available from the self‐help groups and associations of the affected.


39

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55

Appendix A
Studies of the effects of high frequency electromagnetic fields on the cellular level
Abbreviations
neg.

negative finding

n.s.

not statistically significant

pos.

positive finding

s.s.

statistically significant

partly some findings
#

disagreement with the conclusions of the authors

?

unknown; not provided; unreliable

56


Table A.1 Genotoxic effects of high frequency electromagnetic fields
Frequency

Modulation

Power Flux Density / SAR

Exposure duration

Studies subject / Method

Result

Ref.

2,45 GHz

cw

10 – 20 W/m2
0,6 – 1,2 W/kg

2h

Rat, in vivo

pos., s.s.

Lai & Singh 1995

2,45 GHz

PM, 500 Hz

10 – 20 W/m2
0,6 – 1,2 W/kg

2h

Rat, in vivo

pos., s.s.

Lai & Singh 1995

2,45 GHz

PM, cw

20 W/m2
1,2 W/kg

2h

Rat, in vivo

pos., s.s.

Lai & Singh 1996

2,45 GHz

PM, 500 Hz

20 W/m2
1,2 W/kg

2h

Rat, in vivo

pos., s.s.

Lai & Singh 1996

2,45 GHz

PM, 500 Hz

20 W/m2
1,2 W/kg

2h

Rat, in vivo

pos., s.s.

Lai & Singh 1997

2,45 GHz

cw

0,7 – 1,9 W/kg

2 h – 24 h

Glioblastoma Cells
(Human), in vitro

neg.?

Malyapa et al.
1997a

2,45 GHz

cw

0,7 – 1,9 W/kg

2 h – 24 h

Fibroblasts (Mouse), in
vitro

neg.?

Malyapa et al.
1997a

836 – 848 MHz

cw, FM, PM

0,6 W/kg

2 h – 24 h

Glioblastoma Cells
(Human), in vitro

neg.?

Malyapa et al.
1997b

0,6 W/kg

2 h – 24 h

vitro

neg.?

Malyapa et al.
1997b

2h

Rat (Brain), in vivo

?

Malyapa et al. 1998

Direct DNA damage

836 – 848 MHz
2,45 GHz

cw

1,2 W/kg
2

814 – 837 MHz

PM, TDMA, 50 Hz

8 – 90 W/m
2,4 – 26 W/kg

1 h – 10,67 h

T-Lymphoblasten

pos., s.s.

Phillips et al. 1998

2,45 GHz

cw

10 W/m2
1,18 W/kg

120 d, 2 h/d – 200 d, 2 h/d

Mouse (Brain, Testicles),
in vivo

pos., s.s.

Sarkar et al. 1994

1,7 GHz

cw

500 W/m2

30 min

Mouse (Testicles), in vivo

pos.

Varma & Traboulay
1977


57

Frequency

Modulation


Exposure duration


Result

Ref.

Influences on DNA synthesis and repair
350 MHz

cw

10 – 100 W/m2
0,039 – 4,5 W/kg

1h–3h

Fibroblasts (Human), in
vitro

unclear, partly pos.

Meltz et al. 1987

350 MHz

PM, 5,0 Hz

10 – 100 W/m2
0,039 – 4,5 W/kg

1h–3h

vitro


Meltz et al. 1987

850 MHz

cw

10 – 100 W/m2

1h–3h

vitro


Meltz et al. 1987

850 MHz

PM, 5,0 Hz

10 – 100 W/m2

1h–3h

vitro


Meltz et al. 1987

1,2 GHz

cw

10 – 100 W/m2

1h–3h

vitro


Meltz et al. 1987

1,2 GHz

PM, 80 kHz

10 – 100 W/m2

1h–3h

vitro


Meltz et al. 1987

836,55 MHz

PM, TDMA, 50 Hz

0,9 – 90 W/m2
0,00015 - 0,059 W/kg

4 h – 14 d

Glioma-Cells (Rat), in
vitro

pos., s.s.

Stagg et al. 1997

Chromosome aberrations
2,45 GHz

cw

?

?

Mouse (bone marrow), in
vivo

pos.

Banerjee et al. 1983

2,45 GHz

cw

400 W/m2

6 d, 30 min/d

Rat, in vivo

pos.

Beechey et al. 1986

7,7 GHz

cw

300 W/m2

15 - 60 min

Fibroblasts (Chin.
Hamster), in vitro

pos., s.s.

Garaj-Vrohac et al.
1990

7,7 GHz

cw

5 W/m2

15 - 60 min

Fibroblasts (Chin.
Hamster), in vitro

pos., s.s.

Garaj-Vrohac et al.
1991

7,7 GHz

cw

5 – 300 W/m2

10 min

Lymphocytes (Human), in
vitro

pos., s.s.

Garaj-Vrohac et al.
1992

0,4 MHz – 20 GHz

cw, AM, PM

Human, in vivo

pos.#, n.s.

Garson et al. 1991

Egg Cells (Chinese
Hamster)

pos., partly s.s.

Kerbacher et al.
1990

2,45 GHz

58

PM, 25 kHz

2

490 W/m
33,8 W/kg

2h


Frequency

Modulation


Exposure duration


Result

Ref.

2,45 GHz

cw

104 – 193 W/kg

20 min

vitro

neg.

Lloyd et al. 1984

2,45 GHz

cw

4 – 200 W/kg

20 min

Lymphocytes (Human)

neg.

Lloyd et al. 1986

2,45 GHz

cw

75 W/kg

30 – 120 min

vitro

pos.

Maes et al. 1993

954 MH

PM, 217 Hz, GSM

Occupational exposure

Lymphocytes, Human, in
vivo

pos., s.s.

Maes et al. 1995

954 MHz

217 Hz, GSM

15 W/m2
1,5 W/kg

2h

vitro

pos., s.s.

Maes et al. 1995

935,2 MHz

PM/GSM, 217 Hz

0,3 – 0,4 W/kg

2h

vitro

pos., n.s.

Maes et al. 1997

9,4 GHz

PM, 1000 Hz

1 – 100 W/m2

2 w, 3 d/w, 1 h/d

Mouse, in vivo

pos., s.s.

Manikowska et al.
1979

2,45 GHz

cw

0,05 – 20 W/kg

2 w, 6 d/w, 30 min/d

Mouse, in vivo

pos., s.s.

Manikowska-Czerska
et al. 1985

2,55 GHz

cw

2W/kg

20 min

DNA (E.coli), in vitro

pos.

Sagripanti &
Swicord 1986

2,0 – 8,75 GHz

cw

10 W/kg

5 min – 25 min

DNA, in vitro

pos., s.s.

Sagripanti et al.
1987

2,45 GHz

cw

100 W/m2

120 d 6 h/d

Spermatogonia (Mouse), in neg.
vivo

Saunders et al. 1988

2,45 GHz

cw

50 W/m2
12,46 W/kg

90 min

vitro

pos., n.s.

Vijayalaxmi et al.
1997

2,45 GHz

cw

750 W/m2

5 – 30 min

Chinese Hamster (Corneal
Epithelium), in vivo

pos, s.s.

Yao 1978

2,45 GHz

cw

15,2 W/kg

RH5- and RH16-Cells
(Kangaroo-Rat), in vitro

pos., s.s.

Yao 1982


59

Frequency

Modulation


Exposure duration

PM, 24,4 Hz

Changing exposures on the pastures


Result

Ref.

Micronuclei
154 – 162 MHz

2

Cow (Erythrocytes) in vivo pos., s.s.

Balode 1996

10 min

vitro

pos., partly s.s.

d'Ambrosio et al.
1995

2,45 GHz

CW

530 W/m
90 W/kg

2,45

AM, 50 Hz, sin

530 W/m2
90 W/kg

10 min

vitro

pos., partly s.s.

d'Ambrosio et al.
1995

1,25 – 1,35 GHz

?PM

0,1 – 200 W/m2

Occupational exposure

vivo

pos.

Fucic et al. 1992

7,7 GHz

cw

5 W/m2

15 - 60 min

Fibroblasts (Chin.
Hamster), in vitro

pos., s.s.

Garaj-Vrohac et al.
1991

7,7 GHz

cw

5 – 300 W/m2

10 min

vitro

pos., s.s.

Garaj-Vrohac et al.
1992

2,45 GHz

cw

75 W/kg

30 – 120 min

vitro

pos.

Maes et al. 1993

9,0 GHz

cw

70 W/kg

10 min

Lymphocytes (bovine), in
vitro

pos., s.s.

Scarfi et al. 1996

2,45

cw

50 W/m2
12,46 W/kg

90 min

vitro

pos.#, n.s.

Vijayalaxmi et al.
1997 b

2,45

cw

1,0 W/kg

18 mon

Erythroczyten (Mouse
blood / bone marrow)

pos, s.s.

Vijayalaxmi et al.
1997 a

Sister chromatid exchange
380 MHz

PM, 17,65 Hz

80 W/kg

?

vitro

neg.

Antonopoulos et al.
1997

900 MHz

PM/DCS, 217 Hz

208 W/kg

?

vitro

neg.

Antonopoulos et al.
1997

1,8 GHz

PM/GSM, 217 Hz

1700 W/kg

?

vitro

neg.

Antonopoulos et al.
1997

2,45 GHz

cw

?

?

Mouse (bone marrow), in
vivo

neg.

Banerjee et al. 1983

60


Frequency

Modulation


Exposure duration


Result

Ref.

2

2,45 GHz

PM, 25 kHz

490 W/m
33,8 W/kg

2h

Egg Cells (Chinese
Hamster), in vitro

neg.

Ciaravino et al.
1987

2,45 GHz

PM, 25 kHz

490 W/m2
33,8 W/kg

2h

Egg Cells (Chinese
Hamster), in vitro

neg.

Ciaravino et al.
1991

2,45 GHz

cw

104 – 193 W/kg

20 min

vitro, Add. caffeine

pos., s.s.#

Lloyd et al. 1984

2,45 GHz

cw

75 W/kg

30 – 120 min

vitro

neg.

Maes et al. 1993

954 MHz

PM/GSM, 217 Hz

1,5 W/kg

2h

vitro

pos., s.s.

Maes et al. 1996

935,2 MHz

PM/GSM, 217 Hz

0,3 – 0,4 W/kg

2h

vitro

pos., partly s.s.

Maes et al. 1997

2,45 GHz

cw

100 W/m2

120 d 6 h/d

Spermatogonia (Mouse), in neg.
vivo

Saunders et al. 1988

2,45 GHz

AM, 100 Hz

40 – 80 W/kg

2 h –6 h

Escherichia coli, in vitro

partly pos., s.s.

Anderstam et al.
1983

2,45 GHz

AM, 100 Hz

40 – 80 W/kg

4h–7h

Salmonella typhimurium,
in vitro

neg.

Anderstam et al.
1983

3,07 GHz

PM, 500 Hz

95 W/kg

1h


neg.

Anderstam et al.
1983

3,07 GHz

PM, 500 Hz

75 - 100 W/kg

2 h – 2,5 h

in vitro

neg.

Anderstam et al.
1983

9,4 GHz

cw

600 W/m2
23 W/kg

30 – 120 min


neg.

Dardalhon et al.
1981

9,4 GHz

cw

600 W/m2
23 W/kg

30 – 120 min

Saccharomyces cerevisiae, partly pos., s.s.
in vitro

Dardalhon et al.
1981

9,4 GHz

cw

10 – 600 W/m2

330 min

Saccharomyces cerevisiae, pos.
in vitro

Dardalhon et al.
1985

Mutations


61

Frequency

Modulation


Exposure duration


Result

Ref.

2,45 GHz

AM, 100 Hz

130 W/kg

5,7 h

in vitro

partly pos, s.s.

Hamnerius et al.
1985

3,10 GHz

PM, 500 Hz

90 W/kg

6h

in vitro

partly pos., n.s.

Hamnerius et al.
1985

2,45 GHz

AM, 100 Hz

110 W/kg

6h

Drosophila melanogaster,
in vivo

neg.

Hamnerius et al.
1985

3,10 GHz

PM, 500 Hz

60 W/kg

6h

in vivo

neg.

Hamnerius et al.
1985

2,375 MHz

cw

150.000 – 250.000 W/m2

25 – 300 min

in vivo

partly pos., s.s.

Marec et al. 1985

2,45

PM, 25 kHz

480 W/m2
30 W/kg

bis 63 h

Leukaemia-Cells (Mouse),
in vitro

pos./neg., partly s.s.

Meltz et al. 1989

2,45 GHz

PM, 25 kHz

650 – 870 W/m2
40 – 40,8 W/kg

4h

Leukaemia-Cells (Mouse),
in vitro

neg.

Meltz et al. 1990

62


Table A.2 Effects of high frequency electromagnetic fields on cellular processes
Frequency

Modulation

Power Flux Density SAR

Exposure Duration

Examines Subject Method

Result

Ref.

Gene transcription and gene translation
890 – 915 GHz

PM/GSM, 217 Hz

0,3 – 7,5 W/kg

4h

Brain (Rat), in vivo

pos., partly s.s.

Fritze et al. 1997 a

835,62 MHz

FM/cw

0,6 W/kg

4d

Fibroblasts (Mouse), in vitro

partly pos., s.s.

Goswami et al. 1999

847,74 MHz

PM/CDMA, 50 Hz

0,6 W/kg

4d

Fibroblasts (Mouse), in vitro

partly pos., s.s.

Goswami et al. 1999

836,55 MHz

2

PM/TDMA, 50 Hz

0,9 – 90 W/m
0,00026 – 0,026 W/kg

20 – 100 min

Pheochromocytoma Cells (Rat), in vitro

pos., s.s.

Ivaschuk et al. 1997

380 MHz

PM, 17,65 Hz

80 W/kg

?

Lymphocytes (Human), in vitro

neg.

Antonopoulos et al. 1997

900 MHz

PM/DCS, 217 Hz

208 W/kg

?


neg.


1,8 GHz

PM/GSM, 217 Hz

1700 W/kg

?


neg.


Cell-Cycle

2

2,45 GHz

PM, 25 kHz

490 W/m
33,8 W/kg

2h

Egg Cells (Chinese Hamster), in vitro

neg.

Ciaravino et al. 1991

2,45 GHz

cw

5 – 25 W/kg

2h

Egg Cells (Chinese Hamster), in vitro

pos., s.s.

Cleary et al. 1996

9,4 GHz

PM, 1,0 kHz

1 – 100 W/m2

2,45 GHz
2,45 GHz
2,45 GHz

cw
cw
cw

2 w 5 d/w 1 h/d

Mouse, in vivo

pos., s.s.

Manikowska et al. 1979

100 W/m

2

6x1 h


neg.

Pazmany et al. 1990

100 W/m

2

3x1 h


neg.

Pazmany et al. 1990

100 W/m

2

5h


pos., s.s.

Pazmany et al. 1990


63

Table A.3 Effects of high frequency electromagnetic fields on cell transformation and cell proliferation
Frequency

Modulation


Exposure Duration

Studied Subject Method

Result

Ref.

Cell Transformations (including neoplastic)
2,45 GHz

PM, 120 Hz

4,4 W/kg

24 h

vitro

partly pos., s.s.

Balcer-Kubiczek &
Harrison 1985

2,45 GHz

PM, 120 Hz

4,4 W/kg

24 h

vitro

partly pos., s.s.

Balcer-Kubiczek &
Harrison 1989

2,45 GHz

PM, 120 Hz

0,1 – 4,4 W/kg

24 h

vitro

partly pos., s.s.

Balcer-Kubiczek &
Harrison 1991

2,45 GHz

cw

0,8 – 12,3 W/kg

5d

vitro

neg.

Czerska et al. 1992

2,45 GHz

PM, 1000 Hz

0,8 – 12,3 W/kg

5d

vitro

pos., s.s.

Czerska et al. 1992

2,45 GHz

cw

50 W/m2

Lymphocytes (Mouse)

pos.

Smialowicz et al. 1979

Cell Communication
836,55 MHz

PM, TDMA, 50 Hz

0,3 – 30 W/m2
0,00015 - 0,015 W/kg

28 d

vitro

partly pos., s.s.

Cain et al. 1997

Cell Proliferation
2,45 GHz

AM, 100 Hz

40 – 80 W/kg

2 h –6 h


partly pos., s.s.

Anderstam et al. 1983

2,45 GHz

AM, 100 Hz

40 – 80 W/kg

4h–7h

in vitro

partly pos., s.s.


3,07 GHz

PM, 500 Hz

95 W/kg

1h


partly pos., s.s.


3,07 GHz

PM, 500 Hz

75 - 100 W/kg

2 h – 2,5 h

in vitro

partly pos., s.s.


900 MHz

PM/GSM, 217 Hz

0,55 – 2,0 W/m2
0,075 – 0,270 W/kg

10 d 2 h/d

Lymphocytes (Rat,
(Sprague-Dawley), in vivo

neg.

Chagnaud & Veyret
1999

2,45

cw

5 – 50 W/kg

2h

Blut (Human),
Lymphocytes, in vitro

pos., s.s.

Cleary et al. 1990 a

2,45

cw

5 – 75 W/kg

2h

Glioma-Cells, in vitro

pos. s.s.

Cleary et al. 1990 b

64


Frequency

Modulation


Exposure Duration

Studied Subject Method

Result

Ref.

2,45 GHz

cw

5 – 50 W/kg

2h

T-Lymphocytes (Mouse,
CTLL-2), in vitro

pos., s.s.

Cleary et al. 1996

2,45 GHz

PM/PCS, 50 Hz

5 W/kg

2h

T-Lymphocytes (Mouse,
CTLL-2), in vitro

pos., s.s.

Cleary et al. 1996

2,45 GHz

?

?

15 s – 5 h

Myeloma- and HybridomaCells (Mouse), in vitro

?, Methode fragwürdig

Dorp et al. 1998

150 MHz

AM, 72 Hz, 217 Hz, 1100 Hz

1,6 kV/m
5,4 µT


pos., partly s.s.

Grospietsch et al. 1995

2,45 GHz

AM, 100 Hz

130 W/kg

5,7 h


pos, s.s.

Hamnerius et al. 1985

3,10 GHz

PM, 500 Hz

90 W/kg

6h


pos., s.s.

Hamnerius et al. 1985

836,55 MHz

PM, TDMA, 50 Hz

0,9 – 90 W/m2
0,00015 - 0,059 W/kg

4 h – 14 d

Glioma-Cells (Rat), in vitro neg.

Stagg et al. 1997

960 MHz

PM, GSM, 217 Hz

0,0021 W/kg

30 min

transform. EpithelAmnion-Cells (Human), in
vitro

Velizarov et al. 1999

pos., (s.s)


65

Appendix B
Studies of the effects of high frequency electromagnetic fields on the central nervous system
(Blood-Brain-Barrier)
Abbreviations
neg.

negative finding

n.s.


pos.

positive finding

s.s.


#


?


66


Table B.1 Effects of high frequency electromagnetic fields on the central nervous system
Frequency

Modulation


Exposure duration


Result

Ref.

2

2h

Rat (Wistar)

pos.

Albert 1979

2h

Hamster (Chin.)

pos., s.s.

Albert & Kerns 1981

4h

Rat (Wistar)

pos., partly s.s.

Fritze et al. 1997 b

4h

Rat (Tac:N(SD)sBR)

partly pos, n.s.

Gruenau et al. 1982

4h

Rat (Tac:N(SD)sBR)

partly pos, n.s.

Gruenau et al. 1982

30 min – 2 h

Rat (Sprague Dawley)

pos., s.s.

Neubauer et al. 1990

2,8 GHz

cw

100 W/m

2,45 GHz

cw

100 W/m2
2,5 W/kg

900 MHz

PM/GSM, 217 Hz

0,3 – 7,5 W/kg

2,8 GHz

cw

100 – 400 W/m

2,8 GHz

PM, 500 Hz

2

10 – 150 W/m2
2

2,45 GHz

PM, 100 Hz

100 W/m
2 W/kg

1,3 GHz

cw

3 – 30 W/m2

20 min

Rat (Wistar)

pos., s.s.

Oscar & Hawkins 1977

1,3 GHz

PM, 5 Hz

0,3 – 0,5 W/m2

20 min

Rat (Wistar)

pos., s.s.


20 min

Rat (Wistar)

pos., s.s.


30 min

Rat (Sprague-Dawley)

partly pos., s.s.

Preston et al. 1979

1,3 GHz

PM, 1000 Hz

1 – 10 W/m

2
2

2,45 GHz

cw

1,0 – 300 W/m

915 MHz

cw

0,3 – 5,0 W/kg

2h

Rat (Fischer 344)

pos., s.s.

Salford et al. 1994

915 MHz

PM, 8 Hz

0,016 – 0,16 W/kg

2h

Rat (Fischer 344)

pos., s.s.

Salford et al. 1994

915 MHz

PM, 16 Hz

0,03 – 2,1 W/kg

2h

Rat (Fischer 344)

pos., s.s.

Salford et al. 1994

915 MHz

PM, 50 Hz

0,3 – 5,0 W/kg

2h

Rat (Fischer 344)

pos., s.s.

Salford et al. 1994

915 MHz

PM, 200 Hz

0,4 – 2,9 W/kg

2h

Rat (Fischer 344)

pos., s.s.

Salford et al. 1994


67

Appendix C
Studies of the Carcenogenic Effects of High Frequency Electromagnetic Fields in Animal
Experiments
Abbreviations
neg.

negative finding

n.s.


pos.

positive finding

s.s.


#


?


68


Table C.1 Animal experiments regarding the carcenogenic effects of high frequency electromagnetic fields
Frequency

Modulation


Exposure duration


Result

Ref.

836,55 MHz

PM/TDMA, 50 Hz

0,74 – 1,6 W/kg

24 mon 4 d/w 2 h/d

Rat (Fischer 344)

neg.

Adey et al. 1999

900 MHz

PM/GSM, 217 Hz

0,55 – 2,0 W/m2

2 w, 2 h/d

Rat, Cancer, total

neg.

Chagnaud et al. 1999

2,45 GHz

PM, 800 Hz

0,15 – 0,4

25 mon

Rat, Cancer, total

pos., s.s.

Chou et al. 1992

2,45 GHz

cw

0,3 W/kg

18 mon, 7 d/w, 20 h/d

Mouse (C3H/HeJ), Cancer,
total

neg.

Frei et al. 1998 a

2,45 GHz

cw

1,0 W/kg

78 w, 7 d/w, 20 h/d

Mouse (C3H/HeJ), Cancer,
total

partly pos., n.s.

Frei et al. 1998 b

835,62 MHz

FM, cw

0,75 W/kg

150 d, 5 d/w, 4 h/d

Rat (Fischer 344), B16
Melanoma

partly pos., n.s.

Higashikubo et al. 1999

835,62 MHz

PM/CDMA, 50 Hz

0,75 W/kg

150 d, 5 d/w, 4 h/d

Rat (Fischer 344), B16
Melanoma

neg.

Higashikubo et al. 1999

929,2 MHz

PM/TDMA, 50 Hz

0,58 – 0,8

6 w, 5 d/w, 90 min/d

Rat (Fischer 344), Liver
cancer

neg.

Imaida et al 1998 a

1,439 GHz

PM/TDMA, 50 Hz

0,453 - 0,680 W/kg

6 w, 5 d/w, 90 min/d

Rat (Fischer 344), Liver
cancer

neg.

Imaida et al. 1998 b

900 MHz

PM/GSM, 217 Hz

2,6 – 13 W/m2
0,008 – 4,2 W/kg

18 mon 30 min/d

Mouse (transgenic Eµ-Pim1),
Lyphomas

pos., s.s.

Repacholi et al. 1997

915 MHz

PM, 4 – 217 Hz

0,0077 – 1,0 W/kg

2-3 w 5d/w 7h/d

Rat (Fischer 344), Brain
Tumor

partly pos., n.s.

Salford et al. 1993

2,45 GHz

cw

10 W/m2
1,2 W/kg

max. 46 w, 6 d/w, 2,5 h/d

Mouse (C57BL/6J), B16
Melanoma

partly pos., n.s.

Santini et al. 1988

2,45 GHz

PM, 25 Hz

10 W/m2
1,2 W/kg

max. 46 w, 6 d/w, 2,5 h/d

Mouse (C57BL/6J), B16
Melanoma

partly pos., n.s.

Santini et al. 1988

2,45 GHz

cw

50 – 150 W/m2
2 – 8 W/kg

12 mon 6d/w, 2h/d

Mouse (C3H/HeA), Cancer,
total

pos., s.s.

Szmigielski et al. 1982

2,45 GHz

cw

50 – 150 W/m2
2 – 8 W/kg

5 mon 6d/w, 2h/d

Mouse (Balb/c), Skin Cancer

pos., s.s.

Szmigielski et al. 1982


69

2,45 GHz

cw

50 – 150 W/m2

6 mon, 2 h/d

Mouse (Balb/c), Hautcancer

pos., s.s.

Szudinski et al. 1982

435 MHz

PM, 1,0 kHz

10 W/m2
0,32 W/kg

21 mon

Mouse (C3H/HeJ), Chest
tumors, Ovarian tumors

partly pos., s.s.

Toler et al. 1997

2,45 GHz

cw

100 W/m2
11 W/kg

5 mon, 6 d/w, 3 h/d

Mouse (Balb/c), Intestinal
cancer

partly pos., n.s.

Wu et al. 1994

70


Appendix D
Epidemiological Studies of the health Risks of HF EMFs


71

Table D.1

Overview of the results of epidemiological studies regarding exposures in the high frequency spectrum and health risks

Column 1: studied illness
Column 2: Exposure situation
Column 3: Reliability of the exposure classification:
‐

3: Source of exposure and quantity clearly identified,

‐

2: Method of exposure clearly identified

‐

1: HF‐exposure probable

Column 4: Relative Risk (R.R.), Explanations see text
Column 5: Statistical significance of the findings:
‐

s.s.: statistically significant(R.R.=1 outside of  95 %‐trust interval, or. p<0,05

‐

n.s.: statistically not significant

Column 6: Literatur reference
Column 7: Comments:
‐

R: Values in the Column R.R. obtained by conversion (reciprocal value, proportion) of other numerical values or via the interpretation of
diagrams

‐

*: Paper listed in the literature references of Appendix E

72


Illness

Exposure

Exp.
class.

R.R.

stat. Sign. References

C

All illnesses, morbidity

MW, Radar, Military

2

1,18

n.s.

Robinette et al. 1980

R*

All Illnesses, morbidity

MW, mobile
telecommunications

3

0,93

n.s.

Rothman et al. 1996

Cancer, total, morbidity

MW, Radar, Military

2

1,50

n.s.

Robinette et al 1980

R*

Cancer, total, Incidence

RF, Radio, women

2

1,2

s.s.

Tynes et al. 1996

*


RF/MW, Military

2

2,07

s.s.

Szmigielski 1996

*


HF, Radio and TV transmitters, local residents

3

1,09

s.s.

Dolk et al. 1997 a

*


HF, place of work

1

2,0

n.s.

Lagorio et al. 1997


RF/MW, Radar and Radio, Police

2

0,96

n.s.

Finkelstein 1998

*

Multiple Myelome

HF, Radio and TV transmitter, local residents

3

1,23

n.s.

Dolk et al. 1997 a

*

All Illnesses

Cancer, total

Brain tumors, total and tumors of the nervous system, total
Brain-Tumors, total, Morbidity

HF, Place of work

1

1,54

n.s.

Lin et al. 1985

Brain-Tumors, Glioblastomas and Astrocytoma, Morbidity

HF, Place of work

1

2,15

s.s.

Lin et al. 1985


HF, Place of work, Men

1

0,38

n.s.

Milham 1985


RF/MW, Place of work, Men

2

2,3

s.s.

Thomas et al. 1987


RF, Amateur Radio Users

2

1,39

n.s.

Milham 1988

Brain-Tumors, total, Incidence

HF, Place of work

1

2,9

s.s.

Törnqvist et al. 1991

Brain-Tumors, Glioblastomas, Incidence

HF, Place of work

1

3,4

s.s.



RF, Place of work, Men

2

0,61

n.s.

Tynes et al. 1992


RF, Radio, Women

2

1,0



1

2,4

s.s.

Beall et al. 1996


RF/MW, Military

2

1,39

s.s.

Grayson 1996


Tynes et al. 1996

*

*

*

73

Illness

Exposure

Exp.
class.

R.R.


C


HF/MW, TV transmitters and others
residents (adults)

3

0,89

n.s.

Hocking et al. 1996

*


HF/MW, TV and other transmitters, Local
residents/ Adults

3

0,82

n.s.

Hocking et al. 1996

*


residents/child.

3

1,0

Hocking et al. 1996

*


residents/child.

3

1,3

n.s.

Hocking et al. 1996

*

Tumors des Nervensystems einschl. Hirntumors, Incidence

RF/MW, Military

2

1,91

s.s.

Szmigielski 1996

*


HF, Sender Radio and Fernsehen, Local residents 3

1,29

n.s.

Dolk et al. 1997 a

*

Brain-Tumors, maligne, Incidence


1,31

n.s.

Dolk et al. 1997 a

*



2

0,84

n.s.

Finkelstein 1998

*


MW, Mobil telecommunications, Mobile phones

3

1,20

n.s.

Hardell et al. 1999

*

Brain-Tumors, Expos.seite, Incidence

MW, Mobilradio, Handy

3

R 2,45 n.s.
L 2,40 n.s.

Hardell et al. 1999

*

MW, Radar, Military

1

2,1

s.s.

Holly et al. 1995

Cancer der Atmungsorgane, Morbidity

MW, Radar, Military

2

2,59

s.s.


Lungencancer, Morbidity


1

0,80

n.s.

Milham 1985

Lungencancer, Incidence

RF, Radio, Women

2

1,2

n.s.

Tynes et al. 1996

*



1,01

n.s.

Dolk et al. 1997 a

*



2

0,66

s.s.

Finkelstein 1998

*

HF, Place of work

1

2,9

n.s.

Demers et al. 1991

Cancer, Eyes
Melanome, Augen, Incidence
Cancer of the respiratory system, lung cancer
R*

Chest cancer, Men
Brustcancer, Mönner, Incidence

74


Illness

Exposure

Brustcancer, Men, Incidence

Exp.
class.

R.R.


C


1,64

n.s.

Dolk et al. 1997 a

*

Brustcancer, Women, Morbidity

HF, Place of work

2

1,15

s.s.

Cantor et al. 1995

*

Brustcancer, Women, Incidence

RF, Radio, Women

2

1,5

s.s.

Tynes et al. 1996

*

Brustcancer, Women, Incidence


1,08

n.s.

Dolk et al. 1997 a

*

Cancer des lymphat. and des blutbild. Systems, Morbidity

MW, Radar, Military

2

1,98

n.s.


R*

Cancer des lymphat. and des blutbild. Systems, Morbidity


1

1,37

n.s.

Milham 1985

Cancer des lymphat. and des blutbild. Systems, Incidence


1,21

n.s.

Dolk et al. 1997 a

*

Cancer des lymphat. and des blutbild. Systems, Incidence

RF/MW, Military

2

6,31

s.s.

Szmigielski 1996

*

Leukaemia, total, Morbidity

HF, Place of work

1

1,11

n.s.

Milham 1982


RF, Amateur radio user

2

1,91

s.s.

Milham 1985 a



1

1,02

n.s.

Milham 1985 b


RF Amateur radio user

2

1,24

n.s.

Milham 1988

Leukaemia, total, Incidence

HF, Military

1

2,4

s.s.

Garland et al. 1990


HF, Place of work

1

0,8

n.s.



RF, Place of work, Men

2

2,85

s.s.

Tynes et al. 1992


RF, Radio, Women

2

1,1

n.s.

Tynes et al. 1996

*


RF/MW, TV and other transmitters, Local
residents/ Adults

3

1,17

n.s.

Hocking et al. 1996

*


residents/ children.

3

2,32

s.s.

Hocking et al. 1996

*


RF/MW, TV and other transmitters , Local
residents/

3

1,24

s.s.

Hocking et al. 1996

*

Breast cancer, Women

Cancer of the lymphatic and blood forming systems, total

Leukaemia, total


75

Illness

Exposure

Exp.
class.

R.R.


C

Adults

residents/ Children.

3

1,58

s.s.

Hocking et al. 1996

*



1,83

s.s.

Dolk et al. 1997 a

*

Leukaemia and Non-Hodgkin-Lymphoma, total, Incidence


1,25

n.s.

Dolk et al. 1997 a

*



2

0,6

n.s.

Finkelstein 1998

*


residents/
children.

3

1,47

n.s.

McKenzie et al. 1998

*

Acute Leukaemia, total, Morbidity

HF, Place of work

1

2,39

n.s.

Milham 1982

Acute Leukaemia, total, Morbidity


1

2,12

n.s.

Milham 1985

Acute Unspez. Leukaemia, Morbidity

RF, Amateur radio users

2

1,76

n.s.

Milham 1988

Acute Leukaemia, total, Incidence

HF, TV and Radio transmitters, Local residents

3

1,86

n.s.

Dolk et al. 1997 a

Lymphat. Leukaemia, total, Morbidity


2

0,77

n.s.

Milham 1985



2

1,03

n.s.

Milham 1988


residents/ Adults

3

1,39

s.s.

Hocking et al. 1996

*


residents/ children.

3

2,74

s.s.

Hocking et al. 1996

*

Lymphat. Leukaemia, total, Incidence

residents/ Adults

3

1,32

s.s.

Hocking et al. 1996

*


residents/ children

3

1,55

s.s.

Hocking et al. 1996

*

Acute Leukaemia, total

*

Lymphat. Leukaemia, total

76


Illness

Exposure

Exp.
class.

R.R.


C


residents /children.

3

1,53

n.s.

McKenzie et al. 1998

*

Acute Lymphat. Leukaemia, Morbidity


2

1,20

n.s.

Milham 1988

Acute Lymphat. Leukaemia, Incidence


3,57

n.s.

Dolk et al. 1997 a

Chron. Lymphat. Leukaemia, Morbidity


2

1,43

n.s.

Milham 1985

Chron. Lymphat. Leukaemia, Morbidity


2

1,09

n.s.

Milham 1988

Chron. Lymphat. Leukaemia, Incidence

HF, Place of work

1

1,3

n.s.


Chron. Lymphat. Leukaemia, Incidence


2,56

s.s.

Dolk et al. 1997 a

Myelo. Leukaemia, total, Morbidity


2

2,81

s.s.

Milham 1985



2

1,40

n.s.

Milham 1988


residents/ Adults

3

1,01

n.s.

Hocking et al. 1996

*


residents/child.

3

1,77

n.s.

Hocking et al. 1996

*

Myelo. Leukaemia, total, Incidence

residents/ Adults

3

1,09

n.s.

Hocking et al. 1996

*

Myelo. Leukaemia, total, Incidence

residents/child.

3

1,73

n.s.

Hocking et al. 1996

*

Acute Myelo. Leukaemia, Morbidity


2

2,89

s.s.

Milham 1985

Acute Myelo. Leukaemia, Morbidity


2

1,76

s.s.

Milham 1988

Acute Myelo. Leukaemia, Incidence

HF, Place of work

1

2,1

n.s.


Acute Myelo. Leukaemia, Incidence

HF, Radio, TV, Local residents

3

1,02

n.s.

Dolk et al. 1997

Acute Lymphat. Leukaemia

*

Chron. Lymphat. Leukaemia

*

Myelo. Leukaemia, total

Acute Myelo. Leukaemia


*

77

Illness

Exposure

Exp.
class.

R.R.


C

Chron. Myelo. Leukaemia, Morbidity


2

2,67

s.s.

Chron. Myelo. Leukaemia, Morbidity


2

0,86

Chron. Myelo. Leukaemia, Incidence

HF, Radio and TV transmitters, Local residents

3

1,23

n.s.

Dolk et al. 1997

*

Leukaemia, non-lymph. and non-myelo., Morbidity

residents/ Adults

3

1,57

s.s.

Hocking et al. 1996

*

Leukaemia, non-lymph. and non-myelo., Morbidity

residents/child.

3

1,45

n.s.

Hocking et al. 1996

*

Leukaemia, non-lymph. and non-myelo., Incidence

residents/ Adults

3

1,67

s.s.

Hocking et al. 1996

*

Leukaemia, non-lymph. and non-myelo., Incidence

residents/child.

3

1,65

n.s.

Hocking et al. 1996

*

Lymphosarkome, Morbidity


1

0,73

n.s.

Milham 1985

Lymphome, excl. Lymphosarkoma, Morbidity


1

3,42

n.s.

Milham 1985

Hodgkin-Syndrome, Morbidity


2

1,23

n.s.

Milham 1988

Other malignant illness of the lymphat. tissues, Morbidity


2

1,62

s.s.

Milham 1988

Lymphomas, total, Incidence

RF, Radio, Women

2

1,3

n.s.

Tynes et al. 1996

*

Hodgkin-Syndrome, Incidence


2

0,84

n.s.

Finkelstein 1998

*

Non-Hodgkin-Lymphoma, Incidence


3

0,66

n.s.

Dolk et al. 1997 a

*

Testicular cancer, Incidence

RF/MW, Place of work

2

3,1

s.s.

Hayes et al. 1990

Germ cell-Carcinoma, Seminoma


2

2,8

n.s.

Hayes et al. 1990

Germ cell-Carzinome, others


2

3,2

s.s.

Hayes et al. 1990

Chron. Myelo. Leukaemia
Milham 1985
Milham 1988

Leukaemia, non-lymph. and non-myelo.

Lymphomas, Hodgkin-Syndrome

Testicular cancer

78


Illness

Exposure

Exp.
class.

R.R.


C


MW, Radar, Police

2

6,9

s.s.

Davis & Mostofi 1993

*



2

1,33

s.s.

Finkelstein 1998

*

RF, Radio, Women

2

1,9

s.s.

Tynes et al. 1996

*

Skin Cancer, Malignant Melanoma, Incidence

RF, Radio, Women

2

0,9

n.s.

Tynes et al. 1996

*

Skin Cancer, total, Incidence

RF/MW, Military

2

1,67

n.s.

Szmigielski 1996

*

Skin cancer, Malignant Melanoma, Incidence


3

1,43

n.s.

Dolk et al. 1997 a

*

Skin cancer, Malignant Melanoma, Incidence


2

1,37

s.s.

Finkelstein 1998

*

Cardio vascular diseases, Morbidity

MW, Radar, Military

2

1,09

n.s.


R*

Cardio vascular diseases, Morbidity


2

0,70

s.s.

Milham 1988

Abnorm. Hearbeat rate variability

RF/AM, Radio transmitters, Place of work

2

1,6

s.s.

Bortkiewicz et al. 1996

*

Abnormal ECG

MW

2

2,9

?

Zhao et al. 1994

R

Cardio vascular complaints

MW

2

3,2

?

Zhao et al. 1994

R

reduced Fertility, reduced Sperm count

MW, Place of work

2

1,20

s.s.

Lancranjan et al. 1975

R

reduced Fertility, immob.
Spermatozoa

MW, Place of work

2

1,39

s.s.


R

reduced Fertility, normal Spermatozoa

MW, Place of work

2

1,18

s.s.


R

reduced. Fertility, reduced Sperm count

MW, Military

2

2,70

s.s.

Weyandt et al. 1996

R

reduced Fertility, reduced sperm count

MW, Radar

2

1,54

n.s.

Hjollund et al. 1997

R

reduced Fertility, immob. Spermatozoa

MW, Radar

2

1,58

n.s.

Hjollund et al. 1997

R

reduced Fertility, reduced Sperm count

MW, Radar

2

1,10

n.s.

Schrader et al 1998

R

Cancer of the uterus
Cancer of the uterus, Incidence
Skin cancer

Heart and cardio vascular diseases

Infertility, reduced fertility, Men


79

Illness

Exposure

Exp.
class.

R.R.


C

KW, Place of work, Physiotherapie, Mothers

2

1,7

n.s.

Larsen et al. 1991 a

*

Infertility, reduced. fertility, Women
reduced. fertilityt

Miscarriages, Stillbirths, Malformations and other abnormalities of newborns
Malformations and perinatal death

KW, Place of work, Mother

2

2,36

s.s.

Källén et al 1982

Miscarriage

MW, Place of work, Mother

2

1,28

s.s.

Ouellet-Hellstrom &
Stewart 1993

*

Miscarriage

KW, Place of work, Mother

2

1,07

n.s.

Ouellet-Hellstrom &
Stewart 1993

*

Tumors of the nervous system

HF, Place of work, fathers

1

2,01

n.s.

Cole Johnson & Spitz 1989


Radar, Place of work, fathers

2

2,3

s.s.

Smulevich et al. 1999

*

Alzheimer’s, Morbidity

HF, Place of work

1

1,5

n.s.

Savitz et al. 1998

*

Parkinson’s Disease

HF, Place of work

1

-

Savitz et al. 1998

*

Amyotrophic Lateral Sklerosis

HF, Place of work

1

-

Savitz et al. 1998

*

Cancer, Offspring (parental exposure)

Neurodegenerative Diseases

Disturbances of motoric and psychological reactions, Unwellness
Reduced stamina, Boys

MW, Radar

2

1,38

s.s.

Kolodynski & Kolodynska
1996

R*

Reduced stamina, Girls

MW, Radar

2

1,38

s.s.

1996

R*

reduced memory, Boys

MW, Radar

2

1,09

s.s

1996

R*

Reduced memory, Girls

MW, Radar

2

1,12

s.s

1996

R*

Reduced concentration, Boys

MW, Radar

2

1,23

s.s.

1996

R*

80


Illness

Exposure

Exp.
class.

R.R.


C

Reduced Concentration, Girls

MW, Radar

2

1,20

s.s.

1996

R*

Extended reaction time, Boys

MW, Radar

2

1,07

n.s.

1996

R*

Extended reaction time, Girls

MW, Radar

2

1,12

s.s.

1996

R*

Unwellness. ('Neurosis')

MW

2

3,2

?

Zhao et al. 1994

R


81

Appendix E (only available in German)
Extracts of our database (EMFbase)
Important research papers relevant to the assessment of health risks resulting from exposure to the electromagnetic fields of mobile
telecommunications under the aspect of precautionary health protection

82


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