Limited Exposure To Magnetic Fields

Volume 15 No.
3 2004
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Chilton, Didcot,
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Working in partnership with the
Health Protection Agency
Documents
of the NRPB
Review of the Scientific Evidence
for Limiting Exposure to
Electromagnetic Fields (0300 GHz)
iii
Contents
Review of the Scientific Evidence for Limiting Exposure to
Electromagnetic Fields (0300 GHz)
Abstract 1
Executive Summary 3
Background 3
Guidelines ongoing developments 3
EMFs and health 4
Exposure guidelines 5
Scientific basis 5
Scientific uncertainty and caution 5
Recommendations for quantitative restrictions 6
Aspects of further precaution 7
Power frequency fields 7
Radiofrequency fields 8
1 Introduction 9
Background 9
Development of exposure guidelines 10
Structure of document 12
Acknowledgements 12
2 Development of Exposure Guidelines 13
Epidemiology 14
Bias and confounding 14
Statistical power 14
Hypothesis testing or hypothesis generating 15
Epidemiological interpretation 15
Biology 16
Human studies 17
Animal studies 17
Cellular studies 18
Experimental interpretation 18
Dosimetry 19
Computational modelling of the human body 19
3 Static Electric and Magnetic Fields 21
Epidemiology 21
Epidemiological uncertainties 22
Summary 22
Review of the Scientific Evidence for Limiting Exposure to Electromagnetic Fields (0300 GHz)
iv
Biology 22
Human studies 22
Electric fields 22
Magnetic fields 23
Summary 24
Animal and cellular studies 25
Electric fields 25
Magnetic fields 25
Cancer 25
Reproduction and development 26
Neurobehavioural effects 27
Cardiovascular effects 28
In vitro effects of very intense fields 29
Biological uncertainties 29
Summary 30
4 Electromagnetic Fields of Frequencies Below 100 kHz 31
Epidemiology 31
Cancer 31
Residential exposures 31
Occupational exposures 32
Neurodegenerative diseases 33
Suicide and depressive illness 34
Cardiovascular disease 34
Other diseases 35
Reproductive outcome 35
Summary 37
Biology 38
Effects of surface charge and induced electric fields and currents 39
Surface electric charge responses 39
Acute electrophysiological responses 40
Stimulation effects in high fields 41
Electrophysiological studies of weak field effects 42
Volunteer studies of weak field effects 44
Other possible effects 47
Cancer 47
Volunteer studies 47
Animal studies 48
Cellular studies 51
Animal studies 55
Volunteer studies 56
Cognitive studies 57
Electrical activity of the brain 57
Sleep 58
Hypersensitivity and mood states 59
Effects on cardiac activity 59
Contents
v
Animal studies 60
Neurotransmitter function 60
Electrical activity 61
Field detection 62
Arousal and aversion 62
Learned tasks 63
Summary 66
Dosimetry 67
Induced current densities from low frequency magnetic fields 67
Computational methods 67
Calculations of induced fields 68
Induced current densities from low frequency electric fields 70
Calculations of induced fields 70
Dosimetric uncertainties 71
Summary 73
5 Electromagnetic Fields of Frequencies Above 100 kHz 74
Epidemiology 74
Cancer 74
Other health outcomes 76
Effects of heat on mortality and morbidity 76
Biology 78
Whole-body heating 79
Circulatory adjustments to heat stress 80
Physiological limits on heat exposure during physical work 81
Physiological responses in healthy volunteers exposed to RF EMFs 81
Heat-related disorders in adults 82
Heat-related mortality of adults at the population level 83
Temperature regulation during pregnancy, in neonates and in children 84
Effects of heat exposure on cognitive performance 85
Effects of heat on the development of the embryo and fetus 86
Localised heating 88
Other possible effects 90
Effects on cancer 90
Human studies 91
Animal studies 91
Cellular studies 94
Human studies 98
Subjective symptoms 98
Cognitive performance 99
Electrical activity of the brain 100
Sleep 100
Cardiovascular function 101
Animal studies 102
Gene expression 102
vi
Bloodbrain barrier 102
Electrical activity 103
Neurotransmitters 103
Learned and other behaviours 104
The eyes 105
Summary 108
Dosimetry 110
SAR calculations 110
Calculations of whole-body averaged SAR 110
Localised SAR 112
Thermal dosimetry 113
Heating of the skin 114
RF contact burns 115
Thermal response times 115
Heating of the eye 116
Heating of the head 117
Microwave auditory effect 119
Whole-body exposure and heat stress 120
Averaging mass 120
Dosimetric uncertainties 121
Summary 122
6 Scientific Uncertainty 125
EMF health risk assessment 125
Evidence and uncertainties 126
EMF exposure guidelines and caution 126
International initiatives 127
EMF exposures and further precaution 127
The Precautionary Principle 128
European dimension 128
UK dimension 130
Precautionary measures 131
WHO precautionary framework 131
Application to EMFs 133
7 Conclusions and Recommendations 135
Introduction 135
General conclusions on the science 136
Exposure circumstances 136
Static electric and magnetic fields 136
Occupational exposure 137
General public exposure 137
Recommendation 137
Contents
vii
Electric and magnetic fields of frequencies below 100 kHz 137
Reference levels 139
Recommendations 139
Time-varying EMFs of frequencies above 100 kHz 139
Whole-body 142
Partial-body 142
Whole-body 144
Partial-body 144
Recommendations 146
Further precautionary measures 146
Recommendation 146
Future development of exposure guidelines 147
Static magnetic fields 147
Power frequency surface charge effects 147
Weak induced electric field effects 147
Whole-body SAR 148
Localised SAR 148
Dosimetry and reference levels 148
8 References 149
Appendices
A Weak Electric Fields Group 197
B Weak Electric Fields: Developments Subsequent to Appendix A 205
C Summary of ICNIRP Exposure Guidelines 206
Glossary 210
This report from NRPB reflects understanding and evaluation of the current scientific evidence as
presented and referenced in this document.
REVIEW OF THE SCIENTIFIC EVIDENCE
FOR LIMITING EXPOSURE TO
ELECTROMAGNETIC FIELDS (0300 GHz)
ABSTRACT
This document reviews the scientific evidence relating to possible adverse health effects of exposure to
electromagnetic fields (EMFs) in the frequency range 0300 GHz. It provides the basis of NRPB advice
on quantitative restrictions on exposure and other measures to avoid adverse effects. It explores recent
evidence on the possibility of variations in sensitivity between different groups in the population.
The preparation of this review has been carried out at the request of the Department of Health and has
particularly examined the issues of uncertainty in the science and aspects of precaution. In developing
this review, NRPB has taken advice from individual UK and international scientific experts, and from
published comprehensive reviews by expert groups. It sought advice from an ad hoc expert group on
weak electric field effects in the body and gave careful consideration to the views expressed in response
to a consultation document on its proposed advice issued in May 2003. It has also listened to the
concerns raised at a public open meeting on power lines in December 2002.
Having considered the totality of the scientific evidence in the light of uncertainty and the need for a
cautious approach, NRPB recommends that restrictions on exposure to EMFs in the UK should be based
on the guidelines issued by the International Commission on Non-Ionizing Radiation Protection
(ICNIRP) in 1998. This provides for basic restrictions on exposures of members of the public that are a
factor of five lower than for those who are occupationally exposed.
PREPARED BY A F MCKINLAY, S G ALLEN, R COX, P J DIMBYLOW, S M MANN, C R MUIRHEAD,
R D SAUNDERS, Z J SIENKIEWICZ, J W STATHER AND P R WAINWRIGHT
3
Executive Summary
BACKGROUND
1 The National Radiological Protection Board (NRPB) has the responsibility for
providing advice on exposure guidelines for electromagnetic fields (EMFs) in the
frequency range from 0 to 300 GHz. In 1993, NRPB published a comprehensive review
of epidemiological and experimental data relevant to the assessment of health effects
from exposure to EMFs and provided advice on limiting exposure. This advice gave
similar exposure guideline values for workers and members of the public. NRPB
subsequently reviewed its advice in 1999 following publication of exposure guidelines
by the International Commission on Non-Ionizing Radiation Protection (ICNIRP) with
restriction values for workers broadly similar to those of NRPB but which also included
more restrictive values for members of the public. At the time NRPB saw no scientific
evidence for changing its previous advice.
2 Between 1993 and 1999, many studies addressing exposure to EMFs and possible
effects on health had been published and NRPB had carried out continuous surveillance
of these through scientific reviews carried out by its own staff and through the
independent Advisory Group on Non-ionising Radiation (AGNIR), ICNIRP, the World
Health Organization (WHO), and expert bodies in other countries. Since 1999, when
NRPB last published advice on EMF exposure guidelines, there have been further
comprehensive reviews carried out including those from AGNIR, an Independent Expert
Group on Mobile Phones (IEGMP), ICNIRP and the International Agency for Research on
Cancer (IARC), and other national bodies. During this period the question of scientific
uncertainty and its role in the development of EMF exposure guidelines has also been
further addressed by NRPB and others.
GUIDELINES ONGOING DEVELOPMENTS
3 Since 1999, recommendations as to the further development of exposure
guidelines and their implementation within the frameworks of national and international
policy on EMFs and health have been promulgated by a number of bodies.
4 WHO has launched an initiative aimed at achieving a harmonised international
approach to the development of guidelines, a keystone of which is that exposure
guidelines should be based on thorough reviews of the science. ICNIRP, NRPB and
expert committees in other countries concerned with the development of exposure
guidelines have already adopted this approach.
5 The European Commission has urged the need for harmonisation of standards for
protection within the European Union (EU). A Recommendation to EU Member States
on the limitation of exposure of the general public to EMFs in the frequency range from
0 to 300 GHz was passed on 12 July 1999 by the Council of the European Union and
published in the Official Journal of the European Communities. In its preamble, the
Recommendation states that measures with regard to electromagnetic fields should
4
afford all Community citizens a high level of protection: provisions by Member States
in this area should be based on a commonly agreed framework, so as to contribute
to ensuring consistency of protection throughout the Community. The UK supported
the Recommendation.
6 In May 2000, IEGMP published a report on mobile phones and health. This report
contained a recommendation to government to adopt, as a precautionary approach,
the general public exposure guidelines of ICNIRP for mobile telephony. The
government responded positively to this recommendation and the Board of NRPB
supported the governments response. The Board noted that it had foreseen in its
statement of 1999 that, in the absence of direct scientific evidence, government may
take other factors into account in establishing generally accepted exposure guidelines
for the public. Moreover, in issuing the Boards supportive statement it was recognised
that the Boards advice would be further developed following detailed consideration of
the IEGMP recommendation, taken together with other relevant information. Support
for the IEGMP recommendation has additionally been expressed by various other
UK bodies in connection with planning issues concerning the development of tele-
communications masts. These include the (then) Department of the Environment,
Transport and the Regions, the Welsh Assembly Government, the Scottish Executive,
and the Department of the Environment for Northern Ireland. Recommendations to
adopt parts of the ICNIRP exposure guidelines had also previously been made by the
Select Committee on Science and Technology and the Scottish Parliament Transport
and the Environment Committee in their reports on mobile telecommunications.
EMFs AND HEALTH
7 This document is a review of the scientific data relating to possible adverse health
effects of exposure to EMFs and the conclusions that NRPB draws from these data with
respect to providing advice on quantitative exposure restrictions, other measures to
avoid such effects and aspects of further precaution.
8 This review covers epidemiological studies as well as experimental biology,
volunteer studies and dosimetry. These play important individual and collective roles in
identifying possible adverse effects on health and in providing information on the need
for, and appropriate levels of, protection. In evaluating the possible risks from exposure
to EMFs and the basis for providing guidance on limiting exposure, consideration has
been given to uncertainties in the scientific data and a cautious approach has been
adopted in their interpretation.
9 In developing this review, NRPB gave careful consideration to the views expressed
in response to a consultation document on its proposed advice issued in May 2003. NRPB
is aware of, and sympathetic to, concerns about EMFs and health expressed by members
of the public through both individual and media enquiries to which it responds. NRPB
welcomed the positive response from members of the public and others who partici-
pated in an open discussion meeting on power lines that it organised at the National
Exhibition Centre, Birmingham, in December 2002. It also values the information about
issues raised at the open meetings held around the country by IEGMP.
Executive Summary
5
EXPOSURE GUIDELINES
Scientific basis
10 The review of scientific information on possible health effects considers
information published since previous NRPB reports in 1993 and 1999. It also takes
account of advice from AGNIR and recent reports issued by other expert bodies,
including ICNIRP and WHO. The review has covered epidemiological studies as well as
experimental biology, volunteer studies and dosimetry. Taken together, these areas of
the science play an essential role in identifying possible adverse effects on health and in
providing information on appropriate exposure guideline levels.
11 A major difficulty in the development of EMF exposure guidance is that interpretation
of studies of potential health effects is controversial. There exists a spectrum of opinion
within the scientific community and elsewhere. Recognising this, various national and
international expert bodies have undertaken major reviews of the scientific literature,
which have, by and large, achieved a wide degree of consensus.
12 This review by NRPB staff examines the scientific evidence taking account of the
major reviews and individual studies that address specific issues. NRPB concludes that
there are scientific data indicating appropriate quantitative restrictions on exposure.
These data derive from experimental studies related to effects of EMFs on the central
nervous system and effects of heating on the body. The nature of such effects and the
mechanisms underlying them are reviewed in this document. The recommended
quantitative restrictions on exposure and also recommendations for further investigation,
where relevant, are derived from data on these effects. A cautious approach has been
adopted in the interpretation of these scientific data.
13 Evidence of effects associated with EMF exposure, but where the scientific data are
insufficient either to make a conclusive judgement on causality or to quantify appropriate
exposure restrictions, derives principally from epidemiological studies and from some
experimental studies. The main, but not sole, subject of such research has been cancer.
These studies have been reviewed extensively by expert groups, including AGNIR, and
they are summarised and further reviewed in this document. NRPB concludes that
currently the results of these studies on EMFs and health, taken individually or as
collectively reviewed by expert groups, are insufficient to derive quantitative restrictions
on exposure to EMFs.
14 However, such studies, together with peoples concerns, provide a basis for
considering the possible need for further precautionary measures in addition to the
application of quantitative restrictions on exposure to EMFs.
15 The recommendations in this document are not concerned with exposures of
patients carried out under medical supervision or with possible electrical interference
with implantable medical devices such as pacemakers. The recommendations do not
address detailed aspects of applying the guidelines to specific exposure situations.
16 In the light of ongoing research, NRPB is committed to monitoring the results of
scientific studies on EMFs and health and to revising its advice when appropriate.
Scientific uncertainty and caution
17 All scientific investigations are subject to uncertainties, as is the interpretation of the
studies relevant to judgements on likely adverse health effects. An example of the latter
arises when the results of animal studies are extrapolated to possible effects in people
6
because of inter-species and inter-strain differences that can exist. Even the results
from well-designed and well-conducted epidemiological and experimental studies have
uncertainties that can be statistically quantified, but may not always be explained. In
addition, not all studies are well designed and executed and this should also be taken
into account when assessing the available information.
18 It is necessary therefore, in examining published studies, to identify criteria for
assessing the strength of the experimental evidence. The more important criteria in this
context are the adequacy of the experimental design, statistical analysis of the data, and
the avoidance of possible confounding factors that might otherwise result in a misleading
or erroneous conclusion. It is a fundamental principle of scientific investigation that
effects described in one laboratory should be repeatable in the same and in other
laboratories, provided the correct procedures and protocols are followed. Replication
of an effect by an independent laboratory considerably strengthens the view that any
effect observed represents a true response and not an experimental artefact, a chance
observation, or the result of a systematic error present in the experiment. Major factors
in assessing the evidence include: the strength of evidence from an individual experiment;
consistency between studies in the same or different laboratories; doseresponse
relationships; and plausibility and coherence. These factors are consistent with the
guidelines formulated by Bradford Hill for the assessment of the strength of epidemio-
logical evidence of adverse health effects.
19 To ensure that exposure guidelines provide general community protection, the health
risk assessment includes recommendations based on the above factors and on scientific
uncertainties. An intrinsic part of the EMF risk assessment process is the exercise of
caution. The degree to which caution is applied in the interpretation of the scientific
evidence is a matter of judgement and should be consistent.
20 Generally, occupational exposure concerns healthy adults working under
controlled conditions. These conditions include the opportunity to apply engineering
and administrative measures and, where necessary and practical, provide personal
protection. For members of the public, similar controls do not generally exist and
individuals of varying ages have widely varying health status and responses to exposures
to EMFs. NRPB judges, on the basis of recent evidence, that the potential for such
differences in response needs to be taken into account in recommending exposure
guidelines for the public alongside those for workers.
Recommendations for quantitative restrictions
21 The recommendations for quantitative restrictions on EMF exposure set out in this
document have been developed by NRPB following a thorough review of the science,
whilst noting the advantages of harmonisation of approaches to the development of
exposure guidelines as expressed by WHO and the EC.
22 In recommending the quantitative exposure restrictions, judgements have been
made as to the degree of uncertainty in the scientific data on the adverse effects on
which such restrictions are based and how this indicates the choice of the restriction
values. The basic restrictions on exposure recommended in this document for preventing
direct adverse health effects of exposure to EMFs and other recommendations for
limiting the occurrence of indirect effects (eg shock and burn) include such considera-
tions and, overall, they reflect a cautious approach.
Executive Summary
7
23 Judgements have also been made concerning the degree to which exposure should
be additionally restricted where increased susceptibility is expected on scientific
grounds, but where, because there is a lack of specific scientific data, the degree of
susceptibility cannot currently be precisely determined. These judgements form the
basis of recommendations for more restrictive exposure values for members of the
public compared with those for workers.
24 Where the science has pointed to a need for NRPB to revise its extant advice it has
done so. However, given the uncertainties in the science, there appears to be neither
scientific justification nor, considering harmonisation of approaches to exposure
guidelines, any practical merit in recommending new restrictions that are close to those
of ICNIRP but differ from them.
25 This approach leads to the recommendation to adopt the ICNIRP exposure
guidelines.
26 Further, NRPB noted the advice provided by an ad hoc expert group on effects of
weak electric fields and by other experts attending a ICNIRP/WHO workshop on weak
electric field effects in the body. As a result, it has concluded that internal electric field
strength is the appropriate dosimetric quantity with which to express basic restrictions
for low frequency electric and magnetic fields. This judgement and other similar ones
based on uncertainties and new scientific data are intended to stimulate scientific
discussion towards the future development of EMF exposure guidelines.
ASPECTS OF FURTHER PRECAUTION
27 NRPB generally supports the concepts in the WHO initiative on a Precautionary
Framework for Public Health Protection. It considers that, with further development,
such a framework can be an effective tool for considering the possible need for
precautionary measures in relation to health in general and EMF exposure in particular.
28 The government should consider the need for further precautionary measures in
respect of exposure of people to EMFs. In doing so, it should note that the overall
evidence for adverse effects of EMFs on health at levels of exposure normally experi-
enced by the general public is weak. The least weak evidence is for the exposure of
children to power frequency magnetic fields and childhood leukaemia.
Power frequency fields
29 In the context of possible adverse health effects from EMFs, the conclusions of
published expert scientific reviews have identified only one reasonably consistent
epidemiological finding of an adverse health outcome associated with exposure to
EMFs at levels lower than exposure guidelines: that is an apparent increased risk of
childhood leukaemia with time-weighted exposure to power frequency magnetic fields
above 0.4 T. It is the view of NRPB that the epidemiological evidence is currently not
strong enough to justify a firm conclusion that such fields cause leukaemia in children.
30 In 2002, IARC classified power frequency magnetic fields as a possible carcinogen.
31 The view of NRPB is that it is important to consider the possible need for further
precautionary measures in respect of exposure of children to power frequency
magnetic fields.
8
Radiofrequency fields
32 In 2003, AGNIR examined possible health effects of exposure to radiofrequency
(RF) fields, with an emphasis on studies conducted since the IEGMP review in 2000.
AGNIR noted that there are many sources of RF fields at work, at home, and in the
environment but recent emphasis in health-related studies has been on mobile
phones and broadcast transmitters.
33 AGNIR also noted that studies reviewed by IEGMP suggested possible cognitive
effects of exposure to RF fields from mobile phones, and possible effects of pulse-
modulated RF fields on calcium efflux from the nervous system. AGNIR concluded that
the overall evidence on cognitive effects remained inconclusive, while the suggestions
of effects on calcium efflux had not been supported by more recent, better conducted
studies. The biological evidence suggested that RF fields do not cause mutation or
initiate or promote tumour formation, and the epidemiological data overall do not
suggest causal associations between exposures to RF fields, in particular from mobile
phone use, and the risk of cancer. AGNIR noted that exposure levels from living near to
mobile phone base stations are extremely low, and concluded that the overall evidence
indicates that they are unlikely to pose a risk to health. With respect to possible risks to
childrens health, AGNIR noted that little has been published specifically on childhood
exposures to RF fields and no new substantial studies had been published since the
IEGMP report.
34 Overall, AGNIR concluded that, in aggregate, the research published since the
IEGMP report does not give cause for concern and that the weight of evidence now
available does not suggest that there are adverse health effects from exposures to RF
fields below guideline levels. In reaching these conclusions, AGNIR noted that the
published research on RF field exposures and health has limitations and mobile phones
have only been in widespread use for a relatively short time. The possibility therefore
remains open that there could be health effects from exposure to RF fields below
guideline levels; hence continued research is needed.
35 From its own review and the advice from AGNIR above, NRPB concludes that the
scientific evidence for RF fields causing adverse health effects at levels to which the
general public are normally exposed is much weaker than that for power frequency
magnetic fields. It also notes there is a great deal of ongoing scientific research on RF
fields, in particular mobile telephony, and health. There is a need to constantly monitor
the results of this research and keep the guidelines under review.
9
1 Introduction
BACKGROUND
1 The National Radiological Protection Board (NRPB) has the responsibility for
providing advice on limiting exposure to electromagnetic fields (EMFs) in the frequency
range from 0 to 300 GHz. In 1993, NRPB published a comprehensive review of
epidemiological and experimental data relevant to the assessment of health effects
from exposure to EMFs and provided advice on exposure restrictions (NRPB, 1993).
This advice gave similar exposure guideline values for workers and members of the
public. NRPB subsequently reviewed its advice in 1999 following publication of exposure
guidelines by the International Commission on Non-Ionizing Radiation Protection
(ICNIRP), which included more restrictive values for the public (ICNIRP, 1998). At the
time, NRPB saw no scientific evidence for changing its previous advice.
2 In May 2000, an Independent Expert Group on Mobile Phones published a report on
mobile phones and health (IEGMP, 2000). This report contained a recommendation to
government to adopt, as a precautionary approach, the general public exposure
guidelines of ICNIRP for mobile telephony. The government responded positively to
this recommendation and the Board of NRPB supported the governments response
(NRPB, 2000). The Board noted that it had foreseen in its statement of 1999 that, in the
absence of direct scientific evidence, government may take other factors into account
in establishing generally accepted exposure guidelines for the public. Moreover, in
issuing the Boards supportive statement it was recognised that the Boards advice would
be further developed following detailed consideration of the IEGMP recommendation,
taken together with other relevant information.
3 The recommendation by IEGMP to adopt the ICNIRP exposure guidelines was put
forward as a precautionary approach to reflect some uncertainties in knowledge about
possible biological effects of exposures to radiofrequency (RF) fields. A recommendation
to adopt the ICNIRP guidelines for RF exposure had already been made by the Select
Committee on Science and Technology (SCST, 1999) and supported by the Scottish
Parliament Transport and the Environment Committee (SPTEC, 2000) in their respective
reports on mobile telecommunications. Support for the IEGMP recommendation has
also been expressed by various other UK bodies in connection with planning issues and
the development of telecommunications masts. These include the (then) Department
of the Environment, Transport and the Regions, the Welsh Assembly Government, the
Scottish Executive, and the Department of the Environment for Northern Ireland.
Furthermore, the ICNIRP guidelines provide the basis for a Council of the European
Union (CEU) Recommendation on limiting exposure of the general public to EMFs (CEU,
1999), which the UK supported. This Recommendation covers the EMF spectrum up to
300 GHz, encompassing static fields and power frequencies (50 Hz in the UK), in addition
to RF fields.
4 This document is a review of the scientific data relating to possible adverse health
effects of exposure to EMFs and the views that NRPB draws from these data with
respect to providing advice on quantitative exposure restrictions, other measures to
avoid such effects, and aspects of further precaution.
10
5 The scientific review covers epidemiological studies as well as experimental biology,
volunteer studies and dosimetry. These play important individual and collective roles
in identifying possible adverse effects on health and in providing information on the
need for, and appropriate levels of, protection. In evaluating the possible risks from
exposure to EMFs and providing guidance on limiting exposure, consideration has been
given to uncertainties in the scientific data and a cautious approach has been adopted in
their interpretation.
6 The recommendations in this document are not concerned with exposures of
patients carried out under medical supervision or with possible electrical interference
with implantable medical devices such as pacemakers. The recommendations do not
address detailed aspects of applying the guidelines to specific exposure situations.
7 In developing this review, NRPB gave careful consideration to the views expressed
in response to a consultation document on its proposed advice issued in May 2003. NRPB
is aware of, and sympathetic to, concerns about EMFs and health expressed by members
of the public through both the individual and media enquiries to which it responds. NRPB
welcomed the positive response from members of the public and others who partici-
pated in an open discussion meeting on power lines that it organised at the National
Exhibition Centre, Birmingham, in December 2002. It also values the information about
issues raised at the open meetings held around the country by IEGMP.
DEVELOPMENT OF EXPOSURE GUIDELINES
8 National and international guidelines for limiting exposure to EMFs have the
objective of preventing adverse effects on health.
9 Guidelines on limiting exposure to EMFs from ICNIRP and NRPB, as well as from
various expert bodies in other countries, have been based on thorough reviews of the
science. This approach necessitates a measure of caution both with respect to
assessing individual studies and their significance in identifying possible adverse effects
on human health and with respect to addressing the uncertainties in the science. These
bodies have all exercised caution in respect of arriving at judgements on exposure
levels for preventing health effects that are supported by the scientific evidence. An
important aspect of this approach is the need to highlight where data are sparse and/or
inconclusive and to identify where further relevant research is appropriate.
10 Epidemiological and biological data together with dosimetric information underpin
the basic framework for exposure restrictions on EMFs and the derivation of external
field strength levels used in assessing compliance with the guidelines.
11 IEGMP supported the approach to the analysis of the scientific data by NRPB and
concluded The balance of evidence to date suggests that exposures to RF radiation
below NRPB and ICNIRP guidelines do not cause adverse health effects to the general
population (IEGMP, 2000, paragraph 6.37). However, it decided to adopt a precautionary
approach in its recommendations on guidelines for exposure to RF fields in the light
of gaps in scientific knowledge concerning RF exposure and the scientific evidence
which suggests that there may be biological effects occurring at exposures below these
guidelines but not necessarily effects that could lead to disease (IEGMP, 2000,
paragraph 6.38).
1 Introduction
11
12 The IEGMP report identified a number of uncertainties related to exposures to RF
fields. IEGMP noted that some information was available that suggested RF fields below
guideline levels may have an effect on brain function. There was concern that if there
are any unrecognised health risks from mobile phone technology then children would
be more likely to be vulnerable. IEGMP also noted that within the general population
there may be people with illnesses that render them unusually susceptible to the
heating effects of RF fields.
13 There are also uncertainties in relation to the effects of extremely low frequency
(ELF) EMFs on the body. The independent Advisory Group on Non-ionising Radiation
(AGNIR, 2001a) has reviewed the possibility that ELF EMFs may be implicated in the
development of cancer. The conclusions of this and other scientific reports (eg IARC,
2002) are discussed in this current document. In addition, AGNIR has addressed
possible effects of power frequency (50/60 Hz) electric fields on diseases of the central
nervous system (AGNIR, 2001b). Further uncertainties related to possible effects on
the functioning of the central nervous system are also discussed in this document.
14 The principal focus of this document is on establishing guidelines for preventing
adverse health effects resulting from direct exposure to EMFs. Where appropriate
scientific data are available on effects due to indirect exposure, such as from electrical
contact with or discharge from an electrically charged object, these are also considered.
Putative effects resulting from the consequences of electric charge on the inhalation of
pollutant particles or their deposition on the skin are not considered in detail in this
document. AGNIR has considered mechanisms for such effects (AGNIR, 2004).
15 NRPB advice on limiting exposure to EMFs is based on the totality of the
scientific evidence and is broadly in line with that from ICNIRP, although some
uncertainties remain.
16 NRPB considers it important to address such uncertainties and has therefore carried
out a comprehensive review of the science that provides the basis for recommending
exposure guidelines. This review is set out in the current document. Consideration is
given to the role of a cautious approach to the interpretation of scientific uncertainties
and to aspects of further precaution.
17 A significant difference between the UK exposure guidelines on limiting exposure
to EMFs and those of ICNIRP and their derivatives (including the CEU Recommendation
for limiting exposure of the general public) is the distinction between workers and the
general public by ICNIRP and the application of further restrictions on exposure for the
latter. Hence, in preparing this document, NRPB has set out to address this specific
issue, ie whether the more restrictive exposure values for the general public are
supported by current scientific knowledge. In order to benefit from additional scientific
and medical expertise, NRPB has consulted various external experts.
18 Advice on limiting exposure includes basic restrictions on exposure which, as far as
possible, address uncertainties in the scientific data related to adverse health effects.
Generally, basic restrictions on exposure are expressed in terms of internal dose
quantities, which usually cannot be measured directly.
19 Computational dosimetry provides the quantitative link between internal dose
quantities for direct effects and external fields that can be measured. Reference levels
are values of external fields that are intended to ensure the basic restrictions are not
12
exceeded. The dosimetry in this document is based on realistic computational
modelling of the human body under conservative exposure conditions.
STRUCTURE OF DOCUMENT
20 In developing this review, NRPB has taken advice from individuals in the UK,
international scientific experts, and from published comprehensive reviews by expert
groups. It has also taken advice from an ad hoc expert group on weak electric field
effects in the body. It has given careful consideration to the views expressed in
response to a consultation document issued in May 2003. It has also listened to the
concerns raised at a public open meeting on power lines in December 2002.
21 The remainder of the document is set out as follows:
(a) the scientific basis for the development of exposure guidelines (Chapter 2) and
specifically the roles of the various scientific and medical disciplines involved,
(b) detailed reviews of the epidemiology, biology and dosimetry of:
(i) static electric and magnetic fields (Chapter 3),
(ii) electromagnetic fields of frequencies below 100 kHz (Chapter 4),
(iii) electromagnetic fields of frequencies above 100 kHz (Chapter 5),
(c) scientific uncertainty (Chapter 6),
(d) conclusions and recommendations (Chapter 7),
(e) references (Chapter 8).
(f) advice from the ad hoc expert group on effects of weak electric fields is given in
Appendix A, and related, more recent developments in weak field effects follow
in Appendix B; the ICNIRP exposure guidelines (ICNIRP, 1998) are summarised in
Appendix C,
(g) a glossary of terms.
ACKNOWLEDGEMENTS
22 NRPB would like to thank the many individuals and organisations that provided
constructive input and comment during the development of this review document and,
in particular, the members of the ad hoc expert group on weak electric fields.
13
2 Development of Exposure Guidelines
1 This chapter examines the role of science in the development of guidelines for
limiting exposure of people to electromagnetic fields (EMFs) to prevent adverse health
effects. Specifically, the role of different medical and scientific disciplines is discussed,
including most importantly epidemiology, biology human, animal and cellular studies
(in vitro) and computational dosimetry.
2 A major difficulty in the development of EMF exposure guidance is that the
interpretation of studies of potential health effects is controversial. There exists a
spectrum of opinion within the scientific community and elsewhere. Recognising this,
various national and international expert bodies have undertaken major reviews of the
scientific literature, which have, by and large, achieved a wide degree of consensus.
3 In principle, the results of studies most closely related to the actual exposure
of people to EMFs and the physiological and/or adverse health effects that might
result from or correlate with such exposures are of greatest importance to the
development of exposure guidelines that is, well-controlled human laboratory and
epidemiological studies.
4 Animal studies are also important, as discussed below, but with caveats as to the
conclusions that might be drawn from them with respect to effects on human health.
5 Cellular studies can provide data that increase knowledge about possible mechanisms
of biological interaction at the cellular and subcellular level in living systems.
6 Computational dosimetry provides both knowledge of the nature of the physical
interactions of EMFs with living matter (people, animals and in vitro preparations) and
knowledge linking the strengths of external fields to which people may be exposed with
those of fields induced in their bodies.
7 Experimental dosimetry plays an important complementary role with computational
dosimetry, but more with regard to the measurement of peoples exposures and
assessing compliance with exposure guidelines than with the development of exposure
guidelines per se.
8 Guidelines for limiting exposure of people to EMFs are intended to provide a
framework for a system of protection by recommending limits, generally termed basic
restrictions, to avoid the adverse health consequences of exposure.
9 Another set of levels, generally termed reference levels (or investigation levels),
is also provided in exposure guidelines. These are expressed as field and electric
current quantities in order to assist the assessment of compliance with the basic
restrictions for particular exposure situations. NRPB advice has not been prescriptive
with regard to setting field limits, in order to allow the health and safety professional
to use the most up-to-date measurement and computational techniques in assessing
compliance with the basic restrictions. This system, first developed by NRPB (1993),
has proved effective in practice and has been adopted by other expert advisory
bodies including the International Commission on Non-Ionizing Radiation Protection
(ICNIRP, 1998).
14
EPIDEMIOLOGY
10 Epidemiology can be defined as the study of the distribution of disease in
populations and of the factors that influence this distribution. In contrast to clinical
medicine where the emphasis is on treating the individual, epidemiology is concerned
with evaluating patterns of disease among groups of individuals. Consequently the
conclusions drawn from epidemiological studies are applicable generally, rather than to
specific individuals.
11 Epidemiology has proved to be of great value in studying the effects of various
agents on human health and, particularly for cancer, in quantifying risks (Doll, 1998).
However, some caveats should be borne in mind when attempting to interpret epidemio-
logical results, as follows.
Bias and confounding
12 Epidemiology is generally observational rather than experimental in nature. In
contrast to controlled studies in which subjects are randomised to receive, say, a
treatment or a placebo, epidemiologists cannot influence who does or does not receive
an exposure. Consequently, epidemiological studies may be affected by bias (ie a
systematic tendency to error as a consequence of the design or conduct of the study)
or confounding (ie spurious findings due to the effect of a variable that is correlated with
both the exposure and disease under study). For example, the quality of information on
exposures obtained directly from diseased people or their relatives may differ from
that obtained from people without the disease; in particular, the recall of past events
may differ between the two groups (recall bias). Alternatively, workers exposed to
EMFs may also be exposed to another agent in the workplace that could influence their
disease risk for example, welding fumes in the case of welders.
13 Epidemiologists generally attempt to address the above problems by choosing
an appropriate form of study, and by conducting and analysing the study well.
However, not all studies are equally good, and it is important to review their strengths
and weaknesses.
Statistical power
14 An important aspect of an epidemiological study is its statistical power, ie the
probability that it will detect a raised risk of given magnitude with a specific degree of
confidence. Statistical power would normally be calculated prior to initiating a study
for example, to evaluate the probability of detecting a doubling of risk, say, using a
significance test at the 5%level. Once a study has been conducted, its precision can be
gauged by the width of the confidence interval for the estimated effect.
15 There are several ways in which the power of a study can be increased. In a
casecontrol study, in which exposures are compared for people with the disease of
interest (cases) and people selected from the same source population who do not have
this disease (controls), efforts could be made to increase the numbers of cases and
controls. For example, the geographical area or the time period over which the study is
to be conducted could be maximised, although there would be practical constraints in
doing so. For a cohort study, in which a group of individuals is followed to determine
their subsequent disease incidence or mortality, the cohort size or the period of
follow-up may be increased, or attention may be focused on a disease with a relatively
15
high baseline rate. Another possibility would be to widen the range of exposures.
However, within a specific locality or workplace, the opportunity to increase power
may often be limited; there would be little gain from including large additional numbers
of people with little or no exposure. Both the precision and accuracy of epidemiological
findings can also be affected by uncertainties in quantifying exposures. In particular,
errors in the assessment of individual exposures which are non-differential (ie unrelated
to disease) and random tend to reduce statistical power, and to bias estimates of
trend in risk with exposure towards zero (Armstrong, 1998). However, such errors
can sometimes lead to a spurious increase in risk estimates (Sorahan and Gilthorpe,
1994). Assessment of exposure to EMFs remains a challenge in epidemiological studies,
particularly of occupational groups (Kheifets, 1999).
16 In view of the above, attempts are sometimes made to combine results from
different studies of the same topic. One approach involves a meta-analysis of published
summary measures from various studies. Whilst meta-analyses are often relatively
easy to perform, they can sometimes be limited by the degree of data available and by
differences in the way in which data from individual studies were collected and
analysed. It is often preferable to undertake a combined analysis based on individual
level data from each of the available studies (Blettner et al, 1999). Whilst each
investigation may be subject to its own particular sources of bias, this approach allows
data from the studies to be analysed in parallel and may identify any lack of
comparability between the studies. The decision on whether to combine results across
studies can then be made in the light of the evidence for inter-study heterogeneity.
Hypothesis testing or hypothesis generating
17 It is important to distinguish epidemiological studies that set out to test a specific
hypothesis, based on a priori evidence that arose elsewhere, from studies that aim to
generate hypotheses about possible risk factors for which any a priori evidence is
weak or absent. It is easier to interpret a correlation found between the presence of a
factor and the risk of disease if there had been prior reason to think that it might
occur. Otherwise, if a range of possible factors is examined without prior preference for
any particular one, then one of them might yield a positive finding simply by chance.
For example, suppose 20 distinct causes of death were analysed using a statistical test
at the 5%level. The probability of a false positive result for any one of these causes
would be 1 in 20, and so it would not be at all surprising to have at least 1 positive result
among the 20 causes of death owing to chance alone. Consequently, a hypothesis
generated in such a way would usually need to be tested in a separate study.
Epidemiological interpretation
18 Epidemiological studies of people exposed to EMFs have the advantage over animal
studies of providing direct information on the health of people subject to such
exposures. Also, the difficulties of low statistical power and multiple hypothesis testing
highlighted in paragraphs 1417 can affect the interpretation of any study requiring
statistical evaluation, and not just epidemiological studies. The observational nature of
epidemiology makes it difficult to infer causal relationships based on epidemiological
studies alone, and such inferences are possible only when the evidence is strong.
Nevertheless, in combination with information from other sources (eg on biological
16
plausibility), epidemiological studies can assist in testing for causality for example,
using the guidelines suggested by Bradford Hill (1965). Therefore, epidemiological
results can provide an input to guidelines for limiting exposure, although the
importance of information from other sources as reviewed in this document should
be recognised. Furthermore, the strengths and weaknesses of both epidemiological and
experimental findings require critical review.
19 In view of the size of the literature and because many of the relevant studies have
previously been reviewed by various scientific committees, this document largely cites
such reviews. However, individual studies are also cited in order to address specific
issues (for example, concerning the strengths or limitations of certain types of study),
or where such studies have been published after earlier reviews were conducted
(for example, recent studies of mobile phone use and cancer). In contrast to the other
reviews cited here, a report by the California Department of Health Services Panel
(Neutra et al, 2002) involved the use of numerical scales of uncertainty to express
judgements that risks might be real. This approach is unlikely, in itself, to provide a
more reliable assessment than a non-numerical approach. Of greater relevance to
understanding the conclusions reached by the Californian Panel is the lack of emphasis
that it placed on experimental findings and its view that certain epidemiological results
could not be attributed to chance, bias or confounding. Examples are cited in Chapter 4.
paragraphs 811 and 1517.
BIOLOGY
20 In this document, biological studies are taken to include laboratory experiments
with volunteers, as well as those with various animal species including rats and mice,
and with cultured cells. Exposure may last from a few minutes in the case of volunteer
studies, to several years in the case of lifetime animal studies. The main objective of
these studies is to determine the sorts of biological responses that occur as a result
of exposure to EMFs, and to evaluate any uncertainties concerning the reliability with
which these responses can be defined.
21 The studies are further evaluated for the rigour with which they are conducted,
their consistency with other experimental results, their biological plausibility and their
coherence, or compatibility with current scientific understanding (see paragraph 28). In
this context, responses that can be attributed to induced electric fields and currents at
low frequencies (up to about 100 kHz) and to heating at higher frequencies are compared
with the present understanding of electrophysiological and thermophysiological
responses. The distribution of sensitivity within the population, particularly those more
susceptible, is identified from this broader literature.
22 Extrapolating from biological effects to possible adverse human health consequences
is not straightforward. Biological effects can be defined as any detectable changes in a
biological system in response, for example, to EMFs but not all effects will necessarily
result in harm. WHO defines health as the state of complete physical, mental and social
well-being, and not merely the absence of disease or infirmity (WHO, 1946). Thus,
deciding whether biological changes have adverse health consequences depends on
whether they affect the mental, physical or general well-being of exposed people, in
17
either the short- or the long-term. Permanent damage to organs and tissues is clearly
harmful, but transient functional changes are more difficult to categorise. In this regard,
the context of the exposure might be important. For example, a transient but marked
perception of the field may be entirely inconsequential in most cases, but could be
expected to reduce the effectiveness of a worker performing a cognitively demanding
task, and be stressful to people chronically exposed.
Human studies
23 Experimental studies using volunteers, including those exposed to EMFs, are
restricted for ethical reasons to the investigation of transient physiological phenomena
which, in the controlled conditions of a laboratory, can be determined to be harmless.
The advantage of volunteer experiments is that they indicate the likely response of other
people exposed under similar conditions. Disadvantages of volunteer studies include
the innocuous nature of the effects that can be investigated, the often short duration of
investigation, and the small number of subjects usually examined. Such experiments
are subject to ethical constraints; the subjects are usually adults screened for medical
fitness and therefore may not reflect the responses of potentially more susceptible
members of society. Within this limited context, however, volunteer studies can give
valuable insight into the physiological effects of exposure to an agent.
Animal studies
24 Animal studies are frequently based on experiments using inbred strains of mice or
rats. The advantage of such studies compared with studies using cells (in vitro studies)
is that they provide information concerning the interaction of EMFs with living systems
which display the full repertoire of body functions, such as immune responses, cardio-
vascular changes and behaviour, in a way that cannot always be achieved with cellular
studies. Individual animals in inbred strains are genetically identical, thus ensuring a
relative consistency of response to the agent in question. Transgenic or gene knockout
animal models of certain diseases have further increased the value of animal studies to
reveal potential adverse health effects. Animal studies are thus usually a more powerful
experimental tool than cellular studies in this context, but typically are more expensive
and time-consuming. Extrapolation of this information to humans cannot, however,
be expected a priori to be straightforward since there are obvious differences in
physiology and metabolism between species as well as differences in life expectancy,
the proliferative capacity of different tissues, DNA repair capacity, and many other
variables. However, at a molecular level, there are many similarities between processes
in animals and humans. For example, animal studies have been very useful in helping
unravel the sequence of genetic events in the development of a number of human
cancers (Balmain and Harris, 2000).
25 Generally, animal studies can be expected to provide qualitative information regarding
potential outcomes, but the data would not be extrapolated quantitatively to give
reliable estimates of risk (UNSCEAR, 1986), for the reasons outlined above. Quantitative
risk estimates applicable to the development of guidance are more properly derived
from human studies. However, IARC (2002) noted that, with regard to cancer in the
absence of adequate data on humans, it is biologically plausible and prudent to regard
agents and mixtures for which there is sufficient evidence of carcinogenicity in
18
experimental animals as if they presented a carcinogenic risk to humans. Moreover,
IARC noted that the possibility that a given agent may cause cancer through a species-
specific mechanism that does not operate in humans should be considered.
Cellular studies
26 Studies carried out at the cellular level are usually used to investigate mechanisms
of interaction with EMFs but are not generally taken alone as evidence of effects in vivo
(in animals or people). There are a number of reasons for this: cells in culture are
removed from the normal constraints of growth in vivo, the culture medium is usually
provided with supplements to enable the cells to grow, and quite often the cell lines
used are derived from various types of cancer because of their ability to grow for long
periods in culture. AGNIR (2001a) noted that cellular studies are often used as a pre-
screen to identify agents that are suitable for entry into long-term testing on animals or
in human studies because they are relatively inexpensive and rapid.
Experimental interpretation
27 It is clearly necessary at the outset to identify criteria for assessing the strength of
the experimental evidence to be discussed. The more important criteria in this context
are the adequacy of experimental design, statistical analysis of the data, and the
avoidance of possible confounding that might otherwise result in a misleading or
erroneous conclusion (Repacholi and Cardis, 1997). It is a fundamental principle of
scientific investigation that effects described in one laboratory can be repeated in the
same and in other laboratories, providing the correct procedures and protocols are
followed. Thus replication of an effect by an independent laboratory considerably
strengthens the view that any effect represents a true response.
28 More general criteria for assessing the strength of evidence from a number of
studies for a particular experimental outcome would include:
(a) strength of evidence from an individual experiment, which would include the
adequacy of the experimental design, the avoidance of potential confounding and
the use of appropriate statistical analysis,
(b) consistency, which could here include experimental replication as well as similarity
of outcome in different experiments,
(c) doseresponse relationship, the identification of which would clearly strengthen
the view that the agent in question was interacting in a systematic way with a
biological process,
(d) plausibility and coherence, by which is meant that the suspected causation is
biologically plausible and that it does not seriously conflict with current
scientific understanding.
29 These criteria can, of course, only serve as a guide to judgement. On the one hand,
failure to comply does not of itself invalidate the outcome but would, in general,
indicate a lack of robustness and perhaps warrant further experimental investigation.
On the other hand, concurrence with one or more criteria would strengthen the overall
weight of the evidence for a particular outcome. Bradford Hill (1965) has formulated
similar guidelines for the assessment of the strength of epidemiological evidence for an
association between environmental factors and undesirable health effects.
19
DOSIMETRY
30 Computational dosimetry provides a link between external non-perturbed EMFs
and the fields induced within the body. This points to the choice of reference levels in
relation to basic restrictions.
31 Computational techniques may also be used to relate specific energy absorption
rate (SAR) to temperature rises within the body, thereby helping to indicate basic
restrictions on SAR which will avoid adverse heating effects.
32 Maxwells equations describe the mutual interaction of electric and magnetic fields,
and their interaction with materials in time and space. The approach to deriving
reference levels is to solve these equations numerically in fine resolution, anatomically
realistic models of the body.
Computational modelling of the human body
33 Fine resolution, anatomically realistic models of the body are usually derived from
medical imaging data and are referred to as voxel (volume pixel) phantoms. The
phantom structure is a three-dimensional array of voxels, each of which has an
identifying tag denoting the discrete tissue type or the surrounding air. The main groups
working on human dosimetry for EMF exposure guideline development are at NRPB,
the University of Utah (USA), the University of Victoria (Canada) and Brooks Air Force
Base (USA). A description of their human phantoms is given below.
34 The NRPB male phantom is called NORMAN. A complete description of the
acquisition of the medical imaging data and its segmentation into tissue types can be
found in Dimbylow (1996, 1997a). The raw MRI data were acquired from a series of
continuous partial-body scans of a single subject. The blocks of data were conjoined
by rescaling, translation and rotation to form an entire body. The MRI slices were
256 256 pixel images in the axial plane. The data volume was rescaled and
interpolated to produce cubical voxels with sides of around 2 mm. The 8-bit grey scale
images were segmented unambiguously into discrete tissue types. The phantom was
normalised to be 1.76 m tall and to have a mass of 73 kg, the values for reference man
in ICRP Publication 89 (ICRP, 2002). Hence, the name was derived from NORmalised
MAN. The height fixes the vertical voxel dimension, 2.021 mm, and the horizontal
dimensions, 2.077 mm, are then fixed by the mass. There are 8.3 million voxels in the
body. There were originally 38 different tissues types: skin, fat, muscle, tendon, bone,
trabecular bone, blood, brain, spinal cord, cerebrospinal fluid, eye, sclera, humour, lens,
oesophagus, stomach wall, stomach contents, duodenum, small intestine, lower large
intestine, upper large intestine, pancreas, gall bladder, bile, liver, spleen, kidney, bladder,
urine, prostate, testis, male breast, thymus, thyroid, adrenals, heart, lung, air and
background domain. An evaluated review of the dielectric properties of all the tissue
types in NORMAN was performed by Gabriel (1995) and Gabriel et al (1996ac). A
4-Cole-Cole dispersion model was fitted to the data for each tissue type to parameterise
the conductivity and permittivity as a function of frequency.
35 A phantom developed at the University of Utah (Furse and Gandhi, 1998) was
based on MRI scans of a male volunteer of height 1.76 m and mass 64 kg. The MRI
scans were taken with a resolution of 3 mm along the height of the body and 1.875 mm
for the orthogonal axes in the cross-sectional planes. The mass was thought to be
somewhat low for an average man and so the cross-sectional dimensions were
increased to 1.974 mm to produce a new mass of 71 kg. In some of their work it was not
20
possible to run the 1.974 1.974 3.0 mm resolution model of the whole body and so
3 3 2 voxels were combined (taking the dominant tissue in each group) to obtain
a coarser 5.922 5.922 6.0 mm model. The MRI sections were converted to images
involving 31 tissue types: fat, muscle, bone, compact bone, cartilage, skin, brain, spinal
cord, nerve, cerebrospinal fluid, intestine, spleen, pancreas, blood, heart, parotid gland,
eye humour, eye sclera, eye lens, liver, kidney, lung, bladder, stomach, ligament, testes,
spermatic cord, prostate gland, erectile tissue, pituitary and pineal gland.
36 A phantom used at the University of Victoria (Dawson et al, 1997) was developed
from a head and torso model from the Yale Medical School (Zubal et al, 1994). The
body model was completed by attaching legs and arms to the Yale model based on
representations obtained by applying segmentation algorithms to CT and MRI data from
the Visible Human Project at the US National Library of Medicine. The limb dimensions
were scaled to match the torso, and additional manual editing was done in the planes of
attachment. The height of the final model was 1.77 m with an estimated mass of 76 kg.
The original model resolution is 3.6 mm. A 3 3 3 median filtering algorithm was
applied to this model to develop a lower resolution model composed of 7.2 mm cubic
voxels. This phantom will be referred to as the UVic phantom in this document.
37 The Brooks Digital Anatomical Man (Mason et al, 1999) was based on photographic
data from the Visible Human Project created by the National Library of Medicine and
the University of Colorado Health Sciences Center. A segmented dataset based on the
photographic images was created by a collaboration between the National University of
Singapore and Johns Hopkins University. Each of the 1878 axial slices was coded by hand
into a palette of colours that represented 39 tissue types. The initial anatomical dataset
was at a resolution of 1 mm but this was rescaled to 3 mm to perform SAR calculations.
The development of EMF exposure guidelines builds upon comprehensive
reviews of the scientific evidence relevant to possible adverse health effects
in people.
Epidemiological studies provide evidence most closely related to the exposure of
people to EMFs and the adverse health effects that might result from or correlate
with such exposures. It is difficult to infer causal relationships based on
epidemiological studies alone, but such inferences are possible when the
evidence is strong. In combination with information from other sources (eg on
biological plausibility), epidemiological studies can assist in testing for causality.
Epidemiological results therefore provide an input to guidelines for limiting
exposure and, as with experimental studies, the strengths and weaknesses of
these findings require critical review.
Laboratory volunteer studies provide useful information when well controlled,
but are restricted in terms of the endpoints that can be examined and the
exposures that can be used.
Experimental studies on animals are important, with reservations as to the
conclusions that might be drawn with respect to possible effects on human health.
Cellular studies can provide an understanding of possible mechanisms of
biological interaction.
Computational dosimetry provides information on the physical interactions of
EMFs with people and quantitatively links the strength of external fields with
those fields induced in their bodies.
21
3 Static Electric and Magnetic Fields
1 In this chapter scientific data relevant to the development of exposure guidelines
for static electric and magnetic fields are addressed. Specifically, epidemiological
studies, biological studies and physical interactions are reviewed.
EPIDEMIOLOGY
2 Epidemiological studies have focused on workers exposed to static magnetic fields
of up to a few millitesla (mT), and the children of such workers. IARC (2002) has
reviewed studies of cancer among such workers. In general, these studies have not
pointed towards elevated cancer risks, although the number of studies was limited,
the numbers of cancer cases were often small, and there was a paucity of information
on individual exposure levels. Perhaps the most detailed study was conducted by
Ronneberg et al (1999), who used job-exposure matrices to estimate exposures in
cohorts of workers at an aluminium smelter. No association was found between the risk
of brain cancer or cancers of lymphatic and haematopoietic tissue and either static or
power frequency (50/60 Hz) magnetic fields. However, the numbers of cases at the
higher exposure levels were small (Ronneberg et al, 1999).
3 There is little information on other health outcomes among workers exposed to
static fields. A small study showed no association between the occurrence of sick leave
caused by musculoskeletal disorders and exposure to static or power frequency
magnetic fields at an aluminium plant, although the data were limited (Moen et al, 1996).
However, there is anecdotal evidence unsupported by epidemiology that in conditions
of low humidity the associated static electric fields arising from work with visual
display units (VDUs) may aggravate existing skin problems and the strain of the actual
work may give rise to skin problems among those with a predisposition to them
(AGNIR, 1994).
4 Previously, NRPB (1993) noted that only a few studies of groups with occupational
exposure to static magnetic fields had been performed. Measurements of field levels
were generally not available; an exception is a study of workers at a chloralkali plant
exposed to fields of up to 30 mT for whom no increased cancer risk was found, although
the number of workers was small (Barregard et al, 1985). Some studies have examined
reproductive outcome for workers involved in the aluminium industry or in magnetic
resonance imaging (MRI). Mur et al (1998) and Kanal et al (1993) did not find decreased
fertility for either male or female workers, respectively. Irgens et al (1999) reported a
decreased proportion of males among the offspring of aluminium workers, particularly
women, although the potential impact of occupational exposures other than magnetic
fields was unclear. In contrast, Kanal et al (1993) found no clear association between
work in MRI by females and the gender of offspring, premature delivery, low birth
weight or spontaneous abortion, although the low response rate in this study severely
limited inferences.
22
Epidemiological uncertainties
5 The studies cited above have predominantly been of exposures of up to a few tens
of mT. No studies of high quality have been carried out of workers occupationally
exposed to fields greater than 1 T.
Summary
6 Studies of workers exposed to static magnetic fields up to several tens of millitesla
do not overall demonstrate raised health risks. However, the number of studies, their
size and the information on exposure levels are generally limited. There is some
suggestion that static electric fields associated with work with VDUs may aggravate
existing skin conditions.
BIOLOGY
7 Static electric and magnetic fields exist as natural phenomena. Static electric fields
develop through the accumulation of electric charges on the surface of objects for
example, on clouds where the electric potential differences may exceed the dielectric
breakdown threshold of air resulting in lightning discharges. Typical values range
between 500 and 1200 kV m
1
but may be lower in certain circumstances (Weast,
1980). A static magnetic field of around 2070 T exists over the surface of the Earth
and is implicated in the orientation and migratory behaviour of certain animal species.
8 There has been a fragmentary and incoherent approach to investigating the biological
consequences of exposure to static electric or magnetic fields, and in many areas the
data are insufficient to draw conclusions regarding the possibility of health effects,
especially following chronic exposure. Although the effects of static magnetic fields
have been investigated to a much greater extent than those of static electric fields, this
database is not exhaustive. The earlier literature has been summarised by WHO (1987),
Kowalczuk et al (1991) and ICNIRP (1994, 1997), while more recent studies have been
reviewed by Repacholi and Greenebaum (1999), IARC (2002) and ICNIRP (2004).
9 It is clear that for exposure to static electric fields the major consequences result
from perception of the field and from spark discharges induced by touching objects at a
different electric potential. The major consequences of exposure to static magnetic
fields result from the effects of the electric fields induced in living tissues by movement
within the field. These acute effects depend on the magnitude of the respective field,
and these will be negligible at levels usually experienced by members of the public. This
chapter presents a summary of the studies that have investigated biological effects of
static fields in humans, and using animals and cells.
Human studies
Electric fields
10 Static electric fields interact directly with the body by inducing a surface electric
charge. Indirect effects can also occur when a person is in contact with a charged
conducting object, eg a car exposed to a static field. At sufficiently high voltage the air
will ionise and become capable of conducting an electric current between the charged
body and a person in good electrical contact with the ground. A charged insulated
person touching a grounded object would receive a microshock (spark discharge).
23
These effects may be painful. However, the threshold static electric field values for
such perception will vary depending on the degree of insulation and other factors.
Overall, the results of the few studies that have investigated the effects of static electric
fields in humans do not suggest exposure is associated with significant health effects
(IARC, 2002).
11 Clairmont et al (1989) exposed volunteers to static electric fields up to 40 kV m
1
and reported a threshold for perception of around 20 kV m
1
. This was possibly
associated with corona discharge on the tips of hair shafts. Annoying sensations were
induced above about 25 kV m
1
.
Magnetic fields
12 Ueno and Iwasaka (1999) and ICNIRP (2004) have reviewed the interactions of
static magnetic fields with biological materials. These interactions include magneto-
mechanical effects, effects on electronic spin states in certain types of charge transfer
processes, and electrodynamic interactions with ionic conduction currents. Ionic
currents interact with static magnetic fields as a result of the Lorentz forces exerted on
moving charge carriers. This electrodynamic interaction gives rise to an induced
electric field. An example of such a process is the induction of electric potentials as a
result of blood flow in the presence of a static magnetic field.
13 Prior to the development of MRI techniques, few studies of the effects of static
magnetic fields on volunteers had been documented (see WHO, 1987), although
various anecdotal reports from laboratories using large particle accelerators existed.
However, with the advent of superconducting magnet technology, volunteers could be
routinely exposed to static fields of around 1.5 T or more. Most of the acute effects that
have been reported are consistent with known mechanisms of interaction.
14 Schenck et al (1992) reported dose-dependent sensations of vertigo, nausea and a
metallic taste in the mouth in volunteers exposed to static magnetic fields of 1.5 or 4 T
in an MRI system. These occurred only during movement of the head. In addition,
magnetic phosphenes could sometimes be seen during eye movement in a field of at
least 2 T. These effects are probably attributable to the current induced by movement
within a static field, since vertigo and phosphenes can be induced by weak electric
currents directly applied to the head (eg Adrian, 1977). However, no damage to the
acoustic or vestibular systems were reported by Winther et al (1999) following exposure
of healthy volunteers to 27 mT for 9 hours.
15 Lorentz forces resulting from the movement of charged particles in a magnetic field
will be exerted on ions flowing through nerve membranes in a static field. These could
affect nerve function, although they are unlikely to be of biological significance until
very large fields (around 20 T) are experienced (Tenforde, 1992). A lack of effect on
cognitive performance of volunteers, evaluated using a battery of tasks following
exposure to a static magnetic field of 8 T for 1 hour, was reported by Kangarlu et al
(1999). An earlier study of a large number of volunteers also reported a lack of effect of
MRI exposure involving static magnetic fields of 0.15 T on cognition (Sweetland et al,
1987), although anxiety was increased in the exposed group.
16 Kinouchi et al (1996) noted that the Lorentz force exerted on blood flow generates
an electric potential across blood vessels. In practice, so-called flow potentials are
readily demonstrated in volunteers exposed to static fields greater than around 0.1 T.
Generally, the largest flow potentials occur across the aorta after ventricular contraction
24
and appear superimposed on the T-wave of the electrocardiogram (ECG) (Tenforde,
1992). The latter indicates the repolarisation of ventricular heart muscle when electrical
excitability gradually recovers following contraction (Antoni, 1998). Fibrillation of the
heart potentially fatal asynchronous and irregular cardiac muscle contraction can be
induced only during this vulnerable period. However, the fibrillation threshold is about
1020 times higher than that for cardiac muscle stimulation per se; the latter occurs
during diastole, when cardiac muscle is relaxed. Reilly (1998) estimated the first and
fiftieth percentile ranks for cardiac stimulation in humans due to induced electric fields
to be 5 and 10 V m
1
, respectively.
17 Kinouchi et al (1996) calculated that a static field of around 5 T would induce
maximum current densities around the sino-atrial node of the heart of about 100 mA m
2
(approximately 500 mV m
1
using a general tissue conductivity of 0.2 S m
1
), which is
below the cardiac excitation threshold. In addition, a 5 and 10%reduction in blood flow
in the aorta was predicted to occur in static fields of 10 and 15 T, respectively, due
to magneto-hydrodynamic interactions. However, Kangarlu et al (1999) found that
volunteers exposed to an 8 T field for 1 hour showed no change in heart rate or diastolic
or systolic blood pressure either during or after exposure. The ECG recorded during
exposure was regarded as uninterpretable due to the superposition of the potential
generated by aortic blood flow and smaller potentials generated by blood flow in other
vessels. In addition, vertigo and other sensations were recorded during movement in
this field.
18 More detailed studies by the same group have recently been published (Chakeres
et al, 2003a,b); both were approved by the US FDA Investigational Review Board.
The authors reported that exposure of 25 healthy volunteers, aged between 18 and
65 years, to 8 T static fields (duration unspecified) had no effect on cognitive function
assessed during exposure using seven standard neuropsychological tests (Chakeres
et al, 2003a). The second paper reported a lack of clinically significant effects of
exposure to fields of up to 8 T on heart rate, respiratory rate, systolic and diastolic blood
pressure, finger pulse oxygenation levels, and core body temperature (Chakeres et al,
2003b). There was a statistically significant trend for systolic pressure to increase with
magnetic flux density, but at 8 T this was only 3.6 mm Hg, approximately one-half of
the difference seen in moving from a sitting to a supine body position. In order to
avoid the transient, movement-induced sensations described above (Schenck et al, 1992),
the volunteers were moved very slowly (one or two feet over a few seconds, followed
by a 1530 seconds pause, taking overall about 34 minutes) to move into the magnet
bore. Nevertheless, nine subjects reported sensations of dizziness, and two reported a
metallic taste, assumed to be due to electrolysis of metallic chemicals in the subjects
teeth fillings.
19 One study has examined the effects of exposure to static magnetic fields on
melatonin rhythms in male volunteers. Haugsdal et al (2001) reported that a single,
nocturnal exposure to a static field of 27 mT had no effect on the excretion of
6-hydroxymelatonin sulphate, the major urinary metabolite of melatonin.
Summary
20 For static electric fields, a threshold for perception was reported at around 20 kV m
1
,
and annoying sensations were induced above about 25 kV m
1
. Painful spark discharges
can be expected when a person who is well insulated from ground touches a grounded
25
object, or when a grounded person touches a conductive object that is well insulated
from ground; however, the threshold static electric field values will vary depending on
the degree of insulation and other factors.
21 Vertigo, nausea, a metallic taste and phosphenes can be induced during movement
in static magnetic fields larger than about 2 T. In addition, flow potentials induced in a
magnetic field of this value have been calculated to generate electric fields near the
sino-atrial node of the heart of about 200 mV m
1
during the relative refractory period of
the cardiac cycle, when cardiac excitability is relatively low.
Animal and cellular studies
Electric fields
22 Few recent studies have investigated the biological effects of exposure to static
electric fields. Rats showed aversive behaviour in an electric field of 55 kV m
1
but not
to fields of less than 42.5 kV m
1
(Creim et al, 1993), although exposure to 75 kV m
1
did
not induce taste aversion learning (Creim et al, 1995). Results of earlier studies suggest
rodent behaviours are not significantly modified by exposure to up to 12 kV m
1
(Mse
and Fischer, 1970; Bailey and Charry, 1986). No adverse effects on haematology or on
reproduction and prenatal and postnatal survival were reported following exposure of
mice to fields up to 340 kV m
1
(Fam, 1981).
23 IARC (2002) noted that there was insufficient evidence to determine the carcino-
genicity of static electric fields.
Magnetic fields
24 The biological consequences of exposure to static magnetic fields have been
investigated from a variety of endpoints including effects on cancer, reproduction and
development, and on the nervous system. There are only isolated reports of field
dependent effects using unique exposure conditions, which makes it impossible to
judge the likelihood and generality of any potential health effect.
Cancer
25 There has been some concern that exposure to static magnetic fields may increase
the risk of cancer. However, most studies have been performed in vitro and have
examined effects on cellular processes which, if they malfunction, could contribute to
the development of cancer. While of scientific interest, such changes cannot be used
alone as evidence of effects in vivo. Very few cancer studies per se have been carried
out with the aim of investigating a direct transformation of normal cells into cancer cells.
26 There is no convincing evidence that static magnetic fields are genotoxic (ICNIRP,
2004). No effects on DNA damage were reported in four strains of Salmonella or E coli
exposed at up to 5 T (Ikehata et al, 1999) or on E coli strains disabled for DNA repair
exposed at 3 T (Mahdi et al, 1994). Although a co-mutagenic role was suggested by
Ikehata et al (1999) using E coli exposed to various chemical mutagens, this result was
not supported by Schreiber et al (2001) using wild-type Salmonella bacteria. Exposure
to fields of up to about 1 T did not affect dominant lethal frequency in male germ cells
in vivo (Mahlum et al, 1979), nor the frequency of chromosomal aberrations and sister
chromatid exchanges in cells exposed in vivo or in vitro (Wolff et al, 1980; Cooke
and Morris, 1981; Schwartz and Crooks, 1982; Geard et al, 1984). However, Suzuki
et al (2001) reported a dose-dependent increase in the frequency of micronuclei in
26
mouse bone marrow cells exposed at 3 or 4.7 T, whereas Okonogi et al (1996) reported
exposure of Chinese hamster CHL/IU cells at 4.7 T for 6 hours significantly decreased
the frequency of micronuclei induced by mitomycin c.
27 A lack of evidence for mutagenicity suggests that exposure is not capable of
initiating carcinogenesis. Tumour progression and, by implication, tumour promotion
seem to be unaffected by exposure to static fields of at least 1 T (Bellossi and Toujas,
1982; Bellossi, 1984, 1986). Mevissen et al (1993) reported that exposure to a magnetic
field of 15 mT for 13 weeks did not significantly affect the incidence of chemically
induced mammary tumours, nor did it affect the number of tumours per animal compared
with controls; weight per tumour was, however, significantly increased.
28 Effects of static magnetic fields on cell growth and proliferation have been carried
out using a mixture of in vitro models. No consistent field dependent effects have been
observed using fields of up to 1.5 T (Hiraoka et al, 1992; Linder-Aronson and Lindskog,
1995; Wiskirchen et al, 1999, 2000; Buemi et al, 2001), although acute exposure at
200 mT decreased incorporation of [
3
H]thymidine into the DNA of MCF-7 human breast
cancer cells (Pacini et al, 1999b) and exposure to 7 or 8 T for several days was reported
to induce large inhibitions in growth in various human cancer cells (Raylman et al, 1996;
Oguie-Ikeda et al, 2001). Sabo et al (2002) reported that the metabolic activity of HL-60
cells was reduced by exposure to a 1 T field. In other studies, exposure to 500 mT
modified in vitro expression of activation markers and interleukin release from human
peripheral blood mononuclear cells (Salerno et al, 1999) and immune function was
reduced in mouse macrophages and lymphocytes exposed to fields of 25150 mT for
24 hours (Flipo et al, 1998).
29 Other studies have investigated potential effects on apoptosis using a variety of cell
lines, exposure conditions and measures of apoptosis. No field dependent effects were
reported by Reipert et al (1997), Narita et al (1997) or Fanelli et al (1999), although the
last suggested that magnetic fields may have an inhibitory effect on chemically induced
apoptosis in cell lines in which calcium influx has an anti-apoptotic effect. In contrast,
Blumenthal et al (1997) and Flipo et al (1998) reported that exposure to static magnetic
fields can increase apoptosis.
30 There is little experimental information describing possible effects of chronic
exposure. So far, no long-term adverse effects have become apparent. Exposure to
fields of up to 2 T had no effect on circulating stress hormone levels (Battocletti et al,
1981), haematological profile (Kelman et al, 1983; Osbakken et al, 1986), or on the few
immunological responses investigated (Bellossi, 1983; Kelman et al, 1983; Tenforde and
Shrifrine, 1984). Studies by Jankovic et al (1991, 1993a,b, 1994) with rats suggest that the
field from an implanted magnet may increase immune competence or reverse reductions
in immune function induced by lesions of the locus ceruleus or pinealectomy.
31 Overall, IARC (2002) concluded that there was insufficient evidence to determine
the carcinogenicity of static magnetic fields.
Reproduction and development
32 The possibility that static magnetic fields may affect reproduction and development
has been examined by several researchers. No consistent field dependent effects
have been seen using mammalian species (Kowalczuk et al, 1991; ICNIRP, 2004). Narra
et al (1996) reported slight changes in spermatogenesis and embryogenesis in mice
27
exposed at 1.5 T for 30 minutes, whereas Tablado et al (1996, 1998, 2000) reported that
maturation of sperm movement in mice as well as postnatal testicular and epididymus
development was unaffected by either single, short-term exposure or continuous, long-
term exposure at 0.7 T.
33 Several studies have indicated that implantation and prenatal and postnatal
development of the embryo and fetus are not affected by continuous or discrete
exposure during gestation to fields from 1 to 9.4 T (Sikov et al, 1979; Konermann and
Monig, 1986; Murakami et al, 1992; High et al, 2000). However, Mevissen et al (1994)
reported continuous exposure to a 30 mT field slightly decreased the numbers of viable
fetuses per litter. As a probable consequence of these smaller litter sizes, prenatal
development as measured by skeletal ossification was accelerated, and postnatal
growth up to day 50 was increased. There was no effect on postnatal behaviour.
Inconsistent increases in the development of the pineal gland in chick embryos were
observed by Jove et al (1999) using fields of 18 and 36 mT.
34 Other studies have used MRI fields, which include exposure to intense static fields
usually in the range of 1 to 4 T. Field effects have been reported in mice on fetal growth
and testicular development (Carnes and Magin, 1996) and on craniofacial size and
crown-rump length (Tyndall, 1993). Acute exposure was reported not to affect early
mouse embryo development in vitro (Chew et al, 2001). MRI fields do not appear
to increase the teratogenicity of x-ray induced eye malformations (Tyndall, 1990),
although exposure to MRI fields in combination with acute exposure to ultrasound has
been reported to reduce fetal size and weight (Magin et al 2000) but this may have been
due to stresses associated with the experimental procedure.
35 A few studies have also investigated effects of static magnetic fields on embryo
development using non-mammalian species. Irreversible changes were reported in
developing chick cerebellum by acute or continuous exposure to a 20 mT field (Espinar
et al, 1997). Similarly, exposure to fields of 30 mT (but not 15 mT) delayed the onset of
mitosis and increased exogastrulation (gut evagination) in early sea urchin embryos
(Levin and Ernst, 1997). Inhibition of growth and vitality of amoeba exposed to 71 or
106 mT have also been reported (Berk et al, 1997). However, exposure to 8 T did not
affect early embryonic development of Xenopus toads (Ueno et al, 1994a). No effects
were reported on early chick development following acute exposure to MRI fields (Yip
et al, 1994a,b).
Neurobehavioural effects
36 A number of studies have investigated the effects of exposure to static magnetic
fields on the functions of the nervous system and on behaviour. Such investigations can
provide a sensitive measure of the physiological effects induced by exposure to the field.
37 The evidence from carefully conducted experiments with rodents is that circadian
rhythms (Tenforde et al, 1987) and spontaneous and some learned behaviours (Davis
et al, 1984) are unaffected by chronic exposure at about 1.5 T. This result is consistent
with a lack of effect of exposure up to about 2 T on isolated nerve preparations
(Schwartz, 1978, 1979; Gaffey and Tenforde, 1983) and of exposure to 1.5 T on the electro-
retinogram response of cats and squirrel monkeys (Tenforde et al, 1985). However,
Levine and Bluni (1994) reported that exposure of Harvest mice to a 300 mT field for
30 minutes impaired subsequent performance in a leftright discrimination task.
28
38 Using sensitive patch-clamp methods, no changes in resting membrane potential
were observed in neuroblastoma cells following brief exposures up to 7.5 mT (Sonnier
et al, 2000), although Rosen (1996) reported subtle changes in calcium ion channel
activation in GH3 cells exposed at 120 mT and Wieraszko (2000) reported changes in
the population spike recorded from rat hippocampal slices exposed to fields of 23 mT
for 20 minutes. Morphological and molecular changes were reported by Pacini et al
(1999a) in cultured human neural cells (FNC-B4) exposed for 15 minutes to a 200 mT
field. DNA stability was unaffected.
39 The experimental evidence for an effect of static magnetic fields above 2 T on the
nervous system of animals is equivocal. Using behaviour in a T-maze to evaluate
aversion, Weiss et al (1992) reported that a field of 4 T (but not 1.5 T) was aversive
to rats. Two studies (Thach, 1968; de Lorge, 1979) reported that the performance of
learned tasks by squirrel monkeys was reduced during exposure to static fields
in excess of about 5 T. Changes in the electrical activity recorded from the brains of
squirrel monkeys during exposure to between 2 and 9 T were reported in one study
(Biescher and Knepton, 1966), although it has been suggested (WHO, 1987) that these
responses could be artefacts, possibly due to muscle activity. A temporary increase in
sinus arrhythmia and a decrease in heart rate were observed (Beischer and Knepton,
1964) in squirrel monkeys during acute exposure to magnetic fields between 4 and 7 T,
although a threshold could not be identified. Exposure to 5 T fields for 48 hours has also
been reported to significantly inhibit food and water intake in mice (Tsuji et al, 1996).
Nolte et al (1998) reported that exposure to 9.4 T for 30 minutes could be used as a
stimulus to induce conditioned taste aversion in rats.
40 Small increases in the permeability of the bloodbrain barrier were reported by
Prato et al (1994) following acute exposure of rats to fields of 1.5 or 1.9 T. Similar
changes were observed using conventional MRI fields, although manipulation of the
radiofrequency field and time-varying magnetic field gradient was able to reverse the
observed effect.
41 A number of studies suggest manipulation of the ambient static magnetic field may
disturb the normal melatonin rhythm in rodents (see reviews by Kowalczuk et al, 1991,
and Reiter, 1993). In these studies, night-time inversion or changes in the orientation
of the field at magnetic flux densities approximately equivalent to that of the Earths
magnetic field produced changes in melatonin content in the pineal gland or in enzymes
involved in the metabolism of melatonin weaker or stronger fields, or day-time
exposure, had lesser or no effects. Kroeker et al (1996) reported that neither acute
exposure at 7 T nor medium-term exposure at 80 mT had any effect on nocturnal pineal
or serum melatonin levels in rats. Such phenomena may be linked to the neurobiology
of magnetic field detection utilised in homing and migratory behaviour (Schneider
et al, 1994; see also ICNIRP, 2004, for a review of avian navigation and magneto-
reception in animals). Although melatonin has also been implicated in the physiology of
seasonal reproduction (Reiter, 1980) and in cancer (Stevens, 1987, 1994; see Chapter 4,
paragraphs 4978), these possibilities seem less likely to be of relevance here.
Cardiovascular effects
42 Experiments with mammals, including two primate species exposed to fields of less
than about 2 T, confirm a lack of effect on cardiac function (Gaffey and Tenforde, 1979,
29
1981; Gaffey et al, 1980). In particular, there were no significant changes in heart rate or
arterial blood pressure in monkeys exposed to 1.5 T, although this exposure was
sufficient to generate measurable electric potentials arising from blood flow (Tenforde
et al, 1983).
43 The effects of static fields on localised blood flow have been investigated in several
studies. Small but significant decreases in microcirculation in the skin and concomitant
changes in local and rectal temperature were reported in anaesthetised rats during
acute whole-body exposure to fields of around 8 T (Ichioka et al, 1998, 2000). Similarly,
changes in blood flow and vasomotor tone have been reported in the ears of rabbits
with acute exposure at 110 mT (Ohkubo and Xu, 1997; Okano et al, 1999; Okano and
Ohkubo, 2001), acute exposure at 250 mT (Gmitrov et al, 2002), or subchronic exposure
at 180 mT (Xu et al, 1998). Static fields of about 300 mT applied to the region of the
sinocarotid artery in rabbits have also been reported to affect the control of blood
pressure and increase baroreflex sensitivity (Gmitrov and Ohkubo, 2002a,b). The
mechanism for these effects has not been identified.
In vitro effects of very intense fields
44 Several laboratories have investigated the effects of very intense fields in vitro.
In particular, Ueno and colleagues have reported various changes in the properties of
biological and other materials exposed to 8 T or more, often producing field gradients
of about 50 T m
1
. These include effects on the flow and distribution of water in small
containers (Ueno and Iwasaka, 1994a,b), changes in the behaviour of dissolved oxygen
molecules (Ueno et al, 1994b), effects on fibrin (Iwasaka et al, 1994, 1998), changes in
the orientation of human erythrocytes (Suda and Ueno, 1999) and osteoblasts (Kotani
et al, 2000), increased aggregation of rabbit blood platelets (Iwasaka et al, 2000), and
decreases in the activity of catalase (Iwasaka et al, 2001). In studies from other
laboratories, changes have been reported in the orientation of erythrocytes fixed with
glutaraldehyde in field of 8 T (Higashi et al, 1996) and in the sedimentation rate of
erythrocytes in a field of 6.3 T (Iino, 1997). Possible mechanisms for these and similar
effects have been considered by ICNIRP (2004). Whether any of these phenomena
may occur in vivo has yet to be determined (although see Taoka et al, 1997).
Biological uncertainties
45 It has been demonstrated that magnetic fields at millitesla levels and above can
affect chemical reactions involving radical intermediates in vitro (McLauchlan, 1981;
Grissom, 1995; Walleczek, 1995; Brocklehurst and McLauchlan, 1996; Brocklehurst,
1997). This raises the possibility that such effects might occur on metabolic reactions
involving similar mechanisms, but this has not been demonstrated in vivo and the
implications for human health are not clear (but see Watanbe et al, 1997, and Chigell and
Sik, 1998; see also Adair, 1999, for a discussion of these mechanisms at environmental
field levels). A similar argument applies to the various phenomena that have been
reported in vitro with exposures at 8 T and above.
46 Much of the database consists of largely phenomenological observations, although
the possibility of finding an effect seems to increase with field magnitude, particularly
with exposures above 58 T. There is, however, insufficient evidence at present from
animal and cellular studies to enable the thresholds for long-term effects from chronic
exposure to static magnetic fields to be determined.
30
Summary
47 Cutaneous perception remains the most robust biological consequence of exposure
to static electric fields. A threshold for perception was reported around 20 kV m
1
and
annoying sensations were induced above about 25 kV m
1
. Painful spark discharges can
be expected when a person who is well insulated from the ground touches a grounded
object, or when a grounded person touches a conductive object that is well insulated
from ground. However, the threshold static electric field values will vary depending on
the degree of insulation and other factors. There is some suggestion that electrostatic
fields associated with work with VDUs may aggravate existing skin conditions.
48 Very low frequency electric fields are induced in the body whenever movement of
electrically conductive biological materials, such as blood, occurs in a static magnetic
field. Vertigo, nausea, a metallic taste and phosphenes can be induced during movement
of the head in static magnetic fields larger than about 2 T. In addition, flow potentials
induced by the flow of blood in a magnetic field of this value have been calculated
to generate electric fields of about 200 mV m
1
near the sino-atrial node of the heart
during the relative refractory period of the cardiac cycle, when cardiac excitability is
relatively low.
49 The effects of static magnetic fields have been investigated using a wide variety of
animal models and exposure conditions. Apart from possible field dependent changes
on localised blood flow in the skin, and on neuroendocrine effects associated with
homing behaviour, no consistent effects have been reported using fields below 2 T,
although the possibility of biological effects increases with exposure to fields of 58 T
and above. There is little information regarding possible effects of chronic exposure.
50 There is little evidence suggesting that static magnetic fields of up to about 1 T are
genotoxic, and while many in vitro data suggest that static magnetic fields are not
carcinogenic, few in vivo studies have been carried out. Very few laboratory studies
have investigated the effects of exposure to static electric fields. Overall, the available
data remain insufficient to draw any firm conclusions regarding the carcinogenicity of
static magnetic or electric fields.
The most plausible and coherent set of data from which guidance can be
developed concerns perceptual and annoying responses in static electric fields
and effects resulting from induced electric fields during movement in static
magnetic fields. Other studies reviewed lack plausibility, coherence and
consistency precluding a positive role in this process.
For static electric fields, any annoying and other stressful effects should be
avoided if exposure is below the threshold for cutaneous perception of around
20 kV m
1
. Painful spark discharges can be expected when a person touches an
object at a differing potential. However, the threshold field value under these
circumstances will vary depending on the degree of insulation and other factors
and will require specific assessment.
With regard to static magnetic fields, acute effects on the heart or nervous
system associated with electric fields and flow potentials induced during
movement in the field should not occur if exposures are less than 2 T. Particular
caution should be applied with exposure to fields in excess of about 58 T.
There is insufficient evidence from animal and cellular studies to enable the
thresholds for long-term effects from chronic exposure to static electric or
magnetic fields to be determined.
31
4 Electromagnetic Fields of
Frequencies Below 100 kHz
1 In this chapter, scientific data relevant to the development of exposure guidelines
for time-varying electromagnetic fields (EMFs) of frequencies less than about 100 kHz
are addressed. This range of frequencies is where the dominant and well-understood
interaction processes and adverse health effects are due to electrostimulation of body
tissues from induced internal electric fields and currents, although these processes occur
up to about 10 MHz. However, the reviews summarised in this chapter cover a wide range
of possible biological effects and disease outcomes. Thus this chapter summarises
relevant published epidemiological, biological and computational dosimetry studies.
EPIDEMIOLOGY
2 The following subsections consider epidemiological studies of people exposed to
extremely low frequency (30300 Hz), including power frequency (50/60 Hz), electric
and magnetic fields. These fields will be termed ELF EMFs in this document. Much of
the associated research has examined the risk of cancer, and accordingly particular
attention is given to this area. In addition, other health outcomes have been studied,
including neurodegenerative diseases, suicide and depressive illness, cardiovascular
disease, and reproductive outcome, and findings from these studies are also considered
here. In doing so, references are made to published reviews of the relevant literature,
together with citations to recent publications.
Cancer
3 The Advisory Group on Non-ionising Radiation (AGNIR) has periodically assessed
epidemiological and experimental studies of exposures to ELF EMFs and the risk of
cancer. A comprehensive assessment by AGNIR was recently published (AGNIR,
2001a). Other recent detailed reviews of this issue have also been performed by the
International Agency for Research on Cancer (IARC, 2002) and by the Standing
Committee on Epidemiology of the International Commission on Non-Ionizing Radiation
Protection (Ahlbom et al, 2001).
4 Epidemiological studies reviewed previously by AGNIR (1992) suffered from a lack
of measurement-based exposure assessments. Since then, considerable advances have
been made in methods for assessing exposure. In particular, instrumentation allowing
personal exposure to be measured has become widely available and has been used
in many of the more recently published studies. This has provided a substantially
improved basis for many of the epidemiological studies reviewed by AGNIR (2001a).
Residential exposures
5 Recent large and well-conducted studies have provided better evidence than was
available in the past on the relationship between residential exposures to power
frequency magnetic fields and the risk of cancer. A combined analysis, based on the
32
original data from nine key studies (Ahlbom et al, 2000), suggests that time-weighted
average exposures of 0.4 T or more are associated with a doubling of the risk of
leukaemia in children under 15 years of age. However, the evidence is not conclusive. In
studies in North America, the UK, Germany and New Zealand in which measurements
were made, the extent to which the more heavily exposed children were representative
is in doubt, owing to relatively low response rates for the controls (Ahlbom et al, 2000).
Furthermore, in studies in the Nordic countries (Denmark, Finland, Norway and Sweden),
for which the representativeness of the more heavily exposed children is assured, the
fields were estimated and the results were based on such small numbers that the findings
could have been due to chance. In the UK, very few children (perhaps 4 in 1000) are
exposed to time-weighted average fields of 0.4 T or more and a study in the UK
(UK Childhood Cancer Study Investigators, 1999), with much the largest number of direct
measurements of exposure, found no evidence of risk at lower levels. Nevertheless,
the possibility remains that high and prolonged time-weighted average exposure to
power frequency magnetic fields can increase the risk of leukaemia in children (AGNIR,
2001a). A recent study in Canada (Infante-Rivard and Deadman, 2003) reported a relative
risk of childhood leukaemia following maternal occupational exposure during pregnancy
to magnetic fields that was similar to that from the above combined analysis.
6 A study in the UK did not show an association between childhood cancer and
measurements of electric fields in homes, although the precision of the findings based
on fully validated measurements was generally low (Skinner et al, 2002).
7 Data on brain tumours come from some of the studies also investigating leukaemia
and from others concerned exclusively with these tumours. AGNIR concluded that
these data provided no comparable evidence of an association (AGNIR, 2001a). The
ICNIRP Standing Committee on Epidemiology concurred in this view, and also
concluded that there was no convincing evidence from studies in various countries of a
relationship between childhood lymphoma and residential exposure to EMFs from
nearby power lines (Ahlbom et al, 2001). There have been many fewer studies in adults.
AGNIR found no reason to believe that residential exposure to EMFs was involved in
the development of leukaemia or brain tumours in adults (AGNIR, 2001a). A recent
analysis (Li et al, 2003) reported an association between elevated residential exposure
to power frequency magnetic fields in Taiwan and an increase in the average age at
diagnosis for adult patients with brain tumours, but not for leukaemia or breast cancer
patients; this may represent a chance finding (Li et al, 2003). Also, studies of breast
cancer and residential EMF exposures, based on measurements in the home, have
generally not shown associations (Erren, 2001; Davis et al, 2002; Schoenfeld et al, 2003).
Tynes et al (2003) reported an association between cutaneous malignant melanoma
and estimated residential magnetic field exposures, but information was lacking on
individual exposures to ultraviolet radiation, which is a known risk factor.
Occupational exposures
8 Studies of populations exposed occupationally to EMFs can include groups exposed
generally at much higher levels than members of the public (AGNIR, 2001a). They may
therefore have a greater potential to detect any adverse health effects, although they
can be affected adversely by misclassification of exposures (Kheifets, 1999). Recently
published studies of occupational exposure to EMFs and the risk of cancer are, in the
4 Electromagnetic Fields of Frequencies Below 100 kHz
33
main, methodologically sound, and some of them are based on very large cohorts. AGNIR
concluded that causal relationships between such exposures and an increase in tumour
incidence at any anatomical site were not established (AGNIR, 2001a). The excesses,
where they exist, are generally modest and are largely restricted to the two cancers
noted in the 1992 AGNIR report, namely, leukaemia and brain cancer (AGNIR, 1992).
Conflicting evidence exists for the particular cell types of leukaemia associated with the
greatest risk but acute myeloid leukaemia is the most cited. The evidence of any risk for
brain cancer is conflicting, even that from the most powerful of the studies (AGNIR,
2001a). More recent studies of workers exposed to EMFs have generally not shown
raised risks of leukaemia or brain cancers (Harrington et al, 2001; Sorahan et al, 2001;
Oppenheimer and Preston-Martin, 2002; Willett et al, 2003). A recent association reported
in Canada (Villeneuve et al, 2002) between occupational magnetic field exposure and one
particular type of brain tumour, namely glioblastoma multiforme, is not in accord with
findings from another study conducted in Canada and France (Thriault et al, 1994).
9 Like AGNIR (2001a), the ICNIRP Standing Committee on Epidemiology concluded
that the evidence linking occupational EMF exposure to adult leukaemia or brain tumours
was weak (Ahlbom et al, 2001). In contrast, the California Department of Health Services
Panel (Neutra et al, 2002) placed more weight on the epidemiological findings concerning
adult brain cancers and EMFs. The ICNIRP Standing Committee on Epidemiology
concluded that the evidence for links with occupational EMF exposure was also weak
for breast cancer in men or women (Ahlbom et al, 2001). Furthermore, Erren (2001) has
drawn attention to difficulties of probable misclassification of exposure and of possible
misclassification of disease in interpreting studies of breast cancer. These points are
relevant in view of suggested effects of EMF exposure on melatonin levels, as discussed
further in paragraphs 5052. Findings for some other cancer sites, such as the prostate
(eg Thriault et al, 1994; Charles et al, 2003) and kidney (Hkansson et al, 2002), have
been variable. In addition, the ICNIRP Standing Committee on Epidemiology considered
the results from studies of childhood cancer and parental occupational exposure to
EMFs to be inconsistent and unconvincing (Ahlbom et al, 2001).
10 The findings for breast and prostate cancer discussed above are relevant in view of
suggested effects of EMF exposure on melatonin levels, as discussed in paragraphs 5052.
Reviews of studies of shift workers (Swerdlow, 2003) and of other studies of groups
exposed to differing levels of light (Erren, 2002) have provided some suggestion that
risks of certain types of cancer (eg breast and prostate) may be increased among those
with suppressed melatonin levels due to light exposure. However, the interpretation of
these results is not straightforward, owing to the possibility of confounding. For example,
shift workers or blind persons may differ from reference populations not only in their
exposures to light but also with respect to other determinants of health (Erren, 2002).
AGNIR is currently examining the issue of melatonin, and the implications for assessments
of EMFs and health.
Neurodegenerative diseases
11 AGNIR has reviewed epidemiological studies of ELF EMFs and the risk of neuro-
degenerative diseases (AGNIR, 2001b). These studies were mostly of people with
occupational exposures. AGNIR concluded that there is no good ground for thinking
that exposure to ELF EMFs can cause Parkinsons disease and only very weak evidence
34
to suggest that it could cause Alzheimers disease. The evidence that people employed
in electrical occupations have an increased risk of developing amyotrophic lateral
sclerosis (ALS) is substantially stronger, but this could be because they run an increased
risk of having an electric shock rather than any effect of long-term exposure to the
fields per se. Similar conclusions were reached by the ICNIRP Standing Committee on
Epidemiology (Ahlbom et al, 2001). The California Department of Health Services Panel
(Neutra et al, 2002) tended to favour an association between ALS and ELF EMFs,
whereas Li and Sung (2003) concluded that causal inferences were restricted because
of the lack of direct information on EMF exposures and the incomplete consideration of
other potential risk factors in the workplace. Two recent studies of mortality in occupa-
tional cohorts in Sweden have yielded somewhat conflicting results. Hkansson et al
(2003a) reported raised risks of both ALS and Alzheimers disease in relation to ELF
magnetic fields, whereas in a larger cohort Feychting et al (2003) reported a raised risk
for Alzheimers disease but no increased risk (or even a decreased risk) of ALS in
relation to magnetic fields. It is notable that the results of Hkansson et al (2003a) based
on primary cause of death showed weaker evidence for an association in the case of
Alzheimers disease, whereas the findings for ALS were essentially unchanged. Thus,
the quality of the information on diagnoses may have affected some of these findings,
making their interpretation difficult.
Suicide and depressive illness
12 Risks of suicide and depressive illnesses have been examined in several studies of
people exposed to power frequency EMFs occupationally or residentially. In a meta-
analysis of such studies, Ahlbom (2001) concluded that the support for an association
was weak. In its assessment of this topic, the ICNIRP Standing Committee on
Epidemiology (Ahlbom et al, 2001) drew attention to a subsequent large occupational
study that suggested an association with suicide (van Wijngaarden et al, 2000). A more
recent occupational study, based on job titles recorded on death certificates, also
suggested a weak association with suicide (van Wijngaarden, 2003). However, the
exposure assessment here was not as detailed as that in the occupational studies of
Baris et al (1996), Johansen and Olsen (1998), and van Wijngaarden et al (2000), whose
findings were variable. Overall, the ICNIRP Committee found it difficult to interpret the
literature on suicide and depressive illnesses in relation to EMFs, owing in part to
inconsistency in the findings (Ahlbom et al, 2001).
Cardiovascular disease
13 Several studies have examined cardiovascular disease and mortality among
workers exposed to EMFs. In its review of these studies, the ICNIRP Standing
Committee on Epidemiology concluded that evidence of cardiovascular effects due to
elevated exposure to magnetic fields was weak (Ahlbom et al, 2001). This Committee
also considered that an hypothesised association between such exposures and altered
autonomic control of the heart suggested by some human laboratory studies
remains speculative until corroborating evidence from further large epidemiological
studies becomes available (Ahlbom et al, 2001). Two more recent occupational studies
have not shown links between exposure to magnetic fields and either mortality from
acute myocardial infarction (Sahl et al, 2002) or the incidence of severe cardiac
arrhythmia (Johansen et al, 2002), whereas Hkansson et al (2003b) reported an
association for mortality from acute myocardial infarction.
35
Other diseases
14 In 1994, AGNIR published a review of health effects related to the use of visual
display units (VDUs) (AGNIR, 1994). It found that skin diseases did not appear to be
caused by the EMFs from VDUs, although there was anecdotal evidence unsupported
by epidemiology that in conditions of low humidity the associated static electric fields
may aggravate existing skin problems and the strain of the actual work may give rise to
skin problems among those with a predisposition to them. AGNIR found no evidence
that work with VDUs resulted in a predisposition to the formation of cataracts, although
there was an absence of long-term follow-up studies of users of VDUs. Minor opacities
of the eye lens that do not affect visual acuity are to be expected among a large
fraction of the population whether or not they use VDUs. Similar overall conclusions
were reached by the International Non-Ionizing Radiation Committee (INIRC, now
ICNIRP) of the International Radiation Protection Association in collaboration with the
International Labour Organization (INIRC, 1994).
Reproductive outcome
15 In its 1994 report on health effects related to the use of VDUs, AGNIR reviewed nine
epidemiological studies of spontaneous abortion and VDU use. Of these nine studies,
six found no increase in risk, even in heavy users of VDUs, and three reported some
increase in certain subgroups. The studies that showed no evidence of an increased risk
of spontaneous abortion in VDU users had far fewer problems in their design and
conduct than the ones reporting some increase in risk. Overall the results indicated
that VDU use did not increase the risk of spontaneous abortion. AGNIR also concluded
that the risk of congenital malformations did not appear to be increased in women who
have used VDUs in early pregnancy. However, little information was available on the
association of other adverse outcomes such as low birthweight with maternal VDU
exposure. Some investigators had studied related exposures, such as domestic
exposure to EMFs, and outcome of pregnancy. There was some suggestive evidence
that work with, or the manufacture of, electrical appliances might be associated with an
increased risk of prematurity, but this could be due to chemical exposures rather than
exposure to EMFs. AGNIR concluded that the totality of the epidemiological and
experimental evidence provided no good reason to suppose that low frequency EMFs
encountered through the use of VDUs caused any harm to the fetus in utero (AGNIR,
1994). Similar conclusions were reached at around the same time by INIRC (1994). In a
later review that also took account of more recent studies, the ICNIRP Standing
Committee on Epidemiology found that the existing evidence did not support an
association between maternal exposure to EMFs in the workplace and adverse
pregnancy outcomes (Ahlbom et al, 2001).
16 Several studies have examined reproductive outcomes in relation to maternal
residential exposures. Some of these studies have focused specifically on electrically
heated beds. Concern has been expressed by, for example, the ICNIRP Standing
Committee on Epidemiology about the potential for bias in retrospective studies that
have been conducted (Ahlbom et al, 2001). These concerns relate both to the accuracy
of assessing reproductive outcomes and to the quality of the information available on
exposure. A more recent study by Lee et al (2002) that was largely conducted
retrospectively had low response rates; associations that were reported with some
36
metrics measured at 30 weeks gestation are likely to be due to bias and/or chance,
given the weak correlations with exposures early in pregnancy and the absence of an
association with time-weighted average exposure (AGNIR, 2002). Only a few prospective
studies have been conducted. One such study found no increasing trend in the risk of
spontaneous abortion with intensity of use of electric bed heaters (Lee et al, 2000);
another study gave inconsistent results for spontaneous abortion (Belanger et al, 1998)
but no evidence of effects on birth weight or intrauterine growth retardation (Bracken
et al, 1995) from the use of electrically heated beds. The ICNIRP Standing Committee on
Epidemiology concluded that these studies do not support an association between
maternal exposure to EMFs from heated beds and adverse pregnancy outcomes
(Ahlbom et al, 2001). A subsequent prospective study (Li et al, 2002), which, together
with the study of Lee et al (2002) was given strong weight by the California Department
of Health Panel (Neutra et al, 2002) in its review, reported an association between
spontaneous abortion and personal measurements of magnetic fields. However, the
parameter that provided evidence of a risk namely maximum magnetic field strength
was not chosen a priori on the basis of biological or epidemiological reasons to
believe it might plausibly be of aetiological relevance (Li and Neutra, 2002); the results
were sensitive to the choice of breakpoint, which was made on the basis of the
observed data; and the study was not a standard prospective study as more than half
the spontaneous abortions (and all those at all strongly related to maximum field
exposure) occurred before the measurements were made, the compliance rate was
low, and the possibility of selection bias was not excluded (AGNIR, 2002).
17 There has been little epidemiological research on male fertility in relation to
exposure to power frequency EMFs. The few occupational studies conducted have
examined job titles, but have lacked individual measurements of field levels. Results
from these studies have been variable (eg Lundsberg et al, 1995; Irgens et al, 1999) and
do not provide convincing evidence of an association. Studies of birth defects in relation
to parental occupational exposures and to maternal residential exposures (eg Blaasaas
et al, 2002, 2003) have also been limited by a lack of magnetic field measurements, as
well as by the potential for chance findings due to studying many outcomes.
18 Many of the epidemiological studies of groups exposed to ELF EMFs have been
casecontrol studies. Their retrospective nature has led to concerns in some instances
about the possibility of associated sources of bias. For example, some of the case
control studies of childhood leukaemia and residential exposures that were included in
the combined analysis of Ahlbom et al (2000) may have been affected by the relatively
low response rates for controls. This potential problem did not affect all of the studies in
the combined analysis in particular, studies in the Nordic countries, which were based
on national population registers. However, the statistical precision of findings from the
Nordic studies was limited at higher exposure levels.
19 Follow-up studies of workers based on well-defined cohorts and with objective
measures of exposure and health should also be less susceptible to retrospective
sources of bias. However, there can be difficulties in these studies in estimating
exposures many years after the event. Furthermore, other types of exposure may arise
in the workplace which are correlated with EMF exposure and which may affect the
37
health of workers. An example concerns exposure to welding fumes, which may
increase lung cancer risks among welders (Stern, 1987).
20 Meta-analyses of findings from different studies or more detailed combined
analyses based on the original data from these studies have helped in increasing
statistical precision and in examining the compatibility of findings for example, in
highlighting the inconsistency of results on childhood leukaemia and residential
magnetic field exposure (Ahlbom et al, 2000). However, such analyses have also
highlighted inconsistencies in results between studies, so emphasising the need for
caution when drawing conclusions: for example, concerning depressive illnesses and
EMFs (Ahlbom, 2001).
21 Some studies of reproductive outcome and EMF exposure are likely to have been
affected by biases associated with their retrospective nature, namely, differential recall
of exposure and reproductive history. Consequently, prospective studies that have
been performed of such outcomes whilst rarer than retrospective studies should
generally be more reliable. It should also be noted that several exposure measures and
various outcomes have been considered in some studies. In the absence of a strong
a priori basis for these multiple hypotheses, it is difficult to interpret any positive findings.
Summary
22 There is some epidemiological evidence that time-weighted average exposure to
power frequency magnetic fields above 0.4 T is associated with a small increase in the
absolute risk of leukaemia in children, from about 1 in 20 000 to 1 in 10 000 per year. On
a relative scale, this corresponds to a doubling of the risk. Such exposures are seldom
encountered by the general public in the UK, and the raised risk if it were real would
correspond roughly to an additional two cases of childhood leukaemia per year in the
UK, compared with an annual total of around 500 cases. In the absence of clear evidence
of a carcinogenic effect in adults, or of a plausible explanation from experiments on
animals or isolated cells, AGNIR has concluded that the epidemiological evidence is
currently not strong enough to justify a firm conclusion that such fields cause leukaemia
in children. However, the possibility remains that intense and prolonged exposures to
magnetic fields can increase the risk of leukaemia in children, unless further research
indicates that the finding is due to chance or some currently unrecognised artefact
(AGNIR, 2001a). The ICNIRP Standing Committee on Epidemiology reached a similar
conclusion, and took the view that, among all the outcomes evaluated in epidemiological
research of EMFs, childhood leukaemia in relation to postnatal exposures to fields
above 0.4 T is the one for which there is most evidence of an association. This result is
unlikely to be due to chance but may be, in part, due to bias, and is difficult to interpret
in the absence of a known mechanism or reproducible experimental support (Ahlbom
et al, 2001). The International Agency for Research on Cancer (IARC, 2002) judged that
this finding provided limited evidence for an excess risk in humans exposed at these
levels, and it evaluated ELF magnetic fields as being possibly carcinogenic to humans
(Classification 2B). IARC also concluded that for the vast majority of children, who were
exposed to residential magnetic fields less than 0.4 T, there was little evidence of any
increased risk of leukaemia. Furthermore, IARC considered the evidence for excess
cancer risks of all other kinds, in children and adults, as a result of exposure to ELF
electric and magnetic fields to be inadequate.
38
23 Studies of occupational exposure to ELF EMFs do not provide strong evidence of
associations with neurodegenerative diseases. The only possible exception concerns
people employed in electrical occupations who appear to have an increased risk of
developing amyotrophic lateral sclerosis; however, this may be due to effects of
electric shocks rather than any effect of long-term exposure to the fields per se. Studies
of suicide and depressive illness have given inconsistent results in relation to ELF EMF
exposure, and evidence for a link with cardiovascular disease is weak. Skin diseases do
not appear to be caused by EMFs from visual display units (VDUs), although existing
skin conditions may be aggravated, and work with VDUs does not appear to cause a
predisposition to the formation of cataracts. The overall evidence from studies of
maternal exposure to ELF EMFs in the workplace does not indicate an association with
adverse pregnancy outcomes, while studies of maternal exposure in the home are
difficult to interpret. Results from studies of male fertility and of birth outcome and
childhood cancer in relation to parental occupational exposure to ELF EMFs have been
inconsistent and unconvincing.
The epidemiological evidence indicates that exposure to power frequency
magnetic fields above 0.4 T is associated with a small absolute raised risk of
leukaemia in children (an approximate doubling of the relative risk). However,
the evidence is not strong enough to justify a firm conclusion that such fields
cause leukaemia in children.
There is little evidence to suggest that the risk of childhood leukaemia might be
increased by exposure to ELF magnetic fields of time-weighted average magnetic
flux density below 0.4 T, or that raised cancer risks of other types, in children
and adults, might arise as a result of exposure to ELF magnetic fields.
Information specifically on electric fields is more sparse.
The findings from studies of health outcomes other than cancer have generally
been inconsistent or difficult to interpret.
Workers in electrical occupations do appear to have an increased risk of
developing amyotrophic lateral sclerosis, but this may be due to effects of
electric shocks rather than any effect of long-term exposure to ELF EMFs per se.
Whilst skin diseases do not appear to be caused by EMFs from VDUs, existing
skin conditions may be aggravated by the associated static electric fields.
The results of epidemiological studies, taken individually or as collectively
reviewed by expert groups, cannot be used as a basis for the derivation of
quantitative restrictions on exposure to EMFs.
BIOLOGY
24 The biological effects of low frequency EMFs continue to be studied using a wide
variety of exposure conditions, models and biological endpoints. While this research
has produced some useful information in helping to formulate public health policy, a
number of uncertainties and possibilities remain to be resolved, especially regarding
the consequences of exposure at levels commonly encountered in the environment.
Many of the same controversies that existed a decade ago continue to this day. The
absence of any established mechanism to describe interactions of very weak fields with
living tissue still presents a major hurdle to formulating hypotheses suitable for testing.
39
25 This section presents a summary of the biological effects of time-varying EMFs with
frequencies less than 100 kHz. It takes account of the consensus of the many national
and international scientific expert groups that have comprehensively reviewed the
biological effects literature. These include AGNIR (1994, 2001a), IARC (2002), ICNIRP
(1997, 1999a, 2004), NIEHS (1998, 1999) and NRC (1997).
26 It is clear from these reviews that the effects of surface electric charge and of
induced electric fields and currents represent the most suitable biological bases for
formulating restrictions on human exposure to EMFs. These effects, and the different
susceptibilities of people of varying health status, are summarised here.
27 In addition to these well-understood effects, a large number of other biological
effects have sometimes been reported. Most of these can be grouped together into
effects on cancer and carcinogenic processes, effects on the developing embryo and
fetus, and neurobehavioural effects (although these broad categories are neither
exhaustive nor mutually exclusive). The possibility of field dependent effects in these
areas has also been reviewed by the various scientific expert groups. None of these
effects was considered sufficient to form a suitable basis for deriving quantitative
restrictions on exposure. These studies are summarised here.
Effects of surface charge and induced electric fields and currents
28 An electric charge is induced on the surface of a person (or other living organism)
exposed to a low frequency electric field and this charge alternates in amplitude with
the frequency of the applied field. The effects of the surface electric charge per se are
well understood and have been used in the formulation of guidance on restrictions on
low frequency electric field exposure. The alternation of the surface charge with time
induces an electric field and therefore current flow within the body; in addition,
exposure to a low frequency magnetic field induces internal electric fields and
circulating currents. If of sufficient magnitude, these induced electric fields and currents
can affect electrically excitable nerve and muscle tissue.
29 Guidance on restrictions on exposure to low frequency electric and magnetic fields
has been formulated from a consideration of the basic physiological properties of
electrically excitable tissue, particularly the central nervous system (CNS), and of
physiological responses to relatively intense low frequency magnetic fields. The
evidence for these acute effects is summarised here; a more detailed account of the
electrophysiological evidence was prepared by an ad hoc expert group on weak
electric fields convened at NRPB in November 2001 (Appendix A) and was presented
at an ICNIRP/WHO workshop in March 2003 (ICNIRP/WHO, 2003; Appendix B).
Surface electric charge responses
30 Surface electric charge can be perceived directly through the induced vibration of
body hair and tingling sensations in areas of the body, particularly the arms, in contact
with clothing, and indirectly through spark discharges between a person and a
conducting object within the field. In several studies carried out in the 1970s and 1980s
(summarised by Reilly, 1998, 1999), the threshold for direct perception has shown
wide individual variation; 10%of exposed subjects had detection thresholds of around
25 kV m
1
at 60 Hz, whereas 50% could detect fields of 720 kV m
1
. These effects
were considered annoying by 5% of the test subjects exposed under laboratory
conditions above electric field strengths of about 1520 kV m
1
.
40
31 In addition to showing a wide variation in individual sensitivity, these responses also
vary with environmental conditions, particularly humidity. The studies referred to above,
however, included both wet and dry exposure conditions.
32 It has been estimated that spark discharges would be painful to 7%of subjects who
are well insulated from ground and who touch a grounded object within a 5 kV m
1
field
(Reilly, 1998, 1999), whereas they would be painful to about 50%in a 10 kV m
1
field.
Unpleasant spark discharges can also occur when a grounded person touches a large
conductive object such as a large vehicle that is well insulated from ground and is
situated within a strong electric field. Here, the threshold field strength required to
induce such an effect varies inversely with the size of the conductive object. In both
cases, the presence in the well-insulated person or object of a conductive pathway to
ground would tend to mitigate the intensity of any effect (Reilly, 1998, 1999), as would
the impedance to earth of the grounded object or person.
Exposure to power frequency electric fields causes well-defined biological
responses through surface electric charge effects. These responses depend on
field strength, ambient conditions as well as individual sensitivity, and range
from perception to annoyance.
Thresholds for direct perception by 10% of volunteers ranged between 2 and
5 kV m
1
; 5% found 1520 kV m
1
annoying.
For spark discharges, the discharge from a person to ground is painful to 7% of
volunteers in a field of 5 kV m
1
.
Thresholds for the discharge from an object through a grounded person depend
also on the size of the object and therefore require specific assessment.
Acute electrophysiological responses
33 Studies have been carried out of direct nerve stimulation thresholds in volunteers
by intense, pulsed magnetic fields. The effects of exposure inducing weak electric
fields, below the threshold for direct nerve stimulation, can be assessed from electro-
physiological studies of weak electric field interactions with nerve tissue and studies of
retinal and cognitive function in volunteers.
34 These various effects result from the interaction of the induced electric field with
voltage-gated ion channels. These are ion channels in cell membranes that allow the
passage of particular ionic species across the cell membrane in response to the opening
of a gate which is steeply sensitive to the transmembrane voltage (eg Catterall, 1995;
Hille, 2001; Mathie et al, 2003). Sensitivity is therefore primarily to the transmembrane
electric field and varies widely between different ion channels (Hille, 2001; Saunders
and Jefferys, 2002; Mathie et al, 2003). Many voltage-gated ion channels are associated
with electrical excitability and electrical signalling. Such electrically excitable cells not
only comprise neurons, glial and muscle cells, but also endocrine cells of the anterior
pituitary, adrenal medulla and pancreas, gametes and, with reservations, endothelial
cells (Hille, 2001). All these cells generally express voltage-gated sodium and calcium
channels. Both of these ion channels are involved in electrical signalling and calcium
ions activate a number of crucial cellular processes including neurotransmitter release,
excitation-contraction coupling in muscle cells and gene expression (Catterall, 2000;
Hille, 2001). Some ion channels exist in other, non-excitable tissues such as those in the
41
kidney and liver which show slow electric potential changes but their voltage
sensitivity is likely to be lower (eg Jan and Jan, 1989; Begenisich and Melvin, 1998;
Catterall, 2000; Cahalan et al, 2001; Nilius and Droogmans, 2001). Since voltage-gated ion
channels are steeply sensitive to the transmembrane electric potential, electric field
strength in tissue is a more relevant parameter to relate to electrically excitable cell
thresholds than current density (Blakemore et al, 2003). A similar view regarding the
merits of electric field strength as the more relevant dosimetric quantity had been
expressed previously at a workshop on exposure guidelines for low frequency electric
and magnetic fields (Sheppard et al, 2002), and is incorporated into the IEEE C95.6
standard limiting human exposure to ELF EMFs (IEEE, 2002).
Stimulation effects in high fields
35 Large, rapidly changing, pulsed magnetic fields used in various specialised medical
applications such as MRI and transcranial magnetic stimulation (TMS) can induce electric
fields able to stimulate nervous tissue in humans. Minimum, orientation-dependent
stimulus thresholds for large diameter (20 m) myelinated nerve axons have been
estimated (Reilly, 1998, 1999) to lie around 6 V m
1
at frequencies up to about 13 kHz.
In addition, accommodation to a slowly changing stimulus resulting from slow
inactivation of sodium channels will raise thresholds at low frequencies. In MRI, nerve
stimulation is an unwanted side-effect of a procedure used to derive cross-sectional
images of the body for clinical diagnosis (see Shellock, 2001). In TMS, parts of the
brain are deliberately stimulated in order to produce a transient, functional impairment
for use in the study of cognitive processes (see Reilly, 1998; Walsh and Cowey, 1998;
Ueno, 1999). Threshold rates of change of MRI switched gradient magnetic fields for
perception, discomfort and pain resulting from peripheral nerve stimulation are
extensively reviewed by Nyenhuis et al (2001). Median minimum threshold rates of
change of magnetic field (during periods of less than 1 ms) for perception were generally
1525 T s
1
depending on orientation and showed considerable variation between
individuals (Bourland et al, 1999). These values were somewhat lower than those
previously estimated by Reilly (1998, 1999), possibly due to the constriction of eddy
current flow by high impedance tissue such as bone (Nyenhuis et al, 2001). Thresholds
rose as the pulse width of the current induced by the switched gradient field decreased;
the median pulse width (the chronaxie) corresponding to a doubling of the minimum
threshold (the rheobase) ranged between 360 and 380 s (Bourland et al, 1999).
36 In TMS, brief, localised, suprathreshold stimuli are given, typically by discharging
a capacitor through a coil situated over the surface of the head, in order to stimulate
neurons in a small volume (a few cubic centimetres) of underlying cortical tissue
(Reilly, 1998). The induced current causes the neurons within that volume to depolarise
synchronously, followed by a period of inhibition (Fitzpatrick and Rothman, 2000).
When the pulsed field is applied to a part of the brain thought to be necessary for the
performance of a cognitive task, the resulting depolarisation interferes with the ability
to perform the task. In principle then, TMS provides cognitive neuroscientists with the
capability to induce highly specific, temporally and spatially precise interruptions in
cognitive processing sometimes known as virtual lesions. Reilly (1998) noted
induced electric field thresholds to be around 20 V m
1
. However, Walsh and Cowey
(1998) cited typical rates of change of magnetic field of 30 kT s
1
over a 100 s period
transiently inducing an electric field of 500 V m
1
in brain tissue.
42
37 People are likely to show variations in sensitivity to induced electric fields. In
particular, epileptic syndromes are characterised by increased neuronal excitability and
synchronicity (Engelborghs et al, 2000); seizures arise from an excessively synchronous
and sustained discharge of a group of neurons (Jefferys, 1994; Engelborghs et al, 2000).
TMS is widely used, apparently without adverse effects. However, repetitive TMS has
been observed to trigger epileptic seizure in some susceptible subjects (Wassermann
1998; Fitzpatrick and Rothman, 2000). These authors also reported short- to medium-
term memory impairments and noted the possibility of long-term cognitive effects
from altered synaptic activity or neurotransmitter balance. Contraindications for TMS
use agreed at an international workshop on repetitive TMS safety (Wassermann, 1998)
include epilepsy, a family history of seizure, the use of tricyclic anti-depressants,
neuroleptic agents and other drugs that lower seizure threshold. Serious heart disease
and increased intracranial pressure have also been suggested as contraindications due
to the potential complications that would be introduced by seizure.
Electric field strength in tissue is a more relevant parameter to relate to
electrically excitable cell thresholds than current density. Threshold induced
electric field strengths for direct nerve stimulation lie, in theory, in the range
525 V m
1
; apparent thresholds can be somewhat lower due to the preferential
flow of current through tissues with relatively high electrical conductivity. These
thresholds are likely to be constant between a few hertz and a few kilohertz.
An increased sensitivity of brain nerve tissue to induced electric fields seems
likely to be associated with epilepsy, a family history of seizure, the use of
tricyclic anti-depressants, neuroleptic agents and other drugs that lower seizure
threshold. Serious heart disease and increased intracranial pressure have also
been suggested as contraindications due to the potential complications that
would be induced by seizure.
Electrophysiological studies of weak field effects
38 Cells of the central nervous system are considered to be sensitive to induced ELF
electric fields at levels that are below the threshold for impulse initiation in nerve axons
(Jefferys, 1995; Saunders and Jefferys, 2002; Jefferys et al, 2003; Saunders, 2003). Such
weak electric field interactions have been shown in experimental studies mostly using
isolated animal brain tissue, to result from the extracellular voltage gradients generated
by the synchronous activity of a number of neurons, or from those generated by
applying pulsed or alternating currents directly through electrodes placed on either side
of the tissue. Jefferys and colleagues (Jefferys, 1995; Jefferys et al, 2003) identified
in vitro thresholds of around 45 V m
1
. Essentially, the extracellular gradient alters the
potential difference across the neuronal membrane with opposite polarities at either
end of the neuron; a time constant of a few tens (1560) of milliseconds results from the
capacitance of the neuronal membrane (Jefferys et al, 2003) and indicates a limited
frequency response. Similar arguments concerning the limited frequency response of
weak electric field effects due to the long time constants (25 ms) arising from cell
membrane capacitance have been given by Reilly (2002) regarding phosphene data
and have been incorporated into the IEEE C95.6 standard limiting human exposure to
EMFs up to 3 kHz (IEEE, 2002); see paragraph 46.
43
39 The CNS in vivo is likely to be more sensitive to induced low frequency electric
fields and currents than in vitro preparations (Saunders and Jefferys, 2002).
Spontaneous activity is higher, and interacting groups or networks of nerve cells
exposed to weak electrical signals would be expected, on theoretical grounds, to show
increased sensitivity through improved signal-to-noise ratios compared with the
response of individual cells (Valberg et al, 1997; Sterling, 1998; Adair, 2001). Much of
normal cognitive function of the brain depends on the collective activity of very large
numbers of neurons. Neural networks are thought to have complex non-linear
dynamics that can be very sensitive to small voltages applied diffusely across the
elements of the network (Adair, 2001; Jefferys et al, 2003; ICNIRP, 2004). Jefferys and
colleagues recently reported preliminary results from a study of the effects of 50 Hz
electric fields on the electrical activity of hippocampal tissue in which a large number
of interacting neurons were induced into coherent oscillatory behaviour by the
application of a glutamate receptor stimulant (Saunders, 2003). The weakest applied
sinusoidal field that could modulate the induced electrical oscillation was reported
to be 2 V m
1
(peak-to-peak); further study is in progress. Gluckman et al (2001) placed
the detection limit for network modulation in hippocampal slices by electric fields at
around 100 mV m
1
. Recent experimental work by Francis et al (2003) confirmed a
neural network threshold of around 140 mV m
1
, more sensitive than the average
single neuron threshold of 185 mV m
1
in their study. A lower limit on neural network
sensitivity to physiologically weak induced electric fields has been considered
elsewhere on theoretical grounds to be around 1 mV m
1
(Adair et al, 1998a; Veyret,
2003). The time-course of the opening of the fastest voltage-gated ion channels can be
less than 1 ms (Hille, 2001), suggesting that effects at frequencies up to a few kilohertz
should not be ruled out. Accommodation to a slowly changing stimulus resulting from
slow inactivation of the sodium channels will raise thresholds at frequencies less than
around 10 Hz.
40 People suffering from or predisposed to epilepsy are likely to be more susceptible
to induced low frequency electric fields in the CNS (Blakemore et al, 2003). Jefferys (1994)
estimated that around 1000 neurons are the minimum aggregate for epileptic activity.
41 Other electrically excitable tissues with the potential to show network behaviour
include glial cells located within the CNS (eg Parpura et al, 1994), and the autonomic
and enteric nervous systems (see Sukkar et al, 2000), which comprise interconnected
non-myelinated nerve cells and are distributed throughout the body and gut,
respectively. These systems are involved in regulating the visceral or housekeeping
functions of the body; for example, the autonomic nervous system is involved in the
maintenance of blood pressure. Muscle cells also show electrical excitability; only
cardiac muscle tissue has electrically interconnected cells. However, Cooper et al (2003),
in a review of cardiac ion channel activity, concluded that weak internal electric fields
much below the excitation threshold were unlikely to have any significant effect on
cardiac physiology. EMF effects on the heart (eg Sastre et al, 2000) could nevertheless
result from indirect effects mediated via the autonomic nervous system and CNS
(Sienkiewicz, 2003). Effects on the endocrine system could potentially also be mediated
this way, although the evidence from volunteer experiments indicated that acute low
frequency magnetic field exposure up to 20 T did not influence the circadian variation
44
in circulating levels of melatonin (Warman et al, 2003), nor other plasma hormone levels
(ICNIRP, 2004).
42 Electric fields around 10100 V m
1
generated by physiological and metabolic
processes within the body can affect nerve growth in vitro and in vivo and may play
an important role in normal developmental processes (Nuccitelli, 1992, 2003). Electric
fields of a similar order, generated by passing direct currents between electrodes placed
on either side of the preparation, have been reported to affect development of the
embryonic and neonatal nervous system and nerve regeneration (eg AGNIR, 1994;
Jefferys, 1995; Nuccitelli, 2003). However, other authors (Borgens, 1999; Moriarty and
Borgens, 2001) have reported that electric fields of only 100 mV m
1
can influence the
regeneration of nerve fibres in the spinal cord and that application of an electric field of
320 mV m
1
that alternated in polarity every 15 minutes could affect the density and
orientation of astrocytes in an injured mammalian spinal cord. Generally, however
these processes are far less sensitive to the effects of low frequency fields (Sienkiewicz,
2003) and experimental studies do not reveal adverse EMF effects on mammalian
development (Juutilainen, 2003).
Weak electric field interactions can be demonstrated in CNS tissue in vitro
around 45 V m
1
; time constants are typically around tens of milliseconds.
In vivo, greater susceptibility is predicted due to the larger number of
interacting nerve cells or neural networks; the data available are consistent with
a threshold of 100 mV m
1
. Thresholds may be constant between a few hertz and
a few kilohertz. Electrically excitable tissues with the potential to show network
behaviour include nerve and glial cells of the CNS and the autonomic and enteric
nervous system. People suffering from or predisposed to epilepsy are likely to be
more susceptible to induced low frequency electric fields in the CNS.
Other excitable tissues such as the heart seem less susceptible to the direct effects
of weak induced low frequency electric fields, but may be affected indirectly via
effects on the CNS. Applied static electric fields also affect nerve growth and
regeneration. In addition, static electric fields of typically 10100 V m
1
have
been reported to affect the development of the embryonic and neonatal nervous
system; however, these processes are likely to be less sensitive to the effects of
induced low frequency electric fields. Nevertheless, effects have been seen with
applied static electric fields as low as 100 mV m
1
and at higher values of applied
static electric fields which alternate slowly. These data indicate that a degree of
caution is appropriate when considering the potential susceptibility of the
developing nervous system, both in utero and in neonates and young children to
weak induced time-varying electric fields.
Volunteer studies of weak field effects
43 A number of volunteer studies have been carried out on the effects of magnetically
induced or directly applied low frequency electric currents below levels for direct
nerve stimulation on retinal* function; also on learning, memory and other cognitive
functions. Some of these have involved conditions where the induced or applied
currents were mostly around or above the average bulk endogenous brain tissue
* The neural circuitry of the retina forms part of the central nervous system (Dowling, 1987).
45
current density levels of 110 mA m
2
(Bernhardt, 1988; Wachtel, 1992). The equivalent
electric fields would be around 10100 mV m
1
, assuming a conductivity of brain tissue
of around 0.1 S m
1
. The experimental evidence is summarised immediately below.
Most studies, however, have investigated possible effects resulting from very much
lower levels of exposure; these are summarised in paragraphs 5054 and 86100.
44 The effects of exposure to weak low frequency magnetic fields on human retinal
function are well established. Exposure of the head to magnetic flux densities above
about 5 mT at 20 Hz, rising to about 15 mT at 50 Hz, will reliably induce faint flickering
visual sensations called magnetic phosphenes (Sienkiewicz et al, 1991; Attwell, 2003;
Taki et al, 2003). It is generally agreed that these phosphenes result from the interaction
of the induced electric current with electrically sensitive cells in the retina. Several
lines of evidence suggest the production of phosphenes by a weak induced electric
field does not involve the initial transduction of light into an electrical signal. Firstly,
the amplification of the initial signal generated by the absorption of light takes place
primarily through an intracellular second-messenger cascade of metabolic reactions
prior to any change in ion channel conductivity (Hille, 2001). Secondly, the phosphene
threshold appears unaffected by dark adaptation to low light levels (Carpenter, 1972).
In addition, phosphenes have been induced in a patient with retinitis pigmentosa, a
degenerative illness primarily affecting the pigment epithelium and photoreceptors
(Lvsund et al, 1980).
45 There is good reason to view retinal circuitry as a conservative model for induced
electric field effects on CNS neuronal circuitry in general (Attwell, 2003). Firstly, the
retina displays all the processes present in other CNS areas, such as graded voltage
signalling and action potentials, and has a similar biochemistry. Secondly, in contrast to
more subtle cognitive effects, phosphenes represent a direct and reproducible perception
of field interaction. A clear distinction can be made in this context between the
detection of a normal visual stimulus and the abnormal induction of a visual signal by
non-visual means (Saunders, 2003); the latter suggests the possibility of direct effects
on cognitive processes elsewhere in the CNS.
46 Thresholds for electrically induced phosphenes* have been estimated to be
about 1014 mA m
2
at 20 Hz (Adrian, 1977; Carstensen et al, 1985). A similar value
(10 mA m
2
at 20 Hz), based on studies of magnetically induced phosphenes, has been
derived by Wake et al (1998). The equivalent electric field threshold can be estimated
as around 100140 mV m
1
using a tissue conductivity for brain tissue of about 0.1 S m
1
(Gabriel, 1995). More recently, Reilly (2002) has calculated an approximate 20 Hz
electric field threshold in the retina of 53 mV m
1
for phosphene production. A similar
value (60 mV m
1
) has been reported elsewhere (see Saunders, 2003). Subsequently,
however, Taki et al (2003) indicated that calculations of phosphene thresholds suggested
that electrophosphene thresholds were around 100 mV m
1
, whereas magneto-
phosphene thresholds were around 10 mV m
1
at 20 Hz. More detailed calculation by
Attwell (2003), based on neuro-anatomical and physiological considerations, suggested
that the phosphene electric field threshold in the extracellular fluid of the retina was in
the range 1060 mV m
1
at 20 Hz. There is, however, considerable uncertainty attached
* Carstensen et al (1985) applied an incorrect brain tissue conductivity value (0.01 S m
1
); the correct
value has been used above to calculate phosphene threshold current density.
46
to these values. In addition, the extrapolation of values in the extracellular fluid to those
appropriate for whole tissue, as used in most dosimetric models, is complex, depending
critically on the extracellular volume and other factors. With regard to the frequency
response, Reilly (2002) suggested that the narrow frequency response was the result of
relatively long membrane time constants of around 25 ms (see paragraph 38). However,
at present, the exact mechanism underlying phosphene induction is unknown. It is
not clear whether the narrow frequency response is due to intrinsic physiological
properties of the retinal neurons, as suggested by Reilly (2002) above and by Attwell
(2003) considering active amplification process in the retinal neuron synaptic terminals,
or is the result of central processing of the visual signal (Saunders and Jefferys, 2002;
Saunders, 2003). This issue can only be resolved through further investigation.
47 Two groups (Stollery et al, 1985, 1986, 1987; Preece et al, 1998) have studied the
psychological effects of induced 50 Hz electric fields and currents comparable to those
which at lower frequencies can induce phosphenes (515 mT) studies of volunteers
exposed to lower magnetic flux densities are described in paragraphs 5054. Stollery
et al (1985, 1986, 1987) exposed volunteers on two separate days to a 50 Hz electric
field of 36 kV m
1
; the peak induced current density in the brain was calculated
(Edwards and Pickles, 1985; Edwards, 1986) to be between 10 and 40 mA m
2
(100 and
400 mV m
1
using a conductivity of 0.1 S m
1
). Cognitive function and mood were
assessed using questionnaires and a battery of computer-generated cognitive tests. No
obvious or simple mental deficit resulted from the passage of the current but levels of
arousal and the response time for some tests of linguistically complex (syntactic)
reasoning were significantly affected in one group of subjects but not in another.
Overall the results were inconclusive. More recently, Preece et al (1998) found
significant effects on some aspects of cognitive function in volunteers during exposure
to 50 Hz magnetic fields of 0.6 mT. Current densities induced in the head were
estimated as about 2 mA m
2
, peaking at 6 mA m
2
(20 mV m
1
and 60 mV m
1
using a
conductivity of 0.1 S m
1
). The authors reported that exposure to 50 Hz magnetic fields
caused a decline in numeric working memory sensitivity and a decline in word
recognition sensitivity. In addition, the volunteers were less accurate, although not
slower, than controls on the choice reaction time task. Thus, Preece et al (1998)
reported impairments in three important cognitive functions attention, working
memory and episodic secondary memory during exposures inducing peak electric
fields of between 20 and 60 mV m
1
; the dosimetric rigour with which these values were
derived is not, however, clear.
The retina is considered to be a good model of the sensitivity of CNS tissue to
induced electric fields. Retinal function can be reliably affected by exposure to
ELF magnetic fields and applied electric currents; threshold electric field
strengths in the extracellular fluid of the retina have been estimated to lie
between about 10 and 60 mV m
1
at 20 Hz. There is considerable uncertainty
attached to these values. In addition, their extrapolation to those appropriate for
the whole tissue, as used by dosimetric models, is complex and uncertain. The
mechanisms underlying the variation of the threshold of this perceptual
response with frequency are unknown.
47
Other possible effects
48 In addition to the surface charge effects and electrophysiological responses described
above, the possibility that exposure to low frequency EMFs may induce other biological
effects has continued to be investigated. Many different models, including volunteers,
animals and cultures of cells have been examined using a wide range of tests and
exposure conditions (NIEHS, 1999). However, it is conceptually useful to group all these
studies into three broad categories (Sienkiewicz et al, 1993; NRC, 1997) and to consider
effects on cancer, reproduction and development, and neurobehavioural effects. The
experimental evidence for these possibilities is summarised here. Very detailed reviews,
critiques and summaries of this literature have been published elsewhere by national
and international expert groups (AGNIR, 1994, 2001a; IARC, 2002; ICNIRP, 1997, 1999a,
2004; NIEHS, 1998, 1999; NRC, 1997).
Cancer
49 The majority of the experimental studies conducted over the last ten years investi-
gating the biological effects of EMFs have focused on the carcinogenic potential of
power frequency magnetic fields. Few studies have used electric fields. Most of this
research has been conducted at the cellular and animal level, and studies with volunteers
have tended to concentrate on the effects of exposure on melatonin.
Volunteer studies
50 It has been suggested that chronic exposure to EMFs may disrupt pineal physiology
and decrease circulating levels of melatonin and thereby increase the risk of breast
cancers and other tumours (Stevens, 1987, 1994). Several mechanisms for this have
been postulated, including modulation of immune responsiveness and decreased
scavenging of free-radicals (see Cridland et al, 1996a). AGNIR is currently undertaking a
review of the effects of EMFs on melatonin and breast cancer.
51 The evidence suggests that human melatonin rhythms are not significantly delayed
or suppressed by exposure to magnetic fields (NIEHS, 1998; AGNIR, 2001a; IARC, 2002;
although also see Karasek and Lerchl, 2002). Wilson et al (1990) reported that chronic
exposure to the pulsed fields generated by mains or DC powered electric blankets
had no effect on urinary excretion of the major metabolite of melatonin, 6-hydroxy-
melatonin sulphate. Transient increases in night-time excretion were reported in 7 out
of 28 volunteers in the periods following the onset and cessation of use of one type of
blanket, although the particular relevance of this result is questionable (AGNIR, 2001a).
Similarly, night-time exposure to continuous or intermittent power frequency magnetic
fields for 1 or 2 nights had no effect on melatonin metabolism as measured by salivary
melatonin levels (Griefahn et al, 2002), serum melatonin levels or the excretion of
6-hydroxymelatonin sulphate (Graham et al, 1996, 1997, 2001a,b; Selmaoui et al, 1997;
kerstedt et al, 1999; Crasson et al, 2001; Kurokawa et al, 2003). However, the results
of a study investigating the effects of night-time exposure to 60 Hz fields for 4 nights
(Graham et al, 2000a) suggested a weak cumulative effect of exposure. Exposed subjects
showed more intra-individual variability in the overnight levels of excretion of melatonin
or 6-hydroxymelatonin sulphate on night 4, although there was no overall effect on
levels of melatonin. Hong et al (2001) also reported no significant field dependent
effects on melatonin rhythms in men following 11 weeks of night-time exposure.
48
52 Wood et al (1998) suggested that exposure to circularly polarised power frequency
magnetic fields prior to the night-time rise in melatonin may delay the onset of the rise
by about half an hour, and reduce peak levels possibly in a sensitive subgroup of the
study population. This preliminary study is suggestive of an effect, although it has been
criticised for procedural and other difficulties (AGNIR, 2001a).
53 In addition to laboratory studies, several studies have looked at endocrine function
in humans exposed to power frequency magnetic fields in occupational and residential
settings (Pfluger and Minder, 1996; Burch et al, 1998, 1999, 2000; Juutilainen et al, 2000;
Davis et al, 2001). In a review, IARC (2002) noted that these studies reported some
perturbation in the excretion of 6-hydroxymelatonin sulphate in exposed groups.
However, these small reductions were not consistent across studies and the exposure
parameters differed between studies. IARC (2002) concluded that it was difficult to
distinguish between effects of magnetic fields and those of other environmental
factors. The particular difficulties associated with investigating effects of EMFs on
melatonin are discussed by Warman et al (2003).
54 Finally, a few laboratory studies have investigated effects of magnetic fields on other
endocrine and haematological function and immune system. No field dependent effects
have been seen (Selmaoui et al, 1996) confirming earlier results (see Sienkiewicz et al,
1991; NIEHS, 1998; IARC, 2002).
Animal studies
55 Numerous animal studies have investigated the effects of exposure on carcinogenic
processes. Overall, these studies provide no convincing evidence to support the
hypothesis that exposure to magnetic fields can substantially increase the risk of cancer
(AGNIR, 1994, 2001a; Boorman et al, 2000a,b; McCann et al, 2000; IARC, 2002). The most
recent studies, in particular, are more extensive and generally have been carefully
conducted, often using independent quality assurance procedures. These procedures
were absent or less stringent in many of the earlier studies reporting either positive or
negative effects.
56 A few animal studies have investigated the possibility that magnetic fields induce
DNA damage. Increased DNA strand breaks have been reported in brain cells of
exposed rodents (Lai and Singh, 1997a,b; Svedenstl et al, 1999a,b), but the results are
inconclusive (IARC, 2002) and not supported by results from cellular studies.
57 Several recent large-scale studies have investigated the effects of continuous or
intermittent lifetime exposure to magnetic fields on spontaneous tumour incidence in
rats and mice (Mandeville et al, 1997; Yasui et al, 1997; Boorman et al, 1999; McCormick
et al, 1999; NTP, 1999a). Results were negative with regard to leukaemia, brain cancer
and mammary tumours. Although in one study the incidence of thyroid C-cell
adenomas and carcinomas was elevated in male rats, this result might represent a
chance event following multiple pair-wise comparisons (AGNIR, 2001a). Studies using
transgenic mice (E pim-1 or TSG-Trp53) also reported no significant field induced
effects on spontaneous lymphoma incidence (Harris et al, 1998; McCormick et al, 1998).
In contrast, one study found a high increase in lymphoid hyperplasia and lymphoma in
mice exposed over three generations to an intense travelling magnetic field (Fam and
Mikhail, 1996). However this study appears to have severe methodological and other
flaws (Boorman et al, 2000a; McCann et al, 2000; AGNIR, 2001a; IARC, 2002).
49
58 Similarly, possible promotional or co-promotional effects of magnetic fields have
been examined using a variety of multistage carcinogenesis models. Here the animals
are treated with a carcinogen known to induce a particular cancer, and also exposed to
various EMF intensities, sometimes in conjunction with a known promoting agent.
Studies conducted through the 1990s have reported mainly negative results of
magnetic fields using the classical mouse skin tumour model (McLean et al, 1991, 1995,
1997; Stuchly et al, 1992; Rannug et al, 1993a, 1994; Sasser et al, 1998; DiGiovanni et al,
1999). Another laboratory reported accelerated development of ultraviolet radiation
(UVR) induced skin tumours in transgenic (K2) and normal mice (Kumlin et al, 1998a)
and inhibition of UVR induced apoptosis in mouse skin (Kumlin et al, 2002). Other
studies seeking evidence of promotional effects of magnetic fields on the incidence of
lymphoma and other haemopoietic neoplasias have also reported a lack of field
dependent effects using transgenic (pim-1) or normal mice (Shen et al, 1997; McCormick
et al, 1998; Babbit et al, 2000; Heikkinen et al, 2001a). Lastly, no field dependent effects
were seen on the induction of chemically induced pre-neoplastic foci in the rat liver
(Rannug et al, 1993b,c). In addition, a few animal studies have investigated effects
relevant to the non-genotoxic mechanisms of cancer, but the results are inconclusive
(see also IARC, 2002). Changes in the activity of ornithine decarboxylase (ODC) have
been reported in various tissues after short-term exposure of rodents to magnetic fields
(Mevissen et al, 1995, 1999; Kumlin et al, 1998b) but not after longer exposure periods
(Kumlin et al, 1998b; Sasser et al, 1998; Mevissen et al, 1999).
59 Rat mammary carcinomas represent a standard laboratory animal model in the
study of human breast cancer. Several groups have investigated the possible
promotional effects of magnetic fields on chemically induced mammary tumours in
female rats following an earlier report that suggested long-term exposure increased
incidence and malignancy of tumours (Beniashvili et al, 1991). In an extensive series of
medium-term studies, Lscher, Mevissen and colleagues have reported that magnetic
fields may increase tumour incidence, possibly due to field induced increases on
tumour growth rate. Further, a significant linear correlation was found between increase
in tumour incidence and magnetic flux density (Lscher and Mevissen, 1994, 1995;
Lscher et al, 1993, 1994, 1998; Mevissen et al, 1993, 1996a,b, 1998a,b; Thun-Battersby
et al, 1999; Lscher, 2001). There was, however, considerable variation between
experiments reported by this group in the incidence of tumours in the unexposed
control animals (possibly due to seasonal and other factors) which confounds
interpretation of these data (AGNIR, 2001a). Another study (Fedrowitz et al, 2002)
reported an increase in two cell proliferation markers (bromodeoxyuridine and Ki-67)
in rat mammary gland. In contrast, two studies have reported a lack of an effect of
magnetic fields on chemically induced mammary tumours. One extensive study,
consisting of three large experiments, found no effects following an attempt to repeat
and extend some of the positive effects reported by Lscher and Mevissen (Anderson
et al, 1999, 2000; Boorman, 1999; NTP, 1999b). Sensitivity to detect field induced effects,
however, was not optimal in two of these experiments (AGNIR, 2001a). Another study
found no effects following intermittent magnetic field exposure (Ekstrm et al, 1998).
Therefore the evidence for magnetic field effects on chemically induced mammary
tumours in female rats is inconsistent (IARC, 2002). Finally, the limited evidence
suggests magnetic fields do not cause promotion of neurogenic tumours. One study
50
reported no detectable effects of lifetime exposure following gamma-radiation induced
brain tumours (Kharazi et al, 1999). Another very extensive study found no effects on
central and peripheral nervous system tumours in female rats exposed transplacentally
to a potent chemical carcinogen (Mandeville et al, 2000).
60 The few studies that have investigated the effect of magnetic fields on the growth of
transplanted tumours in rats have not reported any field dependent effects. One study
found no effect on the progression of large granular lymphocytic leukaemia (Sasser
et al, 1996; Morris et al, 1999). Another found no effect on the progression of acute
myeloid leukaemia (Devary et al, 2000).
61 The possibility that exposure to electric or magnetic fields may disrupt melatonin
rhythms, and so increase the risk of cancer (Stevens, 1994; Stevens et al, 1997), has
also received attention using animal models. Early studies using 60 Hz electric fields
(Wilson et al, 1981, 1983, 1986; Reiter et al, 1988) suggested that exposure of rats caused
a significant, if temporary, depression in pineal melatonin levels. The inability of later
studies to reproduce this phenomenon (Sasser et al, 1991; Grota et al, 1994) suggests
that the original positive results may be attributable to artefact or confounding (Brady
and Reiter, 1993; Reiter, 1993). No effects on circulating melatonin levels were seen in
male baboons following several weeks exposure to combined 60 Hz electric and
magnetic fields (Rogers et al, 1995a), although effects were noted in a preliminary study
using an irregular and intermittent exposure schedule (Rogers et al, 1995b).
62 A series of experiments by Kato and colleagues (summarised by Kato and Shigemitsu,
1997) provided some evidence to suggest that subchronic exposure of rats to circularly
polarised magnetic fields, but not elliptically or linearly polarised magnetic fields, may
temporarily depress melatonin production and secretion (Kato et al, 1993, 1994ac).
Interpretation of these studies; however, is complicated by variability in the data between
experiments and the frequent use of inappropriate controls (AGNIR, 2001a). It has
been postulated that reductions in melatonin may produce concomitant increases in
sex hormones. Accordingly, serum testosterone levels were also measured in one of
these experiments, but without any field dependent effect being observed (Kato et al,
1994d). Other studies using rats have provided inconsistent and mostly negative
evidence for magnetic field dependent changes in pineal function (Lscher et al, 1994,
1998; Selmaoui and Touitou, 1995; Bakos et al, 1995, 1997, 1999; Mevissen et al, 1996a,b,
1998a; John et al, 1998; Fedrowitz et al, 2002). Similar results have been observed using
mice (McCormick et al, 1995; Heikkinen et al, 1999). Studies using Suffolk ewe lambs
(Lee et al, 1993, 1995) and Djungarian hamsters (Yellon, 1994, 1996; Truong et al, 1996;
Niehaus et al, 1997; Truong and Yellon, 1997; Yellon and Truong, 1998; Wilson et al,
1999) also provided no consistent evidence that exposure to power frequency
magnetic fields can cause sustained disruptions in melatonin levels. One ex vivo study,
however, suggested field dependent effects may occur. Brendel et al (2000) reported
that melatonin production from isolated pineal glands of Djungarian hamsters, when
stimulated by isoproterenol, was significantly suppressed by exposure to 16.67 or 50 Hz
magnetic fields at 86 T. AGNIR is currently undertaking a review of the effects of EMFs
on melatonin.
63 Lastly, the possibility that exposure to electric or magnetic fields might affect the
progression of tumours via some field induced change in the immune response has
been investigated. Overall, there is little consistent evidence of any inhibitory effect of
51
exposure to power frequency fields on the various aspects of immune system function
relevant to tumour suppression that have been examined. The few studies that have
attempted to correlate possible field induced changes in tumour incidence with significant
changes in immune function have not been successful (AGNIR, 2001a).
64 No effects were seen in mice with long-term continuous or intermittent exposure
to magnetic fields using in vivo assays of T-lymphocyte mediated immune response to
bacterial infection and antigen stimulation (House et al, 1996).
65 Studies using in vitro assays following long-term in vivo exposure to magnetic
fields have also been conducted. Using rats, Mevissen et al (1996b, 1998b) reported a
transient initial increase of spleen T-lymphocyte proliferation in rats after 2 weeks
exposure was followed by a decrease after 13 weeks. Murthy et al (1995) reported a
decrease in peripheral blood B-lymphocyte mitogenic response in a pilot study with
baboons exposed to electric and magnetic fields, but this effect was not reproduced in
the main study using more intense fields.
66 A few studies have been carried out of natural killer (NK) cell function. Exposure
to continuous or intermittent magnetic fields was reported to reduce spleen NK cell
activity in female mice, but not in male mice, or in male or female rats (House et al, 1996;
House and McCormick, 2000). This change in NK cell activity in female mice was not
correlated with field induced changes in spontaneous tumour incidence (McCormick
et al, 1999). In contrast, Tremblay et al (1996) reported that spleen NK cell activity was
enhanced by magnetic field exposure in the same strain of rats used by House et al
(1996) when compared with that of cage control animals but not of sham-exposed
animals. Non-significant reductions in spleen and blood NK cell activity were reported
in SENCAR mice treated with chemical carcinogens as part of a tumour co-promotion
study (McLean et al, 1991). Increased numbers of exposed animals also showed
enlarged spleens and extremely high blood mononuclear cell counts, suggestive of
leukaemia (or lymphoma), although the evidence of immune system neoplasia
appeared weak.
67 The activity in a subgroup of peritoneal macrophages was also investigated by
Tremblay et al (1996). No effects of exposure were seen on two measures of
macrophage activity (production of nitric oxide and tumour necrosis factor), although a
third measure of macrophage activity (hydrogen peroxide release) showed a dose-
dependent increase when compared with cage control animals. Comparison with sham-
exposed animals only produced a significant effect at the higher levels of exposure.
Finally, antibody (B-lymphocyte) cell activity in mice was not affected by exposure to
power frequency or pulsed magnetic fields (House et al, 1996).
Cellular studies
68 Cellular studies have been used primarily to investigate possible mechanisms of
interaction with EMFs. Compared with long-term animal studies, they are relatively
inexpensive and rapid to perform, although this type of study is not generally taken
alone as evidence of effects in vivo (AGNIR, 2001a).
69 Very many cellular studies have investigated the possibility that exposure to EMFs
may induce biological changes that may be relevant to the causation or development
of cancer. As with studies using animals, a wide variety of cell systems, tests and
exposure conditions have been employed. While there have been reports of a few field
52
dependent effects, there is no clear evidence that exposure to magnetic fields of less
than 0.1 mT can affect biological processes (NIEHS, 1998, 1999; AGNIR, 2001a). Further,
the positive effects reported tend to be of small magnitude that questions their
biological significance. Several comprehensive reviews and expert committees have
reaffirmed that low level magnetic fields lack reliably observable genotoxic activity
(McCann et al, 1993; Murphy et al, 1993; Lacy-Hulbert et al, 1998; NIEHS, 1998, 1999;
AGNIR, 2001a).
70 Various studies have investigated the potential of EMFs to act as initiators of
cancers. Several authors have indicated that exposure to either pulsed or continuous
EMFs cannot directly bring about the transformation of cells in culture (Balcer-Kubiczek
et al, 1996; Jacobson-Kram et al, 1997; Saffer et al, 1997) or negatively affect cellular
immortalisation (Gamble et al, 1999; Miyakoshi et al, 2000a). In addition, studies using
the Ames test to identify mutation in bacteria have not found any field dependent
effects using magnetic fields (Nafziger et al, 1993; Tabrah et al, 1994; Suri et al, 1996) or
pulsed electric fields and EMFs (Jacobson-Kram, 1997). In contrast, Miyakoshi et al
(1996a, 1997) reported that exposure to very intense magnetic fields at 400 mT
increased mutation at the hrpt gene locus in human MeWo cells, particularly during
S-phase of the cell cycle. These mutations were suppressed by the action of a wild-type
p53 gene (Miyakoshi et al, 1997). There is also some evidence to suggest that the yield
of mutations caused by exposure to ionising radiation may be enhanced by exposure to
intense (500 T and above) magnetic fields (Miyakoshi et al, 1999; Walleczek et al,
1999) but not by weaker fields (Ansari and Hei, 2000). However, preliminary results
from an attempt to replicate these studies have not proved successful (Michael et al,
2004, and see Lloyd et al, in press). Although some data have suggested that magnetic
fields may increase both single and double strand DNA breaks in rat brain cells exposed
in vivo (Lai and Singh, 1997a), other studies have failed to find evidence for the
induction of DNA breaks or effects on DNA repair in human or animal cells exposed to
electric, magnetic or combined fields (Fairburn and ONeil, 1994; Cantoni et al, 1995,
1996; Jacobson-Kram et al, 1997; McNamee et al, 2000; Hone et al, 2003). Several
authors have used chromosomal damage as a measure of mutagenic potential. A few
studies provided some evidence for small effects with magnetic fields (Nordenson et al,
1994; Yaguchi et al, 1999), although other studies failed to find any effect with either
electric or magnetic fields (Antonopoulos et al, 1995; Galt et al, 1995; Jacobson-Kram
et al, 1997). Other authors have reported mainly negative results using the
micronucleus test (Scarfi et al, 1994; Paile et al, 1995; Lagroye and Poncy, 1997). An
increase in micronucleus formation was reported in a human squamous cell carcinoma
cell line but not in a human amniotic fluid cell line (Simko et al, 1998). In addition,
Cho and Chung (2003) reported that exposure of human lymphocytes to a 60 Hz
magnetic field at 0.8 mT increased the frequencies of micronuclei and sister chromatid
exchanges induced by a chemical tumour initiator. Field exposure alone caused no
cytogenetic changes.
71 Many other studies have investigated the potential of EMFs to act as promoting
agents for cancers using a variety of approaches. Several studies have addressed the
question as to whether magnetic fields have any direct effects on cell proliferation.
Results are mixed. Most studies using magnetic fields have reported no effect (Fiorani
et al, 1992; Cridland et al, 1996b, 1999; Reipert et al, 1996) or relatively small effects
53
(Fitzsimmons et al, 1992; Schimmelpfeng and Dertinger, 1993, 1997), although inhibition
of proliferation has been seen (Nindl et al, 1997). Positive effects have also been
reported (Antonopoulos et al, 1995), especially using pulsed electric fields (Sauer et al,
1997; Wartenberg et al, 1997). It has been suggested that EMFs may stimulate cellular
differentiation without affecting proliferation (Hisenkamp et al, 1997; Landry et al, 1997),
although this possibility has been challenged (Macleod and Collazo, 2000).
72 In contrast, a series of experiments suggests that 50 or 60 Hz magnetic fields may
exert effects on cellular proliferation under very specific circumstances. It has been
reported that exposure above a threshold of 0.21.2 T may cause a small, but
significant, inhibition of the antiproliferative action of melatonin (or tamoxifen) in
several human cancer cell lines, especially MCF-7 breast cancer cells (Liburdy et al,
1993; Harland and Liburdy, 1997; Afzal and Liburdy, 1998; Harland et al, 1998; Liburdy
and Levine, 1998; Blackman et al, 2001; Ishido et al, 2001). However, the robustness of
the original effect has been queried (NIEHS, 1998).
73 A number of studies have also investigated the possibility that EMFs may affect
intracellular calcium ion movements and thereby influence cell signalling pathways.
There is some evidence that these effects may be produced in human Jurkat cells using
magnetic fields of a few millitesla, but they appear to depend critically on the state of
the cells and their environment (Walleczek et al, 1994; Galvanovskis et al, 1996).
Changes in calcium have been reported using weaker fields of 40150 T (Lindstrm
et al, 1993, 1995a,b) but these results could not be replicated (Wey et al, 2000). Studies
using magnetic fields tuned to postulated resonant conditions have not found effects
(Prasad et al, 1991; Coulton and Barker, 1993; Lyle et al, 1997).
74 In addition, field dependent effects on other signalling pathways have been
reported using a variety of models and exposure conditions. The most convincing
evidence relates to changes on the SRC family kinase LYN (Uckun et al, 1995; Dibirdik
et al, 1998), but increased production of superoxide anion O
2
and -glucuronidase
(Khadir et al, 1999) and changes in PI3 kinase (Clejan et al, 1995; Santoro et al, 1997)
have been seen. In contrast, Miller et al (1999) found no effect on the signalling
pathways controlling the expression of the transcription factors NF-kB or AP-1.
75 Many studies have investigated possible field dependent effects on both general
and specific gene expression. While early studies reported short-term increases in
gross transcription (reviewed by NIEHS, 1998; AGNIR, 2001a), a more recent, well-
performed study using 2 mT, 60 Hz magnetic fields found no evidence of differential
expression of any of a very large number of genes (Balcer-Kubiczek et al, 1998).
76 Similarly, the results concerning the effects of EMFs on specific gene expression are
inconsistent. Generally, the magnitude of any changes seen in the more reliable studies
tend to be very small compared with those produced by known causative agents (such
as growth factors or serum), whereas some of the studies reporting larger changes can
be criticised for methodological flaws (Cridland et al, 1996a; AGNIR, 2001a). Some
studies suggest that magnetic fields of 100 T or more may affect the expression of
c-myc, c-fos, and other regulatory genes (Phillips et al, 1992; Gold et al, 1994; Goodman
et al, 1994; Lagroye and Poncy, 1998; Tuinstra et al, 1998) perhaps within frequency,
time and field strength windows. However, the results are difficult to interpret because
the studies have used a wide range of exposure conditions and cell types. Other studies
suggest effects on heat shock and stress proteins (Goodman et al, 1994; Pipkin et al,
54
1999; Junkersdorf et al, 2000; Miyakoshi et al, 2000b) again using intense fields. In
contrast, many studies have not reported any effects on c-myc expression and other
proto-oncogenes (Parker and Winters, 1992; Greene et al, 1993; Reipert et al, 1994;
Desjobert et al, 1995; Miyakoshi et al, 1996b; Harrison et al, 1997; Jahreis et al, 1998;
Loberg et al, 1999). In particular, two very-well-performed studies did not detect any field
dependent increases in gene expression (Lacy-Hulbert et al, 1995; Saffer and Thurston,
1995). Another well-conducted series of experiments found no field dependent effect
on the genes directly involved in cell cycle control (Dees et al, 1996).
77 Given the possibility that magnetic fields may affect intracellular calcium ion
movements, a few studies have sought to determine whether electric fields applied to
the cultures can affect gene expression. Modest changes were seen in c-myc, histone
H2B and hsp70 genes in HL-60 cells exposed at 0.33 V m
1
(Blank and Soo, 1992;
Goodman et al, 1994) and in c-fos expression in prostate tumour spheroids following
exposure to a single pulse at 500 V m
1
(Sauer et al, 1997).
78 Lastly, recent attempts to replicate or extend the results of Litovitz et al (1991)
regarding magnetic field induced stimulation of basal ornithine decarboxylase (ODC)
activity failed to find any evidence for effects on ODC expression (Azadniv et al, 1995;
Balcer-Kubiczek et al, 1996; Cress et al, 1999).
The carcinogenic potential of low frequency magnetic fields has been
investigated in laboratories using a wide range of models and endpoints.
From the results of this research there is no convincing evidence to suggest
that magnetic fields are directly genotoxic or that they can bring about the
transformation of cells in culture. They are therefore unlikely to initiate
carcinogenesis.
Some cellular studies report possible enhancement of genetic change caused by
known genotoxic agents; effects on intracellular signalling, especially calcium
flux; and effects on specific gene expression. Many of these positive effects
involve magnetic flux densities greater than 0.1 mT or induced electric field
strengths greater than about 1 mV m
1
.
However, results from different studies are often contradictory and there is an
almost total failure of independent replication of positive results. Those results
that report a positive effect tend to show only small changes, the biological
consequences of which are not clear.
The results of animal studies do not suggest that magnetic fields can cause
cancer or affect its development.
A large number of well-conducted, good quality studies have not shown any field
dependent effects using a range of tumour models, although the possibility that
exposure may affect chemically induced mammary tumours cannot be dismissed.
The lack of a natural animal model of the most common form of childhood
leukaemia, acute lymphoblastic leukaemia, and similarly of spontaneous brain
tumour, are potential shortcomings of these data.
Laboratory studies with volunteers do not suggest that melatonin rhythms are
affected by acute night-time exposure to magnetic fields. However, the
possibility that changes in melatonin physiology may occur in sensitive
subgroups, and perhaps following prolonged exposure, cannot be ruled out.
The carcinogenic potential of low frequency electric fields has not been
experimentally investigated and cannot be determined.
55
79 Interest has been expressed in the possibility that exposure to low frequency EMFs
may affect fertility, reproduction or prenatal and postnatal growth and development.
This issue has been addressed using both mammals and birds; however, the results
of studies using mammals are more relevant to possible effects on humans. Several
comprehensive reviews are available (Brent et al, 1993; AGNIR, 1994; Juutilainen and
Lang, 1997; Huuskonen et al, 1998a; NIEHS, 1998; Brent, 1999; IARC, 2002; Juutilainen,
2003; ICNIRP, 2004).
Animal studies
80 No recent studies appear to have explored the reproductive and developmental
effects of low frequency electric fields. Earlier studies using rats, mice and miniature
swine (reviewed by AGNIR, 1994; NIEHS, 1998; IARC, 2002; ICNIRP, 2004) indicated that
even intense and chronic exposure over several generations caused no consistent
adverse effects, once the confounding effects of spark discharge had been eliminated.
81 The possible effects of magnetic fields have received much attention. One recent
study assessed the effects of a range of 60 Hz fields on fertility and reproductive
performance in rats over three generations (Ryan et al, 1999). No field dependent
toxicity was observed; fetal viability and body weight were similar in all groups,
and there were no differences between test and control groups in any measure of
reproductive performance (number of litters per breeding pair, percentage of fertile
pairs, latency to parturition, litter size or sex ratio). Similarly, medium-term exposure of
mice to 50 Hz magnetic fields at 25 T before mating produced no effects on fertility
(Elbetieha et al, 2002), although fertility was reduced in rats exposed under the same
conditions (Al-Akhras et al, 2001). Also a single 4-hour exposure of hybrid male mice to
a magnetic field at 1.7 mT was reported to decrease numbers of elongated spermatids
at 28 days after exposure (De Vita et al, 1995). No effects were observed at earlier or
later time points, or using an exposure time of 2 hours.
82 Other recent studies using rodents have indicated that exposure to sinusoidal
power frequency magnetic fields or saw-tooth fields for either a part or the whole
of gestation caused no obvious adverse effects. Early exposure of rats or mice
to 50 Hz fields was without consistent effect on embryo implantation and vitality
(Huuskonen et al, 2001a,b). However, some differences in oestrogen-receptor and
progesterone-receptor densities at some time points were observed in the rat uterus.
Several well-designed studies noted an increase in the incidence of minor skeletal
variants following in utero exposure to power frequency fields up to 30 mT or saw-
tooth fields at up to 15 T (peak-to-peak) (Huuskonen et al, 1993, 1998b; Kowalczuk
et al, 1994; Mevissen et al, 1994; Ryan et al, 2000), although other studies have not
reported this effect (Rommereim et al, 1996; Ryan et al, 1996). In these studies overall,
exposure was without any significant detrimental effect on fetal development or
maternal toxicity.
83 Although results obtained using avian species are not useful for predicting
reproductive effects in humans (Brent, 1999), the effects of exposure to pulsed and
sinusoidal magnetic fields have been investigated using chicken and quail embryos
(eggs). As with earlier studies that were broadly supportive of a field induced increase
in abnormalities (see AGNIR, 1994; ICNIRP, 2004), some recent studies have reported
56
field dependent effects (Terol and Panchon, 1995; Farrell et al, 1997), whereas other
studies have not (Cox et al, 1993). It has also been reported that 50 Hz magnetic fields
at 10 mT may modify the embryotoxic effects of x-rays and chemical teratogens
(Pafkov and Jerbek, 1994; Pafkov et al, 1996). Exposure to the magnetic field before
treatment reduced embryonic death and malformations, while embryotoxicity was
increased when the magnetic field followed the x-ray exposure. Finally, a few recent
studies have investigated the effects of magnetic fields on other non-mammalian
embryos. No malformations were seen using zebrafish embryos (Skauli et al, 2000) and
no consistent changes were reported using Drosophila (Nguyen et al, 1995; Graham
et al, 2000).
84 Behavioural teratology represents a sensitive approach to assess the impact of
potential neurotoxic agents (Lovely, 1988). A number of subtle effects on develop-
mental indices and landmarks have been reported in different studies, but, overall, no
evidence to suggest a consistent pattern of deficits is apparent in recent studies using
rats or mice exposed to magnetic fields (Sakamoto et al, 1993; Sienkiewicz et al, 1994,
1996a). Prenatal exposure to combined electric and magnetic fields had no consistent
effect on somatic growth and cerebral development in rats (Yu et al, 1993), whereas
postnatal exposure was reported to cause transient changes in brain weight and in the
concentrations of DNA and RNA in the cerebellum (Gona et al, 1993).
There is only weak evidence to suggest that low frequency electric or magnetic
fields can adversely affect fertility, reproduction or development in mammals.
Subtle changes in skeletal anomalies and on postnatal landmarks have sometimes
been observed but there is little consistency in the data overall.
85 The brain and nervous systems function by using electrical signals, and may
therefore be considered particularly vulnerable to low frequency EMFs and the resultant
induced electric currents. Substantial numbers of laboratory experiments with volunteers
and animals have investigated the possible consequences of exposure to weak EMFs on
various aspects of nervous system function, including cognitive, behavioural and neuro-
endocrine changes. These studies have been reviewed by NRC (1997), NIEHS (1998),
IARC (2002) and ICNIRP (2004). In general, very few effects have been established, and
even the more robust field induced responses tend to be small in magnitude, subtle and
transitory (Sienkiewicz et al, 1993; Crasson et al, 1999).
Volunteer studies
86 Studies of people have investigated a wide range of possible field induced effects on
brain function and behaviour. These include effects on cognition, the electroencephalo-
gram (EEG), as well as effects on sleep, and the control of heart rate. The possibilities of
electrical hypersensitivity and field induced effects on mood have also been investigated.
Effects on melatonin rhythms are considered in paragraphs 4978 on cancer. The
effects induced by intense exposure to EMFs above the threshold for perception have
been considered in paragraphs 3342 on acute electrophysiological responses.
57
87 Cognitive studies Despite the potential importance of field induced effects on
attention, vigilance, memory and other information processing functions, relatively few
studies have looked for evidence of changes in cognitive ability during or after
exposure to low frequency EMFs. These have been reviewed by NIEHS (1998) and
Cook et al (2002). While few field dependent changes have been observed, it is
important to consider that this type of study may be particularly susceptible to various
environmental and individual factors which may increase the variance of the
experimental endpoint and decrease the power to detect a small effect. This may be
particularly important, since any field dependent effects are likely to be small with fields
at environmental levels (Sienkiewicz et al, 1993; Whittington et al, 1996).
88 The effects of acute exposure to magnetic fields on simple and choice reaction time
have been investigated in several recent studies using a wide range of magnetic flux
densities (20 T 1.26 mT) and experimental conditions. Most studies have not found
any field dependent effects (Gamberale et al, 1989; Cook et al, 1992; Lyskov et al,
1993a,b; Podd et al, 1995, 2002; Preece et al, 1998), although modest effects on speed
(Graham et al, 1994; Whittington et al, 1996; Crasson et al, 1999) and accuracy during
task performance (Cook et al, 1992; Kazantzis et al, 1996; Preece et al, 1998) have been
reported. These data also suggest that effects may depend on the difficulty of the task
(Kazantzis et al, 1996; Whittington et al, 1996) and that exposure may attenuate the usual
practice effects on reaction time (Lyskov et al, 1993a,b; Stollery, 1986).
89 A few studies have reported subtle field dependent changes in other cognitive
functions, including memory and attention (see also Cook et al, 2002). Using a battery of
neuropsychological tests, Preece et al (1998) found that exposure to a 50 Hz magnetic
field at 0.6 mT decreased accuracy in the performance of a numerical working memory
task and decreased sensitivity in the performance of a word recognition task. Similarly,
Keetley et al (2001) investigated the effects of exposure to 28 T, 50 Hz fields using
a series of cognitive tests. A significant decrease in performance was seen with
one working memory task (the trail-making test, part B) that involves visual-motor
tracking and information processing within the prefrontal and parietal areas of the
cortex. Podd et al (2002) reported delayed deficits in the performance of a recognition
memory task following exposure to a 50 Hz field at 100 T. Trimmel and Schweiger
(1998) investigated the effects of acute exposure to 50 Hz magnetic fields at 1 mT. The
fields were produced using a power transformer, and volunteers were exposed in the
presence of a 45 dB sound pressure level noise. Compared with a no-field, no-noise
condition and noise alone (generated using a tape recording) significant reductions in
visual attention, perception and verbal memory performance were observed during
field exposure. The presence of the noise during exposure, however, complicates
interpretation of this study.
90 Electrical activity of the brain Since the first suggestion that occupational
exposure to EMFs resulted in clinical changes in the electroencephalogram (EEG)
was published in 1966, various studies have investigated if exposure to magnetic fields
can affect the electrical activity of the brain. Such methods can provide useful
diagnostic information regarding the functional state of the brain, not only from
recordings of the spontaneous activity at rest but also from recording the sensory
58
functions and subsequent cognitive processes evoked in response to specific stimuli
(evoked or event-related potentials). Nevertheless, neurophysiological studies using
magnetic fields need to be performed with much care and attention since they can
be prone to many potential sources of error and artefact (NIEHS, 1998). Changes in
arousal and attention of volunteers, in particular, can substantially affect the outcome of
these studies.
91 Various studies have investigated the effects of magnetic fields on brain activity by
analysing the spectral power of the main frequency bands of the EEG (Silny, 1986;
Gamberale et al, 1989; Bell et al, 1991, 1992, 1994a,b; Lyskov et al, 1993a; Marino et al,
1996; Schienle et al, 1996; Heusser et al, 1997). These studies have used a wide variety
of experimental designs and exposure conditions, as well as healthy volunteers and
patients with neurological conditions, and thus are difficult to compare and evaluate.
Despite some scattered field dependent changes, most notably in the alpha frequency
band, and with intermittent exposure perhaps more effective than continuous
exposure, these studies have produced inconsistent and sometimes contradictory
results. Nevertheless these possibilities cannot be dismissed, although replicable field
dependent effects seem unlikely.
92 Other studies have investigated the effects of magnetic fields and combined
electric and magnetic fields on evoked potentials within the EEG waveform. There are
some differences between studies, but generally, the early components of the evoked
response corresponding to sensory function do not appear affected by exposure
(Lyskov et al, 1993b; Graham et al, 1999). In contrast, large and sustained changes on a
later component of the waveform (N100) representing stimulus detection may be
engendered by intense exposure at 60 mT (Silny, 1984, 1985, 1986), with lesser effects
occurring using fields at 1.26 mT (Lyskov et al, 1993b), and nothing below 30 T
(Graham et al, 1999). Finally, exposure during the performance of some discrimination
and attention tasks may affect the late major components of the EEG (around P300)
which are believed to reflect cognitive processes involved with stimulus evaluation and
decision making (Cook et al, 1992; Graham et al, 1994; Crasson et al, 1999; see also Sartucci
et al, 1997). There also is some evidence that task difficulty and field intermittency may
be important experimental variables. However, all these subtle effects are not well
defined, and some inconsistencies between studies require additional investigation
and explanation.
93 Sleep The possibility that EMFs may exert a detrimental effect on sleep has been
examined in two studies. Using the EEG to assess sleep parameters, kerstedt et al
(1999) reported that continuous exposure of healthy volunteers to a 50 Hz at 1 T at
night caused slight disturbances in sleep. In this study, total sleep time, sleep efficiency,
slow-wave sleep (stage III and IV), and slow wave activity were significantly reduced by
exposure, as was subjective depth of sleep. Graham and Cook (1999) reported that
intermittent, but not continuous, exposure to 60 Hz, 28 T magnetic fields at night
resulted in less total sleep time, reduced sleep efficiency, increased time in stage II
sleep, decreased time in rapid eye movement (REM) sleep, and increased latency to
first REM period. Consistent with a pattern of poor and broken sleep, volunteers
exposed to the intermittent field also reported sleeping less well and feeling less rested
in the morning.
59
94 Hypersensitivity and mood states It has been suggested that some individuals
display increased sensitivity to EMFs. People self-reporting hypersensitivity may
experience a wide range of severe and debilitating symptoms, including sleep
disturbances, general fatigue, difficulty in concentrating, dizziness, and eyestrain. In
extreme forms, everyday living may become problematical. A number of skin problems
such as eczema and sensations of itching and burning have also been reported,
especially on the face, and, although there may be no specific symptom profile (see
Hillert et al, 2002), increased sensitivity to chemical and other factors often occurs
(Levallois et al, 2002). The responses to EMFs are reported to occur at field strengths
orders of magnitude below those required for conventional perception of the field
(Silny, 1999). Bergqvist and Vogel (1997), Levallois (2002) and ICNIRP (2004) have
reviewed these data.
95 In contrast to anecdotal reports, the evidence from double-blind provocation
studies (Andersson et al, 1996; Arnetz, 1997; Arnetz et al, 1997; Sandstrm et al, 1997;
Flodin et al, 2000; Lonne-Rahm et al, 2000; Lyskov et al, 2001a) indicates that neither
healthy volunteers nor self-reporting hypersensitives can reliably distinguish field
exposure from sham-exposure. In addition, subjective symptoms and circulating levels
of stress-related hormones and inflammatory mediators could not be related to field
exposure. Not all studies dismiss the possibility, however. Two studies have reported
weak positive field discrimination (Rea et al, 1991; Mueller et al, 2002) and another study
reported subtle differences in heart rate and electrodermal activity between normal
and hypersensitive volunteers (Lyskov et al, 2001b). There is some morphological
evidence to suggest that the numbers and distribution of mast cells in the dermis of the
skin on the face may be increased in individuals displaying hypersensitive reactions
(Johansson et al, 1994, 1996; Gangi and Johansson, 2000). Increased responsiveness
was attributed to changes in the expression of histamine and somatostatin and other
inflammatory peptides. Similar effects in the dermis have also been reported following
provocation tests to VDU-type fields in normal, healthy volunteers (Johansson et al,
2001). The possibility that hypersensitivity may be associated with enhanced ability to
perceive electric currents has been suggested by Leitgeb and Schrttner (2003).
96 The possible impact of EMFs on mood and arousal has also been assessed in
double-blind studies in which volunteers completed mood checklists before and after
exposure. No field dependent effects have been reported using a range of field
conditions (Maresh et al, 1988; Cook et al, 1992; Graham et al, 1994; Selmaoui et al, 1997;
Crasson et al, 1999). In contrast, Stollery (1986) reported decreased arousal in one of
two participating groups of subjects when mild (500 A) 50 Hz electric current was
passed through the head, upper arms, and feet. This was done to simulate the internal
electric fields generated by exposure to an external electric field strength of 36 kV m
1
.
Also Stevens (2001) reported that exposure to a 20 Hz, 50 T magnetic field increased
positive affective responses displayed to visual stimuli compared with sham-exposure.
Arousal, as measured by skin conductance, gave variable results.
97 Effects on cardiac activity Studies of the effects of EMFs on field induced changes
in autonomic control of the heart have produced inconclusive results. Although EMFs
appear to have no effect on the electrical activity of the heart (Silny, 1981), a series of
studies from the US Midwest Research Institute have suggested a small (35 beats per
60
minute, bpm), but significant reduction in mean heart rate may occur during and
immediately after exposure to 60 Hz electric and magnetic fields at 9 kV m
1
and 20 T
(Cook et al, 1992; Graham et al, 1994). This response did not occur with exposure
to stronger or weaker fields, and was reduced if the subject was mentally alert, or
following fairly hard exercise when heart rate was elevated (Maresh et al, 1988; Graham
et al, 1990). There were no other consistent effects on a wide battery of sensory and
perceptual tasks. NIEHS (1998) commented that the magnitude of the observed effect
was comparatively small and the biological mechanism underlying the phenomenon
had not been identified. Based on an analysis of cardiac cellular electrophysiology,
Cooper et al (2003) concluded that it was highly unlikely that exposure to ELF fields at
environmental levels could cause direct effects on the heart.
98 In independent studies, no effects on heart rate or blood pressure were seen during
day-time exposure to 50 Hz fields at 0.110 kV m
1
and 115 T

for up to a few hours
(Korpinen et al, 1993; Korpinen and Partanen, 1994a,b, 1996) or at 100 T for 9 minutes
(Whittington et al, 1996).
99 More recently, a change in heart rate variability (HRV) in healthy young men was
found during night-time exposure to an intermittent 60 Hz magnetic field at 20 T
(Sastre et al, 1998) or a 16 Hz field at 28 T (Sastre et al, 2000). HRV results from the
action of various neuronal and cardiovascular reflexes and is correlated with sleep
stage. Continuous exposure or exposure at 1 T had no effect on HRV. Similar responses
were reported in older men, but not women, exposed to 60 Hz fields at 28 T (Graham
et al, 2000b). However, no effects were reported in two subsequent studies using
intermittent exposure to 60 Hz fields at either 28 T (Graham et al, 2000c) or 127 T
(Graham et al, 2000d).
100 In order to clarify these data, a pooled analysis of these studies was carried out
(Graham et al, 2000e). This indicated that the changes in HRV were observed only
in studies where blood sampling had taken place using an implanted catheter. It was
suggested that these procedures might have altered the arousal of the subjects, which
disturbed their sleep and thus affected HRV. This analysis also failed to identify either
magnetic flux density or exposure pattern as a main factor.
Animal studies
101 Various animal models have been used to investigate possible field induced effects
on brain function and behaviour. These include effects on neurotransmitter levels,
electrical activity, field detection and the performance of learned tasks. Other
studies have investigated effects on melatonin rhythms and these are considered in
paragraphs 4978 on cancer. Overall, a few field dependent responses have been
tentatively identified but even the most consistent effects appear small in magnitude
and transient in nature.
102 Neurotransmitter function A number of studies have investigated the potential of
low frequency fields to affect the levels of different neurotransmitters within various
regions of the brain. These data have been most recently reviewed by ICNIRP (2004).
103 Early studies reported effects of both acute and chronic exposure to intense
electric fields on catecholamine and amino acid neurotransmitter levels in some parts
of the brain, but values often stayed within the normal range.
61
104 More recently, Margonato et al (1995) reported that chronic exposure to 50 Hz
magnetic fields at 5 T had no effect on levels of norepinephrine, dopamine and its
major metabolites, or 5-hydroxytrytamine or its major metabolite in the striatum,
hypothalamus, hippocampus or cerebellum. In a companion study, Zecca et al (1998)
reported a similar lack of effects following chronic exposure to combined electric and
magnetic fields at either 1 kV m
1
and 5 T or 5 kV m
1
and 100 T. However, intensity-
dependent changes were reported in the opioid system in the frontal cortex, parietal
cortex and hippocampus, but not in other brain areas investigated.
105 Other studies have also investigated field dependent changes in opioid-related
physiology. In a series of related experiments, Kavaliers, Prato and colleagues have
indicated that various types of low frequency magnetic field may affect the endogenous
opioid systems and modulate the response of animals to the analgesic effects of
injected opiates such as morphine (reviewed by Kavaliers et al, 1994). These responses
are complex, and magnetic fields appear to have a differential effect on the functions of
different opioid receptor subtypes (Kavaliers and Ossenkopp, 1991). There is also
evidence that the mechanism for these effects may involve changes in calcium ion
channel function (Kavaliers et al, 1998a) protein kinase C (Kavaliers et al, 1991) and
nitric oxide (NO) production and NO synthase activity (Kavaliers et al, 1998b). Recent
studies with land snails suggest the field induced analgesic effects depend on the
relative direction of the applied fields (Prato et al, 1995) as well as the presence of light
(Prato et al, 1996, 1997, 2000).
106 In another series of experiments, it was reported that the acute exposure of rats to a
60 Hz magnetic field at 0.75 mT decreased activity in the cholinergic pathways in the
frontal cortex and hippocampus (Lai et al, 1993). These effects were blocked by
naltrexone, but not by naloxone, which was taken as evidence that magnetic fields
affected endogenous opioids only within the CNS. Further studies showed the changes
in cholinergic activity appeared to be mediated by activation of endogenous opioids
(Lai and Carino, 1998). There also appears to be some interaction between exposure
duration and field intensity, such that longer exposures (3 hours) at lower intensity
fields (0.05 mT) could induce changes in cholinergic activity (Lai and Carino, 1999).
107 Several authors have investigated the possibility that prior field exposure might
alter electrical activity in the brain and thus influence the onset or severity of epileptic
seizures induced in rats by electrical or chemical stimulation or by a loud noise.
Generally, the effects that have been reported are consistent with a reduction in
susceptibility to epileptic seizure but are inconsistent between different studies
(ICNIRP, 2004). Recently, Potschka et al (1998) reported that chronic exposure to
50 Hz magnetic fields of 100 T exerted weak inhibitory effects on some seizure
parameters of the kindling model with exposed rats showing a higher threshold for
generalised seizures.
108 Electrical activity A number of animal studies have investigated if acute exposure
to low frequency electric and magnetic fields can affect brain electrical activity as
measured as the EEG or as evoked potentials following presentation of a sensory stimulus
(reviewed by Sienkiewicz et al, 1991; NIEHS, 1998). The results of these studies are
somewhat mixed and difficult to interpret, but none suggests any obvious adverse
health effect (ICNIRP, 2004). Some of these studies may have been confounded by
62
experimental design or artefact it has long been recognised that recording potentials
through electrodes attached to the skull is liable to artefact in the presence of EMFs.
Two more recent studies reported significant EEG changes in rabbits during magnetic
field exposure (Bell et al, 1992) and in rats following magnetic field exposure (Lyskov
et al, 1993a). However, the possibility of artefact or of false positive results complicates
interpretation of both studies (NIEHS, 1998).
109 Field detection It is known that animals can detect the presence of low frequency
electric fields, possibly as a result of surface charge effects (Weigel et al, 1987; although
see Stell et al, 1993). Using appropriate behavioural techniques, a number of studies
using rats (reviewed by NRC, 1997; NIEHS, 1998) indicate that the threshold for field
detection is about 313 kV m
1
. Detection thresholds are similar in a variety of other
species, with thresholds reported at 512 kV m
1
in

baboons (Orr et al, 1995a), 25 kV m
1
in mice, and 35 kV m
1
in birds and miniature swine.
110 Detection thresholds for magnetic fields in animals are less clear and show greater
variability than those for electric fields (ICNIRP, 2004). Using a conditioned suppression
paradigm, Smith et al (1994) reported that rats were able to detect ELF magnetic fields
as low as 200 T, although the validity of this result has been questioned by Stern and
Justensen (1995).
111 Arousal and aversion Initial exposure to power frequency electric fields in excess
of detection thresholds may cause transient arousal and stress responses in rodents
and non-human primates (IARC, 2002). These responses appear to habituate quickly
following prolonged exposure. There is also some evidence that animals may avoid
exposure to intense electric fields, although the strength of this unconditioned
response is too weak to elicit aversive behaviours (Creim et al, 1984; Rogers et al,
1995a). Thus electric fields at levels of up to 65 kV m
1
are not considered to be highly
aversive to non-human primates.
112 Exposure of baboons to combined 60 Hz electric and magnetic fields at 6 kV m
1
and 50 T or at 30 kV m
1
and 100 T did not produce significant changes in social
behaviour (Coehlo et al, 1995) previously seen to be affected by exposure to electric
fields alone (Coehlo et al, 1991; Easley et al, 1991). While it is possible that the magnetic
field may have modulated the electric field induced responses, it was considered that
some of the animals in the later experiment may have become desensitised by prior
subthreshold electric field exposure.
113 Acute exposure to power frequency magnetic fields at up to a few millitesla does
not appear to induce aversive behaviour (Lovely et al, 1992; IARC, 2002). Such results
suggest that the arousal responses observed using electric fields are not caused by
field induced internal electric fields, and may be attributed to body-surface interactions.
One study reported that long-term, intermittent exposure to 50 Hz at 18 mT reduced
behavioural responses (irritability) induced by tactile and somatosensory stimuli in
rats (Trzeciak et al, 1993). Another study reported that exposure to specific combinations
of static and low frequency fields affected exploratory behaviour in rats (Zhadin et al,
1999). Exposure to conditions corresponding to the putative cyclotron resonance for
calcium ions reduced this behaviour, and exposure to such conditions for magnesium
ions increased it.
63
114 Learned tasks Early studies with macaque monkeys reported that exposure to
low frequency electric fields at well below detection thresholds may affect operant
performance see IARC (2002). However, more recent, well-conducted studies
using baboons found exposure to 60 Hz electric fields at 30 and 60 kV m
1
had no
sustained effect on the performance of two operant schedules (Rogers et al, 1995a,b),
although initial exposure may contribute towards producing a temporary interruption
in responding.
115 Similarly, studies using 60 Hz electric and magnetic fields (Orr et al, 1995b) indicated
that combined exposure to 6 kV m
1
and 50 T or to 30 kV m
1
and 100 T had no effect
on operant performance on a delayed match-to-sample task in baboons. This result is
generally consistent with earlier results from other research groups using non-human
primates (reviewed by Sienkiewicz et al, 1991; NIEHS, 1998). However, one study using
rats (Salzinger et al, 1990) suggested exposure to 60 Hz fields of 30 kV m
1
and 100 T
may exert subtle effects on performance that depend on the time of testing within the
lightdark cycle.
116 Several recent studies using the Morris water maze or radial arm maze have
investigated the effects of magnetic fields on spatial memory and place learning. These
studies provide evidence that exposure of rats, mice or voles to power frequency fields
at 100 T and above may modulate task performance (Kavaliers et al, 1993, 1996; Lai,
1996; Lai et al, 1998; Sienkiewicz et al, 1998a,b). Exposure to complex pulsed magnetic
fields may also affect performance (Thomas and Persinger, 1997; McKay and Persinger,
2000). In addition, much evidence has accrued over the last decade (but is still only
available from presentations at scientific meetings) that effects may also occur using
specific combinations of static and time-varying fields (see Sienkiewicz et al, 1998b).
The mechanism for these effects has been partly explored and the changes in
behaviour have been attributed to decreases in cholinergic functions caused by field
induced changes in endogenous opioid activity (Lai, 1996; Thomas and Persinger, 1997;
Lai and Carino, 1998). How the magnetic field may have activated the endogenous
opioid systems is not known.
117 The conditions to produce any of these phenomena are not well defined, and both
deficits and enhancements in performance have been observed and one study did not
report any field dependent effects (Sienkiewicz et al, 1996b). It is feasible that these
differences in outcome may depend on experimental or other variables including the
timing and duration of exposure relative to learning (McKay and Persinger, 2000;
Sienkiewicz et al, 2001). While these results suggest that the neural representations or
processes underlying the performance of spatial memory tasks may be vulnerable to
the effects of magnetic fields, some part of the observed outcome may be attributable
to changes in arousal (IARC, 2002) or in motivation (Thomas and Persinger, 1997).
Nevertheless, the transient nature and small magnitudes of the responses do not
suggest an obvious deleterious effect.
118 Two studies using rodents have investigated the effects of magnetic fields on
recognition memory. Using the field conditions putatively identified as having an acute
effect of spatial memory, Sienkiewicz et al (2001) found no effects on the performance
of an object recognition task by mice. Animals were exposed for 45 minutes to a 50 Hz
field at 7.5, 75 or 750 T. However, Mostafa et al (2002) reported that discrimination
64
between familiar and novel objects was impaired in rats following chronic exposure at
200 T for 2 weeks.
119 Stern et al (1996) failed to replicate the results of earlier studies (Thomas et al, 1986;
Liboff et al, 1989) suggesting exposure to combined static and power frequency
magnetic fields arranged to simulate the cyclotron resonance conditions for lithium
ions significantly impaired operant performance. The earlier positive results were
attributed to possible confounding.
The possibility that exposure to low frequency EMFs may affect neurobehavioral
function has been explored in humans and animal models using a range of
exposure conditions. Few robust effects have been established.
Studies with volunteers exposed to low intensity magnetic fields have produced
only evidence of subtle and transitory effects. Generally, the conditions
necessary to elicit these responses are not well defined at present.
There is some evidence suggesting field dependent effects on reaction time and
reduced accuracy in performance of some cognitive tasks, which is supported by
the results of studies on the EEG.
Other possible field dependent changes are less well defined. Studies investigating
effects on sleep quality have reported inconsistent results. It is possible that these
differences may be attributable in part to differences in design between studies.
Mild changes in cardiac activity have been reported from one laboratory, but
only under highly specific exposure conditions. These changes have not been
independently replicated.
The phenomenon of electromagnetic hypersensitivity has been reported in some
people. However, the suggestion from double blind trials is that the reported
symptoms are unrelated to EMF exposure.
There is convincing evidence that power frequency electric fields can be
detected by animals, most likely as a result of surface charge effects. Exposure
above the detection threshold of about 515 kV m
1
may induce transient
arousal or mild stress, but fields are not considered aversive, even at high
field strengths.
Other possible field dependent changes in animals are less well defined and
generally laboratory studies have produced evidence of only subtle and
transitory effects.
There is evidence that exposure to magnetic fields may modulate the functions
of the opioid and cholinergic systems, and this is supported by the results of
studies investigating effects on analgesia and on the acquisition and
performance of spatial memory tasks.
120 The perceptual and sometimes painful effects of surface charge are well understood.
Laboratory evidence shows the distribution of sensitivity in volunteers, but quantitative
published data are lacking on the occurrence and severity of these effects in workers
and members of the public in the UK.
121 Thresholds for peripheral nerve stimulation by induced electric fields are well
understood; data are accumulating concerning brain tissue stimulation thresholds.
The effects of weak electric fields on nervous tissue, at levels below the threshold
65
for direct stimulation, have been explored in vitro but their possible consequences
in vivo are less well understood. It may be expected that functions of electrically
excitable nerve and muscle tissue that show network behaviour, particularly the
CNS, will be altered by relatively weak fields, but these probable effects need further
experimental investigation.
122 Recommendations on limiting exposure to low frequency EMFs can be based on
an extrapolation of phosphene and other physiological data concerning brain tissue
electrophysiology. Magnetic and electric phosphenes clearly result from interaction of
the induced field with electrically sensitive cells that comprise the neuronal circuitry
of the retina; the threshold and frequency response has been studied in several
laboratories. The retinal circuitry has been taken as a sensitive model of neuronal
circuitry in other parts of the brain. However, the effects of weak electric fields on, for
example, cognitive processes, have not been clearly demonstrated in vivo, nor have
thresholds and their variation with frequency been clearly defined.
123 The results of many of the other studies suggesting that low level, low frequency
EMFs may induce adverse biological responses are beset with uncertainty over their
interpretation, limiting their practical usefulness as a basis for establishing exposure
standards. This uncertainty originates from several sources. Firstly, many of these
studies were performed with inadequate scientific rigour, namely, poor experimental
design, insufficient control of potential artefacts, and inadequate dosimetry and
metrology. Other studies may have inappropriate or incorrect data analysis or have
insufficient statistical power to detect small effects.
124 Another source of uncertainty results from the inconsistency in reported effects
(both within and between laboratories) and from the general lack of attempts to
confirm or replicate reported results. This is as true for studies reporting the absence
of effects as for those reporting the presence of field dependent effects. Many of the
experimental data consist of isolated observations where there have been few attempts
to integrate results between different experiments and experimental models.
125 The view that some responses may occur only under specific conditions of exposure
or are dependent on ill-defined biological factors makes broad generalisations difficult, if
not impossible, to draw. There have been suggestions that the time-weighted, average
field strength, used in many studies as a measure of exposure, is not truly representative
of the effective exposure metric. Some studies have suggested the existence of
frequency and amplitude response windows, and that modulation frequency, exposure
pattern and duration may also influence the experimental outcome. These uncertainties
stem from the absence of a plausible biophysical mechanism of interaction on which an
appropriate exposure metric could be based.
126 Other uncertainties result from an incomplete understanding of the distribution of
sensitivity to EMF effects, particularly of weak induced electric fields, amongst the
population. Specific issues are age-related differences and those resulting from medical
conditions or treatment. In addition, there remains some uncertainty about possible
effects on circadian and other biological rhythms and the implication any effect might
have for human health further study is required. Finally, there is the acknowledged
uncertainty of extrapolating results to humans from data obtained using various animal
species and in vitro experimental models.
66
Summary
127 With regard to effects of surface charge induced by exposure to low frequency
electric fields, exposure to fields less than 5 kV m
1
will have a low risk of painful
discharge from a person to ground. Thresholds for the discharge from an object
through a grounded person depend on the size of the object and therefore require
specific assessment. In environments where appropriate control is possible, the risk
of painful discharge can be minimised by engineering or administrative controls
(including training).
128 The primary means by which electric fields and currents induced in the body by
exposure to external fields interact with biological tissue is through voltage-gated ion
channels situated in cell membranes. The effect is to alter the flux of certain ions, and
the electric potential difference, across the cell membrane leading to subsequent
biological responses. The most sensitive tissues are those comprising interacting
networks of electrically excitable tissue, such as the central, autonomic and enteric
nervous systems. Thresholds of between about 100 and 1000 mV m
1
have been
determined in CNS tissue in vitro. The neural circuitry of the retina is taken as a good
model for induced electric field effects on CNS neuronal circuitry in general.
Thresholds of around 1060 mV m
1
in the extracellular fluid of the retina have been
calculated for the phosphene response of volunteers, but there is considerable
uncertainty associated with these values, and their extrapolation to values appropriate
for the whole tissue, as used by dosimetric models, is complex. These uncertainties
can only be resolved through further experimental and dosimetric investigation.
The threshold for effects in central, autonomic and enteric nervous system tissue
is taken to be 100 mV m
1
, possibly as low as 10 mV m
1
. This spans the range of
values identified by the ad hoc expert group on weak electric fields (Appendix A)
for normal and particularly sensitive individuals. The heart, other muscle tissue and
non-excitable tissues with voltage-sensitive ion channels are expected to show a
lower sensitivity.
129 Sensitivity to electric fields induced within the body will vary within the population.
People who are particularly sensitive will include those with epilepsy, a family history of
seizure, or those using tricyclic anti-depressants, neuroleptic agents and other drugs
that lower seizure threshold. The developing nervous system in utero, and in neonates
and young children, may also be considered more sensitive.
130 The frequency response of these effects is unknown. Ion channel kinetics suggest
that the thresholds may be constant over the frequency range 10 Hz 1 kHz and would
apply to a minimum of 1000 interacting cells, which would occupy approximately
1 mm
3
in CNS tissue.
131 In addition, a number of studies suggest that low frequency EMFs, particularly
magnetic fields in excess of about 100 T, may induce a variety of subtle responses
in biological systems, as well as those attributable to the effects of either surface charge
or the induced electric field. However, the pattern of reported responses is diffuse
and inconsistent. Furthermore, many tend to be small in magnitude and often fail to be
replicated. Overall, none is considered sufficient to provide a coherent framework on
which to base restrictions for human exposures.
67
A critical evaluation has been carried out of biological studies relevant to the
assessment of possible adverse health effects of exposure to low frequency
electric and magnetic fields. With regard to electric fields and currents induced
in the body by these external fields, the most plausible and coherent set of
data from which guidance can be developed concerns weak electric field
interactions in the CNS and other excitable tissues. In addition, these data show
doseresponse relationships. A cautious approach has been used to derive
thresholds for adverse health effects.
Other studies reviewed lack plausibility, coherence and consistency precluding a
positive role in this process.
Thresholds for adverse health effects of the electric fields and currents induced
in the body by exposure to low frequency electric and magnetic fields on the
central, autonomic and enteric nervous systems are judged to be at induced
electric field strengths in the extracellular fluid of around 100 mV m
1
and
possibly as low as 10 mV m
1
. However, there is considerable uncertainty
associated with these values. The frequency response of these effects is not, at
present, clear. Ion channel kinetics suggest that they may occur over the
frequency range 10 Hz 1 kHz and in a minimum of 1000 interacting cells, which
would occupy approximately 1 mm
3
in tissue of the CNS.
People with epilepsy, a family history of seizure, or those using tricyclic
anti-depressants, neuroleptic agents and other drugs that lower seizure threshold
are likely be more sensitive to weak electric field effects than people without
these conditions. The developing nervous system in utero, and in neonates and
young children is also considered more sensitive.
With regard to the effects of surface electric charge, exposure to a power
frequency electric field of less than 5 kV m
1
should not result in painful
discharge from a person to ground. Thresholds for the discharge from an object
through a grounded person depend on the size of the object and therefore
require specific assessment. Exposure to electric fields of less than 15 kV m
1
should not result in unpleasant direct perception effects in people.
DOSIMETRY
and the fields induced within the body. This gives guidance on the choice of reference
levels in relation to basic restrictions.
133 Exposure guidelines provide basic restrictions on induced current density to
prevent effects on CNS functions for frequencies up to 10 MHz.
134 The state-of-the-art approach to deriving reference levels is to solve Maxwells
equations numerically, in fine resolution, anatomically realistic models of the body.
Subsequent sections describe the calculations of induced electric fields and current
densities from low frequency magnetic and electric fields.
Induced current densities from low frequency magnetic fields
Computational methods
135 The first method applied to anatomically complex voxel models of the human body
was the impedance method (Gandhi et al, 1984; Orcutt and Gandhi, 1988; Gandhi and
Chen, 1992; Xi et al, 1994). The target body is split into cuboid cells or voxels, which
are then further differentiated into a three-dimensional network of impedances. The
68
time-varying magnetic field impresses a voltage around the closed loop of each face. A
system of coupled equations for the loop currents on the orthogonal faces of the cells
results and can be solved iteratively. The electric fields along the edges of the cuboid
cell are then obtained to produce an average value in the cell and thence a value for the
current density. More recently the Scalar Potential Finite Difference (SPFD) method
has been introduced (Dawson et al, 1996; Dawson and Stuchly, 1997). This method
incorporates the applied magnetic field source as a vector potential term in the electric
field. This equation for the electric field is then transformed into a scalar potential form,
which is then solved using finite-differences. This continuous equation can be mapped
on to a three-dimensional domain of cells. The finite-difference technique can then be
used to define the potential at nodes where the cells meet in terms of potentials at
neighbouring nodes and the conductivities of neighbouring cells evaluated at half-node
points, ie on the edges half-way between nodes, along with vector potential values at
these half-nodes. The equation for the potential can then be solved iteratively or by
matrix methods. A feature of both methods is that the computational space is confined
to only the voxels of the body. A recent review of numerical methods and interaction
mechanisms can be found in Stuchly and Dawson (2000).
Calculations of induced fields
136 Dimbylow (1998) calculated current density in the fine resolution (2 mm) NORMAN
phantom (see Chapter 2, paragraph 34) for uniform magnetic fields aligned with the
front, side and top of the body for frequencies from 50 Hz to 10 MHz. Both the
impedance and SPFD methods were used to provide mutual corroboration. At 50 Hz
they agreed to within 2%for AP (front-to-back), 3%for LAT (side-to-side) and 1%for
TOP (top-to-bottom) orientation. The scalar potential method requires less computa-
tional memory and is much quicker than the impedance method so this was chosen
to perform the full range of calculations up to 10 MHz. The outer layer of the eye in
NORMAN was not initially differentiated from the humour. The retina is important
because of the induction of phosphenes. Therefore, because the humour and sclera
have quite different conductivities, the outer layer of the eye was reclassified as sclera.
The rear part of this shell was then considered to be the retina for the analysis of
induced current density. Results are presented for the current density averaged over
1 cm
2
in muscle, heart, brain and retina.
137 Dawson and Stuchly (1998) have calculated induced electric fields and current
densities in the modified Yale phantom (the University of Victoria, UVic, phantom see
Chapter 2, paragraph 36) at a resolution of 3.6 mm. The results are given for various
organs in terms of average and maximum values for 60 Hz uniform magnetic fields in
three orthogonal orientations. The SPFD method with an appropriate matrix conditioner
and a conjugate gradient solver were used to model the problem. It is difficult to
compare the two sets of calculations because of the differing averaging methods and
model resolutions. The NRPB calculations with NORMAN have a 2 mm resolution
compared with 3.6 mm for the UVic results, so the maximum values over any voxel will
tend to be greater. Hence for the whole body the maximum from the NORMAN
calculations is 82.2 A m
2
per tesla at 50 Hz for AP orientation compared with 63.7 A m
2
for the UVic results converted to 50 Hz. The corresponding values for the maximum
electric field are 381 against 307 V m
1
. The averages performed in NORMAN are over
69
1 cm
2
, whereas UVic gives maximum and average values in an organ so the NORMAN
values should be intermediate. Converting the UVic data to an applied 1 T field at 50 Hz
gives maximum and average values in the brain of 6.07 and 0.746 A m
2
for AP orientation.
The corresponding electric field values are 60.7 and 8.83 V m
1
. The maximum current
density from Dimbylow (1998) in the brain averaged over 1 cm
2
is 3.59 A m
2
and the
electric field is 44.9 V m
1
(using a conductivity, = 0.08 S m
1
). It can be seen that despite
different resolutions and averaging metrics the two sets of calculations are consistent.
Differences in current density distribution can be attributed to the difference in model
shape especially for the orientation from side to side. The UVic model has hands
clasped in front and in contact with the rest of the body, thus forming longer current
loops in some body regions. In contrast, NORMAN has the arms at the side and not in
contact with the rest of the body.
138 Stuchly and Gandhi (2000) performed a comparison of induced fields for exposure
to 60 Hz applied electric and magnetic fields. The University of Utah group (see
Chapter 2, paragraph 35) used the impedance method on the 6 mm resolution version
of their phantom and the University of Victoria group used the SPFD method on the 3.6
and 7.2 mm versions of their model. The average induced electric field in the brain for a
50 Hz, 1 T field for AP orientation was 9.58 V m
1
for the Utah model, and 8.83 and
9.58 V m
1
for the 3.6 mm and 7.2 mm Victoria models. The average over 1 cm
2
from
the NRPB calculations (Dimbylow, 1998) was 44.9 V m
1
. The corresponding average
induced current density in the brain was 1.95 A m
2
for the Utah model and 1.15 A m
2
for the 7.2 mm Victoria model. The average over 1 cm
2
from the NRPB calculations
was 3.59 A m
2
. Stuchly and Gandhi concluded that the obtained differences for the
dosimetric data of human models exposed to electric and magnetic fields could be
rationally explained (see paragraph 151).
139 Later work by Gandhi et al (2001a) calculated current density averages over 1 cm
2
.
They used the impedance method on the 6 mm version of their model but the region
around the spinal cord was expanded to the original dimensions, 1.974 1.974 3.0 mm.
The current densities were averaged over 1 cm
2
by interpolation from the 6 mm grid.
They obtained values of 2.25 A m
2
for the brain/spinal cord and 7.76 A m
2
for the heart
for an AP orientation, 50 Hz, 1 T field compared with 3.59 and 5.26 A m
2
, respectively,
from the NRPB calculations. The Gandhi et al brain/spinal cord values are 37%lower
than those from NORMAN. This may be due to the coarser resolution calculations and
problems with interpolation on to a 1 cm
2
surface. The heart results are higher because
the Utah phantom uses a composite heart muscle/blood tissue rather than discrete
heart muscle and blood as in NORMAN.
140 Gandhi and Kang (2001) have also calculated current densities from non-uniform
fields from electronic surveillance devices. They scaled the Utah adult model to
represent 10- and 5-year-old children. They found that, for the representative devices
and particular operating conditions chosen, the current density averaged over 1 cm
2
in
the brain/spinal cord was lower than the ICNIRP restrictions for the taller model of the
adult, but may approach or even exceed them for the shorter models of the 10- and
5-year-old children. This is a geometric effect due to the brain for the shorter models
being in considerably higher non-uniform fields from the particular device than the
brain of the taller adult. Other example of application to non-uniform fields can be found
70
in Dawson et al (1999) where realistic postures and configurations of three-phase
current carrying conductors are considered.
Induced current densities from low frequency electric fields
141 The difficulty in calculating the interaction of low frequency electric fields with the
body, as opposed to magnetic fields, is that the body perturbs the applied field and this
perturbation must be accommodated in the specification of the boundary conditions.
The Finite-Difference Time-Domain (FDTD) method (Taflove, 1995) is not usually
applied at low frequencies because the time step is related to the resolution of the
model which means that the number of steps required to reach equilibrium is
proportional to the inverse of the frequency. Furse and Gandhi (1998) applied the FDTD
method on a 6 mm resolution grounded MRI based model. The FDTD scheme was run
at 10 MHz, but using the conductivities appropriate to 60 Hz. The calculated induced
current densities were then linearly scaled with frequency to obtain the values at 60 Hz.
142 Dawson et al (1998) used a hybrid two-stage approach. A low resolution (7.2 mm)
solution was performed by a quasistatic-FDTD algorithm (De Moerloose et al, 1997). In
this steady state quasistatic approximation of FDTD the fields exterior to conductors all
have the same phase as the incident field. Interior fields are of first order and are
proportional to the time derivative of the incident field. If a ramp function is used for the
incident field, all fields will eventually have a linear (exterior) or constant (interior)
behaviour. The resulting surface charge density was extracted from the potentials and
interpolated on to the body surface of the higher resolution model (3.6 mm) to provide
the source term for internal calculations using a scalar potential method (Dawson
et al, 1996).
143 Dimbylow (2000), using NORMAN, solved a potential equation on a series of nested
subgrids decreasing from 32 mm to 2 mm. The outer region of the domain extended
sufficiently so that the perturbation in the applied field, due to the phantom, was small
at the periphery whilst the grid near and in the phantom was small enough to model
the structural details. The solution of the potential equation is divided into two parts.
First, the coupling between the externally applied electric field and the human body,
which is deemed to be a conductor at low frequencies, is calculated to provide the
surface charge. This charge is then used as a boundary condition to calculate the internal
potential and hence induced fields and current densities in the body at a resolution
of 2 mm.
Calculations of induced fields
144 Current density distributions in a fine resolution (2 mm), anatomically realistic
voxel model of the human body have been calculated (Dimbylow, 2000) for uniform,
low frequency vertically aligned electric fields for grounded and isolated conditions
from 50 Hz to 10 MHz. Hybrid FDTD methods were used as well as the nested finite-
difference potential method to provide mutual corroboration. The calculated short-
circuit current for the grounded case at 50 Hz using the potential formulation is 14.8 A
per kV m
1
compared with 14.0 A (a difference of 5%) for the FDTD method and
14.7 A (linearly scaled from 17.6 A at 60 Hz) obtained by Dawson et al (1998) for a
1.77 m, 76 kg phantom and around 14.3 A, similarly scaled from the work by Furse and
71
Gandhi (1998) for a 1.764 m, 71 kg phantom. The FDTD calculations of current density
are within 2%of those from the potential method for the maximum value in any 2 mm
voxel, for both the grounded and isolated cases, and within 9%and 2%for the averages
over 1 cm
2
in the retina for the grounded and isolated cases.
145 Furse and Gandhi (1998) calculated electric fields and currents induced in the 6 mm
version of the Utah model. FDTD calculations were performed at 10 MHz and were
scaled using a quasistatic approximation to 60 Hz. Converting their results to an applied
field of 1 V m
1
at 50 Hz yields minimum, average and maximum values of current
density in the brain of 0.059, 0.157 and 0.694 A m
2
. The Dimbylow (2000) value
averaged over 1 cm
2
in brain/spinal cord is 0.176 A m
2
and the maximum value is
0.413 A m
2
.
146 Stuchly and Gandhi (2000) performed a comparison of induced fields for exposure
to 60 Hz applied electric and magnetic fields. The University of Utah group (Furse and
Gandhi, 1998) used the FDTD method scaled in frequency on the 6 mm resolution
version of their phantom and the University of Victoria group (UVic) used the hybrid
quasistatic FDTD/SPFD method (Dawson et al, 1997) on the 3.6 and 7.2 mm versions
of their model. The average induced electric field in the brain in a grounded phantom
for a 50 Hz, 1 V m
1
field was 0.892 V m
1
for the Utah model (6 mm resolution,
brain
= 0.17 S m
1
), and 0.617 V m
1
for the University of Victoria model (7.2 mm
resolution,
brain
= 0.1 S m
1
). This compares with the average over 1 cm
2
for the NRPB
model of 2.2 V m
1
(2 mm resolution,
brain
= 0.08 S m
1
).
147 Hirata et al (2001) calculated induced electric fields and current densities in a
rescaled adult model to represent a 5-year-old child and these are compared with those
in the full-scale adult, UVic phantom. The calculations were performed with the hybrid
approach (Dawson et al, 1998) and a final resolution of 3.6 mm inside the phantom. All
three dosimetric organ measures (average, 99th percentile and maximum) of the induced
electric field are consistently lower in the organs and tissues of the childs head than in
the adults head. The differences are around 20%and reflect the average field reduction
in the head to 67%of the adult. However, this is not necessarily the case for the rest of
the body, eg the field values in the heart are higher in the child than in the adult. In
conclusion, the volume of the child head and brain is proportionately greater as a
fraction of the total body volume than in adults. This results in a lower average current
density and electric field in the childs head.
Dosimetric uncertainties
148 Sources of uncertainty in EMF calculations include the reliability of numerical
methods, different individual anatomies and postures, resolution and variation in
dielectric parameters.
149 Caputa et al (2002) have looked at the reliability of numerical methods and the
effects of variations in voxel phantoms on power frequency magnetic field dosimetry.
The groups at the University of Victoria and NRPB have calculated the induced electric
fields in both the UVic and NORMAN models using independently developed codes.
A detailed evaluation has been performed for a uniform magnetic field at 60 Hz.
Comparisons of the average (E
avg
), maximum (E
max
) and 99th percentile (E
99
) electric
fields for all the organs in the models show differences of 1% or less for the great
majority of tissues. Only in a few cases the difference reaches 2%. The influence of the
72
body model size and shape including anatomy were investigated by comparing the
original NORMAN model at 2 mm resolution, a rescaled NORMAN at 4 mm, the original
UVic model at 3.6 mm, an expanded UVic model at 1.8 mm, and a 2 mm version of
the Brooks digital anatomical man model. The effect of the size is best illustrated by the
digital anatomical model which has a mass 42%greater than the reference 73 kg of
NORMAN. Correspondingly, the whole-body average electric fields are 44%greater.
This is not unreasonable, since the difference in height of the models is small (0.2%),
thus the increase in volume (mass) is mainly in the horizontal frontal dimensions of the
torso. The actual anatomy of people represented by the models, as well as the accuracy
of the models, both influence differences in dosimetric measures. Relatively small organs
(such as the testes) or thin organs (such as the spinal cord) indicate large differences
in induced electric field strength that can be directly ascribed to the differences in the
shape and size of these organs in the models. Differences in current density distribution
can be attributed to the difference in model shape especially for the orientation from
side to side. The UVic model has hands clasped in front and in contact with the rest of
the body, thus forming longer current loops in some body regions. To the contrary,
NORMAN has the arms at the side and not in contact with the rest of the body.
Regarding the model resolution, the differences for E
avg
and E
99
are relatively small. The
most apparent and consistent factor is the influence of the model resolution on voxel
maximum values. The large values of E
max
for the high resolution models are inherent in
their division into voxels, namely the large current density in the vicinity of the inner
corner of a given organ/tissue boundary layer (Dawson, et al, 2001).
150 A limited set of calculations has been performed at NRPB to investigate the effect
of variations in dielectric parameters. Firstly, applied low frequency magnetic fields
were considered. Here the robust dose quantity is the induced electric field. If all the
conductivities of the body are multiplied by a constant factor, say 2.0, then the induced
electric field will stay the same as before but the induced current density will increase
by a factor of 2.0. The conductivity of the brain alone was changed by factors of 2.0
and 0.5 compared with the Gabriel (1995) value (0.08 S m
1
). This resulted in changes of
23%and +30%in the induced electric field, averaged over 1 cm
2
, and changes of +54%
and 35%in the induced current density. For applied low frequency electric fields the
converse is true and the induced current density is the more robust quantity. If all the
conductivities of the body are multiplied by a constant factor, say 2.0, then the induced
current density will stay the same as before but the induced electric field will decrease
by a factor of 2.0. When the conductivity of the brain alone was changed by factors of
2.0 and 0.5 this resulted in changes of +11%and 13%in the induced current density
and changes of 44%and +73%in the induced electric field.
151 Stuchly and Gandhi (2000) concluded that the differences for the dosimetric data of
human models exposed to low frequency electric and magnetic fields could be
rationally explained. Factors are the accuracy of the numerical method, voxel resolution,
human body model size and posture, organ size and shape, and dielectric properties.
Errors due to numerical methods for average values are around 13%. Larger errors are
associated with maximum values. Smaller errors in average values and larger maximum
values are associated with decreasing voxel size, especially for small organs. Body
posture has a relatively large effect. For applied magnetic fields the induced electric
fields are relatively impervious to the magnitude of the conductivity but it has a strong
73
effect on the induced current density. On the basis of the comparison presented, it is
estimated that the average induced electric field and current density in human organs
are known within a factor of two for exposures of the average man to uniform electric
and magnetic fields at 60 Hz.
Summary
and the fields induced within the body. This gives guidance on the choice of reference
levels in relation to basic restrictions. The usual approach to deriving reference levels
is to solve Maxwells equations numerically, in fine resolution, anatomically realistic
models of the body.
153 The computational methods for applied magnetic fields most suitable to voxel
models are the impedance method and the scalar potential finite-difference (SPFD)
method. A feature of both methods is that the computational space is confined to the
voxels of the body. The difficulty in calculating the interaction of low frequency electric
fields with the body, as opposed to magnetic fields, is that the body perturbs the applied
field and this perturbation must be accommodated in the specification of the boundary
conditions. This problem has been approached by modified frequency scaled FDTD
methods, hybrid FDTD/quasistatic potential calculations and nested grid potential
calculations. A recent review of numerical methods and interaction mechanisms can be
found in Stuchly and Dawson (2000).
154 Induced internal electric fields and current densities have been calculated in a
number of voxel models for applied uniform power frequency magnetic fields and for
electric fields. It is important to consider children in the analysis of non-uniform fields,
eg the magnetic fields from electronic surveillance devices, because the brain may be in
a higher non-uniform field from the particular device than the brain of the taller adult.
155 Stuchly and Gandhi (2000) concluded that the differences for the dosimetric data
of human models exposed to low frequency electric and magnetic fields could be
rationally explained. Factors are the accuracy of the numerical method, voxel resolution,
human body model size and posture, organ size and shape, and dielectric properties. On
the basis of the comparison presented, it is estimated that the average induced electric
field and current density in human organs are known within a factor of two for exposures
of the average man to uniform electric and magnetic fields at 60 Hz.
The usual approach to deriving reference levels is to solve Maxwells equations
numerically, in fine resolution, anatomically realistic voxel models of the body.
The differences for the dosimetric data of human models exposed to low
frequency electric and magnetic fields can be explained in terms of the accuracy
of the numerical method, voxel resolution, human body model size and posture,
organ size and shape, and dielectric properties. It is estimated that the average
induced electric field and current density in human organs are known within a
factor of two for exposures of the average man to uniform electric and magnetic
fields at power frequencies.
It is important to additionally consider children when calculating current
densities from low frequency magnetic devices when the field is non-uniform.
74
5 Electromagnetic Fields of
Frequencies Above 100 kHz
1 In this chapter, scientific data relevant to the development of exposure guidelines
for time-varying electromagnetic fields (EMFs) of frequencies greater than about
100 kHz are addressed. These fields have frequencies in the radiofrequency (RF) range
where the dominant identified and well-understood interaction processes and adverse
health effects are due to the heating of body tissues from induced internal electric
fields and currents. However, other adverse health effects due to electrostimulation of
body tissues are also possible at frequencies up to about 10 MHz and these are
considered in Chapter 4. The reviews summarised in this chapter cover a wide range
of possible biological effects and disease outcomes. Thus this chapter constitutes a
comprehensive summary of relevant published epidemiological and biological studies
and computational dosimetry.
EPIDEMIOLOGY
2 A number of studies have examined the health of people exposed to RF EMFs,
through the use of mobile phones, work, hobbies, or residence near radio or television
transmitters. These studies have been reviewed by a European Commission expert
group (McKinlay et al, 1996; Veyret et al, 1999), French expert groups (Zmirou, 2001;
Aran et al, 2003), the French Senate (Lorrain and Raoul, 2002), the Independent Expert
Group on Mobile Phones (IEGMP, 2000), the Royal Society of Canada (Krewski et al,
2001a,b), the Advisory Group on Non-ionising Radiation (AGNIR, 2001c, 2003), Boice
and McLaughlin (2002), and the Swedish Radiation Protection Authority (SSI, 2003).
Many of these studies have looked at cancer risks, but other endpoints such as pregnancy
outcome have also been considered.
3 Findings from these studies which have focused on the possible non-thermal
health effects of RF EMF exposure are reviewed below. Studies of the effects of heat
on mortality and morbidity are also reviewed, and the relevance of these studies to
thermal health effects of RF EMF exposure is considered.
Cancer
4 A review by Elwood (1999) concluded that the epidemiological evidence linking
RF EMF exposures and cancer was weak in regard to its inconsistency, the design of the
studies undertaken as of that time, the lack of detail on actual exposures, and the
limitations of the studies in their ability to deal with other likely relevant factors. In
addition, there may have been biases in some studies. In its review of occupational
studies and studies near broadcasting facilities, IEGMP (2000) concluded that the overall
balance of evidence did not indicate that RF radiation affected the risk of cancer in
people. However, many of the occupational studies had low statistical power, some had
methodological defects, including little or no exposure assessment, and the types of
5 Electromagnetic Fields of Frequencies Above 100 kHz
75
exposure investigated varied between studies. Furthermore, the studies near radio and
television transmitters had major limitations, including the lack of measured field levels
in the analyses. In addition, at the time of the IEGMP report, there had been few studies
of mobile phones and cancer. Thus, whilst the epidemiological studies conducted up to
the early part of 2000 did not give cause for concern, IEGMP concluded that this research
had too many limitations to give reassurance that there was no hazard.
5 Since early 2000, further studies have been published of cancer in relation to the
use of mobile phones. AGNIR (2001c) reviewed two casecontrol studies of brain
tumours in the USA (Muscat et al, 2000; Inskip et al, 2001) and a cohort study in
Denmark (Johansen et al, 2001). The first two of these studies were hospital based, and
information on mobile phone use was collected through interviews with the study
subjects. In contrast, the Danish study used information from operating companies on
mobile phone use, and so the assessment of exposure was likely to be less precise than
in the American studies. However, whereas the Danish study used a national population
registry as the basis of its cohort, the use of hospital controls in the American studies
might have raised the potential for selection bias. A subsequent casecontrol study in
Finland found that mobile phone use was not associated with brain tumours or salivary
gland cancers overall, but there was a weak significant association between gliomas
and the use of analogue mobile phones; however, this study lacked information on
individual exposures (Auvinen et al, 2002). The casecontrol studies in the USA did not
find associations between mobile phone use and the risk of acoustic neuroma (Inskip
et al, 2001; Muscat et al, 2002), but the small numbers of cases both here and in another
American study (Warren et al, 2003) limited inferences.
6 The preceding studies were generally based on several hundred people with a brain
tumour, plus controls, and had limited opportunity to investigate any effects that might
arise 10 or more years after exposure. In contrast, a recent study in Sweden analysed
data on about 1300 people with a brain tumour and the same number of controls, of
whom several tens had used mobile phones more than 10 years previously (Hardell
et al, 2002). A subsequent paper based on the same study, but with a different method
of analysis, gave similar results (Hardell et al, 2003). A raised brain tumour risk was
found in the Swedish study among mobile phone users, particularly those who reported
using an analogue phone at least 510 years previously. There were also indications
of a similar increase in risk among users of cordless phones based on a long latency.
Furthermore, the risk among analogue mobile phone users which in relative terms
was greatest for acoustic neuroma was not raised to a statistically significant extent
after taking account of the fact that some people had used more than one type of
phone. Since RF exposures from cordless phones are much lower than those from
analogue mobile phones, the raised risks reported in the Swedish study may be due at
least in part to biased recall of phone use 510 or more years previously. Such a bias
might also explain why there tended to be a raised risk for tumours in the side of the
head nearest to where the phone was reported to have been used, but a decreased risk
for tumours in the opposite side of the head.
7 Recent studies of cancer and occupational exposures to RF fields (eg Baumgardt-
Elms et al, 2002; Groves et al, 2002; Kliukliene et al, 2003) have given variable results.
Like earlier studies that have been reviewed, for example, by IEGMP (2000), some of
76
these studies had methodological problems and the method of exposure assessment
varied between them. A report of a raised risk of malignant melanoma of the eye in
relation to the use of RF transmitting devices in Germany (Stang et al, 2001) has been
criticised for the lack of adjustment for possible confounding factors such as exposure
to ultraviolet radiation (Inskip et al, 2001); also, the findings were not supported by a
correlation study in Denmark (Johansen et al, 2002) or by temporal trends in disease
incidence in the USA (Inskip et al, 2003).
8 An analysis reported a statistically significantly raised risk of childhood leukaemia
with proximity to a high power radio station in Rome, with less evidence for an increase
in adult leukaemia (Michelozzi et al, 2002). However, these findings were based on small
numbers of cases. They also differ from results around radio and television transmitters
in Great Britain, where there was some evidence of an increased risk with increasing
proximity for the incidence of adult leukaemia but not childhood leukaemia (Dolk et al,
1997). Furthermore, studies around transmitters such as these are limited by a lack
of exposure data. Such problems were more severe in a recent correlation analysis
of melanoma of the skin and frequency modulation broadcasting in Nordic countries
(Hallberg and Johansson, 2002).
9 In its recent review, AGNIR (2003) concluded that while there have been positive
findings in some studies for risks of specific cancers in relation to mobile phone use or
to occupational or residential RF field exposure (or potential for exposure), no relation
has been shown consistently. There has also not been a convincing demonstration of a
doseresponse or durationresponse relationship. However, AGNIR noted that the
design of the studies has often been deficient. Hence, although the studies do not
suggest a raised risk of cancer, they do not rule one out, especially in relation to large
cumulative exposures to mobile phones and possible effects occurring many years
after their use.
Other health outcomes
10 Several cohort studies of occupational groups exposed to RF EMFs have examined
non-cancer mortality and, in some instances, morbidity. IEGMP (2000) concluded
that these studies did not provide any overall evidence of a hazard. Furthermore,
casecontrol studies of pregnancy in physiotherapists have not, overall, supported a
relation of microwave exposure with spontaneous abortion or other adverse outcomes
(IEGMP, 2000; Krewski et al, 2001a). However, IEGMP concluded that this research had
too many limitations to give reassurance that there was no hazard. It also reviewed
reports of symptoms such as fatigue, headache and feelings of warmth behind the ear
occurring during or shortly after the use of mobile phones, and found it unclear as to
what extent, if any, these symptoms were caused by RF radiation (IEGMP, 2000). AGNIR
(2003) reached similar conclusions.
Effects of heat on mortality and morbidity
11 Various studies of temporal changes in population mortality rates have shown
associations with temperature (eg Keatinge et al, 2000; Curriero et al, 2002). In particular,
episodes of very hot or very cold temperatures are associated with increased mortality,
mainly from cardiovascular disease. Furthermore, it has been suggested that a sudden
and unexpected change of as little as 2C in external temperature, giving no time for
77
adaptive changes, could lead to an extra 1900 heat-related deaths per year in Britain
(Donaldson et al, 2003). However, it should be stressed that these studies of mortality
and temperature have been conducted at a population level, and that individual data
have often been lacking on other factors associated with particularly hot or cold periods
that affect mortality rates, eg the prevalence of influenza or air pollution. In addition,
environmental temperature, humidity and physical exertion would also modify cardio-
vascular responses to additional heat loads. Consequently, it is difficult to use these
population studies of external temperature changes to quantify the mortality that might
be produced by an additional heat load due to RF exposures, although the possibility
of an effect cannot be excluded, particularly in periods of hot weather. This topic is
considered further in paragraphs 2339.
12 A number of studies have indicated adverse effects on human prenatal development
particularly on the central nervous system from maternal hyperthermia (Graham
et al, 1998). However, it has often been difficult to separate any influence of heat
alone from maternal metabolic changes occurring in fevers (Edwards et al, 2003). A few
prospective studies have considered groups exposed to both sources of hyperthermia.
For example, Milunsky et al (1992) reported a raised risk of neural tube defects in
relation to use of a hot tub or sauna, or to a report of fever, in the first trimester of
pregnancy. Although this study was based on a large cohort and used information
on individual exposures collected during pregnancy, the small numbers of cases
limit inferences. Furthermore, when considering RF EMF induced heating, it should be
noted that any adverse effect would be modified by environmental temperature and
physical exertion. Consequently, it is difficult to use the studies of maternal hyper-
thermia to quantify teratogenic effects that might be produced by internal heating due
to RF exposures. Similarly, overheating has been associated with sudden infant death
syndrome (eg Fleming et al, 1990).
13 Many of the epidemiological studies of the potential effects of RF exposure
conducted up to the late 1990s had included either poor measures of exposure or none
at all (Swerdlow, 1999). For example, some studies have used current job title or
distance of place of residence from an RF transmitter as a proxy for exposure. However,
exposures are likely to be heterogeneous between workers with the same job title, and
exposures from transmitters are unlikely to be determined solely by proximity. Some,
although not all, of the recent studies of mobile phone users have been able to collect
more specific information relevant to exposures for example, by asking the study
subjects about their use of mobile phones (Muscat et al, 2000; Inskip et al, 2001). These
studies have included several hundred people with a brain tumour, and therefore had
reasonable statistical power to detect an overall association, although this would have
been reduced by misclassification of exposures. However, the power to address more
detailed issues such as the use of digital as opposed to analogue mobile phones and
risks for specific types of brain tumours has been limited. In addition, given that these
phones have only been used widely in recent years, epidemiological studies of users
provide little information on whether there may be health risks many years after initial
exposure. Another potential difficulty in retrospective studies is the possibility of recall
78
bias, ie whether the subjects ability to recall past exposures differs between those who
developed the disease under study and those who did not.
14 In contrast to the cohort and casecontrol approach used for some of the studies
of RF exposures (particularly of mobile phone users), studies of the health effects of
environmental temperature changes have been based largely on aggregated data.
Consequently, it has not been possible in general to take account of factors at the
individual level that may have influenced the risks of mortality or morbidity. Studies of
prenatal development following maternal hyperthermia have generally used individual-
level data, but it was difficult in many of these studies to separate any effects of heat
per se from those associated with other sources of hyperthermia. The estimation of
risks from RF EMF induced heating is complicated further by the modification of such
effects by environmental temperature and physical exertion.
Epidemiological studies of groups exposed to RF EMFs have been variable in
quality. Some studies have been limited by low statistical power or a lack of
exposure measurements, while others may have been affected by bias.
The overall evidence from the more methodologically sound studies, including
those conducted recently of mobile phone users, does not indicate that RF
exposures increase the risk of cancer. However, the evidence is not conclusive.
In particular, these studies have generally provided little information on whether
risks might be raised many years after exposure, or on some specific types of
exposure, eg from the use of digital mobile phones. One recent large study
reported a raised risk of brain tumours some years after using an analogue
mobile phone, but this finding may be due at least in part to bias in the recall
of phone use.
Studies of occupational RF exposures do not indicate raised risks of non-cancer
mortality or adverse pregnancy outcome, although again it is not possible to
exclude the possibility of a small risk.
Mortality, mainly from cardiovascular disease, has been shown to be raised in
populations exposed to high or low temperatures, and there are indications that
maternal hyperthermia may lead to central nervous systems defects in offspring.
However, for several methodological reasons, it is difficult to use these studies to
quantify effects on mortality and prenatal development associated with internal
heating from RF exposures.
BIOLOGY
15 The biological effects of RF EMFs have continued to be studied using a wide range
of frequencies, modulations and experimental models. Earlier studies tended to investi-
gate frequencies set aside for industrial, scientific and medical use (ISM frequencies)
and to a lesser extent those used in radar and communications. More recently, the
growth and development in personal mobile communications has focused attention on
the frequencies associated with this technology. Heating continues to be the major
effect of exposure to RF EMFs. However, concern has been expressed that exposure at
levels too low to cause significant heating may nevertheless cause detrimental effects
and, in particular, increase the risk of cancer.
79
16 This section presents a summary of the biological effects of RF EMFs with frequencies
from 100 kHz to 300 GHz. These studies have been much examined and assessed.
Notable reviews include those by NCRP (1986), WHO (1993), and an EC expert group
(McKinlay et al, 1996; Veyret et al, 1999). Many other reviews and critiques of this
literature have been published, including those by ICNIRP (1996), the Health Council of
the Netherlands (HCN, 1997, 2000, 2002), AGNIR (2001c), and the Swedish Radiation
Protection Authority (SSI, 2003). Of particular importance are the comprehensive
reviews by IEGMP (2000), Zmirou (2001), the Royal Society of Canada (Krewski et al,
2001a,b), and AGNIR (2003).
17 The consensus remains that the majority of reported effects result from either rises
in tissue or body temperature of about 1C or more, or in physiological and behavioural
responses for minimising the total heat load (Saunders et al, 1997). However,
comparatively few studies have attempted to define more rigorously the basis of
previous guidance (eg NRPB, 1993) namely whole-body and localised heating. There
is, however, an established literature on the physiological effects of heat, and on the
consequences of local temperature rises, summarised recently at a WHO workshop
(WHO, 2003b), from which information relevant to the development of guidance can be
derived. This workshop addressed the effects of heat seen in healthy people and in
those vulnerable to heat stress. Similar conclusions were derived, mostly for healthy
people, by Adair and Black (2003).
18 In addition, some studies have reported biological effects in the apparent absence
of overt heating. While the possibility of non-thermal effects cannot be completely
dismissed, none is considered sufficiently well defined to be used as a basis for
guidance. The possible effects of exposure to RF EMFs at non-thermal levels are also
considered in this chapter.
Whole-body heating
19 RF energy absorbed by the body results in heat due to an increase in molecular
rotational and translational kinetic energy. The absorbed heat energy is distributed
throughout the body by the circulation of blood and is eventually lost to the
external environment. Significant whole-body heating has a major impact on cardio-
vascular physiology and thermoregulatory ability. In addition, the ability to carry out
cognitive tasks is also likely to be compromised before physiological limits of tolerance
are reached.
20 Cardiovascular responses to heat and exercise are central to body temperature
regulation in humans. Except in various pathological conditions and during heavy
exercise, the core body temperature is maintained under a wide range of environmental
conditions at a value of about 37C with a circadian fluctuation of about 0.5C. Heat
gained at rest, during exercise or exposure to RF EMFs has to be compensated by heat
loss and is often accompanied by a small increase in heat storage (Gordon, 1984).
21 Values for whole-body metabolic heat production can vary in the average
population from about 1 W kg
1
at rest to about 10 W kg
1
during heavy exercise, but
may be much higher during sports activities, for example. Typical values for metabolic
heat production for many industrial jobs have been estimated to vary from about
2.5 W kg
1
for light manual work to 6 W kg
1
for heavy manual work (NIOSH, 1980). The
principal heat loss mechanisms in humans are radiant and convective heat loss from the
80
skin through increased skin blood flow and evaporative heat loss from sweat. Heat
storage reflects shifts in both peripheral and core temperatures and occurs, for
example, during heavy exercise or in hot, humid environments. Prolonged rates of
increase in heat storage, such as 0.51.0 W kg
1
for 12 hours, will lead to unacceptable
rises in body temperature (Gordon, 1984). In moderate conditions, however, increased
skin blood flow will increase heat storage through an increase in the temperature of
the peripheral tissues of the body, increasing heat loss without necessarily increasing
core temperature.
22 Humans possess comparatively effective heat loss mechanisms; the principal
effectors are the sweat glands and cutaneous blood vessels (Nadel, 1980, 1984, 1985;
Rowell, 1983; Jessen, 1987). In addition to a well-developed ability to sweat, which in
humans can be produced over most of the body surface, the dynamic range of
blood flow rates in the skin is much higher than in other animal species. Skin blood
flow can increase from approximately 0.20.5 litres per minute in thermally neutral
conditions, to values exceeding 78 litres per minute during severe hyperthermia.
A dense network of capillary loops empties into a capacious sub-papillary venous
plexus that constitutes a large potential blood reservoir. Cutaneous venous volume
rises with increased blood flow so that, at any given flow rate, flow transit time
increases permitting greater heat exchange with the skin. From there, heat is lost to the
environment, mainly through convection and, under more severe heat stress, through
evaporation of sweat.
Circulatory adjustments to heat stress
23 The principal cardiovascular adjustments to heat stress have been described by
Rowell (1983). Supine, resting, healthy volunteers were heated to the limits of their
thermal tolerance (core temperature of about 39C) as cardiac output increased by
6.6 litres per minute. The rise in skin blood flow was found to exceed the rise in
cardiac output because blood flow to other major vascular beds was decreased. Mean
arterial pressure decreased slightly and then recovered, but central venous pressure
decreased markedly.
24 The effectiveness of control of body temperature under heat stress depends on the
threshold and the sensitivity (or gain) of the heat dissipation responses. These vary
widely between individuals and are subject to many factors (Nadel, 1985) including the
time of day, blood volume and the level of physical fitness and acclimatisation to heat.
Sweat rates around 11.5 litres per hour are not uncommon, and may reach up to
2 litres per hour in fit individuals providing a potential evaporative rate of heat loss
in excess of 1 kW (about 14 W kg
1
in a 70 kg human). In the absence of adequate
rehydration this deprives the body of fluid from all body compartments, including the
vascular component (Nadel, 1980, 1984, 1985). Both exercise and dehydration
compromise temperature regulation in hot environments by limiting the blood flow
available to the skin. Reflexes that aid in the maintenance of central circulating blood
volume and blood pressure take precedence, overriding the thermoregulatory signals
for cutaneous vasodilatation and so reducing heat loss to the environment. Reduced
blood volume also decreases the sweating rate at any given body temperature. A loss
of body water of more than 3%of body weight constitutes clinical dehydration and is
81
associated with early signs of heat-related disorders such as light-headedness and
disorientation (Nadel, 1984).
Physiological limits on heat exposure during physical work
25 Consideration of the well-being of healthy workers undertaking manual labour in
hot environments has prompted the development of limits on exposure dependent on
several physiological criteria such as sweat rate, percentage water loss, heat storage
and deep body (core or rectal) temperature. The two main health effects that have
usually been considered are dehydration and heat stroke (heat induced decrements in
cognitive performance are considered elsewhere). Heat stroke (see below) is the most
serious, often fatal consequence of excessive heat exposure and occurs at core
temperatures in excess of 40C (Malchaire et al, 2000). The physiological criteria for
limiting work in hot environments in ISO 7933 (ISO, 1989) have recently been reviewed
(Malchaire et al, 2000, 2002). These authors focused particularly on work that described
the population distribution of rectal temperature in groups of subjects during or after
exposure to heat in various working conditions. They concluded that rectal temperatures
should be restricted to a maximum of 38C in order to minimise the risk of heat-related
disorder. They also noted that a loss of body water of around 23%body weight may
lead to heat stress and heat-related illness, and that there is a need for regular rehydration
and salt intake, since the thirst sensation is not sufficient to ensure that this would
otherwise take place.
Physiological responses in healthy volunteers exposed to RF EMFs
26 The physiological responses of healthy volunteers to RF EMFs have been studied
mostly by two groups of researchers. Shellock and colleagues have examined the
thermoregulatory consequences of acute abdominal exposure to 64 MHz magnetic
fields during clinical magnetic resonance diagnostic procedures, while Adair and
co-workers have looked at the consequences of whole- or partial-body acute RF
exposure at 450 or 2450 MHz.
27 The acute exposure of volunteers to 64 MHz for 30 minutes at whole-body SARs
of 2.7 to 4.0 W kg
1
or 16 minutes at 6 W kg
1
resulted in small increases in body
temperature (0.10.4C), heart rate, and localised sweating and increased skin blood
flow (Shellock et al, 1989, 1994). All of the subjects reported that they felt warm during
the procedure and each of them had visible signs of perspiration on the forehead, chest
and abdomen. Volunteer exposure to 450 or 2450 MHz for 45 minutes at peak SARs
(on the back) of about 6 or 8 W kg
1
at several different environmental temperatures
similarly resulted in vigorous increases in sweating rate on the back and chest (Adair
et al, 1998b, 1999, 2001a,b). These effects were directly related to power density, peak
SAR and environmental temperature.
28 Overall, these studies indicate that adequately hydrated, passive, healthy volunteers
accommodate whole-body RF heat loads of approximately 1 W kg
1
for 45 minutes at
environmental temperatures up to 31C to 6 W kg
1
for at least 15 minutes at ambient
temperatures with increased skin blood flow and profuse localised sweating but with
minimal changes in core temperature. However, whilst increased skin blood flow and
profuse localised sweating also ensured small increases in skin temperature in response
82
to a local peak SAR of about 15 W kg
1
at the exposed site, it is not clear how less
superficial and less vascular tissues might respond.
Heat-related disorders in adults
29 Heat-related disorders are not uncommon in healthy people unaccustomed to hot
environments. Heavy exercise either through work or recreation will further exacerbate
any problem, particularly if water and salts lost through sweat are not replenished. In
addition, people with a history of heat illness, heat injury or heat intolerance and
previous difficulty in acclimatising to the heat are likely to be at increased risk (Kenny,
1985). NIOSH (1986) lists body fat and age as further predictors of heat intolerance
but also acknowledges a high degree of individual variation not accounted for by
these factors. A number of drugs and chemicals have direct effects on the control of
body temperature, or on metabolism or heat production of the body (NIOSH, 1986;
BOHS, 1990). Almost any drug that impairs central nervous system activity, cardio-
vascular reserve or body hydration can reduce heat tolerance (NIOSH, 1986). For
example, drugs such as barbiturates or phenothiazines depress reflex regulation of
body temperature generally, while anticholinergic drugs specifically suppress sweating
and vasodilatation. Alcohol, which interferes with nervous system function and results
in dehydration due to the inhibition of anti-diuretic hormone, has been associated
with heat stroke (NIOSH, 1986). The potential interactions between such drugs and
temperature regulation mechanisms are complex in detail and may depend on a number
of factors (BOHS, 1990).
30 A variety of heat disorders have been distinguished clinically when workers have
been exposed to excessive heat (NIOSH, 1986). These disorders range from simple
postural heat syncope (fainting) to the complexities of heat stroke. A common feature
of all heat-related disorders (except for simple postural heat syncope, which is caused
by blood pooling in the dilated vessels of the skin and lower body) is some degree of
elevated body temperature which may then be complicated by deficits of body water
and salt. Even people with access to food and water, particularly if unacclimatised to
heat, often fail to increase intake of salt and water rapidly enough to prevent substantial
loss of body fluid, and as a result the blood becomes more concentrated (Keatinge et al,
1986). This can cause a condition known as salt-depletion heat exhaustion, which
causes cramps if associated with heavy physical exercise. Similarly, water-depletion
heat exhaustion results from dehydration and is characterised by fatigue, nausea,
headache and giddiness. More seriously, both conditions make the blood more prone to
clot, and this increases the incidence of coronary and cerebral thrombosis in people
with pre-existing roughening of the arteries due to atheroma. This is commonly present
in middle-aged and older people and accounts for the fact that most of the heat-related
mortality from arterial thrombosis occurs in people of these age groups (Donaldson
et al, 2003).
31 These adverse effects of thermoregulatory adjustments, rather than lethal over-
heating of the body, account for the great majority of heat-related deaths in temperate
parts of the world, and probably even in tropical regions, but serious overheating of the
body can occur in hot climates. Heat stroke describes the syndrome produced by over-
heating of the body core. It can be produced in normal people by several hours of
physical exercise in a hot, humid environment close to or above body temperature. If
83
heat loss is insufficient, progressive rise in body temperature above 38C leads to
hyperventilation, to cerebral dysfunction involving irritability and confusion, and
ultimately to cardiovascular collapse and cessation of sweating (Donaldson et al, 2003).
Irritability and headache are important warning signs that body temperature is rising to
dangerous levels. The skin is hot and dry and usually red, and rectal temperatures may
be 40.5C or over (NIOSH, 1986). As body temperature rises further, at about 41C, heat
denaturation of proteins causes damage to the large Purkinje cells of the cerebellum
and cerebral cortex. Selective damage to brain tissue is therefore found in people who
have suffered non-fatal heat stroke (Donaldson et al, 2003). Vascular endothelium,
hepatic and renal cells, and striated muscle are then affected, and almost all cells in the
body are killed if their temperature rises to 50C even for a few minutes.
32 Otherwise, heat stroke in sedentary people is usually associated with impairment
of sweating and vasodilatation, either by drugs or disease (Donaldson et al, 2003). It is
most commonly seen in psychiatric patients receiving drugs such as barbiturates or
phenothiazines which depress reflex regulation of body temperature generally, or
anticholinergic drugs which specifically suppress sweating and vasodilatation. General
autonomic hypofunction due to diabetes is a common cause of heat stroke in
sedentary people. Old age without obvious disability also seems to be associated with
increased liability to heat stroke. Diagnosis is suggested by confusion and headache in
hot conditions, and confirmed by a deep body temperature close to or above 41C.
Heat-related mortality of adults at the population level
33 The most important adverse consequence of heat stress is death, and in practice
the great majority of excess deaths in hot weather are not due to hyperthermia but
to the cardiovascular consequences of heat stress in vulnerable and older people
(Donaldson et al, 2003). Older people appear less effective at maintaining normal body
temperature compared to younger people, due to declines in sweating and blood flow
responses, as well as from decline in the neural control of these responses (Rooke et al,
1994; Anderson et al, 1996). Since these deaths are mostly recorded as due to heart
failure, or coronary or cerebral thrombosis, few of the heat-related deaths are specifically
attributed to heat in death certificates and national statistics. Accordingly, they can only
be assessed by analysis of mortality statistics at the population level.
34 Many studies have shown that in most parts of the world mortality falls to a
minimum at a particular environmental temperature, and rises at temperatures above
(and below) this value (for reviews see, for example, Kalkstein and Greene, 1997;
Martens, 1998; Keatinge et al, 2000; Donaldson et al, 2003). These excess deaths occur
mainly in older people. The simplest approach to quantifying this mortality is to identify
the temperature band at which mortality is lowest; annual heat-related mortality is then
obtained as total excess mortality at temperatures higher than this band. These 3C
temperature bands of minimum mortality are significantly higher in warm regions than
in cold regions (Keatinge et al, 2000). In a study spanning Europe, these authors found
that minimum mortality is, for example, at 14.317.3C in north Finland, 19.322.3C
in London, and at 22.725.7C in Athens. Annual heat-related mortalities per million
among people aged 6574 years (expressed as means and 95%confidence limits) were
304 (126482) in north Finland, 40 (1368) in London (which has few days above the
minimum mortality band), and 445 (59831) in Athens.
84
35 Britain has an unusually low rate of heat-related mortality, but even here total
annual heat-related deaths for the whole UK have been estimated to be about 800 per
year (Donaldson et al, 2001). These authors noted that such calculations cannot be
used directly to quantify mortality that might be produced by internal heating due to
RF EMFs, but they imply that any substantial increase in internal heat production will
substantially increase mortality in hot weather. Donaldson et al (2003) indicated that, in
these circumstances, an additional heat load of around 30% of the normal basal
metabolic heat production, ie about 0.4 W kg
1
, could not be regarded as a trivial
increase, or as safe, but that an additional heat load of around 10%, about 0.1 W kg
1
,
could be regarded as trivial and therefore safe.
Temperature regulation during pregnancy, in neonates and in children
36 During pregnancy, augmentation of cutaneous blood flow serves to remove heat
generated by the increased metabolic demands of gestation (Paul, 1993). Maternal core
body temperature at rest increases slightly during the first half of gestation, probably
due to the thermogenic properties of progesterone, after which it declines to the non-
pregnant level. Recent studies of thermoregulation during moderate exercise under
laboratory conditions indicate that pregnant women maintain thermal balance equally
as well as non-pregnant women. In a study of women exposed to short-term heat stress
in the form of sauna bathing, Vh-Eskeli et al (1991) found comparable increases in
core temperature among non-pregnant subjects and those at 1314 and 3637 weeks
of gestation. During the recovery period, core temperatures were significantly lower in
the late pregnancy group compared with the non-pregnant group, leading the authors
to suggest that heat dissipation may even be modestly enhanced during pregnancy.
37 Pathways for the transfer of heat from the fetus to the mother are through the
umbilical circulation and through the fetal skin, amniotic fluid and uterine wall. Of
these, the umbilical circulation is generally thought to eliminate the bulk (85%) of fetal
heat (Power, 1989; Schrder and Power, 1997). As the maternal and fetal blood flows
are relatively large and the placenta exposes a large surface area with only a thin
barrier, temperature equilibrium is expected to be reached quickly. Fetal temperatures
rise quickly if the umbilical cord is occluded, supporting the importance of this site
of heat exchange. However, other studies show heat exchange to be less efficient
than predicted, probably because of the operation of counter-current heat exchange
mechanisms in the vessels of the umbilical cord and perhaps in the smaller vessels in
the placenta (Power, 1989; Schrder and Power, 1997). Factors affecting the temperature
of the fetus therefore not only include maternal body temperature per se but also
placental blood flow. There is some evidence to suggest that heat stress from vigorous
exercise (Erkkola et al, 1992), heat stress induced by short-term exercise in hypertensive
patients (Pirhonen et al, 1994), and fever (Laburn et al, 1992) will all reduce placental
blood flow.
38 There is also some evidence suggesting that young infants aged 23 months are at
an increased vulnerability to heat stress compared with neonates due to their higher
metabolic rate, better tissue insulation, and slightly lower surface area to mass ratio
(Fleming et al, 1992). In addition, heat stress in young infants may be associated with an
increased likelihood of respiratory apnoea. Several studies have indicated that the
primary cause seems to be the over-wrapping of infants to protect them from cooler
85
environmental temperatures (see Donaldson et al, 2003); additional risk factors may
include acute febrile illness and an unusually warm or heated environment.
39 The main physical difference between children and adults affecting thermoregulation
is the much higher surface area to mass ratio of children. In a warm environment this
allows them to rely more upon increased skin blood flow and heat loss through
convection and radiation, and less upon evaporative cooling. The lower sweating rate of
children is partly due to a lower sensitivity of the sweating mechanism to thermal
stimuli. Nevertheless, during exercise in thermally neutral or warm environments,
children thermoregulate as effectively as adults. When ambient temperatures exceed
body temperature, however, children are more liable to have a higher rate of heat
absorption compared with adults. Also, whilst neither children nor adults sufficiently
replace fluid loss during exercise in the heat, dehydration may have a more detrimental
effect on children because of their greater reliance upon elevated skin blood flow to
dissipate heat (Falk, 1998).
Effects of heat exposure on cognitive performance
40 There is increasing evidence that cognitive function can be adversely affected by
whole-body heat stress, resulting in increased levels of unsafe behaviour and reduced
task performance (see Hancock and Vasmatzidis, 2003). For example, Ramsey et al
(1983) found a clear correlation between heat stress and unsafe behaviour in workers in
two industrial plants. The increased technological complexity of society has greatly
increased the level of mental workload imposed on human operators (Hancock and
Meshkati, 1988), which, in turn, increases the propensity for human error. For these
reasons, various investigators (NIOSH, 1972; Hancock and Vasmatzidis, 1998, 2000,
2003) have advocated the establishment of criteria for worker exposure to heat stress
based primarily on cognitive rather than physiological performance.
41 A large number of volunteer studies have been carried out over the past 40 years.
Most have been in laboratory settings where subjects have performed a variety of
cognitive tasks during exposure to a series of thermally stressful conditions. These
conditions have usually been generated by specifying combinations of environmental
temperature, humidity and exposure duration. Overall, it appears that simple tasks, such
as reaction time and mental calculations, are less vulnerable to heat stress than more
complex tasks, such as vigilance, tracking and multiple tasks performed together
(Hancock, 1981, 1982). Similar results can be seen in studies with primates (eg de Lorge,
1983); reduced performance of operant tasks occurs reliably at body temperature
elevations of 1C or more.
42 In humans, Hancock and Vasmatzidis (1998, 2000, 2003) suggested that short-term
increases in core body temperature of less than 1C can be associated with the onset of
performance decrement for vigilance, dual and tracking tasks. However, a number of
other variables will affect performance of these tasks including the level of skill and
acclimatisation of the subjects. In addition, core body temperature rises were not
measured in the experiments reviewed but were extrapolated from other data. The
precise relationship between increased body temperature and cognitive performance
cannot therefore at present be defined (Goldstein et al, 2003); changes in response from
small temperature increments would be particularly difficult to judge.
86
Heat-related disorders are not uncommon in healthy people unaccustomed to
hot environments. Heavy exercise either through work or recreation will further
exacerbate any problem, particularly if water and salts lost through sweating are
not replenished.
Occupational limits on work in hot environments that are based on physiological
criteria such as sweat rate, percentage water loss and core temperature
recommend that core temperature be restricted to a maximum of 38C in order
to prevent heat-related illnesses.
Cognitive performance will also be adversely affected by a rise in core
temperature, susceptibility rising with the complexity of the task to be carried
out. However, precise thresholds are difficult to define because of complex
interactions with other variables.
The most important adverse consequence of heat stress is death, and in
practice the majority of excess deaths in hot weather are not due to
hyperthermia but to the cardiovascular consequences of heat stress in older
and vulnerable people.
Infants, young children, older people and adults taking certain prescribed
medicines and drugs may be particularly susceptible to heat stress.
Effects of heat on the development of the embryo and fetus
43 The majority of studies of effects of RF EMFs on embryo and fetal development
were carried out in the 1970s and 1980s. The results of such studies can almost
always be attributed to raised internal and/or embryo and fetal temperature (see
paragraphs 8691). The extensive and well-established teratogenic effects of heat on
development in utero were discussed at a WHO workshop (WHO, 2003a) and are
summarised here.
44 Fetal temperature is determined primarily by maternal temperature, since the fetus
has almost no ability to regulate its own temperature (Schrder and Power, 1997).
Calculation reveals fetal heat production of around 3 W kg
1
, about twice the resting
heat production of the adult. A temperature difference of around 0.5C is required to
bring the rate at which heat is produced in the fetus into balance with the rate at which it
is dissipated to the mother. This close coupling of the fetus to the mother may be
regarded as a heat clamp, which effectively prevents the fetus from independently
controlling its body temperature before birth. Reduced placental blood flow (see above)
could, however, be expected to increase the fetalmaternal temperature gradient and is
associated with reduced fetal growth (Edwards et al, 2003).
45 Animal studies have shown that, depending on the extent to which temperature
is elevated above normal and the duration of exposure, heat either will have no
perceptible effect or will kill pre-implantation stage embryos (Edwards et al, 1995,
2003). Embryos with lethal lesions either will result in an unnoticed pregnancy or might
undergo implantation in the uterus and form an early resorption. Surviving embryos
treated during pre-implantation go through gestation to form offspring having normal
birth weight without an increased incidence of anomalies. Pre-implantation losses are
seen for temperature elevations of 1.6 to 1.8C administered to pigs, sheep and mice for
1 day or more.
87
46 Hyperthermia during organogenesis induces various developmental defects which
can be related to the amount by which maternal body temperature was elevated
(Edwards et al, 1995, 2003; Miller et al, 2002). Indeed, the normal body temperatures
of some animals are in the teratogenic range for humans. Direct heating ex vivo has
similar effects. The central nervous system (CNS), which continues to develop in the
fetal period and early postnatal life, seems especially vulnerable (Edwards et al, 1995,
2003). Threshold studies have been carried out in experimental rodents. These have
examined the incidence of cranio-facial and skeletal defects in mice exposed during early
neural tube closure (gestation day 8.5), and microencephaly, reduced cortical thickness
and learning defects in mice exposed during neurogenesis, including corticogenesis
(gestation days 1314). Other studies have examined the incidence of cranio-facial and
skeletal defects in rats exposed during early and mid-neural tube closure (gestation
days 910.5). Further studies have investigated microencephaly and other nervous
system defects. These include the assessment of changes in learning ability in guinea pigs
exposed during early neurogenesis and the formation of the cortical plate (gestation
days 2024). Threshold temperature elevations and doseresponse relationships have
been identified for cranio-facial and skeletal defects in rats, and microencephaly in
guinea pigs. Generally, statistically significant increases in the incidence of heat induced
abnormalities are seen in the laboratory at maternal temperature increases of around
22.5C or more, mostly following exposure for tens of minutes up to an hour or so.
Higher elevations, up to about 5C, were required for shorter durations.
47 Some work has been carried out using other species (eg Edwards et al, 1995, 2003).
Long-term exposure of pregnant ewes to severe environmental heat during mid-
to late-gestation caused severe growth retardation, attributed to reduced maternal
appetite, placental circulation, and maternal and fetal endocrine changes. Few studies of
the effects of heat on the development of primates have been carried out; a number of
teratogenic effects have been reported following repeated elevations of maternal body
temperature by about 2.5 to 4.5C (Edwards et al, 2003).
48 The developing CNS is considered to be the system most sensitive to raised
maternal temperature. Microencephaly requires the smallest amount of heat which, in
guinea pigs, is engendered by a spike elevation of 2.0 to 2.5C, rising over a 60-minute
exposure period before returning to normal levels. Microencephaly can be induced
during neural tube closure and early neurogenesis and, to a lesser extent, during glial
cell proliferation and during neuronal myelination, although in the latter case the deficit
found at birth is made up during postnatal growth. Interestingly, behavioural deficits
were seen in mice and guinea pigs exposed during corticogenesis and additionally in
guinea pigs during glial cell proliferation. Generally, however, microencephaly is a
marker of gross CNS toxicity and would not necessarily account for minor lesions in
specific brain regions, nor abnormal neuronal migration and subsequent abnormalities
in dendritic arborisation. Corticogenesis is particularly susceptible to ionising radiation
(eg UNSCEAR, 1986) and preliminary studies indicate that it is also sensitive to heat, but
few appropriate studies have been carried out. Growth and maturation of the CNS
continue after birth in most animal species, including humans; the extent to which
increased susceptibility to elevated temperature remains during the postnatal and
juvenile period is uncertain.
88
49 Animal studies have also shown that hyperthermia combined with endotoxins,
arsenic, vitamin A, alcohol and aspirin is more effective in causing developmental
defects than when administered alone (recently reviewed by Edwards et al, 2003).
50 With regard to the effects of maternal hyperthermia on human in utero development,
various teratogenic effects have been reported, including neural tube defects such as
cranio-facial abnormalities (eg reviewed by Edwards et al, 1995, 2003; Graham et al,
1998). The defects produced generally resemble those found in experimental animals
when the hyperthermic episode coincides with the comparable sensitive stage of
development, with the CNS being particularly susceptible. Several studies suggest a
threshold maternal temperature elevation to about 39C, a rise of about 2C above
normal, for a significant increase in the incidence of heat induced defects. However, the
rigour with which this value has been established is not clear. In addition, possible subtle
effects on corticogenesis, which involves processes sensitive to heat such as cell
proliferation and migration, have not been explored.
Elevated maternal body temperature during pregnancy can induce various
developmental defects in animals. Direct heating of the fetus has similar effects.
The CNS seems particularly susceptible, both during early stages such as neural
tube closure, and during later stages of early corticogenesis and myelination.
Neural tube defects and microencephaly appear the most sensitive endpoints to
have been reported. The effects of elevated maternal temperature on the
developing CNS, and particularly on the developing cerebral cortex, have not
been fully explored. It is not clear to what extent the increased susceptibility of
the developing CNS to raised body temperature continues during postnatal and
juvenile growth.
In human studies, similar effects have been reported in the offspring of febrile
mothers as well as in the offspring of mothers who used hot tubs or saunas. An
increased incidence of neural tube defects was found associated with such
episodes in some studies; a threshold of about 39C has been reported but the
rigour with which this has been identified is uncertain.
Thresholds may be lowered in people taking certain medications.
Localised heating
51 The extent to which RF absorption in tissues or organs of the body results in localised
peaks of temperature rise in relation to the average rise in core body temperature
depends not only on the local SAR but also on the vascularity and flow of blood through
the tissue or organ in question. Whilst the former is an intrinsic property of the tissue,
the latter can be varied considerably, particularly through the skin and musculature, by
metabolic, endocrine and neural control mechanisms (eg Sukkar et al, 2000). Localised
heating, for example, usually results in vasodilatation and increased blood flow but this
response may be compromised by cardiovascular responses to whole-body heating (see
paragraphs 25 and 26). The distribution of blood flow through organs and tissues is also
likely to be compromised in older people. Whilst cardiac output is maintained in healthy
older people, total peripheral resistance is increased (Ferrari, 2002). Cardiovascular
diseases that will further compromise the circulation, such as peripheral vascular disease,
89
which may be caused, for example, by atherosclerosis or heart failure, are also highly
prevalent in older people (Corti et al, 2001; De Sanctis, 2001; Lakatta, 2002). In addition,
people taking medications such as beta-blockers that affect the peripheral distribution
of blood flow may be compromised in this respect. The implication is that heat would
be less effectively removed from the tissues of these people.
52 Hyperthermia is being used increasingly as an adjunct to radiotherapy or chemo-
therapy in the treatment of tumours (Dahl et al, 1999; Falk and Issels, 2001); in addition,
localised heating results from the use of ultrasound in clinical diagnosis (Barnett et al,
2000). A considerable number of studies of acute exposure have been carried out both
in vitro and in vivo, investigating doseresponse relationships for tissue damage resulting
from localised tissue or whole-body heating. Temperatures have usually ranged between
40 and 45C, sometimes up to 50C or more, for periods lasting from a few minutes to
several hours. The results of such studies have been summarised recently by Dewhirst
et al (2003) and, specifically regarding the CNS, by Sharma and Hoopes (2003).
53 In animal studies and in a very small number of human studies (mostly of skin
damage), cell loss and/or tissue lesions have been induced in a variety of tissues
following whole-body or localised heating. The results from different studies are
variable but in many cases lesions occurred when temperatures exceeded 42C or
so for periods of more than about 1 hour (Dewhirst et al, 2003). This occurred with
increasing rapidity as temperatures rose further so that at around 45C, lesions could
occur within 1030 minutes in many tissues. With regard to the susceptibility of different
animal tissues, the CNS (including the bloodbrain barrier) and the testes seemed the
most sensitive to heat; significant changes were reported to occur after exposure
to temperatures of only 4041C for periods of around 1 hour (Dewhirst et al, 2003).
However, human and pig skin seemed less susceptible to raised temperature than the
skin of animals such as mice.
54 In contrast to the studies of acute exposure, few chronic studies of heat exposure
on different organs or tissues have been carried out. The lens of the eye is regarded as
potentially sensitive to RF EMF induced heating because of its lack of a blood supply
and consequent reduced cooling ability. In addition, the lens tends to accumulate
damage and cellular debris because of a limited capacity for repair. Acute RF heating
(more than about 4143C for 23 hours) can induce lens opacities (cataracts) in
experimental animals (see Saunders et al, 1991). However, the threshold for cataract
induction resulting from chronic exposure to RF EMFs has not been defined. Historically,
cataracts have been associated with chronic, occupational exposure to infrared radiation
(eg Lydahl and Phillipson, 1984) indicating that some degree of caution should be
exercised with chronic exposure to RF EMFs. Male germ cells in the testis have been
known to be heat sensitive for some time; testicular temperatures in most mammalian
species are normally several degrees below body temperature (Saunders et al, 1991).
Repeated heating of the human testis by 35C will result in a decreased sperm count
lasting several weeks (Watanabe, 1959); similar results have been seen in animal studies.
55 Localised tissue damage, which can develop into multi-organ dysfunction, is seen in
people who have suffered from acute heat stroke (Donaldson et al, 2003). At about
41C, heat denaturation causes damage to the large Purkinje cells of the cerebellum and
cerebral cortex, resulting in selective brain damage. Vascular endothelium, hepatic and
90
renal cells, and striated muscle are affected at higher body temperatures. Complications
seen in heat stroke patients include acute respiratory distress syndrome, pulmonary
oedema, rhabdomyolysis (muscle breakdown), acute renal failure, severe electrolyte
disturbances, coagulopathy, disseminated intravascular coagulation, and liver failure.
A number of studies of acute exposure have been carried out on the adverse
effects of raised tissue temperature using animals, often in the context of
providing guidance on ultrasound use or hyperthermia in clinical practice.
Generally, lesions, including those resulting from cell death, occur when tissue
temperatures exceed about 42C for more than about 1 hour.
The CNS and testes appear particularly susceptible to heat induced damage and
show significant changes in cell numbers following exposures at 4041C and
above. These effects are not dissimilar to those seen in acute heat stroke
patients, although, here, whole-body heating can lead to multi-organ dysfunction.
Damage to the liver, kidney, vascular endothelium and muscle tissues in heat
stroke patients has also been reported; body temperatures may have been in
excess of 41C. In these circumstances however, effects on individual tissues may
be confounded by the systemic responses of the whole body to heat.
Few studies have been carried out of the chronic effects of heat on localised
tissue damage. Repeated heating of the human testis by 35C results in a
decreased sperm count lasting several weeks and similar effects have been seen
in animal studies.
The lens of the eye should also be treated as potentially sensitive to heating.
People in whom the function of the cardiovascular system is impaired by disease
or medication are likely to be more susceptible to localised heating of tissues
than people with normal cardiovascular function.
Other possible effects
56 The increase in personal mobile communications over the last decade has focused
attention towards the possible detrimental effects posed by exposure to low level RF
EMFs. Particular interest has been expressed that exposure at levels too low to cause
significant heating may nevertheless increase the risk of cancer, adversely affect
reproduction and development, or impair brain function.
57 These and other possibilities have been much examined and assessed by national
and international expert groups. Of particular note are the recent comprehensive reviews
by an EC expert group (McKinlay et al, 1996; Veyret et al, 1999), the Independent Expert
Group on Mobile Phones (IEGMP, 2000), the Advisory Group on Non-ionising Radiation
(AGNIR, 2001c, 2003), the Royal Society of Canada (Krewski et al, 2001a,b), and a
French expert group (Zmirou, 2001). Aspects of the literature have also been reviewed
by the Health Council of the Netherlands (HCN, 1997, 2000, 2002), STUK (1999), and the
British Medical Association (BMA, 2001). The earlier literature was comprehensively
summarised by WHO (1993).
Effects on cancer
58 The possibility that low level exposure to RF EMFs may increase the risk of cancer is
a major concern and one that has received much attention. Laboratory studies have
addressed this possibility using well-established in vivo and in vitro techniques. The
91
literature on this topic has been extensively reviewed by McKinlay et al (1996), Brusick
et al (1998), Juutilainen and de Seze (1998), Repacholi (1998), Verschaeve and Maes
(1998), Moulder et al (1999), and Krewski et al (2001a,b). Recent studies were reviewed
by Elder (2003a), Heynick et al (2003), and SSI (2003).
Human studies
59 It is clear that RF EMFs lack sufficient energy to disrupt covalent bonds, so there is
no theoretical basis to believe they can cause mutation or other genotoxic effects by
affecting DNA directly.
60 However, as with low frequency fields, it has been suggested that exposure to
RF EMFs might increase the risk of cancer in humans by decreasing circulating levels of
melatonin. While this possibility for low frequency fields has received much attention
(see Chapter 4, paragraphs 4978), very few laboratory studies appear to have explored
this likelihood for RF EMFs. Mann et al (1998b) reported that serum melatonin levels
were unaffected by night-time exposure to pulsed 900 MHz fields at 0.2 W m
2
. Serum
levels of growth hormone and luteinising hormone were also unaffected, although
cortisol production showed a small, transient increase. Radon et al (2001) reported that
repeated exposure for 4 hours to pulsed 900 MHz fields had no effect on salivary
concentrations of melatonin, cortisol or selected markers of immune function. Similarly,
Bortkiewicz et al (2002) reported that acute exposure to pulsed 900 MHz fields during
the evening has no significant effect on urinary levels of 6-hydroxymelatonin sulphate
measured up to 12 hours later.
Animal studies
61 A number of studies with rodents have confirmed that RF exposure does not increase
mutation rates in somatic or germ cells when temperatures are maintained within
physiological limits (IEGMP, 2000). Positive effects reported in some early studies have
been attributed to RF EMF induced elevations in temperature (WHO, 1993).
62 However, Sarkar et al (1994) reported large-scale structural rearrangements in DNA
in brain and testis cells in mice exposed to 2.45 GHz fields at 0.2 W kg
1
for 2 hours per
day for up to 200 days. In addition, Lai and Singh (1995, 1996) reported an increased
number of single- and double-strand DNA breaks in brain cells from rats exposed for
2 hours to continuous or pulsed 2.45 GHz fields at 0.6 or 1.2 W kg
1
. DNA was analysed
using the alkaline microgel electrophoresis assay. Four hours after exposure to the pulsed
fields, the number of strand breaks was increased, while this increase was detected
immediately after the exposure using continuous fields. It is possible that these changes
somehow involve the production of free-radicals, since these effects were blocked
by treatment with melatonin or another free-radical scavenger (Lai and Singh, 1997c).
An attempt by Malyapa et al (1998) to replicate the results of Lai and Singh was not
successful. Rats were exposed to 2.45 GHz continuous fields for 2 hours at a whole-
body SAR of 1.2 W kg
1
. No effects on DNA breaks in hippocampal brain cells were seen
immediately or 4 hours after exposure. Complementary in vitro studies (Malyapa et al,
1997a,b) using 2.45 GHz, 836 MHz or 848 MHz also failed to find any increase in DNA
strand breaks. The positive results reported by Lai and Singh were attributed by
Malyapa and colleagues to confounding caused by the euthanasia procedure or some
unknown aspect of the animal handling.
92
63 Studies have also been performed using other indicators of DNA damage. Overall,
these studies do not suggest that low level microwaves are genotoxic (Brusick et al,
1998; IEGMP, 2000; Krewski et al, 2001a). Some recent animal studies have reported
some positive effects (Balode, 1996; Vijayalaxmi et al, 1997a,b; Sykes et al, 2001),
although other studies have not (Vijayalaxmi et al, 1999, 2001a). Using the Big Blue
mouse model, Takahashi et al (2002) reported a lack of RF EMF induced mutation in the
DNA of brain cells.
64 As part of the assessment of the carcinogenic potential of RF EMFs, various studies
using rats, mice or rabbits have examined whether long-term exposure to RF EMFs
affects longevity and overall health (see WHO, 1993; IEGMP, 2000). Earlier studies
tended to use RF EMFs at thermal levels but, even so, few detrimental effects on health
or physiological status were reported. Liddle et al (1994) reported the lifespan of mice
was shortened by life-long, intermittent exposure to 2.45 GHz continuous fields at
6.8 W kg
1
, but not with exposure at 2 W kg
1
. The decrease in lifespan was again
attributed to the effects of thermal stress. There appear to be no consistent effects of
low level RF exposure on the haematopoietic system (Chou et al, 1992; WHO, 1993;
Jauchem, 1998). Similarly, significant effects on the immune system have been ascribed
to thermal responses or to physiological changes occurring during thermoregulation as
a consequence of exposure (IEGMP, 2000). Some recent studies suggest that exposure
to low level fields at around 1020 GHz may increase the production of tumour
necrosis factor in peritoneal macrophages of tumour-bearing mice (Fesenko et al, 1999;
Novoselova et al, 1999, 2001).
65 Early studies exploring the possibility that RF EMFs might affect spontaneous
tumour incidence tended to suffer from insufficient dosimetry, poor histopathology or
inadequate follow-up (IEGMP, 2000). Better conducted studies using mice prone to the
development of mammary tumours have reported a lack of RF EMF effects (Toler et al,
1997; Frei et al, 1998a,b; Jauchem et al, 2001). La Regina et al (2003) found intermittent
long-term exposure of rats to 835 MHz FDMA or 847 MHz CDMA mobile phone signals
had no effect on spontaneous tumour incidence in any organ.
66 Repacholi et al (1997) reported that the number of tumours in E Pim-1 mice
exposed to 900 MHz pulsed at 217 Hz was about double that expected in unexposed
animals (43%compared to 22%). Animals were exposed twice each day for 30 minutes,
from soon after birth until about 18 months old. The SARs were variable and ranged
from about 0.008 to 4 W kg
1
depending on the age/size of the animals. An attempt to
replicate this study using improved dosimetry and pathology with larger numbers of
animals failed to confirm these results (Utteridge et al, 2002; see also comments by
Utteridge et al, 2003). Exposure for up to 24 months was not associated with any field
dependent increase in lymphoma at SARs from 0.25 to 4 W kg
1
. Generally, it is very
difficult to extrapolate results of such studies using transgenic animals to humans, and
the implications for health are far from clear (IEGMP, 2000; Krewski et al, 2001a).
67 The possibility that RF EMFs may act to enhance or promote the growth of tumours
caused by other agents has received attention. The effects on standard rodent models
of cancer have been tested using a wide range of mobile phone signals and exposure
conditions (Wu et al, 1994; Imaida et al, 1998a,b, 2000, 2001; Chagnaud et al, 1999;
Bartsch et al, 2001; Heikkinen et al, 2001b; Mason et al, 2001; Anane et al, 2003). No
consistent field dependent effects were reported, suggesting exposure does not cause
93
promotional effects. Similarly, studies investigating spontaneous brain and spinal cord
tumours and those induced by prenatal application of chemical carcinogens (Adey et al,
1999, 2000; Zook and Simmens, 2001) have not reported any field dependent increases
in tumour numbers or incidence.
68 The possibility that RF EMFs might affect the progression of tumours has been
investigated following injection of various types of cancer cells into healthy rats and
mice. Positive results in early studies have been attributed to the effects of heat or
other coincidental stress (WHO, 1993). Other studies using both continuous and pulsed
signals suggest that exposure does not affect survival time or enhance the growth of
tumours (Santini et al, 1988; Salford et al, 1997; Higashikubo et al, 1999).
69 A few studies have investigated if RF EMFs affect circulating melatonin levels. Strk
et al (1997) measured melatonin levels in the saliva of cattle in the vicinity of a short-
wave radio transmitter and found no chronic effects, although a possible short-term rise
was noted. Vollrath et al (1997) found that short-term exposure of rats at night or during
the day to continuous or pulsed 900 MHz fields at 0.060.36 W kg
1
had no effect on
pineal melatonin synthesis. Similar results were seen in Djungarian hamsters exposed
at 0.04 W kg
1
and Heikkinen et al (1999) found no effects on melatonin production in
mice chronically exposed to pulsed or continuous 900 MHz fields at 0.35-1.5 W kg
1
.
Imaida et al (1998a,b) reported repeated, daily exposure to 929 MHz and 1.5 GHz fields
for 6 weeks increased day-time serum melatonin levels in rats.
70 Using a microgel electrophoresis assay, Lai and Singh (1997c) reported that
subcutaneous injection of melatonin (1 mg kg
1
) immediately before and after RF
exposure blocked any field induced increases in DNA single- and double-strand breaks
in brain cells of a rat. Animals were exposed for 2 hours to pulsed 2.45 GHz (2 s,
500 pulses per second) at an average whole-body SAR of 1.2 W kg
1
. Similar blocking
effects were reported using the spin-trap compound, N-tert-butyl-alpha-phenylnitrone.
71 Changes in heat shock (hsp) gene expression following exposure to low level
RF EMFs have been investigated using a transgenic nematode worm, Caenorhabditis
elegans. This nematode model carries the bacterial lacZ reporter gene downstream
of the promoter of the hsp16 gene. When these nematodes are exposed to conditions
that would stimulate expression of heat shock protein, they produce -galactosidase
(the product of the lacZ gene) which can be readily assessed. This model has been used
for both aquatic and soil-based toxicity testing. It has been reported that exposure
of C elegans to 330 or 750 MHz fields for 216 hours at 0.5 W elevated expression of
hsp genes, suggesting that exposure induced protein damage in these nematodes
(Daniells et al, 1998). The SAR was estimated at 0.001 W kg
1
(de Pomerai et al, 2000a).
There were no detectable increases in temperature of either the worms or the culture
medium the increase in reported gene activity was considered equivalent to a 3C
increase in temperature. In addition, it was further reported that growth rate and
development into egg-bearing adults was significantly increased by overnight exposure
at 0.5 W, and this growth increase was sustained for 24 hours after cessation of
exposure (de Pomerai et al, 2000b, 2002). Increased expression was also reported in a
preliminary study which used the signals from a digital mobile phone handset to expose
these worms for 7 hours (de Pomerai et al, 1999). These phenomena merit further
study and independent replication; the implications for human health also need careful
consideration (see French et al, 2001).
94
Cellular studies
72 Many cellular studies have investigated the possibility that exposure to RF EMFs
may induce biological changes that may be relevant to the causation or development of
cancer. As with studies using animal models, a wide variety of cell types, endpoints and
exposure conditions have been employed. Overall, the results of these studies are
somewhat mixed, and most reported effects appear to be relatively modest in the
absence of significant heating. These particular studies have been comprehensively
reviewed by several expert groups, including IEGMP (2000) and Krewski et al (2001a,b),
and most recently by Meltz (2003).
73 In general, results from a number of experiments (summarised by WHO, 1993; Brusick
et al, 1998; Krewski et al, 2001a) do not provide convincing evidence that RF EMFs are
genotoxic. Consistent with many studies indicating that exposure to various RF EMFs
does not cause mutation, Gos et al (2000) reported that the mutation rate in yeast was
unaffected by exposure to 900 MHz fields at SARs of 0.13 or 1.3 W kg
1
.
74 Several studies have measured the potential of RF EMFs to induce DNA damage
in vitro using the alkaline microgel electrophoresis assay to measure the incidence of
DNA strand breaks. No consistent field dependent effects have been reported using
various mouse or human cell lines exposed to a variety of frequencies and modulations,
mostly associated with mobile phone technologies (Malyapa et al, 1997a,b; Vijayalaxmi
et al, 2000; Li et al, 2001; Miyakoshi et al, 2001; McNamee et al, 2002a,b; Tice et al, 2002).
In these studies, cells were exposed from 0.6 W kg
1
for 24 hours to 100 W kg
1
for
2 hours.
75 Other studies have explored the effects of RF EMFs on indirect measures of DNA
damage. Effects on chromosomal aberrations have been well investigated. Results
are mixed but many studies suggesting positive effects have been criticised for
confounding due to potential thermal effects (IEGMP, 2000). Better conducted, more
recent studies using human lymphocytes have not reported any field dependent
effects (Vijayalaxmi et al, 1997c, 2001b,c; Maes et al, 2001). Effects on sister chromatid
exchange have also been explored. In a preliminary study, Khalil et al (1993) reported
increases in sister chromatid exchange in human lymphocytes exposed to 167 MHz,
but no field dependent effects have been reported using 2.45 GHz at 75 W kg
1
(Maes
et al, 1993), or using GSM fields around 900 MHz at up to 10 W kg
1
(Maes et al, 1995,
1997, 2001). Further studies have explored effects on micronucleus formation and,
again, results are mixed (IEGMP, 2000). Some studies using mobile phone signals did
not report any effects on human lymphocytes (Vijayalaxmi et al, 2001b,c), human
leukocytes (McNamee et al, 2002a,b; Tice et al, 2002) or mouse fibroblasts (Bisht et al,
2002). A negative result was also reported using human lymphocytes exposed to
2.45 GHz (Vijayalaxmi et al, 1997c). In contrast, increases in micronuclei formation have
been reported in human lymphocytes following exposure to the mobile phone signals
(DAmbrosio et al, 2002; Tice et al, 2002) and to 2.45 or 7.7 GHz fields (Maes et al, 1993;
Zotti-Martelli et al, 2000).
76 Although there is a lack of consistent evidence to suggest that exposure to
RF EMFs has a direct carcinogenic effect, some studies have investigated whether
RF EMFs may act synergistically with known mutagens or promoting agents to enhance
their effect.
95
77 Early studies reported enhancement of latent cellular transformation by 2.45 GHz
fields following exposure to x-rays or benzo[a]pyrene (Balcer-Kubiczek and Harrison,
1985, 1991), although the effect was not replicated using 836 MHz fields (Cain et al,
1997). Similarly, amplification of the genotoxic effects of mitomycin-C reported by
Scarfi et al (1996) and Maes et al (1997) are in contrast to earlier negative results using
chemical carcinogens (see IEGMP, 2000). Pakhomov et al (1997) reported exposure to
61 GHz fields at thermal levels could enhance DNA recombination in yeast cells
exposed to ultraviolet radiation (UVR). In a recent study of neoplastic transformation,
Roti Roti et al (2001) exposed C3H 10T mouse fibroblasts to FDMA-modulated
835 MHz or CDMA-modulated 847 MHz fields for 7 days at 0.6 W kg
1
. The cells were
also irradiated with 4.5 Gy of x-rays. No increases in neoplastic transformation were
reported following exposure to RF EMFs either alone or in conjunction with x-rays.
78 Calcium ions play an important role in many cell signalling pathways. Various
studies have investigated the effects of RF EMFs on calcium ion movement across
the cell membrane, particularly in brain tissues. IEGMP (2000) concluded that the
evidence for an RF dependent effect was contradictory, although the possibility that
such effects may occur with amplitude-modulated signals was considered intriguing.
79 The advent of fluorescent dyes specific for calcium ions has made the real-time
estimation of intracellular calcium concentrations in individual cells possible. Utilising
a specific fluorescent dye, Cranfield et al (2001) exposed human Jurkat cells to a
continuous or pulsed 915 MHz field for 10 minutes at 1.5 W kg
1
. No consistent effects
on mean calcium levels were detected in individual cells, nor were there significant
changes in the percentage of cells showing calcium spikes, spike height or number
of spikes. The single significant field dependent change observed may be attributable
to chance.
80 Studies investigating the effects of RF exposure on the expression of early response
genes, such as c-fos and c-jun, have produced inconsistent results (Ivaschuk et al, 1997;
Goswami et al, 1999).
81 Other studies have also reported field dependent changes in heat shock proteins.
Kwee et al (2001) exposed transformed human epithelial cells to 960 MHz for
20 minutes at 0.002 W kg
1
and found increased levels of hsp70, but not hsp27.
Leszczynski et al (2002) reported an increase in hsp27 in human endothelial cells
exposed to a 900 MHz field for 1 hour at an average SAR of 2 W kg
1
. The number of
phosphoproteins including hsp27 was transiently increased more than three-fold
following exposure. However, statistical analysis of these results was not presented.
Tian et al (2002) found effects of 2.45 GHz on hsp70 expression in glioma cells
using SARs above 20 W kg
1
even when thermal effects were taken into account.
While interesting, replication and confirmation of these studies are needed before any
conclusions can be drawn.
82 Natarajan et al (2002) investigated the effect of high peak power pulsed fields on
nuclear factor kappa B protein, an important regulator of DNA transcription. Human
monocytes were exposed to 8.2 GHz for 90 minutes. The average SAR was 10.8 W kg
1
but 10%of the cells could have been receiving 22 to 29 W kg
1
. An almost four-fold
increase in nuclear factor kappa B activity was observed, which was considered to be
likely due to thermal effects.
96
83 Finally, increased cell proliferation may play a role in carcinogenesis. The studies
investigating whether RF EMFs increase cell proliferation have generally produced
mixed results (IEGMP, 2000; Krewski et al, 2001a).
84 Ornithine decarboxylase (ODC) is an enzyme whose activation is related to cell
proliferation. Most, but not all, tumour promoters increase ODC activity. Transient
changes in ODC levels and activity have been reported in mouse fibroblasts exposed to
835915 MHz fields amplitude-modulated at between 16 and 60 Hz for several hours
at 2.5 W kg
1
(Byus and Hawel, 1997; Penafiel et al, 1997). Earlier studies reported field
dependent effects in human melanoma and two other cell lines using amplitude-
modulated 450 MHz fields at 0.08 W kg
1
(Byus et al, 1988; Litovitz et al, 1993). No
changes in ODC activity were seen using frequency-modulated or unmodulated fields.
However, all the field dependent changes were relatively modest compared to those
induced by established tumour-promoting substances (IEGMP, 2000). No additional
in vitro studies appear to have investigated this phenomenon further. Stagg et al (2001)
found that acute exposure of rats to a pulsed 1.6 GHz field at up to 5 W kg
1
did not
affect ODC levels in brain tissues. Regarding other enzyme systems, too few studies
have investigated potential RF EMF influences to formulate conclusions (Pashovkina
and Akoev 2000; Ivanov et al, 2001; Seaman et al, 2002).
85 Some studies have reported modest increases in proliferation (Cleary, 1997; Stagg
et al, 1997) but other studies have reported either no effects (Gos et al, 1997) or
decreases in cell growth (Kwee and Raskmark, 1998). Using 835 MHz FDMA-modulated
signals or 847 MHz CDMA-modulated signals, Higashikubo et al (2001) reported that
exposure of mouse fibroblasts, C3H 10T cells, or human glioma cells at 0.6 W kg
1
for
up to 100 hours had no field dependent effects on cell cycle parameters, including
transit time through G1, G2, and S phase, and the probability of cell division. Wang et al
(2001) demonstrated an inhibition of proliferation and induction of apoptosis in naso-
pharyngeal carcinoma cells exposed to 42.2 GHz at a power density of 1 mW cm
2
for
30 minutes each day for 4 days.
There is no direct experimental evidence to suggest that RF EMFs may
significantly increase the risk of cancer.
Melatonin levels in humans do not appear to be affected by exposure to RF EMFs
although very few studies have investigated this possibility. The evidence from
animal studies is more equivocal.
Well-performed animal studies clearly show that long-term RF exposure does
not promote the development of specific mammary cancers, colon tumours,
lymphomas or liver cancers. Nor does exposure appear to increase the
development of specific brain and spinal cord tumours, or to affect the
progression of injected tumours. While a few animal studies have reported field
dependent effects, some of these can be criticised for poor experimental
techniques and others may have little relevance to human health.
The majority of cellular studies do not suggest RF EMFs can affect indicators of
DNA damage or repair. However, reports of field dependent increases in the
expression of heat shock genes in the apparent absence of heating justify
further study.
Thus while the results of many laboratory studies strongly indicate the absence
of any increased risk of cancer, some caution still needs to be exercised since it is
not possible to dismiss all possibilities.
97
86 The possibility that RF EMFs may affect fertility, reproduction, and development has
been much investigated. Experimental studies have been reviewed by Jensh (1997),
Verschaeve and Maes (1998), OConnor (1999) and Krewski et al (2001a), and most
recently considered by Heynick and Merritt (2003) and AGNIR (2003).
87 Overall, there is no convincing scientific evidence that exposure to low level RF EMFs
can affect reproduction and development in mammals where consistent effects
have been reported they can be attributable to thermal insults induced by exposure.
Hyperthermia is an accepted teratogen and exposure of pregnant animals to RF EMFs
sufficient to induce elevations of maternal temperature will cause a hierarchy of
responses that depend on the magnitude and duration of the rise in temperature. These
responses range from subtle behavioural changes in offspring and growth retardation,
to gross morphological changes and increased intrauterine deaths (Saunders et al, 1991;
Edwards et al, 2003).
88 Testicular temperatures in mammals are normally several degrees below that of the
rest of the body, and exposure to heat, from RF EMFs (or other sources), can induce
temporary sterility. Recently, Khillare and Behari (1998) reported that male fertility
could be decreased by prolonged exposure to 200 MHz fields, modulated at 16 Hz at
about 2 W kg
1
. However, modest warming may explain these effects (IEGMP, 2000).
89 Studies investigating whether RF EMFs potentiate the teratogenic effects of chemicals
and solvents suggest complex interactions can occur but only using fields at hyperthermic
levels (Nelson et al, 1997a,b, 1999, 2001; Cheever et al, 2001).
90 In a small study, Magras and Xenos (1997) reported that exposure to the various
fields from a commercial antenna park produced a rapid drop in fertility in mice.
Twelve male and female mice were caged outdoors close to the antenna park or in a
nearby village. Exposures ranged between 1.7 and 10 mW m
2
. The animals were mated
five times over six months. It was found that the litter sizes were small compared to
those of animals living in an RF EMF free environment in a laboratory. The last mating
away from the antenna park did not restore litter size. The lack of a concurrent control
group, however, undermines these results, and the possibility that the observed changes
were the result of other stresses in the environment cannot be discounted.
91 Two studies have examined the behavioural consequences of prenatal (and early
postnatal) exposure to RF EMFs. Cobb et al (2000) exposed pregnant rats to ultrawide-
band microwave pulses (300 ps rise time, 1.8 ns pulse width, average whole-body SAR
0.045 W kg
1
) for 2 minutes per day from day 3 to 18 of gestation (and from postnatal
day 1 to 10). Offspring were examined using an extensive battery of developmental
landmarks and functional and behavioural tests, including water maze performance and
operant response. No significant exposure dependent effects were found except on
three metrics (less vocalisation in exposed males, longer medial-to-lateral length of
hippocampus, and lower mating frequency but without change in mating success). The
lack of a consistent aetiology suggested these differences were attributable to chance.
Bornhausen and Scheingraber (2000) exposed freely-moving pregnant rats to pulsed
900 MHz fields continuously from day 1 to 20 of gestation. Whole-body SAR (of dams)
ranged from 0.00175 to 0.075 W kg
1
. Subsequent operant performance of offspring was
assessed as adults using three differential schedules of reinforcement requiring either
high or low rates of responses exposure had no effect on task performance.
98
Although there are few informative studies, the available scientific data do not
suggest that exposure to RF EMFs at levels found in the environment poses any
significant threat to reproduction or development. One study suggesting that low
level exposure decreases fertility in mice contains severe methodological flaws.
92 The brain and nervous system have long been considered sensitive targets for the
effects of exposure to low level RF EMFs. Various claims have been made over many
years suggesting that RF EMFs from a variety of civilian and military sources may cause
adverse changes in an assortment of behavioural or neurological functions. These
include lack of concentration, poor memory, changes in sleep pattern, as well as loss of
appetite and reduced libido. Together these symptoms have sometimes been called
the neurasthenic or microwave sickness syndrome. More recently, exposure to mobile
phones has been suggested to cause similar effects.
93 These possibilities have been much investigated in respect of a variety of endpoints
using a wide range of exposure conditions. The earlier literature was reviewed by
WHO (1993), while more recent studies have been considered by Hermann and
Hossman (1997), Pakhomov et al (1998), DAndrea (1999), IEGMP (2000), Krewski et al
(2001a,b), Zmirou (2001), Hamblin and Wood (2002), Sienkiewicz (2002) and DAndrea
et al (2003a,b).
Human studies
94 Due to the close proximity of the head to a mobile phone handset in normal use, the
tissues and structures within the head may absorb relatively greater amounts of energy
than is absorbed elsewhere in the body. Specific concerns have been expressed about
possible adverse effects on memory, attention or other cognitive functions.
95 The detrimental effects of mobile phone use on driving performance have been
comprehensively reviewed by IEGMP (2000). Impairments in speed or accuracy of
reaction to changing road circumstances have been clearly identified. However, as these
do not appear to be primarily caused by exposure to RF EMFs, they are not considered
further here.
96 Subjective symptoms A wide range of subjective symptoms has been attributed
to exposure to various sources of RF EMFs both at home and at work. Some users of
mobile phones report they suffer a variety of subjective complaints, including headaches
and migraines, fatigue, skin itches, and sensations of warmth (Frey, 1998; Hocking, 1998;
Chia et al, 2000; Hocking and Westerman, 2000; Sandstrm et al, 2001; Santini et al,
2002). Less commonly reported symptoms include dizziness, blurred vision, memory
loss, confusion and vagueness, toothaches, and nausea. Prosaic explanations for some
of these symptoms may exist (Sandstrm et al, 2001).
97 In a single-blind study, Koivisto et al (2001) presented 48 normal individuals with
either real or sham exposure to a pulsed 902 MHz field. Subjects were asked to rate
subjective symptoms and sensations during these sessions. No significant differences
were found between exposure conditions, although fatigue and headaches increased
toward the end of sessions.
99
98 In a double-blind study, Hietanen et al (2002) exposed 20 volunteers, who reported
themselves to be sensitive to RF EMFs, to analogue or digital mobile phone signals.
Blood pressure, heart rate and breathing rate were measured every 5 minutes and
subjects were asked to report any abnormal feelings. Nineteen of the subjects reported
symptoms, most of which were sensations in the head of pain or warmth. However,
more symptoms were reported during sham exposure than real exposure, suggesting
the possibility that the blinding conditions between treatments were not adequate. The
physiological parameters showed no relevant trends, although they tended to decrease
throughout the day.
99 In another double-blind study, Zwamborn et al (2003) explored the effects of
exposure to GSM and UMTS signals on self-reported well-being. Small, but significant,
field dependent effects with UMTS signals were seen in a group of subjects who had
previously reported complaints attributed to GSM fields and in a control group who
had not reported any complaints. No effects were seen using GSM signals either at 900
or 1800 MHz. An explanation based on thermal effects seems unlikely: the maximum
SAR in the head was calculated to be in the region of 0.07 mW kg
1
.
100 Cognitive performance

Several recent studies have examined the effects of
RF EMFs associated with mobile phone use on attention, memory and other cognitive
functions. Overall, these studies only provide weak evidence that subtle changes
in cognitive performance may occur following exposure at levels below those
recommended by ICNIRP (1998) for general public exposure. The underlying effects
may be thermal and result from very small, localised heating of the brain in the areas
beneath the phone.
101 Preece et al (1999) used a copy of a commercial phone with an output of 1 W, and
found that exposure to an analogue 915 MHz field for about 30 minutes significantly
decreased choice reaction time. Non-significant changes were observed using digital
signals. Simple reaction times were unaffected and there were no changes in word,
number or picture recall, or in spatial memory. The changes in choice reaction time
were attributed to an improvement in synaptic function within the angular gyrus or to a
facilitation of neuronal transmission caused by localised heating.
102 Koivisto et al (2000a) used a digital phone with an output of 0.25 W, and found that
exposure to 902 MHz fields significantly decreased response times in simple reaction
time and vigilance tasks. In addition, the time needed to accomplish a mental arithmetic
subtraction task was decreased during exposure. Memory tasks were not examined in
this study. The changes were attributed to localised heating effects exerting a facilitating
effect on cognitive processing in the prefrontal cortex and parietal cortex, especially
in those tasks that require attention or cognitive manipulation in working memory. A
further study (Koivisto et al, 2000b), using a task where the working memory load was
varied, found that exposure again speeded up reaction time, but this effect was only
significant when the memory load was particularly demanding. However, an attempt by
the same group to confirm and extend these results was not successful (Haarala et al,
2003). Using an improved experimental design, no consistent field dependent effects
were observed on reaction times or error rates during the performance of a battery
of nine cognitive tasks. This suggests that the results of the original study should be
treated with some caution.
100
103 Other studies have reported RF EMF effects broadly consistent with the original
results of Koivisto et al or Preece et al, although all of these suffer problems in method
or interpretation which challenge their usefulness. Zwamborn et al (2003) reported
a diffuse and inconsistent pattern of field dependent effects on a range of different
cognitive tasks following very low level, whole-body exposure to GSM and UMTS fields.
Lass et al (2002) reported that exposure to a 450 MHz field modulated at 7 Hz improved
performance of a recognition memory task. Edelstyn and Oldershaw (2002) found that
exposure facilitated cognitive tasks involving attentional capacity and in one task which
involved processing speed. Smythe and Costall (2003) reported a field dependent
improvement in immediate memory in male subjects exposed to an 1800 MHz field: no
effects on memory were seen after about 7 days, or in female subjects at either time.
Lastly, a mild facilitating effect on attention, as measured in paper and pencil tests, was
reported by Lee et al (2001) in adolescent users of mobile phones. Attempts to
replicate these results would be most useful.
104 Electrical activity of the brain Using the fields associated with mobile phones,
most recent electrophysiological studies have failed to find an effect of pulsed RF EMFs
on the spontaneous, awake electroencephalogram (EEG) (Roschke and Mann, 1997;
Hietanen et al, 2000). However, under more demanding experimental conditions, such
as during the performance of memory tasks, possible field dependent effects have
been noted. For example, Freude et al (1998, 2000) reported effects of pulsed 916 MHz
fields on slow brain potentials at right, central and temporo-pariental regions during a
visual monitoring task. Eulitz et al (1998) also found a decrease in spectral power in the
bands 18.7531.25 Hz during an auditory discrimination task. The effect was only present
when subjects processed task-relevant target stimuli and was not present for irrelevant
standard or novel stimuli. It was also found to be specific to the side of the brain directly
exposed to the field. Similarly, in narcoleptic patients, Jech et al (2001) reported effects
on two specific components of the EEG evoked by the presentation of rare (oddball)
stimuli on the right half of the visual field.
105 EEG changes have been reported in healthy volunteers exposed to pulsed 902 MHz
fields during performance of either an auditory task (Krause et al, 2000a) or a visual
memory task (Krause et al, 2000b). Both of these studies found that exposure affected
the 810 Hz band of the EEG which has been associated with attentional demands
(Klimesch et al, 1992). This suggests that RF EMFs may have effects on the cortical
oscillatory systems mediating cognitive processes such as attention (Krause et al,
2000a). Croft et al (2002) reported effects on event-related desynchronisation during an
auditory discrimination task and on resting EEG parameters from a 900 MHz GSM
handset operating in listening mode producing an average power of 34 mW.
106 Sleep The normal, cyclical variations in the functional state of the brain, which
occur during sleep, can be examined and quantified using the EEG. A number of recent
studies have used these techniques to examine the effect fields associated with mobile
phones may have on sleep.
107 An initial report by Mann and Roschke (1996) indicated that exposure to pulsed
900 MHz fields at night decreased the latency to sleep onset. There was also a reduction
in the duration and percentage of rapid eye movement (REM) sleep, and an increase in
101
spectral power density during REM sleep. However, these results could not be repeated
in subsequent studies using a circular antenna exposure system (Wagner et al, 1998,
2000). Borbely et al (1999) found that the intermittent exposure to a GSM-like signal
affected the spectral power in non-REM sleep, with a maximal rise in the 1011 Hz and
13.514 Hz bands of the EEG. REM sleep and sleep onset latency remained unaffected.
Lebedeva et al (2001) found that overnight exposure caused a decrease in the percentage
of slow-wave sleep.
108 Results obtained by Huber et al (2000, 2002) suggest that acute exposure during
waking may affect the subsequent EEG pattern during sleep. Using a pulsed 900 MHz
signal from a mobile phone, exposure at a peak SAR of 1 W kg
1
increased the spectral
power in the 9.7511.25 Hz and 12.513.25 Hz bands of the EEG in non-REM sleep. The
effects persisted, but were maximal during the initial part of sleep. Exposure during
continuous wave fields was without significant effect. Changes in cerebral blood flow
were also measured in the dorsolateral prefrontal cortex following exposure.
109 Cardiovascular function Changes in cardiovascular function are unlikely to occur
in the absence of thermoregulatory responses (Jauchem, 1997; Black and Heynick, 2003).
Early reports from the former Soviet Union suggesting that occupational exposure
to RF EMFs may affect heart rate and reduce blood pressure have been attributed to
chance variation (IEGMP, 2000). Mann et al (1998a) reported that the control of heart
rate was not affected by exposure at night to the fields from a mobile phone.
110 However, in a small study Braune et al (1998) reported that both systolic and
diastolic blood pressure of volunteers was increased by about 5 mm Hg by exposure
for 35 minutes to the signals from a GSM mobile phone held close to the right ear.
Heart rate was slightly lowered by exposure. Since capillary perfusion in the hand was
decreased, it was concluded that exposure had increased vasoconstriction, possibly as
a result of changes to sympathetic activity originating within the brainstem. However,
these effects were not replicated in a subsequent, more extensive study by Braune et al
(2002). This study also addressed the criticisms of Reid and Gettinby (1998) on the
design of the original study. Slow increases in blood pressure were again noted, but
these were independent of RF exposure. In addition, there were no field dependent
changes in serum levels of norepinephrine, epinephrine, endothelin and cortisol, which
affect vasomotor tone.
Laboratory studies with volunteers have only recently begun to investigate the
effects that low level exposure to the fields associated with mobile phones may
have on the brain and behaviour. To date, only subtle and transient effects have
been reported and any implications for health remain unclear.
The available data are too limited to decide if exposure can cause headaches or
other subjective symptoms.
There is some evidence that acute exposure may cause mild facilitation effects
on attentional processes, and decrease reaction times to stimuli, possibly as a
consequence of localised heating of brain tissues. The possibility that the
magnitude of the effect increases with the complexity of the task used is unclear.
Effects on sleep have been reported but remain less well defined. No consistent
changes have been seen on cardiovascular function.
102
Animal studies
111 The possible effects of microwaves on the brain and behaviour have been studied
in animals using a range of methods and techniques, from changes in specific gene
expression in cells, to investigations of changes in learned behaviours. These studies
have been reviewed by Hermann and Hossman (1997), Pakhomov et al (1998), and
DAndrea (1999). RF EMF effects on learning and memory have been considered by
Lai (2001).
Gene expression
112 A few studies have investigated if the induction of stress-related genes and their
proteins increase following exposure to RF EMFs. These genes respond to various
insults, such as ischemia or hyperthermia, and help to minimise potential damage.
Mickley et al (1994) exposed rats to 600 MHz fields at 9.3 W kg
1
and measured
increased c-fos protein expression in various areas of the forebrain, especially in
cortical and periventricular areas. These changes were blocked by an opioid antagonist
and were considered consistent with opioid-mediated stress. In another study, rats
exposed to high peak power ultrawideband pulses (0.252.5 GHz) at a peak electric
field of 250 kV m
1
for 2 minutes did not show any changes in expression of c-fos
protein (Walters et al, 1995). Body temperatures of the animals in this study rose by less
than 0.5C.
113 Fritze et al (1997a) exposed the heads of rats to simulated GSM signals (890915 MHz
pulsed at 217 Hz) at 7.5 W kg
1
and measured changes in the messenger RNAs of
hsp70, c-fos, c-jun, and GFAP using in situ hybridisation histochemistry. Only changes
consistent with brain hyperthermia or immobilisation stress were found either
immediately or 24 hours after exposure. Seven days after exposure, no changes were
observed in the levels of the relevant proteins. Similarly, Morrissey et al (1999)
reported that local exposure of the head of mice to a 1.6 GHz Iridium satellite phone
signal (pulse modulated at 11 Hz with a duty cycle of 4 : 1 and a pulse duration of
9.2 ms) for 1 hour only significantly increased c-fos expression in the forebrain when
the average SAR in the brain exceeded 4.3 W kg
1
. The pattern of c-fos change was
consistent with a thermal stress, thermoregulatory activity, and the effects of restraint.
There were no differences between continuous and pulsed exposures. Stagg et al (2001)
exposed rats for 2 hours to 1.6 GHz Iridium signals using a head-only exposure system
that produced local SARs in the brain of up to 5 W kg
1
. No significant increases in body
temperature were recorded and no field dependent increases in c-fos and c-jun mRNA
were observed.
Bloodbrain barrier
114 The bloodbrain barrier (BBB) serves to protect the brain from potentially harmful
compounds and helps to regulate and control the fluid environment of the brain cells.
About 20 years ago several studies reported that low level exposure to RF EMFs may
alter the permeability of the BBB and cause leakage of molecules from the blood into
the cerebrospinal fluid. Such responses could produce severe and lasting consequences.
However, better controlled studies failed to replicate these findings and the original
observations were ascribed to various confounding factors (see Blackwell and Saunders,
103
1986). Consistent changes in the BBB were only found when physiologically significant
heating was induced (using SARs of more than about 7 W kg
1
).
115 However, some recent studies have again suggested that low level RF exposure
may affect the BBB. Neubauer et al (1990) reported that significant changes occurred
with exposures above 2 W kg
1
for 30 minutes or more. Persson et al (1997) reported
changes that varied with both modulation frequency and SAR. Any changes appeared
largely independent of SAR for continuous fields, whereas there appeared to be an
inverse relationship between effect and SAR for pulsed fields. SARs of around 0.01 W kg
1
produced more than twice as many pathological changes than SARs of 28 W kg
1
which may have produced heating. In an extension of this work, Salford et al (2003)
reported that brief exposure of juvenile rats to 915 MHz fields caused long-lasting
neuronal damage throughout the brain, and especially in the cortex, hippocampus
and basal ganglia. Animals were exposed for 2 hours at SARs of 0.002, 0.02 and
0.2 W kg
1
and damage was reported to increase with increasing SAR. However,
there are a number of caveats with the study and major reservations regarding the
results. These include not only the modest size of study (n = 8/group) and a rather
wide age range of the rats used (1226 weeks of age), but also serious uncertainties
about the metrology and dosimetry. The quantification of damaged neurons was
also highly subjective, and too few data were presented to justify any conclusions.
Overall, replication using improved methods and with tighter control of experimental
variables is necessary before any extrapolation can be made regarding potential human
health effects.
116 In contrast, other recent studies have failed to confirm these changes on albumin
permeability using either single or repeated exposure (Fritze et al, 1997b; Tsurita et al,
2000; Finnie et al, 2001, 2002). Exposure at thermal levels only induced modest and
transitory changes in the BBB. In addition, none of these well-conducted studies
reported any morphological changes in brain tissues.
Electrical activity
117 The electroencephalogram (EEG) is a description of the spontaneous, slow electrical
activity of the brain and can be used to indicate subtle changes in brain function.
Exposure to very low levels of amplitude-modulated fields has been reported to alter
the EEG of the brain in cats and rabbits (see WHO, 1993).
118 Complex changes in spectral power of various bands of the EEG have been
reported in recent studies using rodents, rabbits and cats (Thuroczy et al, 1994;
Chizhenkova and Safroshkina, 1996; Pu et al, 1997; Vorobyov et al, 1997; Ivanova et al,
2000). However, differences in experimental and exposure conditions preclude making
general conclusions on these data, although some of the changes appear to reflect
thermal responses.
Neurotransmitters
119 Changes in various neurotransmitter systems have sometimes been reported in a
number of isolated studies from different laboratories. Many of these data were reviewed
by Hermann and Hossman (1997) who ascribed many of the reported changes to
spurious temperature effects.
104
120 An extensive series of experiments from one laboratory suggests that exposure to
low level RF EMFs may affect cholinergic function in a time-dependent fashion (Lai,
1992). Both pulsed and continuous 2.45 GHz fields could elicit decreases in cholinergic
activity. The threshold with pulsed fields (0.45 W kg
1
, specific absorption per pulse of
0.9 mJ kg
1
) was approximately equal to the rats auditory perception threshold. It was
reported that similar changes in cholinergic function could be induced by stressors such
as noise and acute restraint, suggesting that exposure may be associated with mild
stress. In addition, exposure was found to increase the concentration of benzodiazepine
receptors in the cortex following acute but not repeated exposures (Lai et al, 1992a),
again suggesting an anxiety or stress response. More recent studies have provided
evidence on the involvement of endogenous opioids (Lai et al, 1992b) in the medial
septal nucleus (Lai et al, 1996). Recently, Testylier et al (2002) reported that acute
exposure to RF EMFs may cause sustained decreases in acetylcholine release from the
rat hippocampus.
121 Mausset et al (2001) reported that exposure to 900 MHz fields reduced the GABA
content in the Purkinje cells in the rat cerebellum. Animals were exposed to pulsed fields
at 4 W kg
1
and continuous fields at 32 W kg
1
, suggesting the possibility of thermal effects.
Learned and other behaviours
122 Many data indicate that changes in many well-learned behaviours occur only when
core temperatures are increased by about 1C or more (WHO, 1993). Under some
circumstances, ongoing operant behaviours can be terminated completely above a
threshold corresponding to a whole-body SAR of about 4 W kg
1
. Many factors are
known to modify this value, however, including the frequency of the applied field, the
ambient temperature and relative humidity, and the animal size and species.
123 This heating effect is illustrated by the results of a behavioural study using rats
exposed to microwaves at 600 MHz (Mickley et al, 1994). Significant deficits in the
performance of a working memory task were observed when exposures caused rises
in rectal and brain temperatures of at least 1C. These changes were correlated with an
increase in expression of the c-fos gene in the cortex.
124 However, results of some recent studies appear to challenge this conclusion (see
also DAndrea, 1999). Lai et al (1994) reported that the behaviour of rats performing a
test of spatial memory function in a radial arm maze was severely disrupted by daily
exposure for 45 minutes to pulsed 2.45 GHz fields at 0.6 W kg
1
. Exposure did not cause
a measurable rise in colonic temperature but acquisition was retarded and exposed
animals consistently made more errors than controls. Additional results suggested that
exposure had activated the endogenous opioid systems and so caused a decrease in
cholinergic activity within the hippocampus. In an earlier experiment, Lai et al (1989)
reported that exposure for 20 minutes improved learning for the first 2 days, although
final performance and overall accuracy were not affected.
125 Wang and Lai (2000) placed rats in a Morris water maze immediately after being
exposed to pulsed 2.45 GHz fields at 1.2 W kg
1
for 1 hour. The animals had to learn to
escape from the water by locating a submerged (non-visible) platform. Exposed
animals took longer to find the platform than control animals throughout the training
sessions, and, in contrast to the control animals, spent much time trying to climb the
105
side walls of the maze. In a probe trial without the platform being present, the exposed
animals were reported to have spent less time swimming in the quadrant of the maze
that should have contained the platform. Therefore, it was concluded that exposure had
disrupted spatial reference memory functions and that the exposed animals had to use
other, less efficient, learning strategies to locate the platform. However, statistical
analysis of the probe trial data by one-way analysis of variance revealed no significant
treatment effect, and only post hoc analysis suggested a statistical difference between
the exposed and control animals (see also IEGMP, 2000).
126 In contrast, Sienkiewicz et al (2000) found that exposure of mice for 45 minutes to
pulsed 900 MHz fields at 0.05 W kg
1
had no significant effects on performance in a
radial arm maze. Animals were tested immediately after exposure or following delays
of 15 or 30 minutes. The animals tested without delay took longer to complete the task,
possibly due to some mild stress associated with exposure. Similarly, Dubreuil et al
(2002, 2003) exposed rats to pulsed 900 MHz fields for 45 minutes using a head-only
system before daily testing on various spatial memory tasks (performed using a radial
arm maze or a dry land version of the Morris water maze) or on an object recognition
task. No consistent effects on the performance of any task were seen using average
SARs in the brain of either 1 or 3.5 W kg
1
. In addition, a recent attempt by Cobb et al
(2004) to replicate the study of Lai et al (1994) failed to confirm any field dependent
effects on task performance in a radial arm maze. As in the original study, rats were
exposed using a circularly polarised waveguide to pulsed 2.45 GHz fields at 0.6 W kg
1
for 45 minutes before daily learning trials in a radial arm maze.
127 The hippocampus slice preparation has been much used in neurophysiology to
study mechanisms associated with memory. Using a novel parallel plate waveguide,
Tattersall et al (2001) exposed slices of rat hippocampus to 700 MHz continuous fields
at SARs of between 0.0006 and 0.0044 W kg
1
. Changes were found in the electrically
evoked field potential in CA1 that depended on the magnitude of the SAR low field
intensities produced an increase in the amplitude of the population spike by up to 20%,
but higher intensity fields produced either increases of up to 120%or decreases of up
to 80%. In addition, it was reported that exposure at about 0.0011 W kg
1
reduced or
abolished drug induced epileptiform activity in 36%of slices tested. Any field induced
rises in temperature were too small be detected even using sensitive measuring
equipment. Imposed temperature changes of up to 1C failed to mimic the effects of
the RF EMFs.
128 In a preliminary study, Lscher and Ks (1998) ascribed behavioural and postural
abnormalities observed in a herd of dairy cows to the fields from a nearby TV and
mobile phone transmitter site. However, the lack of concurrent sham-exposed animals
to control for the possible impact of environmental or other factors renders any
interpretation premature.
The eyes
129 The eyes have long been considered sensitive to the effects of localised increases
in temperature, although exposure to RF EMFs must be both prolonged and intense to
cause lasting detrimental effects (WHO, 1993, see also Saito et al, 1998). The effects of
RF fields on the eyes have been reviewed by Elder (2003b).
106
130 A series of earlier studies (summarised by Kues and Monahan, 1992) has indicated
that localised exposure of the eyes of anaesthetised monkeys to pulsed 2.45 GHz
(10 s duration at 100 pulses per second) at an SAR in the eye of 2.6 W kg
1
(specific
absorption of 26 mJ kg
1
per pulse), or more, for several hours resulted in lesions in the
corneal endothelium (Kues et al, 1985). The vascular leakage from the blood vessels of
the iris was increased. Lesions in the cornea were also induced by exposure to continuous
fields at 2.45 GHz, but were less effective compared to pulsed fields. Topical pretreatment
with the ophthalmic drug timolol maleate appeared to reduce the threshold for these
effects to 0.26 W kg
1
(Kues et al, 1992). Intermittent exposure over a 10 week period
resulted in early degenerative changes in the retina, which were also exacerbated by
application of timolol maleate.
131 In contrast, Kamimura et al (1994) were unable to induce corneal, lenticular or
retinal lesions in the eyes of unanaesthetised macaque monkeys exposed to continuous
(but not pulsed) 2.45 GHz fields at levels exceeding the threshold for continuous field
induced corneal damage described by Kues et al (1985). The technique used for the
identification of corneal lesions (specular microscopy) was the same as that used by
Kues et al (1985); the latter authors, however, used histological techniques to confirm
damage to both the cornea and retina, in contrast to Kamimura et al (1994).
132 More recent studies using 1.25 GHz high peak power pulsed fields did not report
signs of retinal degeneration or functional impairment in the eyes of rhesus monkeys
intermittently exposed over a 3 week period at average SARs in the retina of 4 W kg
1
(Lu et al, 2000). However, some evidence of mild injury was seen using average SARs of
8.4 and 20.2 W kg
1
. Similarly, no signs of ocular damage were observed in rabbits or
monkeys exposed to continuous 60 GHz fields at 10 mW cm
2
for either a single 8 hour
exposure or five separate 4 hour exposures (Kues et al, 1999).
The possibility that exposure to RF EMFs may affect neurobehavioural function
in animals has been explored from a number of perspectives using a wide range
of exposure conditions.
There are sporadic reports of field dependent effects but none has been firmly
established.
The least questionnable evidence for low level effects relates to the changes in
cholinergic and opioid activity using whole-body SARs of about 1 W kg
1
,
although the possibility that some of these changes may be due to increases in
stress or anxiety associated with field exposure should be considered. Field
induced changes in cholinergic function might predict effects on learning and
memory but the evidence for such effects is conflicting. Results of two studies
from one laboratory showing performance deficits using pulsed 2.45 GHz fields
were not confirmed in two independent studies using GSM signals. Changes in
excitability of hippocampal slices in vitro following exposure to very weak fields
requires independent verification.
Nevertheless, the possibility that low level exposure may engender behavioural
or cognitive changes in animals under certain circumstances cannot be ruled out
too few tasks and exposure conditions have been examined to formulate
definitive conclusions at this time.
107
133 The effects of heat in healthy adults, through physical work and/or in warm, humid
environments, is well documented and understood; many volunteer studies have
been carried out. However, the distribution of heat sensitivity in the general population
is less well documented. In general, people with certain medical conditions and/or
those taking medication are not eligible in volunteer experiments. These restrictions
are also usually applied to older people, children and pregnant women. With regard
to RF EMF induced whole-body heat loads, there is some uncertainty regarding the
identification of tolerable heat loads in people with varying susceptibilities to heat,
and the way in which these might be modified by physical activity and inclement
environmental conditions.
134 Increasingly, people work in jobs requiring astute cognitive processing. In many
cases, the safety of others depends on the mental alertness of the operator. A large
number of studies have been carried out of the effects of elevated environmental
temperatures on cognitive performance; it is generally agreed that more cognitively
demanding tasks are more susceptible to heat induced performance decrements than
simple mental tasks. However, such effects also depend on other factors, such as
training, as well as ergonomic factors. The susceptibility of cognitive tasks to heat load,
and to raised body or brain temperature, and ways in which other environmental
variables affect susceptibility, are yet to be clearly identified.
135 There is compelling experimental evidence that raised maternal body temperature
will adversely affect pregnancy outcome. The central nervous system (CNS) seems
particularly susceptible and in this respect neural tube defects and microencephaly
have been reported in a number of studies. However, possible effects on the develop-
ment of the cortex, known to be particularly susceptible to other harmful agents, and
the behavioural consequences of these effects on the nervous system have not been
fully explored. There is some evidence that the risk of effects such as neural tube
defects is increased in the offspring of women who experience hyperthermia during
pregnancy, particularly during the first trimester, but the rigour with which this has been
established is less certain. In addition, it is not clear to what extent the increased
susceptibility of the developing CNS to raised body temperature continues during infancy
and early childhood.
136 With regard to localised heating of parts of the body, thresholds for tissue necrosis
resulting from acute exposure to heat have been identified using animal studies in a
number of different tissues. The thresholds for such effects are less clearly identified in
humans. In addition, the cumulative effects in tissues that might result from repeated
exposure are less clear. The long-term consequences of functional change induced by
elevated tissue temperatures, in endocrine glands, or in parts of the brain such as the
pituitary or hypothalamus, are also not fully understood. Further, the impact of disease,
particularly of the cardiovascular system, on a persons ability to dissipate excess heat
from organs and tissues is not well established.
137 The results of other experiments suggesting that low level RF EMFs may induce
adverse biological responses are beset with uncertainty, limiting their practical
usefulness as a basis for establishing exposure standards. This uncertainty originates
from several sources. Firstly, studies may have been performed with inadequate
108
scientific rigour, and have deficiencies in experimental design and lack control of
potential artefacts. Other studies may have inadequate metrology or dosimetry.
Studies may have inappropriate or incorrect data analysis or have insufficient statistical
power to detect small effects. Finally, there is the acknowledged uncertainty of
extrapolating results to living humans from data obtained using various animal species
and in vitro experimental models.
138 As with studies using EMFs, the general inconsistency in reported effects and the
lack of attempts to replicate results are major sources of uncertainty. This applies to
studies reporting effects as well as to studies reporting their absence. Further, the view
that some responses may only occur with specific frequencies or pulsed modulations
makes broad generalisations difficult, if not impossible, to draw. The appropriateness of
using SAR as an exposure metric for non-thermal interactions has also been questioned.
139 Finally, other uncertainties result from an incomplete understanding of the
distribution of sensitivity to RF EMFs amongst the population, particularly age-related
differences and those resulting from medical conditions or treatment.
Summary
140 Heat-related disorders should be avoided in the majority of normal healthy adults,
provided that core body temperature does not rise above 38C. This is likely to prevent
adverse effects on the performance of all but the most demanding cognitive tasks. High
rates of physical activity and/or warm, humid environments will reduce the additional
RF heat loads that most adults can tolerate without exceeding 38C. An RF heat load of
0.4 W kg
1
averaged over the whole body should be sufficiently low that these other
factors can be ignored.
141 Individual susceptibility to heat-related disorders varies considerably in the general
population. Older people and infants and children may be considered particularly
susceptible. In addition, adults taking certain drugs and other chemicals that have direct
effects on the control of body temperature, or on metabolism or heat production of the
body, may also be considered at greater risk. An RF heat load of 0.1 W kg
1
averaged
over the whole body should be physiologically trivial in this context.
142 Exposure of pregnant women to an average whole-body SAR of 0.1 W kg
1
should
not result in adverse effects on the development of the embryo and fetus in utero. The
fetus itself is thought to be in general about 0.5C above maternal body temperature
(the embryo less so) and is to some extent limited in its ability to dissipate heat to the
mother by heat exchange within the umbilical blood vessels. In view of the uncertainty
regarding possible effects of raising fetal temperatures directly through the absorption
of RF EMFs, a rise in embryo and fetal temperature to less than 38C should also not
result in adverse developmental effects. The development of some tissues, such as the
CNS, continues during infancy and early childhood, suggesting that some potential
increased susceptibility may continue during these periods.
143 With regard to localised heating and the susceptibility of individual tissues to heat,
the CNS, the testis and the lens of the eye seem particularly sensitive, the last more
through a limited ability to dissipate heat than a greater sensitivity to heat per se.
Other tissues, such as liver, kidney and muscle, seem marginally less susceptible, but
nevertheless can also be adversely affected by elevated temperature. Temperature
rises in the CNS (ie the brain, retina and spinal cord) to above 38C, of the other tissues
109
of the neck and trunk (with the exception of the testes) to above 39C, and of the
tissues of the limbs to above 40C, may result in localised heat induced damage. The
testes are particularly sensitive to the effects of heat; adverse effects should not occur
in this tissue provided temperature increases are less than 1C.
144 The ability to dissipate heat from locally heated tissues or regions of the body will
depend on their temperature in relation to their surroundings and rate of flow of blood
through the tissue. Both may to some extent be compromised by significant whole-
body heating when the increase in skin blood flow is greater than the corresponding
increase in cardiac output. In addition, people with cardiovascular disease, such as
peripheral vascular disease or heart failure, which will reduce the circulation of blood
through tissues, may be at increased susceptibility to localised heating of tissues by
RF EMFs compared with people with normal cardiovascular responses.
145 In addition, a number of studies suggest that low level RF EMFs may induce a variety
of subtle biological responses. Of particular note are possible effects of pulsed fields
on brain function and on changes in heat shock protein expression. Further work is
needed to examine these and other possibilities, especially to consider if local heating
effects may explain these results. Overall, none of these possible effects is considered
sufficient to provide a coherent framework on which to base quantitative restrictions
for human exposures.
The most plausible and coherent set of data from which guidance can be
developed concerns raised temperatures and the physiological stress induced by
increased heat loads. In addition, these data show doseresponse relationships.
A cautious approach has been used to derive thresholds for adverse health
effects that are scientifically robust.
Other studies reviewed lack plausibility, coherence and consistency precluding a
positive role in this process.
Heat-related disorders should be avoided in the majority of normal healthy
adults, provided that core body temperature does not rise above 38C. High rates
of physical activity and/or warm, humid environments will reduce the additional
RF heat loads that most adults can tolerate without exceeding this rise in body
temperature. An RF heat load of 0.4 W kg
1
averaged over the whole body should
be sufficiently low that these other factors can be ignored.
Some people are potentially susceptible to heat-related disorders. These include
older people, infants, children, pregnant women and other adults taking certain
medications. In addition, the performance of cognitively demanding tasks may
also be vulnerable to increases in heat load or body temperature. An RF heat load
of 0.1 W kg
1
averaged over the whole body should be physiologically trivial in
this context.
With regard to partial-body heating, temperature rises in the head, spinal cord,
embryo and fetus above 38C, in other tissues of the neck and trunk (with the
exception of the testes) above 39C, and in the limbs above 40C, may result in
localised heat induced damage.
The testes are particularly sensitive to the effects of heat. Adverse effects will
not result from temperature increases less than 1C.
People in whom the function of the cardiovascular system is impaired by disease
or medication are likely to be more susceptible to localised heating of tissues
than people with normal cardiovascular physiology.
110
DOSIMETRY
and the fields induced within the body. This gives guidance to the choice of reference
levels in relation to basic restrictions.
147 Basic restrictions on SAR prevent whole-body heat stress and excessive localised
tissue heating.
148 The state-of-the-art approach to deriving reference levels is to solve Maxwells
equations numerically, in fine resolution, anatomically realistic models of the body.
Subsequent sections describe the calculations of whole-body averaged SAR and
localised SAR in the wrist and ankle.
149 Techniques for performing temperature calculations in the body are described and
recent results for each type of exposure, from whole-body to highly localised exposure
of vulnerable organs such as the eye and brain, are reviewed.
SAR calculations
150 The Finite-Difference Time-Domain, FDTD method (Taflove, 1995), provides a
direct solution of the coupled, time-dependent Maxwell curl equations and is ideally
suited for application to voxel phantoms. The method follows the time evolution of the
propagation, reflection and absorption of electromagnetic waves in a domain comprising
the target and surrounding space. The domain is divided into a three-dimensional lattice
of cells that are assigned discrete electrical properties. The components of the electric
field, E, are positioned on the middle of the edges and the components of the magnetic
field, H, are at the middle of the faces of the lattice cells. An explicit second-order finite-
difference procedure then leap-frogs, evaluating E from H and vice versa at alternate
half-time steps until equilibrium has been reached. A domain enclosing the target and a
boundary condition on the surface of the domain must be chosen to mimic numerically
the unbounded region outside the domain by absorbing the outgoing scattered waves.
The perfectly matched layer (pml) based boundary conditions of Berenger (1994) can
produce a very small reflection from the boundary. The technique is based on splitting
the electric and magnetic fields into two in the absorbing boundary region. This gives
additional degrees of freedom for the specification of material parameters. Thus it is
possible to create a non-physical absorbing medium, adjacent to the external mesh
boundary, in which waves of arbitrary frequency and angle of propagation are caused
to decay rapidly while maintaining the velocity and impedance of the media from which
they propagated.
151 The Finite Integration Technique, FIT (Weiland, 1990), constitutes a slightly different
conceptual approach to that of FDTD, but both approaches lead to the same basic
numerical scheme.
Calculations of whole-body averaged SAR
152 The FDTD method has been applied (Dimbylow, 1997a) to the NRPB voxel
phantom (NORMAN) to provide a comprehensive set of whole-body averaged SAR
values for adult, 10-, 5- and 1-year-old phantoms, grounded and isolated in air from
111
1 MHz to 1 GHz for plane wave exposure. It was not then computationally tractable to
perform FDTD calculations directly at a cell size of 2 mm. Therefore, the phantom was
rescaled to produce 6 mm, 1 cm and 2 cm models with the properties of the rescaled
cells being taken as the volume average of the basic component voxels. As the
frequency increases, smaller cell sizes are required so that an adequate sampling of
the waveform is performed. The computational effort required is proportional to
the reciprocal of the fourth power of the cell size. Computing technology has now
advanced to the point where the FDTD calculations can be performed at the basic 2 mm
resolution of NORMAN. This enables the SAR values to be performed over discrete
tissue types avoiding the smearing out of tissue properties in calculations with larger
rescaled voxels. The reduction in the voxel size also allows SAR to be calculated at
higher frequencies.
153 Calculations of the whole-body averaged SAR have been performed (Dimbylow,
2002) from 100 MHz up to 3 GHz by using the basic resolution of NORMAN, around
2 mm. At lower frequencies a 4 mm resolution discrete voxel version was used with an
overlap to 200 MHz and it was found that the whole-body averaged SAR was a robust
quantity with respect to model resolution. The adult phantom was resampled to
represent the heights and masses of reference 10-, 5- and 1-year-old children (ICRP,
2002) whilst retaining the 2.077 mm voxel resolution at the higher frequencies and
4 mm at the lower frequencies. The reference 10-year-old has a height of 1.38 m and a
mass of 33 kg, the 5-year-old has a height of 1.1 m and a mass of 20 kg and the 1-year-old
has a height of 0.75 m and a mass of 10 kg. The whole-body resonance occurs at around
65, 85, 110 and 155 MHz for the adult, 10-, 5- and 1-year-old phantoms under isolated
conditions. The resonance occurs when the height of the body is approximately /2,
where is the wavelength in air. When the phantom is grounded, the reflection in the
ground plane halves the resonant frequency. However, the body is not a thin dipole and
the exact resonant frequencies depend on the anatomy and values of the frequency
dependent dielectric properties. Under grounded conditions the whole-body resonance
occurs at around 35, 50, 65 and 95 MHz for the adult, 10-, 5- and 1-year-old phantoms. In
general, the basic restriction on whole-body averaged SAR is the critical condition
requiring the lowest external field value.
154 Chen and Gandhi (1989) calculated whole-body averaged SAR values from 20 to
100 MHz in the previous Utah half-inch body model derived from slices in an anatomical
atlas. They used a resolution of 2.62 cm. These were continued from 100 to 915 MHz
(Gandhi et al, 1992) at a resolution of 1.31 cm. Tinniswood et al (1998) looked mainly at
the power deposition in the head and neck but also reported whole-body averaged SAR
values. Calculations were performed either at the 2 2 3 mm
3
basic resolution of the
Utah anatomical phantom near resonance or at the lower 6 6 6 mm
3
resolution
version away from resonance. The Gabriel et al dielectric parameters were used and
calculations were performed from 10 to 350 MHz (Gabriel, 1996; Gabriel et al, 1996ac).
The predicted resonance frequencies of 35 MHz for grounded and 60 MHz for isolated
conditions agree well with the NRPB calculations (Dimbylow, 2002). The calculated
resonant SAR values are 94.8 and 74.9 W kg
1
per V m
1
rms for grounded and isolated
conditions. The corresponding values from Dimbylow (2002) are 93.1 and 81.2 W kg
1
per V m
1
, differences of +2 and 8%.
112
155 Mason et al (2000) calculated whole-body SAR from 70 to 2000 MHz at 3 and 5 mm
resolution in the Brooks digital anatomical man model for isolated conditions. At
70 MHz, using the 3 mm version, the predicted value is 71.6 W kg
1
per V m
1
, whilst
at 2000 MHz the value is 14.9 W kg
1
per V m
1
. The corresponding values from
Dimbylow (2002) are 80.0 and 15.6 W kg
1
per V m
1
, differences of 10 and 4%.
Localised SAR
156 The maximum of the induced layer current occurs in the lower limbs for exposure
of the body to a plane wave EMF at frequencies below and around the whole-body
resonance. The ankle region has a narrow cross-section with little high conductivity
muscle. The sections comprise mainly low conductivity bone and fat. Consequently,
there is a channelling of the current through the high conductivity muscle, which
produces high, localised SAR values in the muscle. It is not computationally tractable to
perform FDTD calculations, at the basic 2 mm resolution, at frequencies below 100 MHz.
The localised SAR averaged over 10 and 100 g in the lower limb has been calculated
(Dimbylow, 1997b) for a unit current injected through the open upper boundary of a
partial leg model using a finite-difference solution of the quasistatic potential equation
from 0.1 to 80 MHz. The bottom 220 slices of the whole-body model, NORMAN, were
extracted to make a voxel model of the lower leg.
157 The localised SAR averaged over 10 and 100 g in the lower arm has also been
calculated (Dimbylow, 2001) as a function of the current injected through the open
upper boundary of the arm model. This consists of 147 slices from NORMAN, extending
from a plane through the hand at the knuckles to just below the elbow.
158 The ICNIRP guidelines give limb current reference levels of 100 and 45 mA for
occupational and general public exposure between 10 and 110 MHz to provide
compliance with basic restrictions on localised SAR. The limb current reference level
provides a conservative limitation on the localised SAR, in both the arm and the leg,
calculated using NORMAN.
159 There has been interest in the deposition of energy in the head from mobile
phones. Examples of FDTD calculations of localised SAR from the coupled transceiver-
head geometry can be found in Dimbylow and Mann (1994), Bernardi et al (1996),
Okoniewski and Stuchly (1996) and Watanabe et al (1996).
160 Gandhi et al (1996) looked at energy absorption in the head from /4 and 3/8
monopoles at 835 and 1900 MHz. They used the 1.875 1.875 3 mm
3
Utah model of
the adult head and reduced-scale versions to represent 10- and 5-year-old children.
They found that the 1 g SAR peak value was larger for the smaller models of the
children, particularly at 835 MHz. It was also found that the relative penetration of
energy into the deeper anatomical structures of these smaller models was more
noticeable because they were nearer the source. However, these findings were
contradicted by the work of Schonborn et al (1998). They used the FIT code MAFIA
(CST, 1994). Simulations were performed using head phantoms based on MRI scans
of an adult (voxel size of 2 2 1 mm
3
) and two children (2 2 1.1 mm
3
) of ages
3 and 7 years. Differences in absorption were investigated at 900 and 1800 MHz using
0.45 dipole sources. The results revealed no significant differences in the absorption of
EMFs between MRI-based phantoms of both adults and children and for various linearly
scaled adult phantoms.
113
Thermal dosimetry
161 The thermal effects of EMFs may be gauged by the distribution of temperature rises
within the body. Thermal dosimetry aims to determine these, and to relate them to
other metrics such as SAR or power density. As frequency increases, the penetration
depth of the fields decreases. At frequencies above about 10 GHz, most of the energy is
absorbed within the first few millimetres of tissue, and the temperature rise is well
correlated to the incident power density. At lower frequencies, the SAR is a better
predictor. There is no clear-cut frequency at which SAR ceases to be a useful metric;
there is a transitional region in which both metrics are useful but neither is perfect.
ICNIRP (1998) has chosen 10 GHz as the crossover point between restrictions on SAR
and on power density.
162 The most appropriate computational technique depends on the exposure
conditions. In circumstances where the whole body is exposed at a level which causes
elevation of the core temperature and consequent thermoregulatory responses,
coarsely segmented models of the whole body have been used with some success
(eg Stolwijk, 1970; Charny et al, 1987). The trunk, head and each limb are divided into
a few segments, and each segment is then divided into layers, which are assumed to be
of homogeneous composition (eg skin, fat, muscle, bone). A single temperature is taken
to be representative for each region, and heat capacities and transfer coefficients are
lumped. The advantages of such a model are computational efficiency and the
relatively small number of parameters which need to be determined experimentally.
Central and local thermoregulation can be incorporated in these models. However,
these models are inappropriate when exposure is highly non-uniform.
163 The progress of models for whole-body exposure has not been as rapid as that for
localised or regional exposure. The reason is probably that a comprehensive and accurate
thermal model of man would require precise knowledge of thermoregulation and thermal
properties of every organ. Such parameters can only be obtained by human experi-
mentation, and the number of measurable quantities is not sufficient to solve uniquely
for the large number of unknown parameters in a whole-body model.
164 Most theoretical studies of localised or regional heating use some variant of the heat
equation. This is a partial differential equation which describes the variation of
temperature T(r , t ) as a function of position r and time t . It is obtained by considering
an infinitesimal volume element and equating the rate of change of thermal energy
within it to the total heat flowing into it. In its traditional form, the Pennes bioheat
equation (Pennes, 1948) takes the form:
) T T ( c S Q ) T k .(
t
T
c
b b b
+ + =
(1)
where is the density, c the specific heat capacity and k the thermal conductivity of
the tissue at r , the subscript b indicates the corresponding parameters for blood, Q is
the power generated per unit mass by metabolic processes, S is the specific energy
absorption rate (SAR), and is the blood perfusion rate.
165 The Pennes equation has the great virtue of simplicity. Heat transfer between tissue
and blood is represented by a heat sink term, and only one parameter is needed to
114
describe the blood flow within each tissue. However, it was originally derived on the
assumption that heat transfer mainly takes place in the capillary beds. It has since been
shown to the contrary that the principal site of heat exchange is between the terminal
arterial branches and the pre-capillary arterioles (Chen and Holmes, 1980). Other
authors have replaced the heat sink term with an enhanced effective conductivity
(Weinbaum and Jiji, 1985), modified the heat sink term with an efficiency factor (Brinck
and Werner, 1994), or introduced an explicit description of the vasculature (Kotte et al,
1996). However, comparison with these more recent models shows that for many
applications the traditional Pennes bioheat equation is still a valid approximation.
166 Continuum-based models such as the Pennes equation and its variants are partial
differential equations, and must be discretised before they are solved. The most
widespread discretisation methods are the finite-difference methods and finite-element
methods. Finite-difference methods are computationally simple, but require calculation
of temperatures on a uniform rectilinear grid. Finite-element methods may utilise non-
uniform grids; these can model complex geometries more accurately and sometimes
improve computational efficiency.
Heating of the skin
167 At frequencies greater than about 10 GHz, absorption of electromagnetic energy
takes place mostly in the skin and other superficial tissues. For dosimetric purposes
superficial absorption has certain simplifying features. When the penetration depth
of the field is small compared with the radius of curvature of the body surface, one-
dimensional models of electromagnetic propagation and heat transfer may be used.
168 Blick et al (1997) have measured threshold incident power densities for perception
of microwaves and millimetre waves spanning frequencies from 2.45 to 94 GHz as
well as infrared radiation. They found that thresholds in the microwave region decrease
with increasing frequency, and that thresholds at 94 GHz were similar to those for
infrared radiation.
169 Riu et al (1997) have developed a thermal model for human thresholds of
microwave-evoked warmth sensations. Based on examination of the experimental data
by Blick et al (1997), they concluded that the observed data were consistent with the
hypothesis that perception is triggered by an increase in skin temperature in the region
0.060.08C. The measured threshold power densities P
th
(in mW cm
2
) approximately
fit the curve
68 0
th
100
.
f
P (2)
where f is the frequency in gigahertz. The observed frequency dependence of the
threshold is due to the variation in penetration depth, although this is mitigated by
thermal conduction which plays an important role.
170 A further volunteer study of millimetre wave exposure at 94 GHz was performed
by Walters et al (2000). In a sample of ten volunteers they found the mean threshold of
pain at 1.25 W cm
2
, corresponding to an increase in surface temperature of 9.9C from
a baseline of 34.0C to a threshold temperature of 43.9C during a 3 second exposure.
In the same study, infrared thermography was used to measure the subjects' skin
115
temperature as a function of time. This was then fitted to a simple one-dimensional
thermal model to determine the energy transmission coefficient and penetration depth
of the field. The energy transmission coefficient is the fraction of the incident power
density which penetrates the skin surface; the penetration depth is the depth at which
the transmitted power density has been reduced by a factor 1/e. The experimental
values of these parameters were consistent with the dielectric properties of skin
tabulated by Gabriel (1996). There was, however, a considerable scatter between
experiments and subjects, presumably due in part to variation between individuals,
particularly in skin water content.
RF contact burns
171 Threshold currents for perception and pain were determined experimentally by
Chatterjee et al (1986), from measurements on 367 adult human subjects. Based on the
two areas used for finger contact (25 and 144 mm
2
), the authors suggest that the
variation of threshold current with contact area is consistent with a model that predicts
proportionality with the fourth root of area. For finger contact with an area of 25 mm
2
,
the average threshold for perception in the male population rises with frequency from
about 4 mA at 10 kHz to over 40 mA at 100 kHz, and then stays approximately constant
up to 3 MHz. Pain thresholds are no more than 50%greater than those for perception.
There appears to be a systematic difference in average thresholds between the male
and female population, the thresholds for males being 1.26 times those for females.
Assuming that the mechanism of perception is a threshold SAR causing a sensation of
warmth in the hand or wrist, the threshold current is proportional to the square of the
body dimensions; accordingly the authors predict the values for 10-year-old children
should be 60%of those for adults.
172 Foster and Erdreich (1999) used a simplified spherically symmetric thermal model
to estimate the threshold current for painful heating. Since the current density and SAR
depend on the size of the electrode, this is a critical parameter. For a 1 mm electrode
and a frequency of 1 MHz, they estimated a threshold of 8 mA. They were able to make
only limited comparison between the model and the available measured data (Chatterjee
et al, 1986; Hocking and Joyner, 1992) due to lack of sufficient experimental data given
by those studies. A major source of uncertainty is the distribution of current density
beneath the electrodes.
Thermal response times
173 Using simple one-dimensional thermal models it is possible to identify the thermal
time constants pertaining to heat conduction and convection by blood flow (Foster
et al, 1998; Foster and Erdreich, 1999). These constants determine the time taken for the
temperature to approach a steady state after the source of exposure is switched on or
off. This is an appropriate averaging time for dosimetric purposes. An effective time
constant can be determined by combining the effects of conduction and convection;
conduction dominates for small heated regions (less than a few centimetres), and
convection for larger regions. Since the field penetration depth varies with frequency,
so does the time constant. The authors discussed the relationship between the time
constants and the size of the heated region or penetration depth. The decreasing trend
116
of time constants with frequency from 10 to 300 GHz has been accommodated in national
and international standards and guidelines (IEEE, 1992; NRPB, 1993; ICNIRP, 1998) by a
similar variation in averaging time over that frequency range.
Heating of the eye
174 The eye is a particularly sensitive organ for several reasons. Since the blood flow
within the inner tissues is negligible, one of the major cooling mechanisms is absent.
With prolonged exposure the proteins of the lens can suffer permanent damage leading
to a loss of transparency (cataract). Experimental results using rabbits suggest that the
threshold for cataract formation is a temperature rise of 35C (eg Guy et al, 1975a).
The geometry of the eye, and the discontinuity of the dielectric constants between the
eye and the bony orbit, are such that standing waves may be set up so generating a
localised temperature rise.
175 Most theoretical studies have usually simulated exposure to a plane wave, a nearby
dipole antenna, or various approximations to a mobile phone. Since the average mass of
the adult human eye is 7.5 g (ICRP, 2002), the SAR average over the whole eye is close
to the average over the 10 g region recommended by ICNIRP, and many authors have
chosen to compute the former value. In general, the most significant value in these
computations is the temperature rise within the lens. The calculated temperature rises
are usually greater for the cornea, but due to the natural gradient of temperature as a
function of depth, the absolute temperature is likely to remain less in the cornea than in
the lens.
176 Mokhtech et al (1994) mapped the SAR within the eye exposed to the near-field of a
dipole antenna at mobile phone frequencies (840, 915, 1500 and 1800 MHz). Peak SARs
were almost twice as high at 1500/1800 MHz as at 840/915 MHz. A localised temperature
rise was found to occur in the vitreous humour just behind the lens. The bioheat
equation was used to estimate temperature rises, and their dependence on the distance
of the antenna from the eye was investigated. Antennas were assumed to be radiating
at the power limits specified in the C95.1 standard (IEEE, 1992) for the uncontrolled
environment, namely
=
f
. P
450
4 1
r
(3)
where P
r
is the radiated power in watts and f is the frequency in MHz. Temperature
rises were predicted to reach 2.7C for an antenna 5 mm from the eye, and 0.5C for
an antenna at the exclusion distance 25 mm from the eye. In the latter case the 1 g
averaged SAR could reach 6 W kg
1
.
177 Hirata et al (1999) calculated SAR and temperature rise for plane-wave exposure at
0.66 GHz using FDTD and the Pennes bioheat equation. They found several resonant
frequencies, the strongest being at 1.9 GHz. Some of these resonances were found to
correspond to identifiable standing wave patterns in the eye (whose mass is about 10 g)
or the head. There was a fairly strong correlation between the SAR averaged over the
whole eye and the maximum temperature rise within the eye. The temperature rise is
not simply proportional to the SAR, however, because the tissue dielectric properties
117
are frequency dependent. At resonance the incident power density 10 W m
2
was
found to produce an average SAR of 0.36 W kg
1
and a temperature rise of 0.14C; at
6.0 GHz these fell to about 0.2 W kg
1
and 0.075C.
178 After further development of their model, Hirata et al (2000) found slightly different
results. An additional peak at 1.0 GHz not seen in the earlier results was attributed to
coupling of weak resonances in the eye and head. In the later paper the trend of
maximum temperature was to increase, rather than decrease, with frequency, with the
temperature peak at 1.9 GHz being much reduced. The discrepancy is most probably
due to the introduction in the later work of a convective heat transfer term to represent
heat loss to the blood perfusing the choroid. At 6.0 GHz the results are similar to
those of the earlier paper, since most energy is deposited in the anterior part of the eye
where heat loss is dominated by convection at the cornea. An incident power density
of 50 W m
2
was calculated to produce an SAR of 1.1 W kg
1
, and temperature rises up
to 0.28C in the lens and 0.33C in the cornea. At frequencies above this, heat loss is
dominated by convection at the cornea, and therefore accurate modelling of the
choroidal blood flow is less important.
179 At higher frequencies the absorption is concentrated in the anterior part of the
eye, and standing waves are not observed. Bernardi et al (1998) calculated SAR and
temperature rise for several frequencies between 6 and 30 GHz. Comparing results
using several geometric models of the eye and its surroundings, they found the maximum
SAR significantly increased when scattering from the nose was considered. For a
10 W m
2
vertically polarised plane wave the maximum temperature rises were 0.04C
in the lens at 6 GHz and 0.06C in the cornea at 18 GHz. It is suggested that the use of
spectacles could in some circumstances increase the average SAR by as much as 30%.
The authors concluded that for this frequency range a 10 W m
2
standard provides a
sufficient safety factor, but if the power density were scaled to reach the ICNIRP basic
restriction for general public exposure (2 W kg
1
averaged over 10 g) the lens temperature
could rise by 0.6C. However, this value was obtained at 18 and 30 GHz, frequencies at
which the power density, not the SAR, is restricted by ICNIRP guidelines.
Heating of the head
180 Recent concerns over possible effects of mobile phone usage have motivated
research into microwave exposure of the whole head. These models address not only
thermal effects in the eye, but also sensitive locations in the brain, such as the
hypothalamus, which is the central temperature controller for the body. Most of the
studies concentrate on the calculation of the temperature rise due to direct absorption
of electromagnetic energy in the head. It is important to note that when using a mobile
phone this is only one of the mechanisms that serve to raise the brain temperature;
heat is also generated within the phone and conducted to the head, and pressing the
phone to the ear inhibits heat loss from the skin. Most of these studies utilised FDTD
computations of SAR followed by a finite-difference solution of the bioheat equation.
181 Fujiwara et al (1999) computed temperature rises in the head generated by plane
waves incident in the anteroposterior (AP) direction at 1.5 GHz. Their results are
quoted for an incident power density of 50 W m
2
. Since temperature dependence of
the tissue properties was neglected, the results for 10 W m
2
exposure can simply be
118
rescaled in order to compare with those of other authors. When this is done the peak
temperature rises are 0.07C in the eye and muscle, 0.034C in the brain, and 0.00052C
in the hypothalamus. This last figure is too small to trigger thermoregulatory responses
for incident power densities of 10, 50 or even 100 W m
2
, the reference levels most
often used in international standards. The predicted time evolution of temperature in
each organ is consistent with the hypothesis that all time constants are greater than
6 minutes.
182 Yano et al (2001) followed up the above study, examining the sensitivity of
temperature rise to blood flow in the brain and comparing results for adult and infant
head models. Their infant head model had a depth of 10.5 cm in the AP direction,
compared with 19.25 cm for the adult. For the infant model a distinct localised
temperature rise was observed. Peak values of SAR and temperature were greater in
the adult, but values averaged over the whole brain were greater in the infant because
of this localised increase. The average temperature rise in the infant brain was
three times that in the adult. The maximum temperature rise for a power density of
10 W m
2
was 0.07C for the adult (in the eye) and 0.055C for the child (in muscle).
These corresponded to 1 g averaged SAR values of 0.52 and 0.61 W kg
1
, respectively.
It should be noted that these computations were done with incident plane waves;
highly localised effects are usually much less pronounced when near-field sources
are used.
183 Wang and Fujiwara (1999) calculated temperature rises in the head induced by
a more realistic model of a mobile phone, namely a quarter-wavelength monopole
antenna on a metal box. They considered two frequencies, 900 MHz and 1.5 GHz. When
antenna power is scaled to 1 W, the predicted maximum temperature rises in the brain
are 0.090.15C at 900 MHz, and 0.170.27C at 1.5 GHz. In each case the lower value
was obtained with the handset just touching the ear and the higher with the handset
pressed more closely to the head. The corresponding peak 1 g averaged SAR values
were 1.482.82 W kg
1
at 900 MHz, and 2.154.85 W kg
1
at 1.5 GHz. The corresponding
peak 10 g averaged SAR values were 1.12.05 W kg
1
at 900 MHz, and 1.413.3 W kg
1
at
1.5 GHz. At the IEEE SAR exposure limit for the uncontrolled environment (1.6 W kg
1
averaged over 1 g), the maximum temperature rise in the brain was 0.06C, and at the
ICNIRP basic restriction (2 W kg
1
averaged over 10 g) it was 0.11C.
184 Wainwright (2000) computed temperature rises in the brain using a finite-element
method, using SAR profiles previously calculated by FDTD (Dimbylow and Mann,
1994). The source model was again a monopole on a metal box. Both horizontal and
vertical antenna orientations were considered for a phone at the side of the head, as
well as an antenna position in front of the eye. Temperature rises in the brain for a 1 W
antenna were calculated between 0.14 and 0.4C. For exposure at 1 W kg
1
(averaged
over 10 g) the corresponding temperature rises were between 0.109 and 0.164C. During
subsequent development, the geometry of the model has been refined. The temperature
results have been reanalysed and the highest value calculated is 0.122C (Wainwright,
unpublished data).
185 Van Leeuwen et al (1999) introduced a detailed description of individual blood
vessels in the side of the head adjacent to a closely spaced 915 MHz dipole antenna
simulating a mobile phone. The maximum temperature rise in the brain was predicted
119
to be about 0.11C for a 0.25 W antenna output power, corresponding to an SAR of
0.91 W kg
1
averaged over a 10 g cube, or 1.66 W kg
1
averaged over an arbitrary 10 g
region. They also performed calculations using the Pennes bioheat equation and found
results of the same order. Limited experimental validation was done by measuring skin
surface temperatures using infrared thermography.
186 Gandhi et al (2001b) calculated temperature rises in the head taking into account
the effect of SAR together with conduction from a warm (39C) mobile phone and
reduction of heat loss by a phone held to the ear. Frequencies of 835 and 1900 MHz
were considered. For an input power of 10 W kg
1
, they predicted temperature rises of
0.5C in the brain. Temperature rises in the pinna were found to be around 4.5C due to
conduction and suppression of convection.
187 Bernardi et al (2000) investigated temperature rises in the head with four different
types of antenna on a mobile phone. Their results suggested a maximum temperature
increase in the external part of the brain from 0.100.16C for every 1 W kg
1
of SAR
averaged over 1 g.
188 Hirata and Shiozawa (2003) have calculated the SAR and resultant temperature rise
for a large ensemble of different exposure conditions. The exposure conditions were
characterised by multiple parameters: the phone was pressed against the ear, flattening
it against the head, or not; the frequency was varied over five values between 900 MHz
and 2.45 GHz; polarisation was horizontal or vertical; 18 different antenna feed points
were used on a dipole antenna. Monopole and helical antennas were also examined. By
statistical analysis of these results (a total of 660 cases in all), regression lines were
established relating temperature rise to 1 g and 10 g SAR averages. The authors concluded
that the maximum temperature rise in the whole head was better correlated with the
10 g average, whereas the maximum temperature rise in the brain was better correlated
with the 1 g average. At 2 W kg
1
per 10 g of tissue (the ICNIRP general public basic
restriction) the authors predicted for their worst-case exposure scenario a maximum
temperature rise of 0.25C in the brain.
189 In summary, temperature rises generated in the brain per unit SAR have been
calculated for exposures at mobile phone frequencies. Predictions range from about
0.05 to 0.12C per W kg
1
. Little work has been done on thermal dosimetry in general at
other frequencies. However, at frequencies above about 10 GHz the field penetration
depth is reduced to a few millimetres or less, and significant absorption in the brain is
not expected. At lower frequencies the absorption pattern in the head becomes more
uniform, and anomalously high localised SAR values are unlikely.
190 For the above reasons, and because of the importance of mobile telephony as a
source of exposure, the studies carried out at 8001900 MHz provide the most important
data when recommending restrictions on SAR to avoid thermal effects in the brain.
Microwave auditory effect
191 Under exposure to pulsed microwaves, auditory sensations may be produced
(Guy et al, 1975b; Elder and Chou, 2003). It is now widely accepted that thermoelastic
expansion is the most likely mechanism for this phenomenon.
192 Watanabe et al (2000) used an FDTD method to compute thermoelastic waves
generated by a 915 MHz plane-wave pulse, incident on the back of the head. Dominant
120
frequency components at 79 kHz correspond to resonant frequencies of pressure
waves in the head. A variety of pulse durations were investigated, from 1 to 180 s.
The relative loudness of the acoustic signal was found to have several maxima as a
function of pulse duration, notably at 50 s, which is a half-cycle of the resonant
frequency. The threshold power density for audition was predicted by calculating the
power density that would generate the same peak pressure as the threshold of bone
conduction hearing. The predicted threshold, 3 kW m
2
, is near to that which has been
measured experimentally.
Whole-body exposure and heat stress
193 In view of the large number of unknown parameters in any whole-body thermal
model of man, the best guide to the resulting rise in core temperature is still experimental.
Several simplified models have been used; however, to validate the parameters related
to thermoregulation it is necessary to refer to volunteer experiments in situations where
significant thermoregulatory adjustments are produced for example, in MRI exposures.
194 For example, using a simple two-compartment lumped parameter model, Adair and
Berglund (1986) have calculated that an indefinitely long exposure could be carried out
at a whole-body SAR of 5 W kg
1
without raising core temperature by more than 0.6C,
while 3 W kg
1
would not raise core temperature by more than 0.2C. The standard
parameters of this model are derived from measurement of healthy volunteers;
considerable variation can be expected among individuals, particularly those with com-
promised thermoregulatory systems. As this model was applied to MRI procedures, it
was assumed that the subject wore light clothing (pyjamas). At SAR values greater than
5 W kg
1
skin blood flow was predicted to increase over 25 minutes to its maximal rate
of 90 litres per hour per square metre. This response requires increases in heart rate and
total cardiac output, which could be harmful to subjects with impaired cardiovascular
function. These results are reasonably consistent with the available experimental data
(see paragraphs 2628).
Averaging mass
195 In most guidelines for the limitation of SAR, it is not the spatial peak SAR but some
suitable average that is constrained. The size of the region over which averaging should
be done is a matter of debate. The averaging mass serves two purposes: firstly, it
provides a definition of SAR that is robust and not overly sensitive to slight changes in
exposure setup; secondly, it takes into account the spatial dispersion of the deposited
energy which is provided by heat transfer mechanisms.
196 It is not possible to constrain the maximum temperature rise in the body by limiting
any averaged measure of SAR. A sufficiently concentrated heat source can produce
arbitrarily high temperatures at a point (eg an idealised point source would produce a
singular temperature distribution).
197 However, an acceptable averaging mass can be deduced by considering the
characteristic length scales of heat transfer and expected inhomogeneities in the SAR
distribution. The scale of SAR inhomogeneities is itself determined by several factors,
including the penetration depth of the field (which depends on frequency) and the scale
of those anatomical features that may cause localised increases in absorption. The size
of the averaging region should be no larger than the smallest of these length scales.
121
198 The Pennes bioheat equation contains a natural length scale

b b
c
k
L = (4)
In one-dimensional heat flow this is the distance over which conducted heat flux is
reduced by a factor 1/e due to the heat sink. Here is the density, c the specific heat
capacity and k the thermal conductivity of the tissue, the subscript b indicates the
corresponding parameters for blood, and is the blood perfusion rate. In normally
perfused muscle this is about 14 mm; in more highly perfused brain tissue it is
about 4 mm.
199 A long, thin region or a widely spaced set of disconnected regions may be discounted
since such a region will lose heat by conduction much faster than a compact region,
such as a sphere or a cube. Since any disconnected region can be made connected by
the addition of arbitrarily thin bridges, merely specifying that the region should be
contiguous does not exclude these thermally insignificant regions from the average.
Some dosimetric studies have cited the maximum SAR averages over any 10 g cube;
this quantity is probably a better predictor of temperature rise and thermal effects.
Studies such as that of van Leeuwen et al (1999) have suggested that in some circum-
stances the average over an arbitrary contiguous region may be 50100%greater than
that over a cubic region. This should be considered when defining a procedure for
measuring or calculating SAR in the future development of exposure guidelines.
200 Bearing in mind the above points, the averaging regions should have a compact
shape, such as a sphere or a cube. It is judged that the averaging mass for exposure of
the head should be no greater than 10 g, since this is approximately the size of the
eyeball and localised increases in absorption can certainly be created on this scale (see
paragraphs 174179). At frequencies around 4 GHz, the penetration depth is around a
centimetre and decreases to around a millimetre at 10 GHz. Above this frequency, the
temperature rise is well correlated with the incident power density.
201 The choice of averaging mass is clearly most important for highly localised
exposure. At the other extreme, a uniform SAR distribution gives the same average
whatever mass is used. Some authors have cited results both in terms of 1 g (IEEE,
1992) and 10 g (ICNIRP, 1998) averaging masses. It is reasonable to expect the greatest
differences will be for situations of near-field exposure to an antenna such as a
mobile phone. However, most authors (eg van Leeuwen et al, 1999; Wang and Fujiwara,
1999) find no more than a factor of two between the SAR values calculated in these
two ways.
Dosimetric uncertainties
202 Sources of uncertainty in EMF calculations include the reliability of numerical
methods, different individual anatomies and postures, resolution and variation in
dielectric parameters.
203 Dimbylow (2002) showed that the whole-body averaged SAR is a robust quantity
with respect to model resolution and a comparison with other fine resolution calculations
showed an agreement within 10%.
122
204 The thermal and electrical properties of tissue have been studied extensively using
samples obtained from a variety of animal species. Factors that lead to uncertainty in
measured values of these properties include temperature, degree of hydration, time
since death, inter-species variations and age.
205 Gajsek et al (2001) investigated the dependence of SAR values from 70 to 2000 MHz
on tissue dielectric properties using the 3 mm version of the Brooks digital anatomical
man using the Gabriel et al parameters as the baseline (Gabriel, 1996; Gabriel et al,
1996ac). Gajsek et al found that when they changed the conductivity and relative
permittivity of all tissues either by 0.5 times or by 2.0 times the Gabriel (1996) values,
the whole-body SAR remained within a 20%bound. In contrast, the localised SAR in
organs was substantially influenced by variability in dielectric parameters. Changing the
values of muscle by a factor of two resulted in local SAR ratio changes by a factor of two
in almost 50%of tissue types. They concluded that there is no universal approach to
predicting the relative changes in localised SAR values from variations in dielectric
parameters and each case had to be treated individually.
206 A major source of variation between reported results, especially for near-field
sources such as mobile phone handsets, is the difference between geometries used by
the authors. For example, the SAR and hence temperature rise in the brain is critically
dependent on the distance between the antenna and the brain. The brain temperature
rise for a given SAR depends on exactly where the energy is deposited, and may vary
by a factor of between two and five.
207 Computational models of heating are critically dependent on the use of accurate
values of the blood flow rate (or perfusion) in various tissues and organs. In many cases
these have not been adequately determined for humans. For example, models of heat
transfer in the eye, which have been validated by experimental work on rabbits or non-
human primates, should be applied to people only with caution.
208 Adverse effects due to heating are very dependent on the efficiency of the thermo-
regulatory system. This varies with age and health status (see paragraphs 2935).
People with impaired thermoregulatory or cardiovascular function should be considered
in the development of exposure guidelines.
209 The relationship between temperature rise and SAR, as well as the SAR for a given
external field, may be dependent on age. It is known that the dielectric properties of rat
tissues vary with age (Peyman et al, 2001), and it has been suggested that a similar trend
in human tissues may lead to increased vulnerability of children to RF EMFs from
mobile phones and base stations (IEGMP, 2000). It is to be expected that changes in the
composition of tissues, particularly their level of hydration, will also have consequences
for their thermal properties. Other significant differences in thermal physiology between
adults and children (see paragraph 39) should also be taken into consideration, as should
differences in body morphology. The net effect of all these changes cannot easily be
predicted; it is not clear whether their overall effect is to increase or decrease the effects
of exposure in children. Further research is needed in this area.
Summary
and the fields induced within the body. This gives guidance to the choice of reference
levels in relation to basic restrictions. Exposure guidelines provide basic restrictions on
123
SAR between 100 kHz and 10 GHz to prevent whole-body heat stress and excessive
localised tissue heating. The usual approach to deriving reference levels based on SAR
is to solve Maxwells equations numerically, in fine resolution, anatomically realistic
models of the body. Computational techniques may also be used to relate SAR to
temperature rises within the body, thereby helping to indicate basic restrictions on SAR
which will avoid adverse thermal effects.
211 The Finite-Difference Time-Domain (FDTD) method is well suited for application to
voxel phantoms. The method follows the time evolution of the propagation, reflection
and absorption of electromagnetic waves in a domain comprising the target and
surrounding space. The domain is divided into a three-dimensional lattice of cells that
are assigned discrete electrical properties.
212 The FDTD method has been applied to calculate whole-body averaged SAR for
adults and children from frequencies ranging from 10 MHz up to 3 GHz. The whole-
body resonance of maximum energy absorption occurs when the height of the body is
approximately /2, where is the wavelength in air. When the phantom is grounded,
the reflection in the ground plane halves the resonant frequency. High, localised
SAR values can occur in the wrists and ankles, which have a narrow cross-section with
little high conductivity muscle. Recently there has been interest in the deposition
of energy in the head from mobile phones. There are contradictory reports as to
whether there are significant differences in the absorption of SAR in the heads of adults
and children.
213 The most appropriate computational technique for thermal modelling depends on
the exposure conditions. In circumstances where the whole body is exposed at a level
which causes elevation of the core temperature and consequent thermoregulatory
responses, coarsely segmented models of the whole body have been used. At
frequencies greater than about 10 GHz, absorption of electromagnetic energy takes
place mostly in the skin and other superficial tissues. When the penetration depth of
the field is small compared with the radius of curvature of the body surface, one-
dimensional models of electromagnetic propagation and heat transfer may be used.
Most theoretical studies of localised or regional heating use some variant of the Pennes
bioheat equation. Recent concerns over possible effects of mobile phone usage have
motivated research into microwave exposure of the whole head. Most of these studies
utilised FDTD computations of SAR followed by a finite-difference solution of the
bioheat equation. From the several recent independent computational studies of
mobile phone exposure, it seems that a localised SAR of 1 W kg
1
(averaged over 10 g)
should not cause an increase in brain temperature of more than about 0.12C.
214 The localised SAR averaging mass serves two purposes: firstly, it provides a
definition of SAR which is robust and not overly sensitive to slight changes in exposure
setup; secondly, it takes into account the spatial dispersion of the deposited energy
which is provided by heat transfer mechanisms. An acceptable averaging mass can be
deduced by considering the characteristic length scales of heat transfer and expected
inhomogeneities in the SAR distribution. It is judged that the averaging mass for
exposure of the head should be no greater than 10 g.
215 Sources of uncertainty in calculations include the reliability of numerical
methods, different anatomies and postures, resolution and variation in dielectric and
thermal parameters.
124
The approach to deriving reference levels for RF EMFs is to solve Maxwells
equations numerically, in fine resolution, anatomically realistic voxel models of
the body.
The whole-body averaged SAR is a robust quantity with respect to model
resolution. Comparisons between different voxel model calculations showed an
agreement within 10%. Even changes of the conductivity and relative
permittivity of all tissues, either by 0.5 times or by 2.0 times, still provide
whole-body SAR values within a 20% bound.
The whole-body resonance of maximum energy absorption occurs, for uniform
exposure under isolated conditions, when the height of the body is
approximately half a wavelength in air. When the body is uniformly exposed
under grounded conditions, the reflection in the ground plane halves the
resonant frequency.
Children would generally have higher resonant frequencies than adults due to
their reduced heights and so it is important to include them in reference
level calculations.
For exposure to RF EMFs from mobile phones, there are conflicting reports as to
whether there is a significant increase in the SAR absorbed in the head, and
particularly in the brain, for children compared with adults.
There is an absence of SAR evaluations in pregnant women and related heating
in the embryo and fetus.
From the several recent independent computational studies of mobile phone
exposure, it seems that a localised SAR of 1 W kg
1
(averaged over 10 g) should
not cause an increase in brain temperature of more than about 0.12C.
Other studies have addressed plane-wave exposure of the eye at frequencies up
to 30 GHz. At mobile phone frequencies, the computed temperature rises are
similar to those found in the brain. At higher frequencies the temperature rise
per unit SAR is greater. One study suggests that at 6 GHz, a localised SAR of
1 W kg
1
(averaged over the whole eye) produces a temperature rise of up to
0.25C in the lens.
125
6 Scientific Uncertainty
1 This chapter addresses the interpretation of the scientific data and uncertainties in
the context of identifying and assessing:
(a) effects that can be firmly concluded on scientific grounds as being caused by
exposure to EMFs and where supporting scientific data are sufficient to be able to
quantify appropriate restrictions on exposure,
(b) effects that have been associated with EMF exposure but where the scientific data
are insufficient either to make a conclusive judgement on causality or to quantify
appropriate restrictions on exposure.
2 The former of these two classes of adverse effects is relevant to recommending
quantitative restrictions on exposure to EMFs. The latter is discussed in the context of
the possible need for further precautionary measures.
3 NRPB concludes that there are scientific data indicating appropriate quantitative
restrictions on exposure. These data derive from experimental studies related to effects
of EMFs on the central nervous system at low frequencies and effects of heating on the
body at higher frequencies. The nature of such effects and the mechanisms underlying
them are reviewed in this document. Quantitative restrictions on exposure are derived
from biological information on these effects.
4 Evidence of effects associated with EMF exposure, but where the scientific data
are insufficient to make a judgement on causality or to quantify appropriate exposure
restrictions, derives principally from epidemiological studies and from some experimental
studies. The main, but not sole, subject of such studies has been cancer. These studies
have been reviewed extensively by expert groups, including AGNIR, and are summarised
and further reviewed in this document.
5 NRPB concludes that currently the results of these studies on EMFs and health, taken
individually or as collectively reviewed by expert groups, are insufficient to establish
causality of effect or derive quantitative restrictions on exposure to EMFs. This conclusion
is in accord with the manner in which other expert bodies for example, the International
Commission on Non-Ionizing Radiation Protection (ICNIRP, 1998) have developed EMF
exposure guidelines. However, such studies, together with peoples concerns, provide
a basis for considering the possible need for further precautionary measures in addition
to the application of quantitative restrictions on exposure to EMFs.
EMF HEALTH RISK ASSESSMENT
6 A health risk assessment for EMFs includes the determination of adverse effects on
peoples health as a result of exposure and, where possible, quantitative relationships
between exposures and effects. In principle, such relationships may indicate the
magnitude of the EMF exposure necessary to produce the effect where there is a
threshold for the response and/or the probability of the effect occurring as a function of
exposure. A health risk assessment addresses both possible short-term (immediate)
and long-term (delayed) effects of exposure.
126
Evidence and uncertainties
7 The primary source of information for a health risk assessment is the published
scientific evidence from epidemiological studies, human (volunteer) laboratory studies,
and animal (bioassay) laboratory studies. For better understanding of the biochemical
and biophysical mechanisms that may be involved, the results of in vitro studies
should also be included. Thus, a necessary part of EMF health risk assessment is the
examination of the scientific data in a holistic manner, bringing together and assessing
the evidence from the life sciences. Physical dosimetry provides a link describing and
quantifying fields external to the body (people or animals) in relation to fields induced
inside the body.
8 All scientific investigations are subject to uncertainties, as is the interpretation of
the studies relevant to judgements on likely adverse health effects. An example of the
latter arises when the results of animal studies are extrapolated to possible effects in
people because of inter-species and inter-strain differences that exist. Even the results
from well-designed and well-conducted epidemiological and experimental studies
have uncertainties that can be statistically quantified, but may not always be explained.
Additionally, not all studies are well designed and executed and this should also be
taken into account when assessing the available information. Thus, the risk assessment
process should address these uncertainties in life science and dosimetry data.
EMF exposure guidelines and caution
9 NRPB considers that the exercise of caution based on knowledge and under-
standing of the sources of uncertainty in the scientific data is an intrinsic part of the EMF
risk assessment process. The degree to which caution is applied in the interpretation
of the scientific evidence is a matter of judgement and should be consistent. EMF
exposure guidelines should ensure that general community protection is provided.
In this document, the term precautionary is reserved for measures that might be
considered necessary in addition to quantitative restrictions on exposure derived from
a cautious interpretation of the science.
10 In recommending quantitative restrictions on exposure, NRPB has made judgements
on the degree of uncertainty in the scientific data and how this indicates the choice
of the restriction values. The basic restrictions recommended in this document for
preventing direct adverse health effects of exposure to EMFs and other recommenda-
tions for limiting the occurrence of indirect effects (eg shock and burn) include such
considerations and, overall, they reflect a cautious approach.
11 Judgements have been made concerning the need for exposure to be additionally
restricted where increased susceptibility of groups of people is expected on scientific
grounds, but where, because there is a lack of specific scientific data, the degree of
susceptibility cannot currently be precisely determined. These judgements form the
basis of recommendations for more restrictive exposure values for members of the
public compared with those for workers.
12 Further, NRPB noted the advice provided by an ad hoc expert group on effects of
weak electric fields (Appendix A) and by other experts at an ICNIRP/WHO workshop
on weak electric field effects in the body (Appendix B; ICNIRP/WHO, 2003). As a result,
it has concluded that internal electric field strength is the appropriate dosimetric quantity
with which to express basic restrictions for low frequency electric and magnetic fields.
127
This judgement and other similar ones based on uncertainties and new scientific data
are intended to stimulate scientific discussion towards the future development of EMF
exposure guidelines.
International initiatives
13 WHO has launched an initiative aimed at achieving a harmonised international
approach to the development of EMF exposure guidelines, a keystone of which is that
they should be based on thorough reviews of the science. ICNIRP, NRPB and other
national expert bodies concerned with the development of exposure guidelines have
already adopted this approach.
14 The European Commission has urged the need for harmonisation of standards of
protection within the European Union (EU). A Recommendation to EU Member States on
the limitation of exposure of the general public to EMFs in the frequency range 0300 GHz
was passed on 12 July 1999 by the Council of the EU and published in the Official Journal
of the European Communities (CEU, 1999). The UK supported the Recommendation.
15 In its preamble, the Recommendation states that measures with regard to electro-
magnetic fields should afford all Community citizens a high level of protection: provisions
by Member States in this area should be based on a commonly agreed framework, so as
to contribute to ensuring consistency of protection throughout the Community. This
message is reinforced in the Recommendations explanatory material presented to the
European Council by the Commission, where it states the existing variations and gaps
in provisions and guidelines [in some Member States] contribute to a sense of confusion
and insecurity felt by many Community citizens and undermines confidence in health
protection authorities.
16 The view of the European Council as to the importance of the ICNIRP guidelines,
their scientific basis and the integrity of the ICNIRP approach is explicit:
The Community framework, which draws on the large body of documentation that
already exists, must be based on the best available scientific data and should
comprise basic restrictions and reference levels on exposure to electromagnetic
fields, recalling that only established effects have been used as the basis for
recommended limitation of exposure; advice on this matter has been given by the
International Commission on Non Ionising Radiation Protection and has been
endorsed by the Commissions Scientific Steering Committee.
17 NRPB advice on limiting exposure to EMFs has been developed from the reviews of
the science, as detailed in this document, whilst noting the advantages of international
harmonisation.
EMF EXPOSURES AND FURTHER PRECAUTION
18 The possible need for further precautionary measures with regard to EMF exposure,
in addition to quantitative basic restrictions and reference levels, is considered here.
19 The relevance of adopting further precautionary measures for EMF exposure has
been the subject of considerable debate internationally. An important and controversial
aspect of that debate has been whether the Precautionary Principle is relevant in
addressing possible risks to public health.
128
The Precautionary Principle
20 The Precautionary Principle has been succinctly described in plain English as better
safe than sorry and err on the side of caution and in more political and technical terms
as taking steps to avoid possible environmental or health damage, in the face of
insufficient evidence (Foster, 2002).
21 The basic principles for the Precautionary Principle were enunciated in the World
Charter for Nature adopted by the United Nations General Assembly in 1982 (UN,
1982). It was subsequently incorporated in various international agreements on
environmental protection, including the 1992 Rio Conference on the Environment and
Development (EC, 2000). Principle 15 of the Rio Declaration states that in order to
protect the environment, the precautionary approach shall be widely applied by States
according to their capability. Where there are threats of serious or irreversible damage,
lack of full scientific certainty shall not be used as a reason for postponing cost-effective
measures to prevent environmental degradation.
22 It should be noted that all references in the Rio Declaration are to protection of
the environment and there are no specific references to the health of communities or
individuals. The Rio Principle has subsequently become consolidated in international
environmental law.
23 The World Health Organization offered clarification of the issue in the context of EMF
exposure in 2000 in a backgrounder document on cautionary policies for protection
against EMFs namely, that a principal requirement is that such policies be adopted
only under the condition that scientific assessments of risk and science-based exposure
limits should not be undermined by the adoption of arbitrary cautionary approaches
(WHO, 2000).
24 WHO defines health as a state of complete physical, mental and social well-being
and not merely the absence of disease or infirmity (WHO, 1946). Within this definition,
effects on peoples health due to their perception of the risk, whether real or imagined,
should be addressed. Clearly death is the most severe adverse health outcome but
pain, disability, prolonged discomfort and other endpoints leading to a loss of quality of
life should be considered as relevant.
25 Recently, WHO has produced a draft report on a Precautionary Framework for
Public Health Protection (WHO, 2003a)*. This document sets out an overarching
approach encompassing procedures in managing human health risks that are either
known or uncertain. The document considers the principles of the health risk assess-
ment process and does not specifically address EMFs or any other agents. Aspects of
this are discussed in paragraphs 3848 below.
European dimension
26 The European Commission (EC) has taken a leading role in fostering discussion
on the use of the Precautionary Principle, mainly through the publication of a
Communication from the Commission on the Precautionary Principle (EC, 2000). This
document sets out the EC approach to using the Precautionary Principle: establishing
guidelines for applying it; building a common understanding of how to assess, appraise,
* It should be noted that this document is currently in the form of a draft for comment and may be
subject to change. It therefore does not necessarily represent WHO policy.
129
manage and communicate risks that science is not yet able to evaluate fully; and
to avoid unwarranted recourse to the Precautionary Principle as a disguised form of
protectionism. The stated aim of the document is not to be prescriptive but rather to be
used as general guidance and as an input to the ongoing debate. However, it should be
viewed in the context of a resolution adopted by the European Council on 13 April 1999
urging the EC to be in future even more determined to be guided by the Precautionary
Principle in preparing proposals for legislation and in its other consumer-related
activities and develop as priority clear and effective guidelines for application of this
principle (EC, 2000). The EC-published Precautionary Principle document is part of the
EC response to this resolution.
27 There is an explicit (legal) reference to the Precautionary Principle in the environment
title of the EC Treaty (of Rome) (EC, 2000). Here, the reference of application is again to
the environment but the EC states that this cannot be interpreted as applying only
to the environment. The EC sets out its case for this view on the basis of examples of
case law and policy and arrives at the following conclusion. Although the Precautionary
Principle is not explicitly mentioned in the Treaty except in the environment field, its
scope is far wider and covers those specific circumstances where scientific evidence is
insufficient, inconclusive or uncertain and there are indications through preliminary
objective scientific evaluation that there are reasonable grounds for concern that the
potential dangerous effects on the environment, human, animal or plant health may be
inconsistent with the chosen level of protection.
28 The EC clarified the circumstances of the use of the Precautionary Principle and the
difference between risk and effect as Recourse to the Precautionary Principle pre-
supposes: (i) identification of potentially negative effects resulting from a phenomenon,
product or procedure, and (ii) a scientific evaluation of the risk that because of the
insufficiency of data, their inconclusive or imprecise nature, makes it impossible to
determine with sufficient certainty the risk in question (EC, 2000).
29 In December 2000 at the Nice Summit, heads of government endorsed a General
Affairs Council resolution on the Precautionary Principle (CO-SUR, 2002). This provided
as follows.
Use must be made of the Precautionary Principle where the possibility of harmful
effects on health or the environment has been identified and preliminary scientific
evaluation proves inconclusive for assessing the level of risk.
The scientific assessment of the risk must proceed logically in an effort to achieve
hazard identification, hazard characterisation, and appraisal of exposure and risk
characterisation.
Risk management measures must be taken by the public authorities responsible on
the basis of a political appraisal of the desired level of protection.
All stages must be conducted in a transparent manner, civil society must be
involved and special attention must be paid to consulting all interested parties as
early as possible.
Measures must observe the principle of proportionality, taking account of short-
term and long-term risks; must not be applied in a way resulting in arbitrary or
unwarranted discrimination; and should be consistent with measures already
adopted in similar circumstances or following similar approaches.
130
Measures adopted presuppose examination of the benefits and costs of action and
inaction, and the examination must take account of social and environmental costs
and of the public acceptability of the different options possible.
Decisions taken in accordance with the Precautionary Principle should be reviewed
in the light of developments in scientific knowledge.
UK dimension
30 Risk management is a stated priority of the UK government and a strategy has been
published aiming towards it being an integral part of the business of good government.
In the foreword to a Strategy Unit Report published in November 2002, the Prime
Minister wrote It will rarely be possible for governments to eliminate risks entirely. All
life involves some risk, and innovation brings risks as well as reward so the priority
must be to manage risks better (CO-SUR, 2002).
31 This report effectively sets out the manner in which the UK government should
think about risk and practical steps for managing it better.
32 Specifically on the Precautionary Principle, the report provides a definition and
guidance on its use as follows.
The Precautionary Principle provides a framework for action by governments
where there is a threat of serious or irreversible harm even where there is scientific
uncertainty about the nature and extent of the risk. The UK, along with other
developed countries, is committed to using the Precautionary Principle.
The Principle is based on Principle 15 of the 1992 Rio Declaration, which states:
where there are threats of serious or irreversible damage, lack of full scientific
certainty shall not be used as a reason for postponing cost-effective measures to
prevent environmental degradation.
There is no universally accepted definition of the Precautionary Principle. Since Rio,
it has been included in a number of international agreements in a variety of
formulations that reflect the substantive context and the negotiating circumstances
of the individual agreements.
33 These observations broadly align with the views promulgated by the EC, as
summarised in paragraphs 2629.
34 The UK government commissioned an Inter-departmental Liaison Group on Risk
Assessment (ILGRA) to develop guidance on a more consistent approach to application
of the Precautionary Principle across government (ILGRA, 2002). The key points of
ILGRA guidance are summarised below.
35 ILGRA recommends that the Precautionary Principle should be invoked when:
There is good reason to believe that harmful effects may occur to human, animal or
plant health or to the environment.
The level of scientific uncertainty about the consequences or likelihood of the risk is
such that the best available scientific advice cannot assess the risk with sufficient
confidence to inform decision-making.
36 ILGRA guidance also makes the following recommendations.
The Precautionary Principle should be distinguished from other drivers that require
caution such as societys view on the extent of protection afforded to children or
others considered to be vulnerable, or the wish to ensure that conventional risk
assessment techniques deliberately overestimate rather than underestimate risk.
131
Action in response to the Precautionary Principle should accord with the
principles of good regulation, ie be proportionate, consistent, targeted, transparent
and accountable.
Applying the Precautionary Principle is essentially a matter of making assumptions
about consequences and likelihoods to establish credible scenarios, and then using
standard procedures of risk assessment and management to inform decisions on
how to address the hazard or threat.
Decision-making should bring together all relevant social, political, economic and
ethical factors in selecting an appropriate risk management option.
Invoking the Precautionary Principle shifts the burden of proof in demonstrating
presence of risk or degree of safety towards the hazard creator. The presumption
should be that the hazard creator should provide, as a minimum, the information
needed for decision-making.
Decisions reached by invoking and applying the Precautionary Principle should be
actively reviewed, and revisited when further information that reduces uncertainty
becomes available.
37 NRPB notes particularly the comments by ILGRA on the wish to ensure that
conventional risk assessment techniques deliberately overestimate rather than under-
estimate risk. It is the view of NRPB that EMF health risk assessment and derivation of
quantitative exposure restrictions should generally lean towards the side of caution in
reaching a judgement on quantitative levels of exposure restriction.
PRECAUTIONARY MEASURES
WHO precautionary framework
38 There is no scientific consensus that exposures to EMFs at levels below currently
accepted UK or international exposure restrictions cause cancer or any other disease.
However, it is the view of NRPB that the totality of the scientific data and uncertainty in
knowledge and/or other relevant factors indicate that consideration should be given as
to whether further precautionary measures are needed.
39 A workshop jointly organised by WHO, the EC and the US National Institute for
Environmental Health Sciences (NIEHS) was held in Luxembourg in February 2003 that
specifically addressed this topic. Subsequent to the workshop, WHO has produced a
draft document for comment on a Precautionary Framework for Public Health Protection
(WHO, 2003a)*.
40 NRPB welcomes this initiative to clarify this important issue and the following
paragraphs summarise some of the key points addressed in the WHO draft document.
41 WHO introduces a new term, the WHO Precautionary Principle for Public Health,
which it defines as a concept that allows flexible approaches to identifying and managing
possible adverse consequences to human health even when it has not been established
that an activity or exposure constitutes harm to health.
* It should be noted that this document is currently in the form of a draft for comment and may be
subject to change. It therefore does not necessarily represent WHO policy.
132
42 WHO also describes a WHO precautionary framework for public health protection,
which is an overarching approach encompassing procedures in managing human health
risks that are either known or uncertain.
43 WHO notes that current risk management systems focus on what is known and
therefore science plays a key role. It emphasises that similarly science plays a key role
in its proposed precautionary framework for public health protection and that its use is
not at odds with scientific understanding.
44 As expressed in the draft document, the view of WHO is that current risk manage-
ment has the following aspects.
Overall evaluation is based on the weight-of-evidence. The science must be
rigorous, appropriately multidisciplinary, published in a peer-reviewed journal and
relevant to risk assessment.
Uncertainties can exist at every level of risk assessment: the existence of a hazard,
the magnitude of exposure, and the relationship of dose to disease incidence or
severity. Uncertainties and assumptions necessary for the proper assessment of risk
must be identified and clearly stated.
When evidence does not meet generally accepted conventional scientific
standards, science-informed assumptions or extrapolations are used.
45 WHO notes that its precautionary framework operates from a broader knowledge
base and attempts to illuminate what is not known in addition to what is uncertain. Here
too science plays a key role. The evaluation of both boundaries and gaps in current
knowledge can and should be determined with scientific input.
A description of when key evidence (eg epidemiological or toxicological studies) is
missing or inadequate is especially important.
Failure to demonstrate an adverse health effect in a limited timeframe does not rule
out the possibility that it will occur sometime in the future.
Failure to demonstrate an adverse health effect does not rule out its possible
existence since the test system may be too insensitive to detect an effect.
Identifying what is not known does not mean that actions would have to be
implemented for any and all activities and exposures.
46 NRPB notes that WHO states its precautionary framework is not a basis for extending
or replacing science-based guidelines. Explicitly, WHO states that international guidelines
limiting human exposures are supported by health effects research results that are
consistent, reproducible, confirmed by different laboratories and clearly identify when
exposure to physical, biological or chemical agents is thought to be harmful to humans.
In addition, exposure limits generally incorporate safety factors that allow for uncertainty
in any identified thresholds for established effects. Such approaches remain essential
within the WHO precautionary framework.
47 The approach taken by NRPB in developing its advice on limiting exposure to EMFs
is consistent with these concepts.
48 NRPB generally supports the concepts in the WHO draft document and considers
that, with further development, such a framework can be an effective tool for considering
the possible need for precautionary measures in relation to health in general and EMF
exposure in particular.
133
Application to EMFs
49 In the context of possible adverse health effects from EMFs, the conclusions of
published expert scientific reviews have identified only one reasonably consistent
epidemiological finding of an adverse health outcome associated with exposure to
EMFs at levels lower than exposure guidelines: that is an apparent increased risk of
childhood leukaemia with time-weighted average exposure to power frequency
magnetic fields above 0.4 T. It is the view of NRPB that the epidemiological evidence
that prolonged exposure to power frequency magnetic fields above 0.4 T is associated
with a small absolute raised risk of leukaemia in children (an approximate doubling of
the relative risk) is, at present, an observation for which there is no sound scientific
explanation. This is consistent with the conclusions of the Advisory Group on Non-
ionising Radiation (AGNIR, 2001a). There is no clear evidence of a carcinogenic effect of
extremely low frequency EMFs in adults, and no plausible biological explanation of the
association from experiments with animals or from cellular and molecular studies.
Alternative explanations for this association are possible; for example, potential bias in
the selection of control children with whom leukaemia cases were compared in some
studies, and chance variations resulting from small numbers of individuals affected.
Thus any judgements developed on the assumption that the association is causal would
be subject to a very high level of uncertainty.
50 The International Agency for Research on Cancer (IARC) has classified power
frequency magnetic fields as a possible carcinogen (IARC, 2002).
51 Public concern about possible risks from exposure to power frequency magnetic
fields is also important and must be addressed. NRPB is aware of, and sympathetic to,
the concerns about EMFs and health expressed by members of the public through both
the individual and media enquiries to which it responds. NRPB welcomed the positive
response from members of the public and others who participated in an open discussion
meeting on power lines that it organised at the National Exhibition Centre, Birmingham,
in December 2002.
52 Because of the uncertainty cited above, and in the absence of a doseresponse
relationship, NRPB has concluded that the data concerning childhood leukaemia cannot
be used to derive quantitative guidance on restricting exposure.
53 NRPB concludes that it is important to consider the possible need for precautionary
measures with respect to exposure of children to power frequency magnetic fields.
54 AGNIR examined possible health effects of exposure to radiofrequency (RF) fields
(AGNIR, 2003), with an emphasis on studies conducted since the review by the
Independent Expert Group on Mobile Phones in 2000 (IEGMP, 2000). AGNIR noted that
there are many sources of RF at work, at home, and in the environment but recent
emphasis in health-related studies has been on mobile phones and broadcasting masts.
55 AGNIR also noted that studies reviewed by IEGMP suggested possible cognitive
effects of exposure to RF fields from mobile phones, and possible effects of pulse-
modulated RF fields on calcium efflux from the nervous system. AGNIR concluded that
the overall evidence on cognitive effects remained inconclusive, while the suggestions
of effects on calcium efflux had not been supported by more recent, better conducted
134
studies. The biological evidence suggested that RF fields do not cause mutation or
initiate or promote tumour formation, and the epidemiological data overall do not
suggest causal associations between exposures to RF fields, in particular from mobile
phone use, and the risk of cancer. AGNIR noted that exposure levels from living near to
mobile phone base stations are extremely low, and concluded that the overall evidence
indicates that they are unlikely to pose a risk to health. With respect to possible risks to
childrens health, AGNIR noted that little has been published specifically on childhood
exposures to RF fields and no new substantial studies had been published since the
IEGMP report.
56 Overall, AGNIR concluded that, in aggregate, the research published since the
IEGMP report does not give cause for concern and that the weight of evidence now
available does not suggest that there are adverse health effects from exposures to RF
fields below guideline levels. In reaching these conclusions, AGNIR noted that the
published research on RF exposures and health has limitations and mobile phones have
only been in widespread use for a relatively short time. The possibility therefore remains
open that there could be health effects from exposure to RF fields below guideline
levels; hence continued research is needed.
57 From its own review and the advice from AGNIR above, NRPB concludes that the
scientific evidence for RF fields causing adverse health effects at levels to which the
general public are normally exposed is much weaker than that for power frequency
magnetic fields. It also notes there is a great deal of ongoing scientific research on RF
fields, in particular mobile telephony, and health. There is a need to constantly monitor
the results of this research.
135
7 Conclusions and Recommendations
In establishing quantitative restrictions on exposure to electromagnetic
fields (EMFs), a range of values is possible; particularly when taking account
of uncertainties in the responses of different groups of individuals in the
general population. The review of current scientific knowledge by NRPB
staff, the adoption of a cautious approach to the interpretation of these
data, and a recognition of the benefits of international harmonisation,
combine in a recommendation to adopt the ICNIRP exposure guidelines for
occupational and general public exposure to EMFs between 0 and 300 GHz.
INTRODUCTION
1 Scientific evidence related to biological effects of electromagnetic fields (EMFs) and
possible consequential adverse effects on human health has been reviewed in this
document. In evaluating the basis for providing guidance on limiting exposure and
possible risks from exposure to EMFs, consideration has been given to uncertainties in
scientific data and a cautious approach has been adopted in their interpretation.
2 The review has covered epidemiological studies as well as experimental biology,
volunteer studies and dosimetry. These play important individual and collective roles in
identifying possible adverse effects on health and in providing information on the need
for, and appropriate levels of, protection.
3 Based on the review, this chapter summarises the NRPB conclusions and
recommendations including:
(a) the basis for providing quantitative restrictions on exposure of people to EMFs,
(b) basic restrictions on exposure to EMFs to avoid direct effects,
(c) advice on limiting possible indirect effects of exposure (shock and burn),
(d) reference levels, which are measurable quantities for assessing compliance with
basic restrictions or for assessing the possibility of shock and burn,
(e) the possible need for further precautionary measures in relation to EMF exposure
and health.
4 The recommendations are not concerned with exposures of patients carried out
under medical supervision or with possible electrical interference with implantable
medical devices such as pacemakers. They do not address detailed aspects of applying
the guidelines to specific exposure situations.
5 A number of recommendations are made which are specifically aimed at developing
guidance through research in key areas where continuing uncertainty limits the rigour
with which appropriate restrictions on exposure can be formulated.
6 NRPB is committed to ongoing monitoring of the results of scientific studies on EMFs
and health and to revising its advice when appropriate.
136
GENERAL CONCLUSIONS ON THE SCIENCE
7 NRPB concludes that there are scientific data indicating the need for appropriate
quantitative restrictions on exposure. These data derive from experimental studies
related to effects of EMFs on the central nervous system (CNS) and effects of heating
on the body. The nature of such effects and the mechanisms underlying them
have been reviewed in this document. The quantitative restrictions on exposure and
recommendations for further investigation, where relevant, are derived from data on
these effects.
8 Evidence of other possible effects associated with EMF exposure derives principally
from epidemiological studies and from some experimental studies. The main, but not
sole, subject of such studies has been cancer. These studies have been reviewed
extensively by expert groups, including AGNIR, and are summarised in this document.
It is concluded that currently the results of these studies on EMFs and health, taken
individually or as collectively reviewed by expert groups, are insufficient either to make
a conclusive judgement on causality or to quantify appropriate exposure restrictions.
This conclusion is in accord with the manner in which other expert bodies for
example, ICNIRP (1998) have developed EMF exposure guidelines.
9 However, such studies taken together with peoples concerns provide a basis for
considering the possible need for further precautionary measures in addition to the
application of quantitative restrictions on exposure to EMFs.
EXPOSURE CIRCUMSTANCES
10 The basic restrictions on exposure to EMFs recommended in this document
distinguish between occupational and general public exposure situations. This is a
departure from previous NRPB advice and is supported by this review of the science.
11 NRPB notes exposure in occupational situations will generally be to healthy adults
working under controlled conditions. These conditions include the opportunity to
apply engineering and administrative measures and, where necessary and practical,
provide personal protection.
12 NRPB also notes the general public includes people of all ages and widely varying
health status, and exposure is likely to occur under uncontrolled conditions.
STATIC ELECTRIC AND MAGNETIC FIELDS
13 The perception threshold for static electric fields is around 20 kV m
1
, and annoying
sensations can be induced above about 25 kV m
1
. Painful spark discharges can arise
when a person who is well insulated from ground touches a grounded object, or when
a grounded person touches a conductive object that is well insulated from ground;
however, threshold static electric field values will vary depending on the degree of
insulation and other factors.
14 Where static electric fields cause annoyance, or pain from electrostatic discharge, it
is important to reduce the possibility of occurrence of these effects.
137
15 Vertigo, nausea, a metallic taste and phosphenes can be induced during movement
in static magnetic fields larger than about 2 T; in addition, flow potentials induced
in a magnetic field of this value have been calculated to generate electric fields of
about 200 mV m
1
near the sino-atrial (pacemaker) node of the heart during the relative
refractory period of the cardiac cycle, when cardiac excitability is relatively low.
16 NRPB concludes that acute adverse responses will not occur for exposure to static
magnetic fields of less than 2 T.
17 There is insufficient evidence from animal and cellular studies to determine long-
term health effects due to chronic exposure to static magnetic fields.
Occupational exposure
18 On the basis of the evidence on acute effects, and the uncertainty concerning long-
term effects, NRPB considers a cautious approach to restricting exposure to static
magnetic fields is merited.
19 NRPB concludes that restricting whole-body time-weighted average exposure to
a magnetic flux density of 200 mT is appropriate for occupational exposure to static
magnetic fields with an instantaneous ceiling of 2 T. For exposure of the limbs, a ceiling
of 5 T is appropriate.
General public exposure
20 NRPB supports the cautious approach adopted by ICNIRP in setting its basic
restrictions on static magnetic fields for the general public, ie a time-weighted average
magnetic flux density of 40 mT for whole-body exposure.
21 NRPB considers that exposures in excess of 40 mT are appropriate for occasional
access to special facilities under controlled conditions provided that the occupational
exposure restrictions are not exceeded.
Recommendation
22 The ICNIRP exposure guidelines should be used for restricting occupational and
general public exposure to static magnetic fields (see Appendix C).
ELECTRIC AND MAGNETIC FIELDS OF FREQUENCIES BELOW
100 kHz
23 The most plausible and coherent set of data from which guidance can be developed
concerns weak electric field interactions in the CNS and certain other electrically excitable
tissues. A cautious approach has been used to indicate thresholds for adverse health
effects that are scientifically plausible. Data on other possible health effects examined
lack plausibility, coherence and consistency. There is a need for key uncertainties in
these data to be addressed through further research and scientific discussion.
24 The primary means by which the induced electric fields and currents interact with
biological tissue is through voltage-gated ion channels situated in cell membranes. The
effect is to alter the flux of certain ions, and the electric potential, across the cell
membrane leading to subsequent biological responses. The most sensitive tissues
are those comprising interacting networks of electrically excitable tissue, such as the
138
central, autonomic and enteric nervous systems. The heart, other muscle tissue
and non-excitable tissues with voltage-sensitive ion channels are expected to show a
lower sensitivity.
25 Thresholds of around 100 mV m
1
1
, have been
identified for effects in the central, autonomic and enteric nervous systems, spanning
the range identified in Appendix A for most adults and for potentially susceptible
individuals. However, it is recognised that there is considerable uncertainty associated
with these values, which is not possible to resolve without further experimental
and dosimetric investigation. It is considered appropriate to apply these threshold
values over a broad frequency range (approximately 10 Hz 1 kHz) and to a minimum
of around 1000 interacting cells, which would occupy approximately 1 mm
3
in tissue of
the CNS.
26 Precise comparison of basic restrictions expressed in terms of induced electric field
strength with those expressed in terms of induced current density requires computational
modelling employing tissue- and frequency-dependent values of electrical conductivity.
In the absence of such data, simple comparisons can be made with existing guidelines
assuming a fixed chosen value of electrical conductivity.
27 When a person is in an electric field, is ungrounded and comes into contact with a
grounded object there is the possibility of occurrence of a spark discharge at the point
of contact between the person and the object. For fields external to the body greater
than about 5 kV m
1
, there is the likelihood of such discharges being painful. The extent
to which this is a problem in practice is unclear and further investigation is merited.
28 When a person is in an electric field and comes into contact with an ungrounded
object there is the possibility of occurrence of a spark discharge at the point of contact
between the object and the person. For such situations, the probability and the magnitude
of the effect depend on the field strength and the size of the ungrounded object.
29 NRPB concludes that a restriction of the induced electric field in the tissue of the
central, autonomic and enteric nervous systems to less than 100 mV m
1
is adequate to
protect most adult members of the population*.
30 The value of 100 mV m
1
was derived primarily from a consideration of weak
electric field effects in the CNS and corresponds approximately to the existing ICNIRP
basic restriction on current density of 10 mA m
2
, assuming an electrical conductivity
value of CNS tissue of 0.1 S m
1
.
31 NRPB concludes that 10 mA m
2
is an appropriate basic restriction on induced
current density in the CNS for occupational exposure.
32 In respect of general public exposure, those exposed might include people
potentially susceptible to electrical stimulation, ie people with epilepsy, a family history
of seizure, or using tricyclic anti-depressants, neuroleptic agents and other drugs that
* It is acknowledged that setting aside the lower range of uncertainty, based on phosphene data,
facilitates international harmonisation. A cautious approach is nevertheless maintained at power
frequencies and above through the application of a flat frequency response between 10 and 1000 Hz.
139
lower seizure threshold. It should be noted that some workers may have these
conditions, and that seizure is a CNS phenomenon, not autonomic or enteric. The
ad hoc expert group (Appendix A) considered that such sensitive people should be
adequately protected at lower induced electric field strengths, possibly about a factor
of five lower than for normal adults. In addition, the group considered that this
reduction factor would be adequate to protect the developing nervous system in utero,
and in neonates and young children. NRPB concludes that a restriction of the induced
electric field in the tissue of the CNS to less than 20 mV m
1
is adequate to protect these
members of the population.
33 The value of 20 mV m
1
was derived from a consideration of weak electric field effects
in the CNS and corresponds approximately to the existing ICNIRP basic restriction on
current density of 2 mA m
2
, assuming an electrical conductivity value of CNS tissue
of 0.1 S m
1
.
34 NRPB concludes that 2 mA m
2
is an appropriate basic restriction on induced
current density in the CNS for general public exposure.
Reference levels
35 Calculations have been carried out by NRPB, to judge the appropriateness of the
reference levels for occupational and general public exposure to electric and magnetic
fields of frequencies less than 100 kHz (Figures 1 and 2). These calculations indicate that
the reference levels are appropriate for use at the initial stage of assessing compliance
with the relevant basic restrictions on induced current density.
Recommendations
36 The ICNIRP basic restrictions on induced current density should be used for
restricting occupational and general public exposure to electric and magnetic fields of
frequencies less than 100 kHz.
37 The ICNIRP reference levels should be used at the initial stage of assessing
compliance with basic restrictions on exposure.
38 Further investigations of compliance, that are indicated by exceeding these
reference levels, should use the most up to date dosimetry data.
TIME-VARYING EMFS OF FREQUENCIES ABOVE 100 kHz
39 The most plausible and coherent set of data from which guidance can be developed
concerns raised temperatures and the physiological stress induced by increased heat
loads. A cautious approach has been used to derive thresholds for adverse health effects
that are scientifically plausible. Other studies reviewed lack plausibility, coherence and
consistency. There is a need for key uncertainties in these data to be addressed through
further research. In particular, the distribution of increased sensitivity to the effects of
heat in members of the population is not well defined at present.
40 The exposure metric for restricting exposure to fields of frequencies between
100 kHz and 10 GHz is specific energy absorption rate (SAR), unit W kg
1
. For frequencies
between 10 and 300 GHz, because of diminishing penetration into the body, the exposure
metric is incident power density, unit W m
2
.
140
FIGURE 1
(a) Comparison of
the ICNIRP
occupational
reference level and
NRPB quasistatic
calculations of the
electric field strength
required to produce
a current density
equal to the ICNIRP
basic restriction on
induced current
density with
averaging over
1 cm
2
in the brain,
spinal cord and
retina
(a)
(b) Comparison of
the ICNIRP
occupational
reference level and
NRPB quasistatic
calculations of the
magnetic flux
density required to
produce a current
density equal to the
ICNIRP basic
restriction on
induced current
density with
averaging over
1 cm
2
in the brain,
spinal cord and
retina
(b)
141
FIGURE 2
(a) Comparison of
the ICNIRP general
public reference
level and NRPB
quasistatic
calculations of the
electric field strength
required to produce
a current density
equal to the ICNIRP
basic restriction on
induced current
density with
averaging over
1 cm
2
in the brain,
spinal cord and
retina
(a)
(b) Comparison of
the ICNIRP general
public reference
level and NRPB
quasistatic
calculations of the
magnetic flux
density required to
produce a current
density equal to the
ICNIRP basic
restriction on
induced current
density with
averaging over
1 cm
2
in the brain,
spinal cord and
retina
(b)
142
Whole-body
41 NRPB considers that limiting whole-body radiofrequency (RF) induced heat load
to less than 0.4 W kg
1
will prevent heat-related disorders. For most adults it is
unnecessary to additionally account for high rates of physical work and/or hot, humid
environments.
Partial-body
42 With regard to partial-body (localised) heating, limiting the rise in the temperature
of the head and spinal cord, to 38C, of the other tissues of the neck and trunk (with the
exception of the testes) to 39C, and of the limbs to 40C, should avoid any heat
induced damage in the tissues of these regions of the body. For the testes, the increase
in temperature should be limited to 1C, because of their greater sensitivity to heat.
NRPB concludes that occupational basic restrictions on exposure should be aimed at
limiting localised temperature rises to these values.
43 There are still relatively few dosimetric studies linking localised temperature
increases and SAR in most parts of the body. However, with respect to exposure of
the head from the use of mobile phones, there is a growing body of computational
work available. These studies provide reassurance as to the very low localised
temperature increases that might arise from the use of a mobile phone and insight on
the relationship between temperature rise and SAR in this case. The results indicate a
range of localised temperature increases of 0.05 to 0.12C in the brain from a localised
SAR of 1 W kg
1
. The highest of this range of values indicates that, in order to limit the
temperature in all parts of the brain to 38C (corresponding to a temperature rise of 1C
above baseline), the SAR in the head, averaged over any 10 g cube, should not exceed
about 8 W kg
1
.
44 Studies of heating in the eye suggest that an SAR of 1 W kg
1
averaged over the eye
may lead to a temperature rise of up to 0.25C in the region of the lens. Therefore, these
studies indicate that in order to limit the temperature in the eye to 39C, the SAR
averaged over 10 g should be limited to about 8 W kg
1
.
45 Calculations on possible temperature rises in the head and eye indicate the need to
restrict localised SAR to about 8 W kg
1
averaged

over a 10 g cube. These calculations
also indicate that the highest average SAR over any contiguous 10 g mass is typically
at least 50%greater than this. Adequate protection is therefore afforded by restricting
localised SAR in the head and trunk to 10 W kg
1
averaged over any contiguous 10 g
mass. However, given the range of published dosimetric data relating temperature
rise with localised SAR, further dosimetric studies addressing this topic should be
carried out.
Reference levels
ICNIRP external power density and limb current reference levels for occupational
exposure to plane wave EMFs of frequencies greater than 100 kHz (see Figure 3). These
indicate that, to different degrees, the reference levels for occupational exposure are
appropriate for use at the initial stage of assessing compliance with basic restrictions
on SAR.
143
FIGURE 3
(a) Comparison of
the ICNIRP
occupational
reference level and
NRPB plane wave
calculations of the
power density
required to produce
a whole-body SAR
equal to the ICNIRP
basic restriction
(a)
(b) Comparison of
the ICNIRP
occupational
reference level and
NRPB calculations of
the induced ankle
current required to
produce a maximum
localised SAR
averaged over 10 g
anywhere in the leg
equal to the
corresponding
ICNIRP basic
restriction
(b)
144
Whole-body
47 General community protection, including for people potentially susceptible to heat
related disorders, will be assured if the whole-body RF heat load is below an SAR of
about 0.1 W kg
1
. This will provide protection to older people, infants, children, pregnant
women, other adults taking certain medications and to people undertaking cognitively
demanding tasks.
48 For frequencies between 100 kHz and 10 GHz this agrees reasonably well with the
ICNIRP exposure guidelines basic restriction of 0.08 W kg
1
for the general public.
Partial-body
49 With regard to partial-body (localised) heating, limiting the rise in temperature of
the head and spinal cord, and of the embryo and fetus, to 38C, of the other tissues
of the neck and trunk (with the exception of the testes) to 39C, and of the limbs to
40C, should avoid heat induced damage in the tissues of these regions of the body. For
the testes, the increase in temperature should be limited to 1C, because of their greater
sensitivity to heat. NRPB concludes that general public basic restrictions on exposure
should be aimed at limiting localised temperature rises to these values.
50 Computational studies have been published on temperature rises that might arise
from exposure of the head associated with the use of mobile phones. These studies
provide insight on possible temperatures that could result from a localised SAR of
2 W kg
1
averaged over 10 g mass of tissue. This value is one that has been adopted by
ICNIRP as a basic restriction on localised SAR in the head and trunk for general public
exposure and recommended by the Independent Expert Group on Mobile Phones
(IEGMP), the Department of Health and the Board of NRPB as being appropriate for
restricting exposure associated with mobile telephony. Computational results indicate
localised temperature increases of up to around 0.20.25C could result in the brain
from a localised SAR of 2 W kg
1
. Little work has been carried out on thermal dosimetry
of the fetus or with computational models incorporating reduced organ perfusion rates
as might be relevant to people with cardiovascular or other diseases.
51 Taking into account uncertainties related to partial-body exposure, the above
conclusions on limiting temperature increases associated with general public exposure
to fields of frequencies between 100 kHz and 10 GHz agree reasonably well with the
current ICNIRP basic restriction on localised SAR (2 W kg
1
) and with the recommenda-
tions for restricting exposure associated with mobile telephony from IEGMP and the
Board of NRPB.
Reference levels
external power density and limb current reference levels for general public exposure to
plane wave EMFs of frequencies greater than 100 kHz (see Figure 4). They suggest that
the ICNIRP reference levels for general public exposure are generally conservative for
assessing compliance with basic restrictions on SAR. However, the exception is for the
exposure of small children under worst-case exposure conditions at frequencies between
about 50 and 100 MHz and above about 1 GHz.
145
FIGURE 4
(a) Comparison of
the ICNIRP general
public reference
level and NRPB
plane wave
calculations of the
power density
required to produce
a whole-body SAR
equal to the ICNIRP
basic restriction
(a)
(b) Comparison of
the ICNIRP general
public reference
level and NRPB
calculations of the
induced ankle
current required to
produce a maximum
localised SAR
averaged over 10 g
anywhere in the leg
equal to the
corresponding
ICNIRP basic
restriction
(b)
146
53 NRPB considers that the appropriateness of the field reference levels for exposure
of the general public needs to be reviewed for frequencies between about 50 and
100 MHz and above 1 GHz. Nevertheless, given the conservative assumptions used to
derive the basic restrictions for the general public and the assumption of optimal
coupling to the field in deriving the reference levels, it is considered appropriate to use
the ICNIRP reference levels at present.
Recommendations
54 The ICNIRP basic restrictions on whole-body and localised SAR should be used for
restricting occupational and general public exposure to EMFs of frequencies greater
than 100 kHz.
55 Electrical effects on body tissues are also possible at frequencies above 100 kHz
and up to about 10 MHz; hence basic restrictions to prevent these effects should apply
up to 10 MHz.
56 The ICNIRP reference levels should be used at the initial stage of assessing
compliance with basic restrictions on exposure.
57 Further investigations of compliance, that are indicated by exceeding these
reference levels, should use the most up to date dosimetry data.
FURTHER PRECAUTIONARY MEASURES
58 The background and indicators for considering the possible need for further
precautionary measures are discussed in Chapter 6.
59 There remain concerns about possible effects of exposure of children to power
frequency magnetic fields. The view of NRPB is that it is important to consider the
possible need for further precautionary measures in respect of exposure of children to
power frequency magnetic fields.
60 With respect to RF exposures and health, NRPB noted the conclusions of the
AGNIR report on RF fields and human health (AGNIR, 2003).
61 NRPB concludes that the scientific evidence for RF fields causing adverse health
effects at levels to which the generally public are normally exposed is much weaker
than that for power frequency magnetic fields. It also notes there is a great deal of
ongoing scientific research on RF fields, in particular on mobile telephony, and health.
There is a need to constantly monitor the results of this research and keep the
guidelines under review.
Recommendation
62 The government should consider the need for further precautionary measures
in respect of exposure of people to EMFs. In doing so, it should note that the overall
evidence for adverse effects of EMFs on health at levels of exposure normally experi-
enced by the general public is weak. The least weak evidence is for the exposure of
children to power frequency magnetic fields and childhood leukaemia.
147
FUTURE DEVELOPMENT OF EXPOSURE GUIDELINES
63 Recommendations for studies of the possible effects of EMF exposure, including
epidemiological studies, especially in relation to cancer, reproductive and behavioural
effects, have been given in a number of recent reviews (eg AGNIR, 2001a,c, 2003; Ahlbom
et al, 2001). The following recommendations are specifically aimed at developing
guidance through research in key areas where continuing uncertainty limits the rigour
with which appropriate restrictions on exposure can be formulated.
Static magnetic fields
64 Epidemiological studies should be carried out of the long-term risks to health of pro-
longed occupational exposure to static magnetic fields. Additional studies of occupational
health, for example using questionnaires, to derive indices of health status should also
be considered. These studies in human populations should be complemented by long-
term animal studies in static fields in excess of 2 T.
65 Further study should be carried out of the potential long-term effects of static
magnetic fields greater than 1 T on potentially susceptible metabolic reactions, such as
those in which radical pairs are transiently generated. These should be complemented
by volunteer and in vitro studies of magnetic field induced changes in metabolism using
modern, molecular approaches such as genomics, proteomics and metabolomics.
66 The degree to which vertigo, nausea and other acute effects are a feature of
occupational exposure to fields in excess of 2 T should be investigated.
Power frequency surface charge effects
67 Further exploration of the thresholds for surface electric charge effects induced by
exposure to power frequency electric fields should be carried out in both occupational
situations and those encountered by the general public.
Weak induced electric field effects
68 The susceptibility of the brain and other electrically excitable tissue to weak electric
field interactions remains largely unexplored. Further study of the mechanism of phos-
phene induction and its frequency response through neurophysiological investigation
of induced electric field effects on retinal neuronal circuitry, and similar studies of the
threshold and frequency response of neural networks in other brain tissue, are required
to clarify the degree to which phosphene data can be extrapolated to the rest of the brain.
69 These studies would be usefully supplemented by further macrodosimetric and
microdosimetric investigation of the induced fields and currents in the retina in volunteer
studies of phosphenes.
70 Volunteer studies are required to identify behavioural and cognitive functions
affected by exposure. Animal models should be used to supplement these data.
71 The degree to which sensitivity may be increased in people with conditions such as
epilepsy should be investigated through neurophysiological and behavioural investiga-
tion using in vitro and animal models of these conditions.
72 For time-varying fields of frequencies less than 100 kHz, there is a growing consensus
that the appropriate dosimetric quantity with which to express basic restrictions on EMF
exposure should be induced electric field strength. Such recommendations were made
at an EMF Exposure Guidelines Science Workshop held in Brussels (Sheppard et al,
2000) and have been incorporated into the IEEE standard on limiting human exposure
148
to EMFs up to 3 kHz (IEEE, 2002). Similar recommendations were made to NRPB by an
ad hoc expert group (Appendix A) and at a recent ICNIRP/WHO workshop (Appendix B;
Blakemore et al, 2003). This represents a change from the practice used by many
bodies concerned with the development of EMF exposure guidelines (eg ICNIRP, 1998;
NRPB, 1999) where, for this frequency range, basic restrictions are expressed in terms
of induced current density.
73 In the further development of EMF exposure guidelines, consideration should be
given to the basic restrictions for time-varying electric and magnetic fields of frequencies
up to 100 kHz being based on limiting electric field strength internal to the body.
Whole-body SAR
74 The distribution of heat sensitivity in the general population is not well understood;
in particular, there is some uncertainty regarding the heat loads that people with varying
susceptibilities to heat can tolerate. Raised maternal body temperature can adversely
affect prenatal and possibly early postnatal development, particularly that of the CNS,
but thresholds have not been rigorously identified. More quantitative studies should
be carried out, especially on development of the cerebral cortex, during prenatal and
postnatal exposure using both morphological and functional endpoints.
Localised SAR
75 With regard to localised heating, acute animal studies have shown that tissue necrosis
can be induced when local temperatures exceed 41C for an hour or more. Further
studies should be carried out of the effects of prolonged and/or chronic exposure at
lower temperatures, especially those that might result from functional changes induced,
for example, by heating of the brain or endocrine glands.
76 For exposure to mobile phones, there are conflicting reports as to whether there is
a significant increase in the SAR absorbed in the head, and particularly in the brain, for
children compared to adults. This is an area where clarification is needed.
77 Further work should be carried out to provide more knowledge of the quantitative
relationship between localised temperature increases and SAR in the head and eye, trunk,
embryo and fetus including using models incorporating reduced organ blood perfusion
rate. Particular attention should be given to the acquisition of reliable measurements of
the thermal parameters of human tissues, including perfusion rates.
78 The metric used in the ICNIRP guidelines the SAR average over any 10 g of con-
tiguous tissue does not distinguish between compact and diffuse patterns of heating
which are likely to have different thermal effects. The consequences of a cubic averaging
region for exposure guidelines should be investigated.
Dosimetry and reference levels
79 An important requirement in future dosimetry is the development of an adult female
voxel model and also child models which are not simply scaled adults, along with the
appropriate age-dependent tissue dielectric parameters.
80 The appropriateness of the field reference levels for exposure of the general public
needs to be reviewed for frequencies between about 50 and 100 MHz and above 1 GHz
(see paragraphs 52 and 53).
81 Induced electric fields need to be calculated averaged over a 1 mm cube in the
brain, spinal cord and retina for low frequency electric and magnetic field exposures.
149
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197
Appendix A
WEAK ELECTRIC FIELDS GROUP
Position statement on weak electric field effects in humans and
their implications for standards, following a meeting held at NRPB
(22 November 2001), and subsequent discussion and correspondence
Members
Professor C Blakemore FRS (University of Oxford) (Chairman)
Professor D Attwell FRS (University College, London)
Professor J Jefferys (University of Birmingham)
Dr J Tattersall (Dstl, Porton Down and University of Southampton)
Dr R Saunders (NRPB, Chilton)
Dr Z Sienkiewicz (NRPB, Chilton)
Dr J Stather (NRPB, Chilton)
Purpose
The remit of the ad hoc expert group on effects of weak electric fields was to review
the neurophysiological evidence for effects of induced electric fields and currents that
could provide a basis for revised guidance on human exposure to time-varying electric
and magnetic fields below 100 kHz.
Summary
The specific issues addressed included the suitability of the neuronal circuitry of
the retina as a model for neuronal circuitry in the central nervous system (CNS), the
evidence for weak electric field interactions in brain tissue in vitro, effects on coupled
networks of neurons and extrapolation in vivo, effects on the developing nervous
system, sensitive subgroups and the implications for standards. Many of these issues
were raised in the discussion of the paper by Saunders and Jefferys (2002) and the
earlier review by Jefferys (1995).
Suitability of the retina as a model for electric field interactions with
the CNS
There was general agreement with the evidence and conclusions reached by
Dr Saunders and Professor Jefferys in their joint paper cited above. In particular, the
retina was considered to be a good, albeit especially sensitive, model for CNS neuronal
circuitry*. Phosphenes can be reliably produced by electric fields induced in the retina
or directly applied via electrodes; minimum threshold current densities (at 20 Hz) have
been estimated by several authors (Adrian, 1977; Carstensen et al, 1985; Wake et al,
1998) as around 1014 mA m
2
; if the conductance of retinal tissue is assumed to be
similar to that of brain tissue, about 0.1 S m
1
(Gabriel, 1995), the equivalent threshold
electric field value in the retina can be estimated as approximately 100140 mV m
1
.
These values are, however, subject to some uncertainty: the calculation by Wake et al
* Described, for example, by Shepherd (1998).
198
(1998) was based on high retinal conductivity of 1.5 S m
1
(Wake, personal communi-
cation, 2002). Adrian (1977) provided an order-of-magnitude threshold, based on a
homogeneous head, and Carstensen et al (1985) used a 1600-element model of the
head in which the retina was not accurately modelled, although the result was described
as moderately robust to changes in model parameters.
Several lines of evidence suggested that the phototransduction apparatus was not
involved in the induction of phosphenes by induced weak electric fields: Carpenter (1972)
had shown that phosphene threshold did not show the dark adaptation behaviour
characteristic of photoreceptors, and a study cited by Saunders and Jefferys indicated
phosphenes could be induced in a blind patient suffering with a degenerative condition
(retinitis pigmentosa) affecting the pigment epithelium and photoreceptor layer. Other
properties favoured the retina as a sensitive indicator of weak electric field interactions
with CNS neuronal circuits, namely: its peripheral location, its highly ordered structure,
and the predominantly non-spiking (ie graded, electrotonic) behaviour of many of its
neuronal elements, namely the horizontal, bipolar and (most) amacrine cells, as well as
the photoreceptors. These various factors, and the tight electrical coupling that exists
between some groups of retinal cells, were thought to render the retina relatively
sensitive but not unrepresentative of the response of other CNS neuronal circuits to
induced electric fields.
Highly ordered regions of the CNS such as the cerebral cortex, hippocampus and
cerebellum, with tightly aligned dendritic fields and restricted extracellular space, would
favour weak electric field interactions (Faber and Korn, 1989; Jefferys, 1995; Saunders
and Jefferys, 2002) compared with more diffuse structures such as the thalamus or
striatum. The group noted that the anisotropy exhibited by these tissues is likely to
engender a degree of directional sensitivity to induced electric fields, which is unlikely
to be accounted for in the measurement of the dielectric properties of these tissues.
Weak electric field effects on the adult CNS
The evidence concerning weak electric field effects in CNS (predominantly
hippocampal) tissue in vitro, summarised by Jefferys (1995) and more briefly by Saunders
and Jefferys (2002), was considered. Jefferys (1995) concluded that weak induced
fields of the order of 4 V m
1
could affect excitability and synchronicity in neuronal
tissue; however, it was noted at the meeting that this response appeared to vary linearly
with the applied field. Subsequently, effects have been reported at induced electric
fields as low as 400 mV m
1
(Francis et al, 2000). Recently, Gluckman, Schiff and
colleagues (Gluckman et al, 2001) using an in vitro model of epilepsy, reported
detection limits for modulation of single neurons and networks by electric fields near
the 100 mV m
1
range. Consideration should also be given to the possible effects of
electric fields on glia as well as on neurons since:
(a) on theoretical grounds, spatially extended cells may be more sensitive to external
electric fields,
(b) glial cells form a large network interconnected by gap junctions,
(c) recent work has shown that [Ca]
i
elevations in glia can trigger release of the
neurotransmitter glutamate from glia (Parpura et al, 1994; Hassinger et al, 1995;
Bezzi et al, 1998, 2001).
Appendix A: Weak Electric Fields Group
199
The relevance of these in vitro data to possible effects on the CNS in vivo was
discussed. In general, support was expressed for the view taken by Saunders and Jefferys
(2002) that thresholds were likely to be lower, both as a result of the higher levels of
spontaneous activity, and of the potential involvement of large, interacting groups of
nerve cells (neural networks). In particular, much of normal brain function depends on
the collective activity of very large numbers of neurons; network modelling is widely
used in the investigation of neuronal behaviour in the central nervous system*. It was
noted that the integration of a very weak effect on a large number of interacting nerve
cells would result in an increase in signal-to-noise ratio proportional to the square root
of the number of interacting cells, assuming independent noise. It is thought that the
minimum number of cells involved, for example, in epileptic activity in the hippocampus is
about 1000 (Jefferys, 1994) with a volume of approximately 0.51 mm
3
.
The potential frequency response of these weak field effects was discussed.
Attention was drawn to the view that the limited frequency response of phosphenes
results from time constants for synaptic activity (around 20 ms) that are about 100 times
longer than those associated with, for example, peripheral nerve activity (Reilly, 1999;
IEEE, 2002). However, many kinds of neuronal dendrites do not necessarily satisfy
passive cable theory (Tagaki, 2000). They contain voltage-gated ion channels capable of
propagating transient potentials, which may additionally modulate dendritic function.
The group expressed the opinion that effects at frequencies up to a few kilohertz
should not be ruled out, since the kinetics of the fastest voltage-gated ion channels can
be less than 1 ms.
Members of the group noted that the tissue on which conductivity measurements
were made was dead and therefore the conductivity values would not take account of
changes resulting from, for example, increases in ion channel activity that occur in living
tissue. However, the variation of conductivity with frequency was thought to be of
greater significance. It was noted that Gabriel et al (1996) found a four-fold increase in
brain conductivity over the frequency range 10 Hz 100 kHz.
The group noted that the muscle tissue of the heart was an electrical network
(syncytium), driven by pacemaker cells situated in the sino-atrial node, and may be
expected to show similar weak electric field sensitivity. Reference was made to the
(rather inconclusive) work of Graham, Cook and colleagues at the Midwest Research
Institute on heart rate variability during EMF exposure (eg Graham et al, 2000a,b). Other
relevant tissues capable of network behaviour were thought to include the autonomic
and enteric nervous systems (comprising non-myelinated nerve cells, ganglia and
plexuses distributed over the body and gut involved in regulating the visceral or house-
keeping functions of the body).
Theoretical studies
Several papers by Weaver, Astumian, Adair and colleagues that explored the
theoretical limits of biological thresholds to induced electric fields were noted. An early
paper (Weaver and Astumian, 1990) suggested a lower limit for detection by membrane
macromolecules of 100 mV m
1
. More recently, Weaver et al (1998) calculated a mini-
mum threshold of around 10 mV m
1
for an elongated cell and Adair et al (1998) suggested
* See, for example, Jefferys et al, 1996; Rubin and Terman et al, 2000; Whittington et al, 2000.
200
a minimum theoretical sensitivity of 1 mV m
1
for systems in which integration of an
induced electrical signal takes place over a large number of cells.
Weak electric field effects on the developing CNS
Endogenous direct current (DC) electric fields and currents generated by
physiological and metabolic processes within the body can affect nerve growth in vitro
and in vivo and it has been suggested (Nuccitelli, 1992) that they may play an important
role in the guidance of normal developmental processes. The potential for induced
electric fields to affect the developing nervous system was discussed. The group
considered the developing nervous system, both in utero and in neonates and young
children, as potentially susceptible to induced time-varying electric fields. The
considerable number of papers reporting the involvement of DC electric fields of the
order of 10100 V m
1
in development of the embryonic and neonatal nervous system
and in nerve regeneration was noted (eg AGNIR, 1994; Jefferys, 1995; Rajnicek et al,
1998). Recently, however, Borgens (1999) reported that DC electric fields of only
100 mV m
1
can influence the regeneration of nerve fibres in the spinal cord. In addition,
Moriarty and Borgens (2001) noted that application of a DC electric field of 320 mV m
1
that alternated in polarity every 15 minutes could affect the density and orientation of
astrocytes in an injured mammalian spinal cord.
The effect seems to depend to some degree on the surface charge of the substrate,
suggesting that the electric current may interact with the way that the neuronal mem-
brane and surface interact. The galvanotropisms may be due to localised membrane
depolarisations, caused by the field, leading to calcium influx, which affects growth cone
extension (Bedlack et al, 1992). Endogenous electric fields may also play an important role
in guiding nerve development and enhancing repair (Borgens, 1982). These reactions all
occur for cell depolarisations below the threshold for initiating nerve impulses but it is
worth pointing out that spontaneous and stimulus-evoked impulse activities are believed
to play a crucial role in local competition between growing axons and the distribution
of synaptic boutons on target cells (Shatz, 1990). Any tendency of applied fields to
modulate impulse activity could conceivably modify these competitive processes.
Sensitive groups in the population
Epilepsy is characterised by increased neuronal excitability and synchronicity;
seizures arise from an excessively synchronous and sustained discharge of a group of
neurons (eg Jefferys, 1994; Engelborghs et al, 2000). It was thought to predispose
individuals suffering from this disorder as at potentially increased risk from induced
electric field effects compared with most individuals. Other characteristics likely to
increase sensitivity to weak, induced electric fields include a family history of seizure,
the use of tricyclic anti-depressants, neuroleptic agents and other drugs that lower seizure
threshold and people with serious heart disease or with increased intracranial pressure
(Wasserman, 1998). In addition, the potential interference with various medical prosthetic
devices was noted.
Voltage-gated ion channels in non-excitable tissues
The group considered that most cells in the body would possess voltage-gated ion
channels capable of responding to a weak electric field. Voltage-gated potassium
channels are fairly ubiquitous and play a central role in controlling cell membrane
201
potential; voltage-gated sodium channels are less common but also affect membrane
potential (Jan and Jan, 1989). At least four different classes of anion (chloride) channels
exist in secretory epithelia, one of which responds to hyperpolarisation, another
ubiquitous class is activated by cell-swelling (volume-regulated anion channel) and serves
to control cell volume (Nilius and Droogmans, 2001). Generally, many different types of
ion channel exist, some of which are voltage sensitive; ion flow through any channel,
however, can affect membrane potential generating a signal which can activate other
intracellular processes.
Calcium channels are widespread and are particularly important in transducing
membrane signals into an increase in the intracellular second messenger [Ca
2+
] thereby
activating many crucial intracellular processes including gene expression. Voltage-
gated calcium channels in particular mediate calcium ion entry in response to membrane
depolarisation (Catterall, 2000). Typical functions activated by these channels include
neurotransmitter release and dendritic Ca
2+
transients in neurons, excitation-contraction
coupling in muscle cells, hormone secretion in endocrine cells (Catterall, 2000), and
secretion in other secretory epithelia (Begenisich and Melvin, 1998). Other types of
calcium channel, such as calcium-release-activated calcium channels, which also show
some voltage dependence, are involved in lymphocyte function (Cahalan et al, 2001).
Intracellular Ca
2+
signalling is also central to many of the functions of vascular endothelial
cells, such as the release of vasoactive factors, the regulation of macromolecule
transport and endothelial proliferation, and can be modulated by various factors including
changes in membrane potential (Nilius and Droogmans, 2001). Such signals have been
shown to propagate through gap junctions to neighbouring endothelial cells.
Thus, a variety of cellular functions in non-excitable tissue are likely to respond to
changes induced in cell membrane potential by induced electric fields. However,
the sensitivity would probably be less than that of excitable cells, the membranes of
which provide voltage- and time-dependent non-linearities more likely to amplify small
signals. In addition, there will be no integration of these effects over a network of
interacting cells comparable to that exhibited by neuronal circuitry.
Conclusions implications for standards
The group considered that a level of exposure that would avoid potentially adverse
effects should be set at the lower end of the recorded thresholds for phosphene
induction, which is around 100 mV m
1
1
. It was thought
that this should be sufficient to protect normal adults against the potentially adverse
effects on the function of the central, autonomic and enteric nervous systems, and on
the heart, all of which can be expected to show network behaviour. Other tissues
showing voltage-sensitive ion channels are expected to show a lower sensitivity.
Members of the population potentially susceptible to electrical stimulation include
people with epilepsy, people with a family history of seizure, or using tricyclic anti-
depressants, neuroleptic agents and other drugs that lower seizure threshold, and
people with serious heart disease or with increased intracranial pressure. These people
should be adequately protected at lower induced electric field strengths, possibly about
a factor of five lower than for normal adults. In addition, these values were thought
adequate to protect the developing nervous system in utero, and in neonates and
young children.
202
It was thought that the appropriate level of exposure would apply over a broad
frequency range (approximately 10 Hz 1 kHz) and that the averaging volume would
be based on a minimum of 1000 interacting cells, approximately 1 mm
3
in most nerve
tissue. Conversion of the appropriate voltage threshold to a current density threshold
depends on knowing the tissue conductivity at the frequency of interest.
Research priorities
Further neurophysiological investigation was recommended, particularly on the
sensitivity of network activity for instance on epileptic discharges and physiological
oscillations, and on the underlying mechanisms, whether directly on neuronal excitability
or on signalling molecules such as nitric oxide. [The current research programme of
Professor Jefferys on these effects, funded by the Department of Health, was noted.]
The investigation of the threshold and frequency response for these phenomena up to
1 kHz and beyond was considered valuable.
It would also be helpful to identify more rigorously the threshold electric field in the
retina for phosphene induction through better dosimetric modelling of relevant volunteer
studies. [Professor Blakemore noted that one of his research students was comparing
the effects of phosphene induction in the retina by applied electric fields with that induced
in the visual cortex by transcranial magnetic stimulation.] In addition, the identification of
the responsive elements within the retina to weak induced electric fields was considered
useful; this could be achieved relatively easily through neurophysiological investigation.
Further exploration of possible cognitive effects was also considered likely to be
of value.
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Appendix B
WEAK ELECTRIC FIELDS:
DEVELOPMENTS SUBSEQUENT TO APPENDIX A
ICNIRP/WHO Workshop, NRPB, 2003
The report (Appendix A) of an ad hoc expert group that advised NRPB about the
potential health effects of physiologically weak electric fields, induced in the body by
EMF exposure, stimulated an ICNIRP/WHO workshop held at NRPB in March 2003*.
The workshop chair, Professor Blakemore FRS, also chaired the expert group, most
members of which also attended the workshop. In addition, the workshop included
participants with expertise in biophysics, ion channel function, synaptic function, brain
function and cognitive behaviour, cardiac physiology, neuro-endocrinology and develop-
mental biology.
The workshop considerably extended and supplemented the views expressed by
the ad hoc expert group both by the presentations and discussion, summarised in the
rapporteurs reports, and by the subsequent workshop papers. Many comparable views
were expressed. In summary, the main developments to the output of the ad hoc
expert group are as follows.
(a) Voltage-gated ion channel properties, pre- and post-synaptic ion channel clustering
and neural networks were identified as examples of mechanisms by which physio-
logically weak but coherent electric signals might be amplified. This effect would be
emphasised in convergent pathways, which, for example, characterise the retina
and the neuronal input to Purkinje cells in the cerebellum.
(b) Although the retina was still thought a good albeit precautionary model of the
sensitivity of central nervous system tissue to induced electric fields, the uncertainties
in threshold values and their variation with frequency were emphasised.
(c) Detailed calculation based on neuro-anatomical and physiological considerations
suggested a phosphene electric field threshold in the extracellular fluid of the retina
to be in the range 1060 mV m
1
at 2025 Hz (whereas in Appendix A it was expressed
as 50100 mV m
1
in retinal tissue).
(d) It was noted that volunteers participating in cognitive studies, which had not
produced any clear, unambiguous field dependent effects, had usually been exposed
at levels at which the induced electric fields in the brain will have been comparatively
low compared to those that induce phosphenes.
(e) The heart, neuroendocrine organs and embryo and fetal development were
considered less sensitive to the direct effects of induced electric fields, although it is
possible that such effects may be mediated indirectly via interactions with the CNS.
(f) Potentially sensitive individuals were considered to be those with epilepsy and
related conditions in which neuronal excitability in the CNS is increased. The greater
sensitivity of children regarding electrostimulation was also noted.
* ICNIRP/WHO (2003). Proceedings International Workshop: Weak Electric Field Effects in the Body
(M H Repacholi and A F McKinlay, eds). Radiat Prot Dosim, 106(4).
206
Appendix C
SUMMARY OF ICNIRP EXPOSURE GUIDELINES
Exposure
characteristics Frequency range
Current density
for head and
trunk (mA m
2
)
(rms)
Whole-body
average SAR
(W kg
1
)
Localised
SAR (head
and trunk)
(W kg
1
)
Localised
SAR
(limbs)
(W kg
1
)
Occupational Up to 1 Hz 40
TABLE C1

Basic
restrictions for time-
varying electric and
magnetic fields for
frequencies up to
10 GHz
1 Hz 4 Hz 40/f
4 Hz 1 kHz 10
1 kHz 100 kHz f

/100
100 kHz 10 MHz f

/100 0.4 10 20
10 MHz 10 GHz 0.4 10 20
General public Up to 1 Hz 8
1 Hz 4 Hz 8/f
4 Hz 1 kHz 2
1 kHz 100 kHz f

/500
100 kHz 10 MHz f

/500 0.08 2 4
10 MHz 10 GHz 0.08 2 4
Notes
(a) f is the frequency in hertz.
(b) Because of electrical inhomogeneity of the body, current densities should be averaged over a cross-
section of 1 cm
2
perpendicular to the current direction.
(c) For frequencies up to 100 kHz, peak current density values can be obtained by multiplying the rms
value by 2 (~1.414). For pulses of duration t
p
the equivalent frequency to apply in the basic
restrictions should be calculated as f = 1/(2t
p
).
(d) For frequencies up to 100 kHz and for pulsed magnetic fields, the maximum current density
associated with the pulses can be calculated from the rise/fall times and the maximum rate of
change of magnetic flux density. The induced current density can then be compared with the
appropriate basic restriction.
(e) All SAR values are to be averaged over any 6-minute period.
(f) Localised SAR averaging mass is any 10 g of contiguous tissue; the maximum SAR so obtained
should be the value used for the estimation of exposure.
(g) For pulses of duration t
p
the equivalent frequency to apply in the basic restrictions should be
calculated as f = 1/(2t
p
). In addition, for pulsed exposures in the frequency range from 0.3 GHz to
10 GHz and for localised exposure of the head, in order to limit or avoid auditory effects caused by
thermoelastic expansion, an additional basic restriction is recommended. This is that the specific
absorption should not exceed 10 mJ kg
1
for workers and 2 mJ kg
1
for the general public, averaged
over 10 g of tissue.
Appendix C: Summary of ICNIRP Exposure Guidelines
207
Exposure characteristics Power density (W m
2
)
General public 10
Notes
(a) Power densities are to be averaged over any 20 cm
2
of exposed area and any 68/f
1.05
-minute period
(where f is the frequency in gigahertz) to compensate for progressively shorter penetration depth
as the frequency increases.
(b) Spatial maximum power densities, averaged over 1 cm
2
, should not exceed 20 times the values
above.
TABLE C2 Basic
restrictions for
power density for
frequencies
between 10 and
300 GHz
Frequency range
Electric field
strength, E
(V m
1
)
Magnetic field
strength, H
(A m
1
)
Magnetic flux
density, B (T)
Equivalent plane
wave power density,
S
eq
(W m
2
)
Up to 1 Hz 163 000 200 000
1 Hz 8 Hz 20 000 163 000/f
2
200 000/f
2
8 Hz 25 Hz 20 000 20 000/f 25 000/f

0.025 kHz 0.82 kHz 500/f 20/f 25/f
TABLE C3
Reference levels for
occupational
exposure to time-
magnetic fields
(unperturbed rms
values)
0.82 kHz 65 kHz 610 24.4 30.7
0.065 MHz 1 MHz 610 1.6/f 2.0/f
1 MHz 10 MHz 610/f 1.6/f 2.0/f
10 MHz 400 MHz 61 0.16 0.2 10
400 MHz 2000 MHz 3f
1/2
0.008f
1/2
0.01f
1/2
f

/40
2 GHz 300 GHz 137 0.36 0.45 50
Notes
(a) f is the frequency as indicated in the frequency range column.
(b) Provided that basic restrictions are met and adverse indirect effects can be excluded, field strength
values can be exceeded.
(c) For frequencies between 100 kHz and 10 GHz, S
eq
, E
2
, H
2
and B
2
, are to be averaged over any
6-minute period.
(d) For peak values at frequencies up to 100 kHz, see Table C1, note (c).
(e) Between 100 kHz and 10 MHz, peak values for the field strengths are obtained by interpolation from
the 1.5-fold peak at 100 kHz to the 32-fold peak at 10 MHz. For frequencies exceeding 10 MHz it is
suggested that the peak equivalent plane wave power density, as averaged over the pulse width,
does not exceed 1000 times the S
eq
restrictions, or that the field strength does not exceed 32 times
the field strength exposure levels given in the table.
(f) For frequencies exceeding 10 GHz, S
eq
, E
2
, H
2
and B
2
are to be averaged over any 68/f
1.05
-minute
period (where f is the frequency in gigahertz).
(g) No E-field value is provided for frequencies <1 Hz, which are effectively static electric fields.
Electric shock from low impedance sources is prevented by established electrical safety procedures
for such equipment.
208
Frequency range
Electric field
strength, E
(V m
1
)
Magnetic field
strength, H
(A m
1
)
Magnetic flux
density, B (T)
Equivalent plane
wave power density,
S
eq
(W m
2
)
Up to 1 Hz 32 000 40 000
1 Hz 8 Hz 10 000 32 000/f
2
40 000/f
2
8 Hz 25 Hz 10 000 4 000/f 5 000/f

0.025 kHz 0.8 kHz 250/f 4/f 5/f
TABLE C4
general public
exposure to time-
magnetic fields
(unperturbed rms
values)
0.8 kHz 3 kHz 250/f 5 6.25
3 kHz 150 kHz 87 5 6.25
0.15 MHz 1 MHz 87 0.73/f 0.92/f
1 MHz 10 MHz 87/f
1/2
0.73/f 0.92/f
10 MHz 400 MHz 28 0.073 0.092 2
400 MHz 2000 MHz 1.375f
1/2
0.0037f
1/2
0.0046f
1/2
f

/200
2 GHz 300 GHz 61 0.16 0.20 10
Notes
(a) f is the frequency as indicated in the frequency range column.
(b) Provided that basic restrictions are met and adverse indirect effects can be excluded, field strength
values can be exceeded.
(c) For frequencies between 100 kHz and 10 GHz, S
eq
, E
2
, H
2
and B
2
are to be averaged over any
6-minute period.
(d) For peak values at frequencies up to 100 kHz, see Table C1, note (c).
(e) Between 100 kHz and 10 MHz, peak values for the field strengths are obtained by interpolation from
the 1.5-fold peak at 100 kHz to the 32-fold peak at 10 MHz. For frequencies exceeding 10 MHz it is
suggested that the peak equivalent plane wave power density, as averaged over the pulse width,
does not exceed 1000 times the S
eq
restrictions, or that the field strength does not exceed 32 times
the field strength exposure levels given in the table.
(f) For frequencies exceeding 10 GHz, S
eq
, E
2
, H
2
and B
2
are to be averaged over any 68/f
1.05
-minute
period (where f is the frequency in gigahertz).
(g) No E-field value is provided for frequencies <1 Hz, which are effectively static electric fields.
Perception of surface electric charges will not occur at field strengths less than 25 kV m
1
. Spark
discharges causing stress or annoyance should be avoided.
Exposure characteristics Frequency range Maximum contact current (mA)
Occupational Up to 2.5 kHz 1.0
2.5 kHz 100 kHz 0.4f
100 kHz 110 MHz 40
TABLE C5
time-varying contact
currents from
conductive objects
General public Up to 2.5 kHz 0.5
2.5 kHz 100 kHz 0.2f
100 kHz 110 MHz 20
Notes
(a) f is the frequency in kilohertz.
(b) These values are set to avoid the possibility of indirect effects of exposure (shock and/or burn).
(c) NRPB notes that equation 11 in the ICNIRP guidelines (ICNIRP, 1998) that deals with the summation
for limb current and contact current for multiple frequency sources was subsequently amended
(ICNIRP, 1999).
Appendix C: Summary of ICNIRP Exposure Guidelines
209
Exposure characteristics Current (mA)
Occupational 100
General public 45
Notes
(a) The general public reference level is equal to the occupational reference level divided by 5.
(b) For compliance with the basic restriction on localised SAR, the square root of the time-averaged
value of the square of the induced current over any 6-minute period forms the basis of the
reference levels.
(c) NRPB notes that equation 11 in the ICNIRP guidelines (ICNIRP, 1998) that deals with the summation
for limb current and contact current for multiple frequency sources was subsequently amended
(ICNIRP, 1999).
TABLE C6
current induced in
any limb at
frequencies
between 10 and
110 MHz
REFERENCES
fields (up to 300 GHz). Health Phys, 74, 494522.
ICNIRP (1999). Guidelines on Limiting Exposure to Non-Ionizing Radiation (R Matthes, J H Bernhardt and
A F McKinlay, eds). Mnchen, ICNIRP 7/99.
210
Glossary
GUIDELINES TERMINOLOGY
Adverse health effect A biological effect which has a detrimental effect on mental, physical
and/or general well being of exposed people, either in the short-term or in the long-term.
Biological effect A measurable change in a biological system in response (for example) to an
electromagnetic field.
Caution In this document the terms caution and cautious are used strictly to describe the
approach taken in evaluating scientific data and in particular the uncertainties associated with these
data and in making judgements as their relevance to exposure restrictions. See also precaution.
Direct effect An effect resulting from the interaction of the human body with an electromagnetic
field to which it is exposed, eg heating of body tissues.
Dosimetry Evaluation of the absorbed dose or dose rate by an object in an electric, magnetic, or
electromagnetic field.
Epidemiology Study of the distribution of disease in populations and of the factors that influence
this distribution.
Indirect effect An effect on the human body resulting from the interaction between an
electromagnetic field and another object, such as a vehicle or other mechanical structure, with
which the body comes into contact, eg shock or burn.
Interference effect An effect on the function of an item of electrical equipment due to interaction
with an incident electromagnetic field.
Medicine Study of factors influencing disease in individuals.
Precaution In this document the terms precaution and precautionary are used strictly in
relation to possible additional measures that might be considered in the light of the existing limited
uncertain evidence of long-term adverse effects of exposure. See also caution.
ELECTROMAGNETIC FIELDS
Frequency The number of cycles per second for a periodically varying quantity. Frequency has
the unit hertz (Hz).
Electric field strength (E) The force on a stationary unit positive charge at a point in an electric
field. The magnitude of the electric field vector (unit V m
1
).
Magnetic flux density (B) The force on a moving unit positive charge at a point in a magnetic field
per unit velocity.
Electromagnetic radiation A flow of energy in a given direction and in the form of an
electromagnetic wave.
Plane wave A wave such that the corresponding physical quantities are uniform in any plane
perpendicular to a fixed direction.
Wavelength () The distance between two successive points of a periodic wave in the direction
of propagation at which the oscillation has the same phase.
Power density (S) The power crossing unit area normal to the direction of wave propagation.
Root mean square (RMS) Certain electrical effects are proportional to the square root of the
mean value of the square of a periodic function; this is known as the effective value or root mean
square value.
Dielectric A class of materials that undergo polarisation.
Specific energy absorption rate (SAR) The rate of absorption of electromagnetic energy per unit
body mass, usually expressed in watts per kilogram.
Glossary
211
BIOLOGICAL TERMS
Acclimatisation (or acclimation) The physiological changes that occur in response to exposure
for a succession of days to an environmental stress, eg heat stress. The changes act to reduce the
physiological strain caused by the heat stress of the environment.
Action potential (nerve impulse or spike) A sudden brief reversal of the local membrane
electrical potential that occurs once a threshold depolarisation has been exceeded and which
quickly propagates down a nerve axon conveying digitally encoded information.
Ames test A widely used test to detect possible chemical carcinogens; based on mutagenicity in
the bacterium Salmonella.
Antigen Any substance, usually (but not always) foreign, that provokes an antigen-specific
immune response, such as antibody-binding.
Antibody A class of proteins produced by (B) lymphocytes that recognises and binds to a
specific antigen, thereby aiding its elimination, or elimination of the agent, such as a bacterium,
expressing it.
Apnoea The cessation of breathing.
Apoptosis A specific form of cell death during which cells degrade their own DNA. Apoptosis
can occur normally during organ formation, or as a result of DNA or cellular damage.
Atheroma A thickening of the walls of an artery by deposits of fatty substance such as
cholesterol.
Atherosclerosis A condition where deposits of fats and minerals form on the wall of an artery and
prevent blood from flowing easily (especially important in the aorta and the coronary, renal and
cerebral arteries).
Autonomic nervous system A part of the peripheral nervous system that regulates the visceral
or housekeeping functions of the body, such as heart-rate and blood pressure. Its cell bodies lie
either in the central nervous system, or in ganglia in other parts of the body.
Basophil A type of white blood cell derived from myeloid progenitor cells that, with mast cells,
mediate inflammatory immune responses through the release of histamine and other chemicals
that cause inflammation.
Blind study A study in which the subject or, in the case of studies using animals, tissues or cell
cultures, the experimenter, is unaware of whether exposure is to the agent under test or to a
neutral or comparison agent until completion of the experiment in order to avoid unconscious
subjective bias affecting the study outcome.
Bloodbrain barrier A physiological barrier comprising endothelial and epithelial cells that
regulates the composition of cerebrospinal fluid of the central nervous system.
Cancer An uncontrolled and abnormal proliferation of cells that causes disease.
Carcinogen An agent that can induce cancer.
Carcinoma A tumour arising from epithelial tissue (eg glands, breast, skin, linings of the urogenital,
intestinal and respiratory systems).
Cell signalling (pathways) A sequence of intracellular changes linking a signalling event, such as
activation of membrane-bound ion channels or ligand-receptors, and a response, such as a change
in gene expression, for example, leading to increased proliferation.
Central nervous system Usually taken to mean the cells, such as neurons and glial cells, of the
brain and spinal cord. It also includes the retina, which is formed as an outgrowth of the forebrain.
Cerebral thrombosis (an occlusive stroke) A condition where a blood clot enters and blocks a
brain artery.
Chromatid One of the two side-by-side replicas (sister chromatids) that result from the
replication of a single chromosome; their separation during cell division results in two
chromosomes.
Chromosome A single molecule of DNA, comprising a large number of genes and other DNA,
together with associated protein molecules that condense during cell division to form a deeply
staining, rod-shaped body.
212
Circadian rhythm A rhythmic oscillation of some physiological functions of the body, such as
body temperature, which have a periodicity of about 24 hours.
Cognition Information processing by the brain, including processes such as attention, perception,
learning, reasoning, comprehending and memory.
Comet assay A single cell electrophoresis assay in which DNA is caused to migrate away from
the nucleus by an applied electric field. The extent of migration gives a measure of DNA damage.
Core (or deep) body temperature The average temperature of tissues lying deep within the
body, which is normally regulated around a set point value of approximately 370.5C, as
distinct from, for example, the temperatures of the skin and peripheral tissues of the limbs, which
are more labile.
Coronary thrombosis A blood clot which blocks one of the coronary arteries, leading to a
heart attack.
Corticogenesis The growth and development of the cerebral cortex.
Diastole The period of relaxation of heart muscle, following contraction (systole).
Differentiation (cellular) The development of a specialised cellular structure and function from
less specialised precursor cells such as stem cells which is generally accompanied by a loss of
proliferative capacity.
Disseminated intravascular coagulation A condition characterised by widespread blood clotting
in the blood vessels throughout all the organs of the body.
Double blind study A volunteer study in which the subject and the experimenter are unaware of
until completion of whether exposure is to the agent under test or to a neutral or comparison agent
experiment in order to avoid unconscious subjective bias affecting the study outcome.
Electrocardiogram (ECG) A recording of the electrical activity of the heart from electrodes
placed on the body.
Electroencephalogram (EEG) A recording of the electrical activity of the brain from electrodes
placed on the head.
Electroretinogram (ERG) A recording of the electrical activity of the retina from electrodes
placed on the surface of the eye and the head.
Electrotonic Graded non-threshold changes in local membrane electrical potential, usually over
the post-synaptic dendritic region and the cell body of a neuron that are generated by excitatory
and/or inhibitory inputs from other neurons, which may trigger an action potential to pass down
the nerve axon.
Embryo The stage of prenatal development between the fertilised ovum and the completion of
major organ development. In humans, this occurs in the first trimester.
Enteric nervous system Comprises the intrinsic neurons of the gut, about the same in number
(approximately 100 million) as those of the spinal cord, and which exhibit a high degree of
independence from the central nervous system.
Epilepsy Epileptic seizures arise from an excessively synchronous and sustained discharge of a
group of neurons; a persistent increase in neuronal excitability is a key feature.
Event-related (or evoked) potential (ERP or EP) A recording of the electrical activity of the brain
after a stimulus event such as a visual or auditory stimulus (resulting in VEPs and AEPs,
respectively). Late components are associated with cognitive processing.
Fibrillation (ventricular) The loss of organised ventricular contractions of the heart.
Fetus (foetus) The stage of prenatal development between the embryo and birth.
Gene expression The production of a functional protein or an RNA molecule from genetic
information (genes) encoded by DNA.
Genotoxin An agent which damages DNA and RNA.
Haematology The study of blood; its formation, its normal composition and function etc and its
pathology.
Glossary
213
Heat syncope Loss of consciousness due to the heat induced pooling of blood in the dilated
vessels of the skin and lower body without an increase in body temperature or cessation of
sweating.
Heat exhaustion A heat-related illness characterised by muscular weakness, distress, nausea,
vomiting, dizziness, pale clammy skin and fainting, usually associated with lack of heat
acclimatisation and physical fitness, low health status and inadequate water intake.
Heat stroke An acute medical emergency arising during exposure to heat from an excessive rise
in body temperature and failure of the temperature regulating mechanism. It is characterised by a
sudden and sustained loss of consciousness preceded by vertigo, nausea, headache, cerebral
dysfunction, bizarre behaviour, and body temperatures usually in excess of 41C.
Implantation The attachment of the early embryo to the uterine wall.
Intravenous Into a vein.
In vitro In glass; experimental studies of cells or tissues, usually in a sustaining oxygenated, fluid
medium.
In vivo In life; experimental studies of processes in living organisms.
Knockout organism A genetically modified organism, often a mouse, which has genetic material
such a gene stably deleted from its genome.
Leukocyte A white blood cell.
Lymphocyte White blood cells produced in lymphoid tissue that initiate adaptive, antigen-
specific immune responses. Some T-lymphocytes are cytotoxic; B-lymphocytes secrete
antibodies.
Macrophage A phagocytic cell derived from myeloid progenitor cells found in various tissues.
Malignant Neoplasms or tumours that have become invasive.
Metastasis Tumour cells that leave their site of origin and migrate to other sites in the body.
Microcephaly (or microencephaly) An abnormally small brain.
Micronucleus Chromosome fragments that have not been lost on cell division.
Mutation A stable heritable change in the DNA at a specific site in the in the genome of a cell by
an agent (mutagen) such as ionising radiation.
Natural killer (NK) cells Lymphocytes that are not antigen-specific but nevertheless bind to and
kill certain tumour and virus-infected cells.
Neonate, neonatal Newly born.
Neoplasm New growth of abnormal tissue.
Neural network Group of interacting neurons.
Neural tube defect A defect of the newly formed precursor of the central nervous system,
commonly anencephaly (failure of brain to develop), encephalocele (cyst of the brain), and spina
bifida (defects in the closure of the neural tube).
Neurogenesis Proliferation of neural cells to form the nervous system.
Neuron(e) Nerve cell, specialised for the transmission of neural information.
Neurotransmitter A neuroactive substance released by a neuron that causes a post-synaptic
response that is relatively quick in onset (less than one millisecond) and short (less than tens of
millliseconds) in duration, as distinct from the more prolonged action of neuromodulators.
Neutrophil Phagocytic white blood cells derived from myeloid progenitor cells.
Oncogene A gene which contributes to cancer in a dominant fashion through the mutation
and/or abnormal expression of a gene (proto-oncogene) involved in regulating cell proliferation.
Operant behaviour Behaviour, such as pressing a lever, which is shaped by rewards (such as
food pellets) or punishment (such as a mild electric shock).
Organogenesis The process of organ formation in developing organisms.
Parturition Birth.
214
Peripheral nervous system (somatic) The part of the nervous system that mainly deals with the
voluntary and conscious aspects of neural control such as voluntary muscle (motor) contraction
and sensations such as those of warmth or pressure. The cell bodies lie within the spinal cord, but
the peripheral nerves (axons) terminate on muscle fibres or in specialised sensory receptors
throughout the body.
Phosphene The perception of flickering light in the periphery of the visual field induced by non-
visual means such as a trans-retinal electric current.
Reinforcement (behavioural) An action such as reward or punishment that increases the
likelihood of a certain behaviour.
Rapid eye movement (REM) sleep A form of sleep occurring for short episodes and associated
with dreaming and brain electrical activity similar to that of alert wakefulness, as distinct from slow-
wave sleep which accounts for 75%of sleep time.
Renal insufficiency Reduced function of the kidney.
Respiratory distress syndrome A syndrome of life-threatening progressive pulmonary
insufficiency in the absence of known pulmonary disease, usually following a systemic insult such
as surgery or major trauma.
Sinus arrhythmia The normal variation of heart rate during the breathing cycle.
Stroke volume The amount of blood pumped out of the ventricle at each heartbeat.
Synapse A junction between two neurons, or between a neuron and a muscle fibre, that allows
the transmission of electrical information, usually by means of a chemical transmitter
(neurotransmitter) released from the presynaptic terminal of one neuron on to the closely
juxtaposed post-synaptic terminal of the other.
Systole The period of contraction of heart muscle following relaxation (diastole).
Teratogen An agent that can cause birth defects.
Thrombosis Blocking of an artery or vein by a blood clot.
Transcription The process whereby RNA is synthesised from a DNA template.
Transcription factor A protein that binds to a DNA sequence with a regulatory function
thereby, directly or indirectly, affecting the initiation of transcription.
Transformation Conversion of cells to a state of unrestrained growth in culture, resembling or
identical with a tumour-forming (tumorigenic) state.
Transgenic organism A genetically modified organism, often a mouse, which has foreign DNA
such as a gene stably integrated into its genome.
Tumour A growth of tissue resulting from abnormal cell proliferation.
Tumour initiator An agent that can produce an initial carcinogenic event such as a mutation.
Tumour progression The process by which initiated and promoted cells become increasingly
malignant.
Tumour promoter An agent that can stimulate the proliferation (clonal expansion) of initiated cells.
Tumour suppressor gene A normal cellular gene involved in regulating cell proliferation whose
mutation and/or abnormal expression can contribute to cancer in a recessive manner.
Vasoconstriction The contraction of blood vessels, making them narrower.
Vasodilatation (or vasodilation) The relaxation of blood vessels, making them wider.
Vigilance tasks Responding to unusual and infrequent stimuli (signals) occurring against a
background of usual and frequent stimuli (events). Vigilance can be either visual or auditory.
Voltage-gated ion channel Cell membrane proteins that allow the passage of particular ion
species across the cell membrane in response to the opening of a molecular gate which is steeply
sensitive to the transmembrane voltage. They are associated with electrical excitability.
Wild-type (gene) The gene that is found in nature or in the standard laboratory stock for a
given organism.
Working memory An active system for temporarily storing and manipulating information
needed in the execution of complex cognitive tasks.
Glossary
215
EPIDEMIOLOGICAL TERMS
Bias A systematic tendency to error as a consequence of the design or conduct of a study.
Casecontrol study An investigation into the extent to which a group of persons with a specific
disease (the cases) and comparable persons who do not have the disease (the controls) differ with
respect to exposure to putative risk factors.
Cohort study An investigation involving the identification of a group of individuals (the cohort)
about whom certain exposure information is collected, and the ascertainment of occurrence of
diseases at later times. For each individual, information on prior exposure can be related to
subsequent disease experience. Cohort studies may be conducted prospectively or
retrospectively. See retrospective study.
Combined analysis Analysis of data pertaining to the same topic that have been collected in
several different studies. Usually based on individual level data from each of the available studies,
rather than on the published findings. See meta-analysis.
Confidence interval (CI) An interval calculated from data when making inferences about an
unknown parameter. In hypothetical repetitions of the study, the interval will include the
parameter in question on a specified percentage of occasions (eg 90%for a 90%confidence
interval).
Confounding Spurious findings due to the effect of a variable that is correlated with both the
exposure and disease under study.
Meta-analysis Analysis of data pertaining to the same topic that have been collected in several
different studies. Usually refers to an analysis based on published findings from individual studies,
rather than on the original data sets. See combined analysis.
Non-differential measurement errors Errors in exposure assessment that do not depend on
whether or not someone develops the disease under study.
Prospective study An epidemiological study in which data on exposures and disease outcome
are collected as the events occur, unlike a retrospective study (see below). Some cohort studies
are conducted prospectively.
Relative risk The ratio of the disease rate in the group under study to that in a comparison group,
with adjustment for confounding factors such as age, if necessary.
Retrospective study An epidemiological study in which data on exposures and disease outcome
are collected some time after the event, unlike a prospective study (see above). Examples include
casecontrol studies and some cohort studies.
Significance level The probability of obtaining a result at least as extreme as that observed in the
absence of a raised risk. A result that would arise less than 1 in 20 times in the absence of an
underlying effect is often referred to as being statistically significant.
Statistical power The probability that, with a specified degree of confidence, an underlying effect
of a given magnitude will be detected in a study.

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