vvEPA
United States Health Effects Research
Environmental Protection Laboratory
Agency Research Triangle Park NC 27711
September 1984
Final Report
Research and Development
Biological Effects of
Radiofrequency
Radiation
600883026F
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EPA-600/8-83-026F
September 1984
Biological Effects of
Radiofrequency Radiation
Edited by
Joe A. Elder and Daniel F. Cahill
Health Effects Research Laboratory
Research Triangle Park, North Carolina 27711
Health Effects Research Laboratory
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina 27711
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Disclaimer
This document has been subjected to the Agency's required peer and policy
review and approved for publication. Mention of trade names or commercial
products does not signifiy official endorsement.
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Foreword
The many benefits of our modern, developing industrial society are accompanied
by certain hazards. Careful assessment of the risk of existing and new man-
made environmental hazards is necessary to establish sound regulatory policy.
Environmental regulations enhance the quality of our environment in order to
promote the public health and welfare and the productive capacity of our
nation's population.
The Health Effects Research Laboratory conducts a coordinated environmental
health research program in toxicology and clinical studies. These studies
address problems in air pollution, radiofrequency radiation, environmental
carcinogenesis, and the toxicology of pesticides, as well as other chemical
pollutants. The Laboratory participates in the development and revision of air
quality criteria documents on pollutants for which national ambient air quality
standards exist or are proposed, provides the data for registration of new
pesticides or proposed suspension of those already in use, conducts research on
hazardous and toxic materials, and is primarily responsible for providing the
health basis for radiofrequency radiation guidelines. Direct support to the
regulatory function of the Agency is provided in the form of expert testimony and
preparation of affidavits as well as expert advice to the Administrator.
The intent of this document is to provide a comprehensive review of the scientific
literature on the biological effects of radiofrequency radiation. The purpose of
this effort is to evaluate critically the current state of knowledge for its
pertinence and applicability in developing radiofrequency-radiation exposure
guidelines for the general public.
F. G. Hueter, Ph.D.
Director
Health Effects Research Laboratory
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Abstract
This document presents a critical review of the available literature on the
biological effects of radiofrequency (RF) radiation. The objective was to
summarize and evaluate the existing database for use in developing RF-
radiation exposure guidance for the general public.
The frequency range of concern in this document is 0.5 MHz to 100 GHz, which
includes nearly all the significant sources of population exposure to RF radiation,
except 60-Hz electrical power systems. Research reports that are judged to be
credible according to a set of objective criteria are examined for the relation
between the RF energy absorbed and the presence or absence of biological
effects. The reported consequences of the interaction between RF radiation and
biological systems are examined from two perspectives: whole-body-averaged
specific absorption rate (SAR) and RF-energy-induced core-temperature
increases.
The existing database provides sufficient evidence about the relation between
RF-radiation exposure and biological effects to permit development of exposure
limits to protect the health of the general public. It has been concluded from this
review that biological effects occur at an SAR of about 1 W/kg; some of them
may be significant under certain environmental conditions.
IV
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Contents
Page
Foreword iii
Abstract iv
Figures ix
Tables xiii
Acknowledgment xvi
1. Introduction 1-1
(Daniel F. Cahill and Joe A. Elder)
2. Approach 2-1
(Joe A. Elder and Daniel F. Cahill)
2.1 General Approach 2-1
2.2 Specific Approach 2-1
2.3 Major Sections 2-1
3. Physical Principles of Electromagnetic Field Interactions 3-1
3.1 Elements of Electromagnetic Field Theory 3-1
(William T. Joines)
3.1.1 Electromagnetic spectrum 3-1
3.1.2 Wave propagation 3-1
3.1.3 Wave modulation 3-4
3.2 RF-Field Interactions with Biological Systems 3-6
(Claude M. Weil and James R. Rabinowitz)
3.2.1 Scattering and absorption of electromagnetic
waves 3-6
3.2.2 RF dosimetry definitions 3-11
3.2.3 Analytical and numerical RF-electromagnetic
interaction models 3-13
3.2.4 Mechanisms of RF interaction with biological
systems 3-19
3.3 Experimental Methods 3-25
(Claude M. Weil and Joseph S. Ali)
3.3.1 Exposure methods used in biological
experimentation 3-25
3.3.2 Animal holders 3-40
3.3.3 Densitometric instrumentation 3-42
3.4 Dosimetric Methods 3-47
(James B. Kinn)
3.4.1 Whole-body dosimetry 3-47
3.4.2 Regional dosimetry 3-48
3.4.3 Unresolved issues 3-49
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Contents (Continued)
Page
4. Effect of RF-Radiation Exposure on Body Temperature 4-1
4.1 Thermal Physiology 4-1
(Christopher J. Gordon)
4.1.1 Temperature regulation 4-1
4.1.2 Effect of RF radiation on thermophysiological
effectors 4-13
4.1.3 Body temperature regulation during
RF-radiation exposure 4-18
4.1.4 Effect of body size on thermoregulatory
sensitivity to RF radiation 4-22
4.1.5 Unresolved issues 4-27
4.2 Numerical Modeling of Thermoregulatory Systems in Man ... 4-29
(Ronald J. Spiegel)
4.2.1 Heat-transfer models 4-29
4.2.2 RF-radiation/heat-transfer models 4-30
4.2.3 Numerical results 4-32
4.2.4 Unresolved issues 4-33
5. Biological Effects of RF Radiation 5-1
5.1 Cellular and Subcellular Effects 5-1
(John W. Allis)
5.1.1 Effects on molecular systems 5-3
5.1.2 Effects on subcellular organelles 5-4
5.1.3 Effects on single cells 5-6
5.1.4 Unresolved issues 5-9
5.2 Hematologic and Immunologic Effects 5-13
(Ralph J. Smialowicz)
5.2.1 Hematology 5-13
5.2.2 Immunology 5-18
5.2.3 Unresolved issues 5-27
5.3 Reproductive Effects 5-29
(Ezra Berman)
5.3.1 Teratology 5-29
5.3.2 Reproductive efficiency 5-37
5.3.3 Testes 5-38
5.3.4 Unresolved issues 5-41
5.4 Nervous System 5-43
(Michael I. Gage and Ernest N. Albert)
5.4.1 Morphological and physiological observations ........ 5-44
5.4.2 Blood-brain barrier studies 5-46
5.4.3 Pharmacological effects 5-48
5.4.4 Effects on neurotransmitters 5-49
5.4.5 Unresolved issues 5-50
5.5 Behavior 5-53
(Michael I. Gage)
5.5.1 Naturalistic behavior 5-54
5.5.2 Learned behavior 5-55
5.5.3 Interactions with other stimuli 5-60
5.5.4 Unresolved issues 5-61
vi
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Contents (Continued)
Page
5.6 Special Senses 5-64
(Joe A. Elder)
5.6.1 Cataractogenic effects 5-64
5.6.2 Unresolved issues 5-69
5.6.3 Auditory effects 5-70
5.6.4 Unresolved issues 5-75
5.6.5 Human cutaneous perception 5-76
5.6.6 Unresolved issues 5-78
5.7 Endocrine, Physiological and Biochemical Effects 5-79
(Charles G. Liddle and Carl F. Blackman)
5.7.1 Endocrine effects 5-79
5.7.2 Clinical chemistry and metabolism 5-81
5.7.3 Growth and development 5-84
5.7.4 Cardiovascular system 5-85
5.7.5 Biological effects of low-frequency modulation of
RF radiation 5-88
5.7.6 Unresolved issues 5-92
5.8 Genetics and Mutagenesis 5.94
(Carl F. Blackman)
5.8.1 Effects on genetic material of cellular and
subcellular systems '. 5.95
5.8.2 Effects on genetic material of higher-order
biological systems 5.99
5.8.3 Unresolved issues 5-100
5.9 Life Span and Carcinogenesis 5-106
(William P. Kirk)
5.9.1 Life span 5-106
5.9.2 Carcinogenesis 5-108
5.9.3 Unresolved issues -5-111
5.10 Human Studies 5-112
(Doreen Hill)
5.10.1 Occupational surveys/clinical studies 5-112
5.10.2 Mortality studies .5-114
5.10.3 Ocular effects 5-116
5.10.4 Congenital anomalies and reproductive
effects 5-119
5.10.5 Unresolved issues 5-121
6. Summary and Conclusions 6-1
(Joe A. Elder)
6.1 Major Conclusions and Generalizations 6-1
6.2 Specific Absorption Rate 6-3
6.3 Core Temperature 6-7
6.4 Summary 6-9
References R-1
Glossary G-1
VII
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Contents (Continued)
Page
Appendix
A. Science Advisory Board Subcommittee on the Biological
Effects of Radiofrequency Radiation A-1
B. Authors B-1
viii
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Figures
Number Page
3-1 Far-field electromagnetic wave at a particular instant in time 3-3
3-2 Power density vs. distance along axis from antenna aperture 3-4
3-3 Interaction of RF radiation with electrical conductors,
biological tissue, and electrical insulators 3-6
3-4 Energy distribution in proximity to man at 1 GHz at the chest
plane contour presentation 3-7
3-5 Dielectric data for tissues in RF range 0.01 to 10 GHz 3-8
3-6 Illustration of object size vs. wavelength dependence 3-9
3-7 Calculated whole-body average SAR vs. frequency for three
polarizations in a prolate spheroidal model of a human 3-10
3-8 Absorption dependence on various ground and multipath
factors 3-12
3-9 Penetration depth as a function of frequency 3-16
3-10 ARD distribution in core of 6-cm radius multilayered
sphere at 1650 MHz 3-17
3-11 Curve fitting of SAR data for a prolate spheroidal model of
man for three basic orientations 3-18
3-12 Effect of a capacitive gap on average SAR between the man
model and the ground plane 3-18
3-13 A realistic block model of man 3-19
3-14 Absorption for man block model standing on ground plane 3-20
3-15 The real component of the complex permittivity of
muscle as a function of frequency 3-21
3-16 EPA 2450-MHz anechoic chamber facility or 2.45-GHz
far-field exposure facility 3-26
3-17 EPA 2450-MHz anechoic chamber facility: diagram of the
microwave exposure facility 3-27
3-18 Diagram of absorber-lined horn 3-28
3-19 Diagram of a point-source compact range 3-28
3-20 Miniature anechoic chamber facility 3.30
3-21 Photograph of tapered exposure chamber at EPA facility 3-31
3-22 Facility for simultaneous exposure of 10 animals with
minimal inter-animal interaction 3-33
IX
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Figures (Continued)
Number Page
3-23 Monopole-over-ground plane irradiation facility 3-33
3-24 Coaxial air-line system for high power exposures of
cell cultures 3.35
3-25 Parallel-plate (microstrip) exposure system 3-36
3-26 Block diagram of complete RF near-field synthesizer 3-36
3-27 EPA 100-MHz rectangular strip line or Crawford cell 3-37
3-28 Exposure chamber of the circularly polarized 915-MHz
waveguide facility 3.37
3-29 Exposure chamber with associated instrumentation for the
970-MHz circularly polarized waveguide facility at EPA 3-38
3-30 VHP resonant cavity facility 3-39
3-31 SRI multimodal cavity facility for primate irradiation 3-40
3-32 Water-supply system for exposure chamber 3.42
3-33 Samples of commercially available survey meters for
measuring RF electric-field strength 3-44
3-34 Microprocessor-controlled twin-well calorimeter 3-48
4-1 Simple neural model of thermoregulation in a mammal for
predicting the motor responses to short-term changes in
ambient or body temperature 4-2
4-2A Current view of the principal systems employed in the
regulation of body temperature (from Werner 1980) 4-4
4-2B Overall relationship of the sensory, controller, effector, and
passive system components of the the thermoregulatory
system. Note that the overall structure of Figure 4-2A is
retained (modified from Werner 1980) 4-4
4-3 Effect of body mass on thermal.conductance of various
mammals 4-6
4-4 Blood flow vs. skin temperature 4-7
4-5 Effect of age on the preferred ambient temperature of mice 4-8
4-6 Effect of Ta on evaporation, conductance, metabolic rate, and
rectal temperature of dogs acclimatized to summer and winter 4-8
4-7 Effect of T. on evaporation, conductance, metabolic rate, and
rectal temperature of the rhesus monkey under unanesthetized
and ketamine-anesthetized conditions 4-8
4-8 Temperature distributions in the human body at Ta's of
20 and 35°C 4-9
4-9 Effect of skin temperature on sweating 4-10
4-10 Effect of calorimetric temperature on rectal and skin
temperature, heat loss, heat production, evaporation, and
conductance in men and women 4-10
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Figures (Continued)
Number Page
4-11 Effect of exercise on heat loss, metabolic rate, and tympanic
temperature of humans ,... 4-11
4-12 Relationship between body temperature and set point during
pyrogenesis 4-12
4-13 Power densities at 2450 MHz necessary to raise the rectal
temperature by 1 °C in 60 min for the rat, squirrel monkey, and
rhesus monkey 4-12
4-14 Examples of change in tail skin temperature in restrained mice
exposed to 2450 MHz at 25°C and SAP of 10.6 W/kg
or 20.0 W/kg 4-14
4-15 Evaporative water loss of mice exposed to 2450 MHz
for 90 min 4-15
4-16 Change in the rate of sweating from the foot of a squirrel monkey
exposed for 10 min to 2450 MHz; the parameter is ambient
temperature 4-15
4-17 Oxygen consumption and carbon dioxide production of rats
immediately after a 30-min exposure to 2450 MHz at a
T. of 24°C 4-16
4-18 Ventilatory frequency and preferred Ta of mice during exposure
to 2450 MHz inside a waveguide-temperature gradient
system 4-17
4-19 Mean Ta selected by one squirrel monkey exposed to
2450-MHz RF radiation 4-17
4-20 Effects of 5-HT injections on mice for various ambient
temperatures and various power densities at 2450 MHz 4-19
4-21 Example of the triphasic rectal temperature response of a
dog exposed to 2790-MHz RF radiation at a power density
of 165 mW/cm2 4-21
4-22 Effect of an increasing THI on the lethal dose of RF radiation
(2450 MHz) in mice 4-23
4-23 Relationship between the surface area:body mass ratio and
the body mass of various mammals 4-24
4-24 Relation between metabolic rate and body mass of resting
mammals under thermoneutral conditions 4-25
4-25 Relation between mass and percent increase in whole-body
heat loss necessary to maintain normothermia in mammals
exposed to RF radiation at three SARs 4-26
4-26 Effect of body mass on the maximum rate of nonevaporative
heat loss relative to resting metabolism in mammals during
exercise at a Ta of 20°C 4-26
4-27 Relationship between SAR and Ta on the activation of
various thermoregulatory effectors and elevation in body
temperature in five animal species 4-26
4-28 Block diagram for one segment of the thermal model 4-31
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Figures (Continued)
Number Page
4-29 Incident power density vs. exposure duration to obtain
a hot spot 4-33
5-1 Arrhenius plot of Na* efflux 5-8
5-2 Summed incidence of abnormal and nonviable chick embryo
eggs exposed to 2450-MHz radiation 5-30
5-3 Cross-sectional sketch of the human and the rabbit eye 5-66
5-4 Time and power-density threshold for cataractogenesis in
rabbits exposed to near-field 2450-MHz radiation 5.57
5-5 Distribution of energy absorption rate per mW/cm2 incident
power density in the rabbit's eye and head exposed to
2450-MHz radiation 5-67
5-6 Distribution of energy absorption rate per mW/cm2 incident
power density in the rabbit's eye and head exposed to
918-MHz radiation , 5-67
5-7 Linear regressions of eye score on age for workers exposed to
microwave radiation and controls 5-118
XII
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Tables
Number Page
3-1 Radiofrequency Bands 3-2
3-2 Proposed System of RF Dosimetric Quantities, Definitions,
and Units 3-14
3-3 Range of Resonant Frequencies of Man and Animals Irradiated
by Plane Waves in Free Space at 1 mW/cm2 with Long Axis
Parallel to Electric Field 3-15
3-4 Dielectric Permittivities for Various Tissues 3-21
3-5 Energy Units for RF Radiation 3-22
4-1 Partitioning of Heat Loss in Humans as a Function of
Ambient Temperature Under Still Air Conditions 4-10
4-2 Approximate Normal and Lethal Core Temperatures of
Some Birds and Mammals 4-22
4-3 Steady-State Temperatures in a Human Body After
Exposure to 80- and 200-MHz RF Fields 4-32
5-1 Classification of Cellular and Subcellular Experiments 5-1
5-2 ' Summary of Studies Concerning RF-Radiation Effects on
Molecular Systems 5-3
5-3 Summary of Studies Concerning RF-Radiation Effects on
Subcellular Systems 5-5
5-4 Summary of Studies Concerning RF-Radiation Effects on
Single Cells 5-7
5-5 Summary of Studies Concerning Hematologic Effects of
RF-Radiation Exposure 5-15
5-6 Summary of Studies Concerning Immunologic Effects
(In Vivo) of RF-Radiation Exposure 5-19
5-7 Summary of Studies Concerning Immunologic Effects
(In Vitro) of RF-Radiation Exposure 5-26
5-8 Conversion of J/g to W/kg 5-31
5-9 Summary of Studies Concerning Teratologic Effects of
RF-Radiation Exposure 5-37
5-10 Summary of Studies Concerning Reproductive Effects of
RF-Radiation Exposure 5-38
5-11 Summary of Studies Concerning Effects of RF-Radiation
Exposure in Testes of Mice and Rats 5-41
5-12 Summary of Studies Concerning RF-Radiation Effects on
the Nervous System 5-50
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Tables (Continued)
Number Page
5-13 Summary of Studies Concerning RF-Radiation Effects on
Behavior 5-62
5-14 Summary of Studies Concerning Ocular Effects of
Near-Field Exposures 5-65
5-15 Summary of Studies Concerning Ocular Effects of
Far-Field Exposures 5-65
5-16 Summary of Studies Concerning Auditory Effects of
RF Radiation in Humans 5-71
5-17 Summary of Studies Concerning Threshold Values for
Auditory-Evoked Potentials in Laboratory Animals 5-76
5-18 Summary of Studies Concerning Human Cutaneous
Perception of RF Radiation 5.77
5-19 Summary of Studies Concerning RF-Radiation Effects on
Endocrinology 5-80
5-20 Summary of Studies Concerning RF-Radiation Effects on
Clinical Chemistry and Metabolism 5-83
5-21 Summary of Studies Concerning RF-Radiation Effects on
Growth and Development 5-86
5-22 Summary of Studies Concerning RF-Radiation Effects on
Various Aspects of Cardiac Physiology 5-87
5-23 Summary of Studies Concerning Biological Effects of
Low Frequency Modulation of RF Radiation 5-93
5-24 Summary of Studies Concerning Genetic and Mutagenic
Effects of RF-Radiation Exposure 5-103
5-25 Summary of Studies Concerning RF-Radiation Exposure
Effects on Life Span/Carcinogenesis , 5-107
5-26 Summary of Prausnitz and Susskind Data 5-107
5-27 Summary of Selected Human Studies Concerning Effects of
RF-Radiation Exposure 5-113
5-28 Distribution of Years of Exposure for 226 Radar Workers 5-113
5-29 Age Distribution of 226 Microwave Workers and 88 Controls ... 5-113
5-30 Microwave Exposure Levels at the U.S. Embassy in Moscow 5-115
5-31 Number of Deaths from Disease and Mortality Ratios by Hazard
Number: U.S. Enlisted Naval Personnel Exposed to Microwave
Radiation During the Korean War Period 5-116
5-32 Classification by Military Occupation of World War II and
Korean War Veterans With and Without Cataracts, Based on
Discharges from VA Hospitals 5-117
5-33 Estimated Relative Risk of Cataracts Among Army and
Air Force Veterans by Age Group and Occupation 5-117
5-34 Paternal Radar Exposure Before Conception of Index Child 5-120
XIV
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Tables (Continued)
Number Page
6-1 Selected Studies Reporting "No Effects" at SARs
< 10 W/kg Grouped by Biological Variable 6-5
6-2 Selected Studies with Reported "Effects" at SARs
< 10 W/kg Grouped by Biological Variable 6-6
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A cknowledgment
The authors thank Jan Parsons and Carole Moussalli, Northrop Services, Inc., for
editorial review of this document. The authors wish to express special
appreciation to Dr. Don R. Justesen for his editorial comments on an earlier draft
and Dr. Charles Susskind for his editorial assistance on the final draft.
XVI
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Section 1
Introduction
Daniel F. Cahill
Joe A. Elder
The goal and purpose of this document is review and
evaluation of the available scientific information on the
biological effects of radiofrequency (RF) radiation. To
address this broad topic most effectively and to
present the information in the most useful form,
several guidelines and simplifying assumptions were
adopted. It is in the selection and employment of
these guidelines and assumptions that differences of
opinion are most likely to arise. These guidelines and
assumptions are as follows:
1. The frequency range of interest is defined as 0.5
MHz to 100 GHz. This range includes nearly all the
frequencies that serve as significant sources of
population exposure (e.g., AM, FM, land mobile,
and amateur radio; UHF and VHFTV; and air traffic
control radar).
2. The general public is the population of concern.
Therefore, far-field exposures are the more usual
condition, rather than the near-field exposures
commonly associated with the workplace.
Wherever possible, the impact on all ages is
considered, not only on healthy adults, who are of
principal concern in occupational-exposures.
3. Dose rate is defined by the specific absorption rate
(SAR), which is used to normalize the rate of RF
energy input into biological systems across this
frequency range. The SAR is the mass-normalized
rate at which the energy of an electromagnetic
(EM) field is coupled into an absorbing body; the
units are watts per kilogram (W/kg). Inherent in
the use of a single, whole-body-averaged SAR
value is a disregard of nonuniform RF energy
deposition patterns and possible local SAR values
in excess of the average. However, the data that
describe the distribution patterns of RF energy in
biological systems over a frequency band as broad
as 0.5 MHz to 100 GHz are far too incomplete at
this time to be directly useful.
4. In reports of pulsed RF-radiation exposure
experiments the time-averaged SAR is considered,
although controversy exists as to whether some
biological effects are functions of the temporal
pattern of energy delivery or only the result of total
energy input.
5. We have accepted "no effects" data in credible
reports as highly valuable in our review of the state
of knowledge in this area. Both "effects" and "no
effects" studies are used to determine the extent
of the biological interactions of RF radiation.
6. We are assuming that data derived from the use of
experimental mammalian systems have relevance
for the human situation.
7. This document presents only the biological effects
of RF radiation. The benefits of RF radiation are
not considered, and therefore no benefit/risk
analysis is undertaken.
A draft of this report (Cahill and Elder 1983) was
published in June 1983 and transmitted to EPA's
Science Advisory Board (SAB) for review of its
scientific and technical merit (Federal Register
1983a). The initial review by the SAB Subcommittee
of the Biological Effects of Radiofrequency Radiation
was held on September 22-23, 1983 (Federal
Register 1983b); the second review occurred on
January 24-25, 1984 (Federal Register 1984). A list
of the Subcommittee members is given in Appendix
A.
The June 1983 draft was a critical review of the
literature on the biological effects of radiofrequency
radiation through 1980. The present document is a
revision of the June 1983 draft and is based on the
comments and suggestions of the Subcommittee,
and includes a number of post-1980 references that
were considered important to the conclusions of the
present review of the biological effects of RF radiation
by both the authors and by the Subcommittee
members.
j-j
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Section 2
Approach
Joe A. Elder
Daniel F. Cahill
2.1 General Approach
Although a comprehensive literature review is
useful, it is even more desirable if the body of
literature is consolidated, analyzed, and synthesized
into a statement or statements that relate the
presence or absence of biological effects to a
meaningful exposure parameter such as dose rate
(SAR). To this end, our general approach is essentially
as follows:
1. The reports are evaluated for their scientific
quality and utility. Acceptable reports contain
adequate descriptions of appropriate physical and
biological systems and tests.
2. The credible reports are then examined for the
relation between the RF energy absorbed and the
presence or absence of biological effects in the
experimental systems.
2.2 Specific Approach
The literature evaluated for this document includes
English-language publications, numerous English
translations of Soviet research reports obtained
through the U.S. Joint Publications Research Service,
and selected technical reports translated from Polish,
French, Italian, and Russian.
The extant literature base numbers over 5000
citations, but considerably fewer are valuable
in developing exposure guidelines for the following
reasons.
1. A large fraction of the literature is available only in
Slavic languages.
2. The research reports are uneven in quality and
usefulness because authors often failed to
include sufficient experimental details to allow
reviewers to estimate critical exposure parameters
such as incident field intensity, dose rate, or dose.
3. In many review articles, equal currency is given to
the conclusions from properly designed and
executed studies and to those from less stringently
conducted research. Because these uncritical
reviews have contributed to the general confusion
over the health risks associated with RF radiation.
we have relied on original research papers rather
than review articles and have chosen to be highly
selective in our review.
In reviewing the literature we first evaluate
descriptions of frequency, exposure parameters, RF
source, experimental species, age, sex environmental
and biological controls, and the statistics employed;
and whether actual data are displayed or merely
referred to in the text. Many pre-1970 reports are
deficient in one or more of these key areas and are
either rejected outright if the flaws are judged fatal, or
are segregated into the category of reports with
"unresolved issues." Reports that provide adequate
descriptions of these parameters are further
scrutinized for the appropriateness of biological
systems, tests, sample sizes, controls, and statistics
employed, as well as substantiation of their
conclusions. Reports that clear this second hurdle are
credible reports, but are considered usable only if
biological results are linked explicitly or implicitly to
SAR data from the description of the exposure
parameters. Reports that fail to provide these
parameters are also assigned to the "unresolved
issues" category.
2.3 Major Sections
Four major sections follow. They are Physical
Principles of Electromagnetic Field Interactions (Sec.
3), Effect of RF-Radiation Exposure on Body
Temperature (Sec. 4), Biological Effects of RF
Radiation (Sec. 5), and Summary and Conclusions
(Sec. 6).
The first part of Sec. 3 presents some introductory
information on electromagnetic field theory. Next,
RF-field interactions with both simple and complex
biological objects, such as the human body, are
discussed and, most important, definitions of RF
dosimetric terms are given. The mechanisms of RF
interactions with biological systems, particularly
molecular systems, are discussed. The remaining two
major subsections described experimental methods
and dosimetric methods used in state-of-the-art
research on the biological effects of RF radiation.
Since the absorption of RF energy by biological
species can lead to an increase in the temperature of
body tissues, it is important to understand how
2-1
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animals, including man, regulate the additional
thermal input of RF-radiation exposure, both
physiologically and behaviorally. Section 4 is an
introduction to the subject of thermoregulation in
both animals and human beings and, in addition,
discusses the specific effects of RF radiation on
thermoregulatory processes. Also, a description is
included of the mathematical models that are being
used to predict increases in temperature and
activation of thermoregulatory effectors in human
beings in simulated RF fields.
Section 5 is a review of the main body of literature on
the biological effects of RF radiation. The section
contains ten subsections, each of which represents a
biological discipline or major research area, ranging
from subcellular systems to human beings. In each of
the ten areas, the conclusions and generalizations
that can be drawn from the review of the literature are
presented.
In Sec. 6, the major conclusions and generalizations
of Sees. 3, 4, and 5 are presented. Next, many of the
reports are tabulated by biological variable and dose
rate (SAR). In summary, the reported consequences
of the interaction between RF radiation and biological
systems are examined from two perspectives (whole-
body-averaged SAR and RF-energy-induced core
temperature increases) in order to analyze, synthesize,
and consolidate the review data into statements that
relate biological effects to a meaningful exposure
parameter (dose rate or SAR).
2-2
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Section 3
Physical Principles of Electromagnetic Field Interactions
3.1 Elements of Electromagnetic Field
Theory
William T. Joines
3.1.1 Electromagnetic Spectrum
3.1.1.1 Frequency, Wavelength, and Velocity
Oscillating electric charges induce an electromagnetic
(EM) field within the region surrounding the charge
source. In turn, this oscillating induction field—often
called the near field—of the source generates an EM
wave that radiates energy from the region surrounding
the charges. The radiated wave consists of coupled
electric and magnetic fields that oscillate at the same
frequency as the source, and the wave propagates
outward from the source at the velocity of light in the
medium. In free space, this velocity is~ 3 x 108 m/s,
whereas in a medium with low EM energy dissipation
the velocity is this value divided by the square root of
the material's dielectric constant relative to that of
free space. In a low-loss material such as fatty tissue,
with a relative dielectric constant of 4, the velocity of
light is 1.5 x 108 m/s. For an EM wave traveling at
velocity v, the wavelength in the medium is the
distance the wave travels in one time period or T = 1 /f,
where f is the oscillation frequency of the wave in
cycles per second, or hertz (Hz). Therefore, the
wavelength ^ is expressed as
* =v/f
The EM spectrum extends from zero to 1025 Hz (or
cycles/s) and includes the ranges of visible light and
ultraviolet (UV), infrared (IR), X, and gamma rays. The
region from zero to 3000 GHz (lower IR range) is
referred to as the RF region (Sams & Co. 1981). The
region of interest here is the RF band from 0.5 MHz to
100 GHz. The wavelengths in free space for this
frequency band range from 600 m to 3 mm.
3.1.1.2 Ionizing and Nonionizing
Electromagnetic Radiation
EM waves of all frequencies carry energy. According
to quantum mechanics, they can also be thought of as
packets of energy called photons. The energy of a
photon is given by
Energy = hf
where h = 6.63 x 10"34 joule seconds (Planck's
constant)
f = frequency
The energy of a photon is thus directly proportional to
the frequency of the radiation. When the frequency
approaches or exceeds 3 x 10'6 Hz (UV), the photon
energies equal or exceed 2x10"18 J, or 12.4 eV, and
become comparable to the binding energy of
electrons to atoms. This high-frequency radiation (X
rays, gamma rays, etc.) is referred to as ionizing
radiation. Since even the weakest chemical bonds
have energies that are several orders of magnitude
greater than those of RF or microwave photons (10~3
eV or less), RF waves are referred to as nonionizing
radiation.
3.1.1.3 Designation of Microwave and
Radiofrequency Bands
Bands of radiofrequencies have been assigned
designations according to frequency or wavelength
as shown in Table 3-1 (Sams & Co. 1981). Typical
uses of the frequencies within a band are also
indicated. Certain radiofrequencies—notably the
industrial, scientific, and medical (ISM) frequencies—
have been assigned by the Federal Communications
Commission for specific applications (Sams & Co.
1981). The ISM frequencies are
13.56 MHz ±6.78 kHz
27.12 MHz± 160kHz
40.68 MHz ± 20 kHz
915 MHz ±25 MHz
2450 MHz ± 50 MHz
5800 MHz ± 75 MHz
22,125 MHz± 125 MHz
3.1.2 Wave Propagation
Power Density, Electric Field, and Magnetic Field
In free space, EM waves spread uniformly in all
directions from a theoretical point source. The
wavefront, or the surface joining all points of identical
phase, is spherical in this case. As the distance from
the point source increases, the area of the wavefront
surface increases as a square of the distance, so that
the source power is spread over a larger area. If power
density is defined as the ratio of the total radiated
power to the spherical surface area enclosing the
source, the power density W is inversely proportional
to the square of the distance from the source, and can
be expressed as
3-1
-------
Table 3-1. Radiofrequency Bands*
Frequency Wavelength
Band Designation
Typical Uses
300-3000 GHz
30-300 GHz
3-30 GHz
0.3-3 GHz
30-300 MHz
3-30 MHz
0.3-3 MHz
30-300 kHz
3-30 kHz
0.3-3 kHz
30-300 Hz
0-30 Hz
1-0.1 mm
10-1 mm
10-1 cm
100-10 cm
10-1 m
100-10 m
103-102m
10-1 km
100-10 km
103-10'km
104-103km
oe-104 km
Supra EHF
(extremely high
frequency)
Extremely high
frequency (EHF)
Super high
frequency (SHF)
Ultra high
frequency (UHF)
Very high
frequency (VHF)
High frequency
(HF)
Medium frequency
(MF)
Low frequency
(LF)
Very low
frequency (VLF)
Voice frequency
(VF)
Extremely low
frequency (ELF)
Sub-ELF
Not allocated
Satellite communications,
radar, microwave relay.
radionavigation, amateur radio
Satellite communications, radar.
amateur, taxi, police, fire,
airborne weather radar, ISM
Microwave point to point,
amateur, taxi, police, fire
radar, citizens band, radio-
navigation, UHF-TV, microwave
ovens, medical diathermy. ISM
Police, fire, amateur, FM,
VHF-TV, industrial RF equipment
diathermy, emergency medical
radio, air traffic control
Citizen band, amateur, medical
diathermy. Voice of America,
broadcast, international
communications, industrial RF
equipment
Communications, radio-
navigation, marine radiophone,
amateur, industrial RF
equipment, AM broadcast
Radionavigation, marine
communications, long-range
communications
Very long range communications,
audiofrequencies, navigation
Voice, audiofrequencies
Power lines, audiofrequencies,
submarine communications
Direct-current power lines
*Sams& Co. 1981.
W = P/477T2 (3-1)
where P = transmitted power
r= distance from the source
An isotropic source radiates uniformly in all
directions in space. In practice, there is no source that
has this property, although there are close approxi-
mations. The inverse-square law (Equation 3-1)
applies also when the source is anisotropic
(directional), as long as the medium is homogeneous
and isotropic (e.g., free space or a medium in which
the velocity of wave propagation does not change
with direction or distance).
An EM wave is also characterized by its electric-field
(E) intensity and its magnetic-field (H) intensity. In an
unbounded medium, the product of E and H is the
power density W, or
W = EH (3-2)
where E is in volts per meter, H is in amperes per
meter, and W is in watts per square meter. If the peak
instantaneous values of E and H are used in
Equation 3-2, then W is the peak power density; if
effective or root-mean-square (RMS) values of E and
H are used, then W is the effective or time-averaged
power density. The ratio of E to H is the intrinsic
impedance of the medium rj (in ohms), or
/7 = E/H (3-3)
where rj is 120w ohms in free space. From Equations
3-1 through 3-3, one can express E in free space at a
distance r from an isotropic source radiating total
power P as
E =V3OP/r (3-4)
The radiated waves that propagate outward from an
RF or microwave source can be confined to travel
along a two-conductor transmission line (coaxial.
3-2
-------
stripline, microstrip, twin lead), or inside a hollow
metal pipe (waveguide). The waves can also be
propagated outward into the space that surrounds a
transmitting antenna, as in communications broad-
casting. In this case, the RF or microwave source
forces electrons to oscillate on the surface of a metal
transmitting antenna and thereby produces EM
waves. This is a reciprocal process, for when these
waves strike a receiving antenna, they force electrons
to oscillate, which typically produces current in the
receiver. This reciprocity phenomenon forms the
basis of EM communication systems. Information can
be placed on an EM carrier in several ways, including
amplitude and frequency modulation of the carrier
wave.
3.1.2.1 Sources of Radiofrequency Radiation
There is widespread interest in possible new
applications of RF energy, especially at microwave
frequencies. The growing number of commercial
applications has led to an increased awareness of
potential hazards due to the energy sources used.
Typical sources of RF or microwave energy are
klystrons, magnetrons, planar triodes, backward-
wave oscillators, and semiconductor devices. In all
these sources, energy is imparted to charged particles
or electrons from a convenient supply, usually a direct
voltage and current. A portion of the energy is then
given up by the charged particles in the form of
oscillations in a tuned circuit. Such sources may
operate to produce (1) continuous (CW) radiation, as
in the case of some communications systems; (2)
intermittent radiation, as in microwave ovpns,
induction heating equipment, and diathermy equip-
ment; or (3) radiation in the pulsed(PW) mode in radar
systems.
3.1.2.2 Plane-Wave, Far-Field, and Near-Field
Concepts
Usually the region that is more than a few
wavelengths from the transmitting antenna is called
the far field. In this region, the spatial relationship
between the electric and magnetic fields in the EM
wave is that shown in Figure 3-1. In this diagram, an
EM wave is propagating in a direction perpendicular
to the motion of the electrons in the transmitting
antenna. The electric field E is always perpendicular
to the direction of propagation and lies in the plane
formed by the line of propagation and the motion of
electrons in the antenna. The direction of the electric
vector periodically changes along the direction of
propagation, and its magnitude forms a sine-wave
function. The magnetic field H, which is always
perpendicular to both the electric field E and the
direction of propagation, traces out a sine-wave
function in the same manner as the electric field E.
Figure 3-1 depicts the situation at a particular instant
in time. The entire wave can be pictured as moving in
the direction of propagation at ~ 3 x 108 m/s.
Figure 3-1. Far-field electromagnetic wave at a particular
instant in time.
Velocity, v
At some distance from the transmitting antenna
(within the far field), the radius of curvature of the
generally spherical wavefronts is large compared
with the diameter of any receiving or detecting object
within the field. At this distance from the antenna the
wavefronts may be treated (for all practical purposes)
as plane surfaces over which the intensity of E and H
is constant. In such regions, E and H form plane
waves. The terms "plane-wave field" and "far field"
are often used interchangeably, although the
distinction between the two terms depends on the
size of the receiving object, as stated above.
At distances less than a few wavelengths from a
transmitting antenna, in the near field, the situation
is somewhat complicated because the maxima and
minima of E and H do not occur at the same points
along the direction of propagation as they do in the
far-field case (Figure 3-1). Near-field exposures
become particularly important when one is consider-
ing radiation from microwave ovens, microwave
diathermy equipment, RF sealers, broadcast antennas,
and microwave oscillators under test. For investiga-
tions into the biological effects of RF-radiation
exposure, studies of exposures in the far field are
usually preferable; field strengths in the nearfield are
more difficult to specify because both E and H must be
measured and because the field patterns are more
complicated.
Incident power density at a given distance from an
antenna may be calculated from the measured
power transmitted by the antenna, the known
antenna gain G, and effective area A of the antenna.
Antenna gain is defined as the power density at a
point in front of the antenna divided by the power
density at the same point if the antenna were
radiating the same total power as an isotropic source.
For any impedance-matched antenna (i.e., one where
all the energy fed to it is transmitted), the ratio of G to
A is
G/A = 47T/M2
(3-5)
3-3
-------
The far-field power density is calculated from the Friis
free-space transmission formula (Mumford 1 961 ) as
W = GP/477T2 = APA*2r2 (3-6)
where ^ = wavelength
P = power output of the antenna
W = power density on a surface at distance r
from the antenna
It is convenient to express the far-field free-space
power density in terms of the power density at the
antenna aperture, i.e., W0 = P/A, and hence P = WoA.
Substituting this expression for Pin Equation 3-6 and
dividing both sides by W0 yields
W/Wo = (A/^r)2 (3-7)
Equation 3-7 may be rewritten as
Figure 3-2. Power density vs. distance along axis from
antenna aperture.
This expression applies in the far-field region, and
the following simple modification makes it applicable
to the near-field region as well:
W/W0 = 4sin2( A/2,* r) (3-9)
This formula applies to uniform irradiation of square,
round, or rectangular apertures or to irradiation that
is tapered in amplitude for round apertures. For other
shapes and tapers, a more complicated analysis is
necessary (Mumford 1961).
Since the power density at the antenna aperture (Wo =
P/A) is greater than the output power P divided by the
cross-sectional area of the aperture, the effective
area A is less than the actual area. For the waveguide
horn and dish antennas commonly used at microwave
frequencies, the effective area ranges from about 50
to 80 percent of the actual area of the cross section.
For a given P, with A determined for the particular
antenna used, W0 = P/A is used in Equation 3-9 to
compute W at any distance r from the antenna
(Mumford 1961).
Equation 3-9 is plotted in Figure 3-2 along with lines
representing the maximum values in the near-field
and the far-field approximations as given by Equation
3-7. In this graph, the relative power density is plotted
in decibels [dB = 1 0logio (W/Wo)] on the ordinate, and
^r/A is plotted logarithmically on the abscissa. Note
the alternate maxima and minima in the near field.
The maxima all are 6 dB above (4 times) the power
density at the aperture. For- a conservative estimate
in possible near-field human exposure situations, the
power density can be approximated as the maximum
value or
W = 4W0 = 4P/a
(3-10)
Figure 3-2 and Equation 3-9 also show that for ^r/A =
1, W = W0, the power density at the antenna
aperture. Hence, a convenient point of demarcation
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between the near field and far field is the distance
from the antenna where
r=A/* (3-11)
The gain of an antenna as used in Equations 3-5 and
3-6 is usually taken to be the gain in the direction of
maximum radiated power. In general, the antenna
will have a radiation pattern that is at a maximum in
front of the antenna on an axial line perpendicular to
the aperture surface. On a surface of radius r from the
antenna, the power density typically decreases as the
off-axis angle increases. The relative power density is
expressed as W(0)/Wma«, where Wmax is the power
density at a given distance along the axis of maximum
radiation, and W(0) is the power density at the same
distance from the center of the aperture but at an off-
axis angle 0. Equations 3-6 through 3-9 apply to
angles off-axis if their right-hand sides are multiplied
by the radiation pattern W(0)/Wma«. While the
radiation pattern may be known or determined, it
does depend upon the type of antenna that is used.
3.1.3 Wave Modulation
3.1.3.1. Amplitude and Frequency Modulation
With an EM wave of a particular frequency serving as
a carrier, information signals at lower frequencies are
superposed onto the carrier through the process of
modulation. Modulation of the carrier can be
accomplished either by continuous variation of one of
the parameters of the carrier (amplitude, frequency,
or phase) or by interruption of the carrier by a process
in which it is chopped into segments (pulse wave or
PW modulation). If the impression of the information
3-4
-------
signal on the carrier causes its amplitude to vary, the Long-range and short-range radars may thus be of
process is called amplitude modulation (AM). If the comparable average transmitted power.
information signal causes a frequency variation of the
carrier at constant amplitude, the process is called
frequency modulation (FM). If the information signal
causes a time-phase variation of the carrier, the
process is called phase modulation (PM). Phase
modulation and frequency modulation are closely
related; both cause a change in the time phase angle
of the carrier (Froehlich 1969).
Since the purpose of modulation is to improve the
overall efficiency of transmission, the carrier
frequency is chosen for its suitability tothe medium in
which it is to be transmitted. Transmitting unmodified
audio signals is theoretically possible; however, the
antenna required to transmit and receive such
signals would be too large to be practical. More
important, unmodulated signals are not transmitted
because no other method exists to separate several
information signals on the same transmission path to
provide multichannel capability. This flexibility is
obtained if carriers of higher frequencies are chosen
and then spaced in frequency so as to prevent
overlap. High-frequency carriers are also more
suitable for radio propagation. One must then shift
the information signal to a high-frequency range
through the process of modulation. Introducing
frequency translation to information signals provides
a way of separating information channels and
thereby improving the transmission efficiency.
3.1.3.2 Pulse Modulation
One of the more familiar applications of PW
modulation is in radar. Radar is possible because EM
waves at some frequencies are reflected by certain
materials, including metal surfaces and water vapor
in clouds. A radar antenna can transmit and receive,
and it is directional; that is, it transmits and receives
signals in a narrow beam. For most purposes, the
radar antenna sends out short pulses of EM waves
and later receives the reflected pulses. The interval
between the outgoing and incoming pulse is
correlated with the beam direction to pinpoint the
position of the reflecting objects, such as airplanes or
cloud formations. The incoming reflected pulse is
smaller than the outgoing pulse by a factor of millions
and sometimes billions. To detect an incoming pulse
in the presence of atmospheric noise, the power of
the outgoing pulse is made as large as possible.
The duty factor (DF) of a transmitter is the ratio of the
width of the transmitted pulse to the time between
the leading edges of consecutive pulses. Hence,
average power (Pav) is determined from peak power
) by
Pav = (DF)Ppeak
In general, long-range radars have a larger
transmitted pulse power and a longer waiting time
between pulses (lower DF) than short-range radars.
3-5
-------
3.2 RF-Field Interactions with Biological
Systems
Claude M. Weil
James R. Rabinowitz
Consideration of the coupling of RF radiation into
various biological objects (human, animal, etc.) is
important to any study of the biological effects of RF-
radiation exposure. From measurements and
predictions of RF-energy absorption based on
experimentation with laboratory animals, one can
extrapolate data for estimating effects of RF radiation
on humans. Furthermore, an adequate understanding
of the interaction of RF radiation with humans has
been crucial in determining exposure limits recom-
mended in the American National Standards Institute
(ANSI) C95.1 standard (ANS11982). Relating a health
effect to a maximum permissible incident power
density requires an in-depth understanding of the
interaction of RF energy with humans.
3.2.1 Scattering and Absorption of
Electromagnetic Waves
The interaction of EM waves with any irradiated
object is a complex event that forms a large part of the
study of electromagnetism. When an EM wave
propagating in air impinges normal to the surface of
any material with dielectric properties different from
those of air, a reflected wave created at the air
dielectric interface propagates in a direction opposite
to that of the incident wave. This interaction is
illustrated in Figure 3-3 for three materials of
differing electrical properties. At the top of the figure,
an EM wave is shown incident on a metallic
conductor. In this case, virtually all the incident
energy is reflected back to its source by the
conductive plate. At the bottom of the figure, the
energy is shown incident on a slab of low-loss,
nonconductive material (dielectric insulator) where
almost no energy is dissipated within the material. In
that case part of the incident energy is transmitted
through the slab, part is reflected back at the first air-
dielectric interface, and a part is absorbed—a small
amount, since this material exhibits almost no
dielectric losses. An intermediate case, shown in the
middle of Figure 3-3, is the interaction with a
"complex" dielectric. Biological tissue falls between
the conductor and the nonconductor in Figure 3-3;
i.e., it exhibits values of relative permittivity (a
measure of how strongly the. material reflects
energy) and conductivity (how well the material
conducts electrically) that fall between the very high
values for a metallic conductor and the near-zero
values for a dielectric insulator. If the tissue slab is of
sufficient thickness, all incident energy is reflected or
absorbed and no energy is transmitted through the
slab. The mechanism by which RF energy is absorbed
or dissipated within-the tissue slab is discussed in
more detail below.
Figure 3-3. Interaction of RF radiation with electrical
conductors, biological tissue, and electrical
insulators (modified from Sher 1970).
Incident
Microwave
Power
Incident
Microwave
Power
Total
Reflection
Tissue
Part
Reflection
Incident
Reflection
Nonconductor
Part k\\\\NNS* Part
Microwave
Power
Transmission
In general, the reflected and transmitted waves that
surround a dielectric nonplanar object irradiated by
an incident RF wave together comprise what is
termed the scattered field. Scattering by a dielectric
object and any absorption within the object represent
the two basic components of the EM interaction
phenomenon. The degree, to which any object
interacts with an EM field when irradiated by a
uniform plane wave is defined in terms of scattering
and absorption cross sections. These cross sections
represent the cross-sectional area in square meters
of an equivalent flat plate placed normal to the
direction of propagation that totally reflects (in the
case of the scattering cross section) or totally absorbs
(in the case of the absorption cross section) the
radiant energy incident on the plate.
In general, the EM cross section is smaller than the
geometric (optical) cross section that the object
creates when illuminated by a distant light source.
However, under certain conditions—termed reson-
ance—when the wavelength of the incident radiation
is comparable to the physical dimensions of the
object, the scattering and absorption effects are
enhanced, so that both respective cross sections
exceed the geometric cross section. Resonance is a
significant phenomenon that will be discussed in
more detail in the following sections; it can be
explained by the apparent ability of the resonant
3-6
-------
Figure 3-4. Energy distribution in proximity to man at 1 GHz at the chest plane contour presentation; A) vertical.
B) horizontal (Reno 1974).
Radiation
Radiation
Field Amplitude
0.0-0.1 0.1-0.2 0.2-0.3 0.3-0.5 0.5-0.7 0.7-1.0 1.0-1.3 1.3-1.6 1.6-2.0
nj/m3
3-7
-------
object to intercept or "pull in" considerably more of
the energy incident upon it relative to the optical case.
Figure 3-5. Dielectric data for tissues in RF range 0.01 to 10
GHz. a: permittivity, b: conductivity.
The terms "scattering coefficient" and "absorption
coefficient," referring to measures of the efficiency
with which an object scatters and absorbs energy, are
defined as the ratio of the scattering to optical cross
sections and the absorption to optical cross sections,
respectively. Of the two basic measures of interaction,
the absorption coefficient is considerably more
prominent in the interaction of EM waves with
biological bodies. Potentially adverse biological effects
are related to the energy that the body is absorbing,
not to what is scattered. Because absorption rate is
related to internal field strength, it is conceivable that
a biological effect could be related to the field strength
within the tissue. For this reason, most of the
remaining material in this section deals only with the
absorptive aspect of the interaction phenomenon.
Some measurements have been made of the
scattered fields that surround both human subjects
and life-size phantom models exposed to incident
microwave fields (Reno 1974). Although this work
illustrates well the complex scattered fields
surrounding the irradiated subject (see Figure 3-4),
no attempts have yet been made to relate the field
patterns to what the subject is absorbing. Although it
is theoretically possible to determine the energy
being absorbed and the internal distribution from
measurements of the distribution of externally
scattered fields, in practice this determination
remains a difficult task and has not yet been
attempted. Interest in this area is growing, as
evidenced by a recent symposium (IEEE 1980) that
addressed methods of obtaining high-resolution
images of the internal dielectric structure of a
biological target. The methods are based on
techniques of probing the scattered fields created
when the target is irradiated by an RF field. The scope
for future work in this area appears large, particularly
in diagnostic applications.
3.2.1.1 Factors Affecting the Absorption of RF
Energy by an Irradiated Subject
The greater the efficiency of EM energy coupling into
a biological subject the greater the overall whole-
body absorption. The factors that influence the
degree of absorptive coupling are listed below and
will be discussed in turn:
a. Dielectric composition of subject
b. Object size relative to wavelength of incident field
c. Shape or geometry of subject and its orientation
with respect to polarization of incident field
d. Complexity of incident radiation
a. Dielectric composition of subject—As mentioned
previously, absorptive coupling to the irradiated
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subject can take place only if the subject is
composed of dissipative dielectrics of finite
conductivity value. The dielectric properties of all
biological tissues fall into this category, primarily
because their major constituent is water (average
of 70 to 80 percent by mass), which contains
electrically polarizable or dipolar molecules as
well as free ions. The basic mechanism of
dissipation of incident RF energy within these
tissues is that 1) the free rotations induced in the
dipolar water molecules by the externally
3-8
-------
Figure 3-6. Illustration of object size vs. wavelength
dependence. (Object is composed of tissue-like
dispersive dielectric.)
A A
\J\J
Incident wavelength £> object size.
Little power absorption,
uniform internal distribution.
A A
WT7
Wavelength and object comparable in magnitude.
Resonant case with significant absorption;
internal distribution very nonuniform with
"EM hot spots" present.
Penetration
A A
V/T7
Incident wavelength <*object size.
Intermediate absorption with internal
energy deposition largely confined to
object surface.
Poor penetration
impressed electric field are damped out by
collisions with surrounding molecules, and 2)
conduction currents are induced within the tissue
medium because of the presence of free ions.
These phenomena are discussed extensively in
Sec. 3.2.4, Mechanisms of RF Interaction with
Biological Systems.
Over the past 40 years, many measurements have
been made of the dielectric properties of biological
tissues. These data have been collected in the
Radiofrequency Radiation Dosimetry Handbook
(Durney et al. 1978, Tables 9 and 10), as well as in a
more recent paper by Stuchly andStuchly (1980). The
dielectric properties of biological tissues depend to a
considerable extent on the water content of the
tissue; i.e., tissues of high water content (blood, skin,
muscle, brain, etc.) exhibit much higher permittivity
(cf. Sec. 3.2.4.1) and conductivity values than do
tissues of low water content (fat, bone, etc.). As a
result, most incident RF energy tends to pass through
the fatty surface tissues of the body and be deposited
in the deeper tissues such as muscle and brain.
Figure 3-5 illustrates some dielectric data for various
types of tissues in the RF range 0.01 to 10 GHz. Note
that the dielectric properties of tissue are not
constant, but change with frequency. This is an
example of what is termed a dispersive dielectric. For
the case of biological tissues, the dispersive
characteristic above 1 GHz is created by the Debye
relaxation phenomenon in water molecules (discussed
further in Sec. 3.2.4, Mechanisms of RF Interaction
with Biological Systems). In part (b) of Figure 3-5, it is
apparent that conductivity increases by almost an
order of magnitude for all tissues in the frequency
range from 1 to 10 GHz. Because of this fundamental
dielectric property of tissue, microwaves in the
frequency range above about 5 GHz become strongly
attenuated in the increasingly lossy tissue medium.
Consequently, microwave energy of such frequencies
cannot penetrate deeply into body tissues and is
deposited near the body surface. As a result of their
poor penetration capability, microwaves in the
centimetric wavelength region (<6 cm approximately)
are less capable of inflicting potential damage on
internal tissue than are those of longer wavelength (>
10cm).
b. Object size relative to wavelength of incident
field—The second major factor on which energy
absorption depends is the size of the irradiated
object relative to the wavelength of the incident
radiation. Figure 3-6 illustrates that when the
wavelength is much greater than the object size
(see case A at top of figure), the absorptive
coupling is inefficient and little energy is
deposited in the object. For this case, called the
"subresonant" condition, values of the absorption
coefficient lie in the range 0 to 0.5. Case B
illustrates the resonant case, which occurs when
the wavelength and object dimensions are
comparable. For this case, the absorptive
efficiency is markedly improved so that signifi-
cantly more RF energy is coupled into the object
and creates much greater deposition. Absorption
coefficient values in the range 1.5 to 4 are
obtained under resonant conditions. Furthermore,
the incident energy penetrates into the object and
is deposited internally in a characteristically
nonuniform manner, with localized regions of
enhanced energy deposition ("EM hot spots") at
or near the object's center. These effects are
discussed further in later sections of this
document. In case C shown at the bottom of Figure
3-6, the wavelength is much shorter than the
object size. This represents the quasi-optical case,
where the absorptive efficiency is similar to that at
optical wavelengths. The absorption coefficient
3-9
-------
Figure 3-7. Calculated whole-body average SAR vs. frequency
for three polarizations in a prolate spheroidal model
of a human; incident power density = 1 mW/cm2.
Case Field Polarization
I -
A] E//a Vertical
B] H//a* Horizontal
Body
Orientation
10°_ „.-,,-
102 103
Frequency (MHz)
10"
approaches 0.5 under these conditions, which
gives intermediate absorption values that fall
between those achieved with the conditions of
cases A and B. Case C is also characterized by the
inability of the incident energy to penetrate much
beyond the surface of the object (note the
dielectric factors discussed earlier); consequently,
the energy coupled into the object under these
conditions is confined to the object surface.
c. Geometry and orientation of subject—The third
factor on which energy absorption depends is the
shape of the object and its orientation with respect
to the electric-field vector of the incident field.
Most biological subjects used in studying the
biological effects of RF radiation have a charac-
teristic shape that is significantly elongated along
one axis (similarly to humans). Although this
observation may appear to be simplistic, it is of
considerable significance in the discussion of the
interaction of RF waves with such objects. When
the electric-field vector of the incident radiation is
oriented parallel to the major or long axis of the
irradiated subject (e.g., a vertically polarized field
that is incident on a standing human subject),
then the subject absorbs as much as 10 times
more energy at resonance than if the electric-field
vector is oriented parallel to either of the two
minor axes. Figure 3-7 shows absorption
characteristics of a prolate spheroid model of an
average human. The ordinate represents the
whole-body-averaged specific absorption rate
•(SAR; see Sec. 3.2.2, RF Dosimetry Definitions, for
discussion of units), and the abscissa represents
frequency. From Figure 3-7, it is evident that
when the electric-field vector is oriented parallel
to the long axis of the prolate spheriod (electric-
field polarization case), the absorption curve has a
sharp peak at the resonant frequency of ~ 80
MHz. For the other orientations (H- and k-
polarization cases), it is apparent that the
absorption peak is much broader and occurs at
somewhat higher frequencies. Furthermore, the
resonant absorption values for the H and k cases
are considerably lower than that for the E
polarization case. These basic differences in
absorption values hold true in both the subreson-
ant and resonant regions, but not in the above-.
resonant (or quasi-optical) region, where absorp-
tion in the E- and H- polarization cases is
approximately the same.
d. Complexity of incident radiation—The fourth and
final factor on which RF-energy absorption
depends involves the complexity of the incident
radiation. Up to this point, most of the discussions
of RF coupling in biological targets have assumed
the simplest form of free-field exposure, which
involves a unipath plane wave emanating from a
distant source and incident on a subject
suspended in space. (See Sec. 3.1 for definition of
plane wave.) Virtually all the RF-radiation
protection guides and standards in use throughout
the world are based on this rather idealized
assumption. Furthermore, most of the biological
experimentation involving free-field exposures in
anechoic chambers attempts to simulate this
idealized concept. However, real-world, actual
exposure conditions are far more complex.
One complicating circumstance arises in the near
field. It is readily apparent that the most intense target
exposure with the resulting greatest potential for
injury would occur close to the RF-radiation source.
However, in this near field, the plane-wave
assumptions that are true for the far field of the
source's radiating antenna no longer hold. As
discussed in Sec. 3.1, the near field is characterized
by complex EM field properties: the E and H fields are
no longer in space quadrature (E and H vectors
separated by 90°), and the value of the E/H ratio
(termed the wave impedance) differs greatly from the
constant value 377 Q that characterizes the far field.
3-10
-------
In the near field, the power density concept is
meaningless in its usual sense. For an object placed
in the near field of an antenna the interaction is
exceedingly complex because every type of antenna
possesses near-field characteristics that are unique
to that type of radiator. Consequently, every
phenomenon involving near-field exposures must be
individually analyzed and characterized. Although it
is possible to predict the spatial field distribution in
the near field of an antenna, this distribution cannot
be used as a basis for predicting the absorptive
properties of an object placed in this field because the
object will substantially alter that field distribution, as
well as alter the radiating charateristics of the
antenna itself. When an object is placed in the near
field, it interferes with the basic purpose for which
most antennas are designed: the efficient transfer of
RF energy from source to far field. An object in the
near field tends to load the antenna capacitively,
which creates an impedance mismatch if the antenna
was originally well matched to free space. Asa result
the antenna reflects some of the transmitter energy
output back to the source. In general, for an antenna
that radiates well in free space, the closer the object is
to the antenna, the greater is the mismatch
condition, and the poorer is the transfer of radiated
energy to the far field. Consequently, it is reasonable to
conclude that whole-body-averaged SAR values in
the near field do not greatly exceed those existing at
the beginning of the far field, although there may be
regions within the object of high energy deposition.
The limited data available from EM models involving
near-field exposure (see Sec. 3.2.3) seem to confirm
this conclusion.
A secondary aspect of near-field exposures involves
the unwanted exposure to leakage fields emanating
from RF devices, such as microwave ovens, RF heat
sealers, and diathermy units, which are not intended
to radiate energy beyond their immediate surroundings.
Such leakage fields are complex, and exposure
invariably takes place in the near zone of the leakage
source. Nevertheless, the limited data available from
near-field exposures of EM models to leakage fields
seem to show that whole-body-averaged SAR values
are lower than might otherwise be expected because
of the leakage-source and near-field interaction
effects.
Another aspect of real-world exposures is the so-
called multipath problem. People usually stand on
the ground and are not suspended in space as in the
idealized exposure concept; furthermore, they
frequently stand close to buildings or to other
reflective surfaces. This situation creates the
multipath problem, in which a subject is exposed to
scattered as well as to direct energy. Some of the
effects are illustrated in Figure 3-8, which shows that
there is a considerable enhancement in energy
absorption occurring for various multipath conditions.
These effects have been illustrated by means of the
prolate-spheroid representation of a 70-kg man. To
compute the SAR of man for the nonresonant
condition, the optical cross-sectional area of the
prolate spheroid is first multiplied by the power
density (10 mW/cm2), and then the resultant 38 W is
divided by 70 kg to give an SAR of 0.54 W/kg. Note
that when the model is in contact with a conducting
ground plane, there is a doubling of the resonant
whole-body energy absorption compared to that of
free-space (Case II vs. Case I). Furthermore, if the
model is standing at a distance in front of the
reflecting plane that corresponds to an eighth of the
incident wavelength (Case V, 0.125,*), there is a
tenfold increase in absorption relative to that of free
space. Even greater increases are recorded when the
model is placed at a critical point inside a 90° corner
reflector (Cases IV and VI). The enhanced absorption
is a result of the reflector producing an enhanced field
strength at the position of the object and not due to
interaction between object and reflector.
In addition to these multipath effects, enhancement
of energy absorption can occur because of proximity
effects that are created when two or more subjects are
simultaneously irradiated. Gandhi et at. (1979) have
found that when subjects are spaced by a critical
separation of 0.65,*, a 50-percent enhancement in
absorption can occur. Coupling of RF energy into
biological systems is discussed further in the
Radiofrequency Radiation Dosimetry Handbook
(Durney et al. 1978, pp. 27-40).
3.2.2 RF Dosimetry Definitions
Dosimetry is the measurement or estimation of RF
energy or power deposition in an irradiated subject,
including the internal distribution of that deposited
energy. In recent years, the terminology describing
dosimetric assessment has been evolving. Prior tothe
mid-seventies most investigators used terminology
that appears to have been conveniently borrowed
from the ionizing-radiation field and that employed
the same cumulative dosage concept (Youmans and
Ho 1975; Justesen 1975). Many investigators felt
that this terminology was inappropriate for use with
nonionizing or RF radiation because energy absorption
in this case is not considered a cumulative
phenomenon in a way that has been accepted for
ionizing radiation (Susskind 1975; Guy 1975).
Consequently, a new terminology was proposed that
did not use the word "dose." The now widely
accepted term "specific absorption rate" (SAR) was
first reported in the literature by Johnson (1975);
however, the term evolved from joint discussion by
members of Scientific Committee 39 of the National
Council on Radiation Protection and Measurement
(NCRP). (This meeting, chaired by George Wilkening,
took place at the Battelle Research Center in Seattle,
Washington, on June 23,1975, with members Frank
Barnes, Curtis Johnson, Arthur Guy, Charles
3-11
-------
Figure 3-8. Absorption dependence on various ground and multipath factors (Gandhi etal. 1977). Note that these data are based on
experimental measurements.
Rate of Whole-Body Absorption (WBA) in Watts for a
Prolate Spheroid Model of Man (weight = 70 kg, height = 1.75 m) at 10 mW/cm3
WBA
SAR
Nonresonant conditions
38 W
(no reflectance)
19W
(50% reflectance)
Case I. At resonance for free space.
0.54 W/kg
0.27 W/kg
0
151 W
2.1 6 W/kg
f = 62-68 MHz
Case II. At resonance for conditions of electrical
contact with the ground plane.
2 x 151= 302 W
4.31 W/kg
f = 31-34 MHz
Case III. At resonance for placement in front
of a flat reflector.
O
d = 0.125
4.7 x 151= 710 W
10.14 W/kg
f = 62-68 MHz
WBA
SAR
Case IV. At resonances for placement in a 90° corner reflector.
d= 1.5A
27x151 =4077W
58.24W/kg
f = 62-68 MHz
Case V. At resonance in electrical contact with
ground plane, in front of a flat reflector.
d =0.125 A
2 x 710= 1420 W
20.28 W/kg
f = 31-34 MHz
Case VI. At resonance in electrical contact with
ground plane in a 90° corner reflector.
d = 1.5
2 x 4077 = 81 54 W
11 6.48 W/kg
f = 31 -34 MHz
3-12
-------
Susskind, Saul Rosenthal, Karl Illinger, and Ronald
Bowman attending. The committee members agreed
to publicize the new term as much as possible in their
publications to promote wide acceptance. Members
Johnson, Susskind, and Guy published comments
concerning SAR in 1975.) NCRP (1981) has formally
recommended adoption of the term SAR in RF
dosimetry. NCRP has also endorsed use of the term
"specific absorption" (SA) for the absorbed energy
per unit mass (referred to earlier as "dose").
Table 3-2 lists the various RF dosimetric quantities in
general use, together with their definitions and units.
Although the terms (particularly SA and SAR) for
some of these quantities have now gained widespread
acceptance, other terms, particularly dealing with the
volume-normalized power or energy absorption, have
only recently been proposed and have not yet gained
wide acceptance.
The mass-normalized and volume-normalized
absorption rates are directly related through the
localized or whole-body-averaged tissue mass
density p, that is, absorption-rate density, ARD =
p(SAR), where p is in kilograms per cubic meter. Most
biological tissues are composed largely of water, so
that it is reasonable to assume a unity tissue density
value. In this case, the two quantities are numerically
equivalent. This approach has been adopted by many
investigators engaged in predictive EM modeling (see
Sec. 3.2.3, Analytical and Numerical RF-Electro-
magnetic Interaction Models), where the model is
composed of some homogeneous tissue with average
physical and dielectric characteristics that are
representative of the various tissues of the body being
modeled. For example, all the SAR data given in the
familiar Radiofrequency Radiation Dosimetry Hand-
book were derived this way; the assumption of a unity
average tissue density is specifically stated (Durney
et al. 1978).
A subset of two additional values exists for both the
mass-normalized and volume-normalized quantities
listed in Table 3-2: (a) the whole-body-averaged
value, which represents the overall absorption or
absorption rate divided by the total mass or volume of
the subject; and (b) the localized value, which
describes the absorption or absorption rate in an
incrementally small mass or volume at some given
point within the subject. The localized ARD is
mathematically defined by the expression
-------
Table 3-2. Proposed System of RF Dosimetric Quantities. Definitions, and Units*
SI Unit
Quantity and Definitions
Name
Symbol
Other Units Used
Whole-Body Absorption
(formerly integral dose)
The total EM energy absorbed
by the irradiated subject
Whole-Body Absorption Rate
(formerly integral dose rate)
The time rate of total EM energy or
total power absorption by the
irradiated subject
Specific Absorption
(formerly dose)
The mass-normalized EM energy absorbed
by the irradiated subject
Specific Absorption Rate
(formerly dose rate)
The mass-normalized rate of energy
or mass-normalized power absorbed by
the irradiated subject
Absorption Density
(also absorbed energy density
or energy density, dissipated)
The volume-normalized EM energy
absorbed by the irradiated subject
Absorption Rate Density
(also absorbed power density,
density of absorbed power, heating
potential, etc.)
The volume-normalized rate of EM energy
or volume-normalized power absorbed by
the irradiated subject
joule
watts
joules
per
kilogram
wans
per
kilogram
joules
per
cubic
meter
watts
per
cubic
meter
W
J/kg
W/kg
J/m3
W/m3
millijoules (mJ)
(1 mJ = 10'3J)
calories
(1 cal = 4.187 J)
Milliwatts (mW)
(1 mW = 10~3W)
cal/min
mj/g
cal/g
mW/g
cal/g-min
mJ/cm3
mW/cm3
(1 mW/cm3 =
103 W/m3)
"Throughout this table, "absorption" refers to RF-energy absorption.
corresponds to a whole-body-averaged SAP of ~ 1 to
1.4 W/kg. To determine the power density level of
incident radiation that will create this exogenous heat
load in man, a detailed knowledge of human RF-
absorption characteristics is required. At the time the
first RF-radiation protection guide was proposed in
the early 1950s, virtually no data existed on the RF-
absorption characteristics of humans; the assumption
had to be made that the EM absorption cross section
for humans was equivalent to man's geometric cross
section, which is ~ 1 m2 (i.e., a unity absorption
coefficient was assumed). From this calculation came
the well-known exposure limit of 10 mW/cm2.
During the past 10 years or so, a considerable
accumulation of data based largely on human
interaction modeling has been developed (discussed
later in this section). These data showed that under
resonant conditions, the RF-absorption cross section
of humans can be 4 to 8 times greater than the
geometric cross section. Thus, at resonance, the RF-
absorption rate for humans can potentially exceed the
BMR by this factor when exposure is to incident
radiation levels of 10 mW/cm2. Such a situation
clearly constitutes an excessive thermal burden for
exposures of indefinite duration. Thus, EM modeling
has played a significant role in demonstrating that,
under certain conditions, the originally recommended
exposure limit is potentially unsafe, and in providing
an objective basis for the revision of that guideline.
The second reason for the importance of EM
modeling is that it provides us with a method of
extrapolating absorption data from animal experi-
ments for application to humans. From the prolate
spheroid representation for humans and animals, a
considerable amount of data has been compiled on
whole-body-averaged SAR vs. frequency characteris-
tics for several species. These data are given in the
Radiofrequency Radiation Dosimetry Handbook
(Durney et al. 1978); highlights of this material are
presented in Table 3-3, which shows the resonant
frequency range (long axis oriented parallel to E field)
and the whole-body-averaged SAR at resonance,
normalized to an incident field level of 1 mW/cm2 for
five different species, including humans. The data
given in Table 3-3 enable a researcher readily to
determine for a particular animal species the
resonance frequency range to be used during
experimentation. For example, to simulate human
resonance in adult rats, exposure would have to be
in the frequency range of 600 to 700 MHz. This is an
example of "frequency scaling," or adjusting the
frequency at which an experimental animal is
3-14
-------
exposed in order to approximate certain given
conditions of human exposure. In addition, differences
in the whole-body-averaged SAR between the two
species must be considered; from the last column of
Table 3-3, it is evident that, at resonance, the whole-
body SAR for the rat is 3 times that of a human. Thus,
if a certain SAR value is obtained in a rat when
exposed at a 10-mW/cm2 level, roughly 3 times that
level, or 30 mW/cm2, is needed to obtain the same
SAR value in humans (resonant condition for both).
The data shown in Table 3-3 can be likewise used to
determine whether a given exposure frequency falls
in, above, or below the resonance range for humans.
As was discussed earlier, these three categories
lead to fundamental differences in absorption as well
as patterns of internal energy deposition. Most likely
a corresponding difference in biological effects will be
seen in several frequency ranges, with the resonant
range representing the potentially most hazardous
condition because of the high absorption efficiency
and highly nonuniform internal deposition of energy.
As already emphasized, proper simulation of a given
human exposure scenario by means of experimental
animals requires the use of (1) frequency scaling to
ensure that the type of interaction taking place is
roughly comparable (i.e., subresonant, resonant, or
supraresonant); and (2) appropriate adjustment of the
incident exposure level to obtain a specified whole-
body-averaged SAR or, where possible, a given
localized SAR in some specified target organ. To
check for the possibility of any effects that might be
specific to a particular frequency to which humans
are being exposed, animals must necessarily be
exposed to that same frequency. Given such an
experiment, the use of frequency scaling is obviously
inappropriate.
3.2.3.1 Model Details
Gandhi (1980) and Durney (1980) published excellent
reviews on EM modeling, summarizing most of the
major research contributions to 1980 and detailing
the status of the EM modeling field at that time. The
material that follows does not duplicate these
reviews, but instead traces the historical development
of EM models with emphasis on the increasing
complexity of such models and their application. Only
a few relevant publications in the field are cited; the
reader is referred to Gandhi's and Durney's reviews
for more complete details, as well as to the
Radiofrequency Radiation Dosimetry Handbook
(Durney et at. 1980, pp. 42-44), which contains a
comprehensive literature survey of all theoretical and
experimental modeling work performed to 1 979. The
reader is also referred to the original publications for
further details of the mathematical techniques used
to solve the various problems that are discussed
below.
Table 3-3. Range of Resonant Frequencies of Man and
Animals Irradiated by Plane Waves in Free Space
at 1 mW/cm2 with Long Axis Parallel to the
Electric Field*
Species
Man (av)
Woman (av)
Child (10 years
old}
Rhesus monkey
(seated)
Dog (beagle)
Guinea pig
Rat (medium)
Mouse
Average
Weight
(kg)
70
61
322
35
135
0.58
032
002
Average
Length
(m)
1 75
1.61
1 38
004
006
0.02
0.02
0.007
Resonant
Frequency
(MHz)
70-80
80-90
90-100
300-350
200-250
550-600
600-700
2400-2600
RMR
(W/kgl
1 26
1.15
2.00
2.36
1.72
3.83
4.8
6.5
Average
SAR
(W/kg)
0.25
025
035
030
016
055
075
072
•Data derived from Durney et al (1978).
Planar and spherical models—The earliest model
considered involved the one-dimensional solution to
the planar tissue slab irradiated by a plane wave
(Schwan and Li 1956). The slab is infinitely wide and
can contain several layers of various tissues.
Although the solution to this problem is straight-
forward, the model is restricted in its application
because it does not account for the obvious closed-
form shape of all human and infrahuman bodies.
This particular model is valid only when the
wavelength is small compared to the system size, as
depicted earlier in Figure 3-6, case C; for human
irradiation, such wavelengths correspond to fre-
quencies above approximately 3 GHz. The concept of
"penetration depth" has been developed on the basis
of this one-dimensional model. The penetration depth
is the depth within the tissue slab at which the RF
power has been attenuated to a value of 1 /e2 and is
shown as a function of frequency in Figure 3-9.
Strictly speaking, this concept applies only to this
particular planar model; however, if prudently applied
the concept has an approximate qualitative meaning
for other configurations. It is unfortunate that the
concept has been extensively borrowed and is often
inappropriately used in discussions of RF absorption
in nonplanar models where the wavelength is either
longer than or comparable to the object size. The
penetration depth concept can be accurately applied
only when the wavelength is small compared to the
object size.
The next level of complexity involves two-dimensional
solutions of the infinitely long cylinder with circular,
elliptical, and arbitrary cross sections; some of these
models are of homogeneous tissue and others are
multilayered (Ho 1975). These models are primarily
intended to simulate RF heating in human limbs
under conditions of plane-wave irradiation from a
rectangular applicator in contact with the cylindrical
model, which is of particular interest to diathermy
practitioners. Ruppin (1979) examined a lossy-
dielectric cylinder model placed in front of a perfectly
conducting plane (i.e., a multipath configuration). His
data show both enhancement and reduction of
3-15
-------
average SAR relative to the isolated cylinder,
depending on the conditions of irradiation. Cylindrical
models were also used extensively for SAR
calculations in the second edition of the Radiofre-
quency Radiation Dosimetry Handbook (Durney et al.
1978).
The first attempts at three-dimensional solutions
involved homogeneous spheres of tissue-equivalent
dielectrics. Although it is only a poor approximation to
the actual shape and heterogeneous dielectric
composition of humans and experimental animals,
the sphere model has been used extensively because
of the ready availability of solutions based on the
classical Mei theory involving spherical wave
functions (Stratton 1941). These methods can be
readily programmed on high-speed machines that
yield data on the EM absorption cross section and on
the distribution of localized ARD for homogeneous
spheres (Kritikos and Schwan 1975). (Some
approximations made by Kritikos and Schwan [1975]
can be used in the subresonance or Rayleigh region
and the supra-resonance or quasi-optical region,
which greatly simplifies these computations.) This
work demonstrated that a highly nonuniform
absorption distribution is obtained under resonant
conditions, including the formation of relatively
intense "EM hot spots" near the sphere's center
(Figure 3-10). Other workers (Weil 1975) have used a
multilayered spherical model that consists of several
concentric layers of different tissues representing an
idealized model of an adult, child, or monkey head
exposed to plane-wave radiation. However, this
concept has obvious limitations because the
spherical model is spatially isolated rather than
attached by the neck to the body's trunk. Results for
the multilayered sphere were similar to those
obtained for the homogeneous sphere with the
exception that, in the supraresonance region,
enhanced absorption was noted in the multilayered
model. This enhancement is caused by the presence
of the surrounding layers of skin and fat, which
appear to provide an impedance transformation
mechanism by which energy transfer into the sphere
is increased. A recent paper by Barber et al. (1979)
has shown that a planar model can accurately predict
this enhancement effect for any three-dimensional
nonplanar shape, and that the layering enhancement
factor can be applied to any nonlayered object, such
as a human model, to predict trve absorption
characteristics of the layered object.
The effects of altering irradiation from plane wave to
near field on the absorption characteristics of
multilayered sphere models were investigated by
Hizal and Baykal (1978). They found that EM hot spots
continue to occur when the model is excited near
resonance in the near field of a loop antenna, but not
when similarly excited by a dipole antenna.
Figure 3-9. Penetration depth as a function of frequency (data
from Table 3, Oumey et al. 1978).
100
0.1
10
100 1000
Frequency (MHz)
10000
Prolate spheroidal and ellipsoidal models—Since
prolate spheroids and ellipsoids are much better
approximations to actual human and animal shapes,
use of these models was a logical next step to solving
this problem. Although one can in principle obtain
solutions to the prolate spheroid and ellipsoid
problem in spheroidal and ellipsoidal wave functions in
the manner already accomplished for the sphere, in
practice this approach has not been possible because
of many mathematical difficulties. Consequently,
workers have resorted to using several different
approximation techniques, further details of which
may be found in Durney's review (1980). Such
methods have provided accurate data on absorption
in the subresonant and near-resonant region, as
well as in the supraresonant or quasi-optical region.
These data have been compiled in tbeRad/ofrequency
Radiation Dosimetry Handbook (Durney et al. 1978,
pp. 75-106) in whole-body-averaged SAR vs.
frequency plots for many animal species. However,
under some conditions, there is a gap at the resonant
and immediate post-resonant regions, where these
approximations no longer hold. Using approximate
data derived from antenna theory and experimental
observations, investigators have bridged this gap with
the aid of curve-fitting techniques. This approach is
illustrated in Figure 3-11, which shows SAR data for
a prolate spheroidal model of man for the three basic
orientations of the model's long axis relative to the E,
3-16
-------
Figure 3-10.
6.0 cm
1650 MHz
E-Plane
ARD distribution in core of 6-cm radius
multilayered sphere at 1650 MHz (Weil 1975).
IS 170
-70,
H, and k vectors. Note the strong orientation effect
discussed earlier. Durney et al. (1978, 1979) have
also developed a useful empirical formulation that
describes the E-field polarization curve shown in
Figure 3-11. It can be programmed on a hand
calculator and yields reasonably accurate SAR data
for a prolate spheroidal model of any size of
eccentricity.
As discussed earlier, an isolated model, regardless of
shape, suspended in space is an inappropriate
representation of the real-life conditions under which
humans are exposed. A prolate spheroidal model in
contact with or in close proximity to a conductive
ground plane is an obvious improvement over the
isolated model. Iskander et al. (1979) have analyzed
such a model by both antenna and circuit theory. In
this model, the finite separation between feet and
ground created by the usual presence of footwear can
be accounted for by a lossy capacitor in the equivalent
electrical circuit of the prolate spheroid. From
Iskander's data (Figure 3-12), it is apparent that the
primary effect of the ground plane is to shift the SAR
curve for the isolated model to the left with only a
slight evident increase in peak SAR. The resonant
frequency of the prolate spheroidal model of man is
shifted from ~ 75 MHz to 45 MHz when the model is
in perfect contact with a conducting ground plane; the
intermediate case shown, in which resonance occurs
at 55 MHz, represents imperfect contact between
model and ground plane due to a 3-cm lossy gap. The
latter case is probably the most realistic of the three
considered. Iskander er al. also concluded that when
the model is separated from the ground plane by a gap
of 7.5 cm or more, the whole-body SAR values are
essentially the same as those for the isolated model
It is evident from oral presentations at recent (1978-
1980) scientific meetings that much effort is being
devoted to analyses of the absorption of prolate
spheroid and other models in the near field of an
antenna. Iskander et al. (1980) have studied such a
problem for a prolate spheroid model of man in the
near field of a short electric dipole at 27 MHz. They
found that average SAR values in the near field tend
to oscillate about the constant value predicted for
plane-wave irradiation. There are also significant
alterations in the internal distribution of deposited
energy in the near field.
As discussed previously, the data developed on
prolate spheroidal and ellipsoidal models have played
an important role in extrapolating RF absorption data
from lower animals to man. Yet these data have
limitations: the solutions are not exact but are
approximations, and yield data that are accurate
enough (±10 percent)for most practical applications.
Furthermore, with the exception of the subresonant
region (long-wavelength analysis. Figure 3-11),
existing solutions provide data on only the whole-
body absorption characteristics of this model. No data
are yet available on the three-dimensional ARD
distribution and EM "hot spot" formation potential in
the resonant and immediate supraresonant region.
Such data would be of potential value to those
engaged in experimentation with rodents because of
the close similarity between the rodent shape and the
prolate spheroid.
Human block models—Although prolate spheroidal
and ellipsoidal models are reasonably accurate
representations of many laboratory animals, partic-
ularly rodents, that is not true of the primates,
including man, because the appendages(head, arms,
and legs) are much larger and more significant. The
importance of these appendages is underscored by
experimentation on saline-filled dolls and scaled-
down human phantoms (Guy et al. 1977), which
showed relatively intense localized absorption in the
ankles, legs, and neck. Since it was impossible to
confirm the localized effects with the prolate
spheroidal model, attempts were made to develop a
more realistic human model in which numerous
cubical cells form a so-called block model of man
(Figure 3-13). The EM solution to this type of
sophisticated problem is realized through the solution
of a large system of simultaneous equations and
matrix inversion or iterative techniques. Further
mathematical details are given in Durney's review
(1980). Such solutions can be obtained only by use of
dedicated large-scale computing facilities with
expensive memory capability. Furthermore, because
of finite limits in the average memory capacity of all
but the largest computers, the number of cubical cells
3-/7
-------
Figure 3-11. Curve fitting of SA R data for a prolate spheroidal
model of man for the three basic orientations of
the model's long axis relative to the E, H, and k
vectors of an incident plane wave (1 mW/cm2
power density). Taken from Ourney et al. (1978).
10°H
Figure 3-12. Effect of a capacitive gap on average SAR
between the man model and the ground plane
(Iskander et al. 1979).
10-'
cc
W ID'2
S,
2
0)
10-3
H//r =
E//a
k//a
Long wavelength analysis
-«- EBCM
Empirical relation
Estimated values
• • Cylindrical model
-*—*• Geometrical optics
technique
10'
102 103 104
Frequency (MHz)
106
that can be used to make up the model is limited. The
accuracy and resolution of the solutions depend on
cell size. In the work of Chen and Guru (1977), a
maximum of 108 cells was used, whereas Hagmann
et al. (1979a) used 180 cells. These limits inevitably
reduce the spatial resolution with which the localized
absorption distribution can be determined in the
model, and they place an upper limit on the frequency
range over which solutions are valid. (This range does
include the resonant and immediate supraresonant
region.) Since this technique readily allows for
differences in the dielectric properties of individual
cells in the models, it is possible to approximate the
inhomogeneous tissue properties of the human body,
but there isa limit to howfinely such inhomogeneities
can be modeled.
Figure 3-14 shows some data obtained for the human
block model (Figure 3-13) when it stands on a ground
plane and is irradiated by a vertically polarized plane
wave. The curve labeled "whole body" gives the
whole-body-averaged SAR throughout the model,
IV
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1 io-i
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«
1
E
_o
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of 10-2
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-------
human and infrahuman heads (Rukspollmuang and
Chen 1979). The Hagmann er a/, data show strong
localized absorption at the front and back of the neck
and in the center-based region of the skull; localized
SAR values are two and four times the whole-body
average.
RF absorption in block models when irradiated under
near-field conditions is being studied by some
workers. Chatterjee et at. (1980) reported a study
involving the near-field interaction of the human
block model (Figure 3-13) with the measured
leakage-field distribution of an industrial RF heat
sealer operating at 27 MHz. Their data show that
averaged and localized SAR values are much lower
for near-field exposure than is the case for plane-
wave exposure at equivalent power density levels.
3.2.3.2 Accuracy
As discussed already, this document and the 1982
ANSI guideline (ANSI 1982) recommend frequency-
dependent exposure limits that have been derived
mostly from the EM modeling data just described. The
validity of this approach therefore depends strongly
on the accuracy of these data. One may conclude that
the accuracy of the whole-body-averaged absorption
data is good (certainly within ±10 percent). The good
agreement obtained between data for the human
prolate spheroidal and block models appears to
support this contention. However, the accuracy of the
localized absorption data is probably inferior. This is
particularly true of the block models where accuracy
is probably no better than ± 50 percent, because of
Figure 3-13. A realistic block model of man (Hagmann era/.
1979a).
the limitations on numbers of blocks available. On the
other hand, localized absorption data for the spherical
model, as well as those available for the prolate
spheroid, are more accurate, since they were derived
by more rigorous techniques.
3.2.3.3 Unresolved Issues
The need for additional modeling has been discussed
by Durney (1980). Improvements and refinements in
existing block models are needed, especially in spatial
resolution and accuracy; the same is also true in
modeling tissue inhomogeneities. In coming years, a
new generation of "superpower" computers with
greatly enhanced computational speeds—an order-
of-magnitude increase over existing machines—will
undoubtedly become available for scientific studies.
Such computers will almost certainly be used to
refine existing EM absorption models, particularly in
spatial resolution problems and in solving more
complex problems that hitherto have not been
attempted because of computer limitations.
As Durney (1980) emphasized, there is still a need
for more solutions to near-field interaction problems,
since the near field more frequently represents the
real-life situation to which people are exposed.
Though models involving near-field irradiation are
considerably more complex than are those for the far
field (plane wave), it should be possible to attempt the
solutions of these based on our existing knowledge of
plane-wave solutions.
3.2.4 Mechanisms of RF Interaction with
Biological Systems
Biophysical models that relate molecular structure to
the interaction of RF radiation with biological systems
provide a base for understanding the potential
hazards of this type of RF radiation and for designing
relevant experiments. The purpose of this section is to
review these interactions and, where possible, to
discuss the changes in structure and biological
function that may result.
3.2.4.1 Complex Relative Permittivity
The molecular-level interactions may be averaged
over a macroscopic biological sample and character-
ized by an average interaction parameter called the
complex relative permittivity (£*) of the sample. This
interaction parameter facilitates discussion of the
effects of a biological sample on thermodynamic
properties. It is a measure of the capacity of the
charge distribution within the sample to adjust to a
change in an applied electric field. This measure is
composed of two parts, the real component of the
complex permittivity ft') and the imaginary component
of the complex permittivity (f" = a/&>£0). The real
component is a measure of the energy stored in the
charge distribution of the sample by the interaction
with the field. The imaginary component is related to
3-19
-------
Figure 3-14. Absorption for man block model standing on ground plane (Gandhi et al. 1979).
Incident Power Density = 1 mW/crn*
102
Frequency, MHz
the energy dissipated by the field in the sample.
Initially, the dissipated energy may be restricted to
just a few molecular modes within the sample.
Eventually, the dissipated energy will be thermalized,
but temperature gradients may persist within the
sample if the rate of energy dissipation is a function of
position, due to the geometry of the sample or to field
gradients or differences in c" within the system.
Finally, after the RF-radiation exposure has ceased,
the dissipated energy will be equally distributed
throughout the various modes of the sample and will
result in either a change in sample temperature or a
transfer of thermal energy from the sample as well as
possible chemical and structural changes.
The r* of many biological tissues has been measured
by several investigators. Some excellent reviews are
available (Schwan 1957; Johnson and Guy 1972;
Durney et al. 1978, 1980; Stuchly and Stuchly 1980;
and Schwan and Foster 1980). Complex relative
permittivity is a function of frequency over our region
of interest.
Table 3-4 shows the values of e' and c" (abstracted
from Durney et al. 197^., Schwan and Foster 1980;
Stuchly and Stuchly 1980). The dielectric properties
of muscle tissue have been used to characterize the
dielectric properties of all biological tissues with a
high water content (Schwan 1957; Schwan and
Foster 1980). This characterization also serves as an
illustration of some of the underlying phenomena
responsible for f *. Figure 3-15 showsthec' of muscle
as a function of frequency.
It can be seen in Table 3-4 that in the region between
0.5 MHz (the lower end of the range of interest) and
~ 50 MHz, the complex permittivity of muscle
decreases by two orders of magnitude. However,
between 100 MHz and 10 GHz it decreases by < 50
percent; and again, at frequencies above ~ 10 GHz,
but still within the range of interest, the real
component of complex permittivity decreases rapidly.
The imaginary component of the complex permittivity
(O has two components—one due to the movement
of free charges, and the other to the orientation of
either permanent dipoles or dipoles resulting from
the interaction of the field with polarizable microscopic
structures. The former component is proportional to
the inverse of the applied RF-radiation frequency;
energy absorbed this way acts directly to heat the
sample. The modes of absorption of the latter
component relate to the specific structure of
biological molecules and molecular complexes, and
this component has a maximum where the real
3-20
-------
component of the complex permittivity £' is changing
most rapidly with respect to frequency.
Frequency regions with rapidly changing dielectric
parameters indicate that a particular component of
the system, or a particular type of response to the
field, is reaching the limit of its capacity to respond
(i.e., at higher frequencies the field is changing too
rapidly for a particular component to respond). It has
been suggested that the rapid change in the region
below 50 MHz results from polarization effects in
which cellular membranes are charged by the
surrounding electrolytes (Schwan and Foster 1980).
Another response that is limited to this low-
frequency range is the rotation of large dipolar
macromolecules or molecular complexes orienting
with the changing field (Takash'ima and Minikata
1975). The dielectric response below 50 MHz may
result from more than one mechanism. The response
above ~ 5 GHz results from the rotation of water
molecules in the biological systems, and it is similar
to the response seen in pure water. It has been
postulated that a small decrease in c' observed near 1
GHz results from rotation of water molecules
constrained by their interaction with large molecules
and molecular complexes (Schwan 1965; Grant et al.
1968) and, therefore, these water molecules cannot
respond to the field at higher frequencies.
The general features of c* of biological tissues can be
explained in terms of the major molecular and
structural components of the tissues. However,
biological systems are inhomogeneousand inherently
complex at the molecular level, and interaction with a
minor molecular component may have negligible
influence on the dielectric parameters of tissue (an
average property of a macroscopic volume) but may
interfere with the capacity of that minor component to
perform its biological function. Therefore, it is useful
to discuss the specific mechanisms for the absorption
of RF radiation at the molecular level. Furthermore,
since the mechanisms are similar for the major
Table 3-4. Dielectric Permittivities for Various Tissues*
components, this discussion also provides a more
detailed explanation of the interactions responsible
for the complex relative permittivity e*.
3.2.4.2 Mechanisms for RF-Radiation
Absorption at the Molecular Level
Table 3-5 presents information on the energy of an RF
beam relevant to molecular level interactions. The
binding energy of a single electron in a molecule is
typically of the order of tens of electron volts, whereas
excitations of electrons within molecules are of the
order of electron volts, and the energy of a hydrogen
bond is > 0.1 eV. Accordingly, direct linear mecha-
nisms for the absorption of a photon or a few photons
by biological molecules from an RF field cannot
involve changes in electronic or covalent molecular
structure, nor can they involve the breaking of
hydrogen bonds. That does not imply that single
photons cannot cause changes in the structure of
biological molecules or molecular complexes. They
Figure 3-16. The real component of the complex permittivity
of muscle (;') a* a function of frequency (f)
from the values for muscle (Schwan 1957).
4567
Log f (CPS)
8 9 10
Frequency
(MHz)
Tissue
Type
Muscle
Brain
Liver
Bone
Fat
Dielectric
Value
£'
f"
c'
f"
f'
t"
£'
c"
c'
f"
0.1
3 x 104
106
10"
5 x 10"
8.0
0.5
1
2 x 103
10"
2.6 x 103
1.5 x 103
5x 103
10
220
1.2 x 103
240
500
240
800
50
90
400
110
180
90
195
7.2
10.8
12
17
100
75
80
80
95
78
110
10
12
103
54
27
40
16.5
46
18
5.8
1.3
6.0
2.0
104 1.7X104
40 34
21 21
35
15
36
11
4.9
0.7
4.0
0.7
'These values are abstracted from reviews by Schwan and Foster (1980) and Stuchly and Stuchly (1980). The original sources are quoted
therein. The values have been chosen in the middle of the range for experimental values. Reported values may differ from one another by
as much as a factor of 2.
3-27
-------
contain sufficient energy to change the three-
dimensional structure of biological molecules in a
manner that leaves the covalent and hydrogen-
bonded structure intact. The following paragraphs
describe some of the excitations of biological
molecules that can be induced by an RF field and the
changes in three-dimensional molecular structure
that may result.
A change in the rotational energy of dipolar
molecules or molecular segments is a ubiquitous
mode for energy absorption from an RF field by
molecules in a biological system. The absorbing
molecular structure increases its angular momentum
by quantized units. The size of these units and the
characteristic frequencies for absorption depend on
the distribution of mass within that structure. In
general, the more massive the rotating structure, the
lower the characteristic frequencies.
The rotational mode of interaction is relevant through
the entire range of the frequencies of interest for the
purpose of this document. Free rotation of proteins
and other bipolymers are modes for absorption in the
frequency range from 10 kHz to 100 MHz and beyond.
In addition, smaller molecules and molecular
segments absorb at higher frequencies by this mode.
The absorption of energy into free rotational modes
does not lead to structural changes in the absorbing
molecule or segment because it rotates rigidly.
Through collisions with other molecules in the
biological system, this initial increase in rotational
kinetic energy is dispersed throughout the various
molecular motions of the system (i.e., the energy is
thermalized). With this mode of absorption, functional
changes, if any, result only from these local increases
in temperature. In a biological system at normal body
temperatures, an individual molecular species
absorbs over a broad frequency range by this mode
because of its concurrent interaction with other
molecules.
Since water, which has a characteristic frequency for
free rotation near 20 GHz, is the major component of
biological systems, a change in the rotational energy
of water molecules is the principal mechanism for
absorption of microwave radiation at frequencies > 2
GHz. (The frequency range for which this interaction
is likely to be important is broadened by the
interaction of absorbing molecules with surrounding
molecules.) At the lowest frequencies of interest,
changes in molecular rotational motion may also
make a significant contribution to the overall
dielectric properties through the interaction of
microwaves with large molecules.
For many biological molecules, segments as large as
many amino acids or as small as a methyl group have
some rotational freedom, but are constrained both by
covalent bond(s) to the main structure of the molecule
and by electrostatic interactions with other nearby
Table 3-5. Energy Units for RF Radiation
A f Energy-photon
(m) (MHz) (eV)
10*
1.24x10'
3x10"
10
3 x 102
3x 104
2 45 x 103
103
3x 10
1
1.2x 10 *
1 x 10's
4.1 x10"6
1.2x10'7
4.1 xlO'9
molecules. This rotational freedom provides a mode
for the absorption of energy from an RF field.
Although this mechanism is similar to the preceding
one, it has been suggested (Illinger 1970; Rabinowitz
1973) that it can result in changing the equilibrium
position of the rotating segment relative to the main
structure of the molecule and surrounding molecules.
This structural change is probably reversible but
could have consequences for biomolecular function.
The importance of this mechanism for a biological
effect of RF radiation has not been substantiated
experimentally.
More complicated intramolecular motional modes
involve rotation and vibration, bond stretching, and
twisting. These modes also absorb energy from an RF
field and have potentially similar effects on molecular
structure and function. In general, these more
complicated modes are at frequencies above the
range of interest, but there is some suggestion that
they are important near 10 GHz. Prohofsky et al.
(1979) have calculated the stretching modes for an
artificial double-stranded DNA polymer containing
one strand of adenine that is hydrogen bonded to a
strand containing only thymine. They suggest that
absorption of energy into these modes may affect
DNA helix melting and replication. The characteristic
frequencies of these calculated modes are, however,
> 40 GHz.
The amount, of energy required to excite either
rotational or the more complex motional modes is
small with respect to the amount of energy
exchanged in molecular collision at biological
temperatures. This implies that, unless there are
special circumstances (Illinger 1970; Rabinowitz
1973; Prohofsky et al. 1979; Ginzburg 1968), the
molecular configuration that results from the
absorption of energy from the RF field is not unusual.
However, the relative distribution of normally
occurring configurations may be affected by the
absorption of energy. The effect produced may be only
a relative change in a normally occurring process, and
may be reversible on the molecular level. However,
reversibility for the molecular-level absorber does not
imply that the resulting—if any—macroscopic
biological effect is reversible. If the unusual
distribution of states does not return to the normal
distribution as quickly as one would expect from
strictly thermal considerations, then these effects
will be much more important (Fermi et al. 1965).
3-22
-------
Another general mechanism for the interaction of RF
radiation with biological molecules results from the
field-induced migration of ions associated with
biopolymers. The migration may be of positively
charged ions—like protons or other cations—from
one negatively charged site to another within the
same biopolymer (Kirkwood and Schumaker 1952) or
from the polarization of the ionic cloud that surrounds
the biopolymers (Schwarz 1972). The distinction
between these two mechanisms has been made
because in the case of the former, the migration of the
ion(s) may directly affect the function of the
biopolymer if the migrating ion(s) or one of the sites is
directly involved in molecular function. In both cases,
there are effects on the long-range interaction
between biopolymers. The minimum field strength
needed for the first case can be roughly estimated
from the size and shape of biopolymers, and even for
rod-like structures, a field of at least 105 V/m would
be needed. For the second case, the field strength
necessary is smaller and depends on the size of the
surrounding ionic cloud. The frequencies at which
these processes are important depend on the size and
shape of the molecule (Pollak 1965). For sonically
fragmented DNA segments that have a rod-like
structure, broad absorption regions have been found
near 10 kHz and 10 MHz (Takashima 1963; Pollak
1965).
A mechanism has been described for the direct
influence of an RF-electric field on the configuration
of biopolymers (Schwarz 1967). If the interaction of
the field with one configuration of a biomolecular
system is much greater than the interaction with
other configurations, then—in the presence of that
field—a shift in the relative populations of the various
configurations results. The difference in interaction
energy may be due to differences in the dipole
moments or in the polarizabilities between configura-
tions. This mechanism has been demonstrated in the
model protein poly (x-benzyl-L-glutamate), or PBLG
(Schwarz and Seelig 1968). In its random-coil
conformation, PBLG has essentially no dipole
moment, whereas in its helical conformation it has a
large dipole moment (~ 103 Debye). The presence of a
field of sufficient strength can induce a transition
from the coil to the helical conformation, in PBLG this
mechanism is responsible for absorption of energy
near 1 MHz; for the distribution of conformations to
be affected significantly, the field must be greater
than 105 V/m. (If there were systems in which the
change in dipole moment was larger, then the field
needed would be proportionally smaller.(This change
in conformation is not unusual (although the relative
amounts of the two conformations are altered) or
irreversible, but, as previously stated, reversibility
on the molecular level does not necessarily imply that
any resulting, macroscopic, biological effect is
reversible. For instance, the conformations may have
differing biological activities, and the products of
these activities may remain even after the distribution
of the conformations has returned to equilibrium
3.2.4.3 Unresolved Issues
The mechanisms for trre absorption of energy from an
RF field previously discussed have been demonstrated
in solutions of biological molecules, and the response
of macroscopic biological systems to these fields is
consistent with these molecular mechanisms. The
question that remains is: Are any of these mechanisms
likely to impose a potential hazard to human health?
Certainly, if enough RF energy is absorbed and
converted to thermal energy, corresponding biological
effects ensue. Other mechanisms have been
proposed for effects at the molecular level. They
require changes in molecular structure and function
as the result of absorption. It is extremely likely that
some changes in biomolecular structure result when
RF energy is absorbed. But are these changes
functionally significant? Some mechanisms for
biological effects in these circumstances have been
proposed. They are plausible but often not quantitative,
and have not been demonstrated in biological
experiments. Further research to quantitate and
consider these mechanisms experimentally is
urgently needed. Since exposure to RF radiation often
leads to increased temperature, careful studies are
needed to separate effects that are not due to heating
from other concomitant changes in temperature.
Two other general mechanisms at the supramolecular
level need further discussion. A theoretical mechanism
has been proposed for coherent action over long
distances in biological macromolecular systems that
are far from thermal equilibrium (Frbhlich 1968). This
mechanism has been developed to explain the
extraordinarily high catalytic power of enzymes; one
of its consequences is an extremely long-range
interaction between macromolecules. The require-
ments of this model are that the macromolecules
possess a metastable excited state that has a large
dipole moment (> 103 Debye) and that its polar modes
couple with elastic modes. This highly dipolar
metastable state will be stabilized by the migration of
ions and by the structure of the water near the
macromolecular surface. One of the implications of
this model for enzyme action is that interaction with
an EM field that is capable of supplying energy above a
critical rate results in all of the energy going into a
single homogeneous electric vibration of this system
(Frolich 1975). This means that all the other modes
of the system are at or near thermal equilibrium, and
that single mode is far removed. Although it is
unlikely that this redistribution of energy will
increase the rate at which the energy is absorbed by
the system, the biological consequences of putting all
the energy into a single mode that is related to the
functional properties of the system could be
extraordinary. If that single mode relates to enzyme
function or recognition, it could greatly increase
3-23
-------
enzyme function until saturation is reached. The
possibility also exists of re-emission of large amounts
of energy and action at sites remote from the initial
absorber. The specific biological consequences of this
model relative to RF-field effects on biological
systems cannot be well understood until detailed
characteristics of particular biological systems are
included. Some data can be explained by this model
(Grundler et al. 1977); the resultant in vivo vibrational
spectral properties of biological systems also have
been discussed (Illinger 1982).
One of the interesting and relevant consequences of
Frohlich's (1968) model is that the particular
biological result of RF-field interaction with a
biological system may be frequency dependent. It has
been suggested that the range of frequencies where
this process is most likely to be significant is probably
> 30 GHz (Frbhlich 1968, 1975). The actual range of
applicability is uncertain. The effect also may be
important at lower frequencies.
Frohlich's mechanism is general. Its applicability in
real or model biological systems has not been
demonstrated. For potential biological effectsfromRF
fields, it is a possible mechanism for grouping
individual photons or phonons with energies « kT
(the average thermal energy). This process results in
the application of energy in a significant amount (>
kT) at a single locus. Effects resulting from this
process could not be duplicated by addition of the
same amount of energy to the system by a different
process.
Another set of mechanisms at the supramolecular
level has been proposed recently. These mechanisms
are theoretical means for the direct interaction of RF
fields with microscopic biological processes that
depend on naturally occurring electric potentials. In
general, these mechanisms depend on a nonlinear
response to an applied field by the cell membrane.
Barnes and Hu (1977) have proposed that the ion
gradient across a cell membrane can be altered
significantly if PW radiation at 105 V/m peak field
strength or more is applied. This theoretical view
derives from consideration of the balance between
field-driven and thermal currents. Changes in the
time-averaged concentration gradient occur that
depend on the square of the field applied across the
membrane, but not on the frequency of the applied
field. There are larger terms that are frequency
dependent but when averaged over a complete cycle
are zero. This mechanism has not been demonstrated
in a biological system.
Pickard and Rosenbaum (1978) considered a similar
problem and came to the same conclusion for the
time-averaged concentration gradient across the
membrane. In their model, they included unidirec-
tional ion channels through the membrane, and they
postulated that the new concentration gradient is
achieved by the field-induced movement of ions
through these channels. They calculated that, for this
particular method of achieving the concentration
gradient, the frequency of the field must be < 200
MHz if the ions are protons, and < 10 MHz for less
mobile ions. Pickard and Barsoum (1981) have
demonstrated activity across the membrane of a plant
cell that begins at the onset of an RF field greater than
667 V/m with a frequency below 10 MHz. The
immediate response to the field indicates that the
activity is not thermally induced. The activity
demonstrated is consistent with an RF-induced DC
potential across the membrane. This potential could
result from any nonlinear response of the membrane
to the RF field, and it is not clear that any particular
mechanism for that response has been demonstrated.
More data are needed to demonstrate a realistic
microscopic model for this process. It is difficult to
proceed from these mathematical models and this
single experimental demonstration to an assessment
of the importance of this mechanism. The induction of
DC or extra-low-frequency potentials in biological
systems by an RF field could provide significant
mechanisms for the biological effects of RF radiation.
3-24
-------
3.3 Experimental Methods
Claude M. Weil
Joseph S. AH
3.3.1 Exposure Methods Used in Biological
Experimentation
In this section the most commonly used exposure
methods employed in RF biological effects research
are reviewed, and the inherent advantages and
disadvantages of each are discussed. Researchers
have used a diversity of exposure methods; the
chosen method depends on the specialized application
involved, the existing facilities available for experi-
mentation, and the cost of setting up new facilities.
This diversity may have created difficulties in
reproducing biological effects studies, which have, in
turn, fueled controversies on several reported
effects. Whereas an effect may have been noted by
one group who employed a particular form of
exposure system, a second group that carefully
reproduced the experiment in every detail but for the
exposure method might not see the reported effects.
It is possible that basic differences in the exposure
environment may, in some cases, explain this lack of
reproducibility.
In much of the literature, effects have been traditionally
reported as a function of incident power density, the
independent variable. As pointed out by several
prominent workers (King et al. 1970; Johnson 1975),
power density is an inadequate and inappropriate
independent variable for two reasons:
1) Biological effects are logically related to the
internal electric and magnetic fields which are in
turn nonlinear and complex functions of frequency
vs. body size, body shape, and orientation to field
vectors, etc. (See Sec. 3.2, RF Field Interactions
with Biological Systems.)
2) Although meaningful for certain plane-wave-
exposure situations, such as free-field or
transverse electromagnetic (TEM)-mode cells, the
power density concept is no longer applicable in
most other commonly used exposure systems
with complex irradiation fields. Consequently,
meaningful comparisons of the incident field
levels in different types of exposure systems
cannot be made on this basis.
For these reasons, it must be concluded that the
various exposure methods are unique; experimental
results obtained in different exposure environments
cannot be compared except perhaps on a whole-
body-averaged SAR basis, and reproducibility of
experimental data is not guaranteed unless exactly
the same exposure methodology has been used. Even
if equivalency of whole-body-averaged SAR is
achieved, there may still be differences in biological
outcomes for exposures performed in multipath fields
(e.g., a cavity) when compared to plane-wave fields,
which have the same carrier frequency and
modulation parameters.
Although many of the specialized requirements of a
particular experiment are unique, some requirements
are common to almost all experiments. For example,
there is a critical need in virtually all work for
temperature and humidity regulation of the environ-
ment in which animals, biological specimens, etc.,
are located. Such control ensures that the ambient air
temperature and humidity are properly controlled, so
that the possibility of unwanted variability in the
experimental protocol is minimized. Also, airflow is
an important variable, particularly in animal studies
that should be regulated and reported. Two other
important requirements are common to the majority
of experiments involving whole-body or unrestricted
irradiation of animals: (1) an animal population large
enough to allow for statistically reliable conclusions
to be drawn, and (2) an equally large population of
control animals that must be housed during exposure
periods under conditions that are, in every way,
virtually identical to those of irradiated animals
exeept for the presence of RF energy. For certain
critical experiments, there may also be a need for a
population of passive or reference control animals
that are maintained under normal conditions in their
vivarium during the tenure of a study. Much of the
early experimental work on RF biological effects
frequently contained no provision for controls,
involved inadequate numbers of experimental
subjects, and lacked adequate provision for environ-
mental control, and thus yielded data of questionable
validity. It is only within the past decade or so that
researchers have succeeded in correcting most of
these experimental deficiencies in exposure protocol.
Existing exposure methods have been reviewed by
Weil (1977) and Ho et al. (1976); the latter paper
discusses exposure techniques that have been used
at the FDA's Bureau of Radiological Health. The
commonly used methods are categorized into two
groups and considered separately: (1) free-field, and
(2) enclosed. In the former category, the exposure
fields are generated within a reflection-free
environment by a radiating antenna or applicator,
whereas in the latter category, the exposure fields are
those excited within a struture of reflective or
conducting walls.
3.3.1.1 Free Field
Free-field exposure methods were historically the
first to be used in such experimentation and remain
the most commonly used techniques. These methods
involve placing the experimental subject(s) in the
near-field or far-field region of a radiating antenna,
3-25
-------
such as a horn, parabolic dish, or diathermy
applicator. For exposures in the far-field region, all
unwanted scattering of RF energy from the surround-
ing room structure, etc., must be eliminated.
Otherwise, the power density levels at the subject's
location are not well established. A microwave-
absorbing material that wholly or partially surrounds
the experimental subjects must be used to create
what is termed an anechoic chamber. (The term
a jnuic," meaning "without echoes," has been
borrowed from acoustics research.) The design of
anechoic chambers is a specialized art normally
performed by commercial manufacturers of absorbing
material (e.g., Emerson and Cuming, Canton, Mass.).
The anechoic properties of such chambers, which are
defined by the characteristics of the "quiet zone"
where the experimental subjects are placed, is a
function of the reflective properties of the absorbing
material with which the chamber is lined. (Such
properties refer to the degree with which RF energy is
reflected by the material, rather than absorbed.)
Reflectivity is proportional to the incident wavelength,
so that the performance of an anechoic chamber
deteriorates as the frequency of operation is lowered.
A minimum reflectivity of 20 dB (1 percent) is usually
considered essential; the frequency at which this
value is reached then defines the lower frequency
limit of operation for the chamber. Anechoic
chambers perform well at frequencies in the
microwave region of the spectrum (above 500 MHz).
However, satisfactory performance at lower frequen-
cies or longer wavelengths requires using large
blocks of absorbing material formed into long
pyramids or cones. Consequently, a large structure is
needed to house such a chamber, so that the cost of
such a facility rapidly escalates to the point of
nonfeasibility. For all intents and purposes, it is
impractical to contemplate building anechoic
facilities that operate at frequencies below ~ 250
MHz.
Some of the most extensive anechoic chamber
facilities devoted to RF biological effects work are to
be found at the Department of Microwave Research
of the Walter Reed Army Institute of Research, Silver
Spring, Md. Similar conventional anechoic facilities
are found elsewhere; e.g., at the Bureau of
Radiological Health in Rockville, Md. at the U.S.
Environmental Protection Agency in Research
Triangle Park, N.C. (Figures 3-16 and 3-17), at the
U.S. Air Force School of Aerospace Medicine in San
Antonio, Tex., and at the Universities of Pennsylvania,
Utah, and Washington.
The principal advantages—applicable to exposures in
only the far-field zone of an antenna—of the free-field
exposure method are:
• The incident power density to which the subject is
exposed can be well defined to an accuracy of ±1
dB (±20 percent) or less. This makes replication of
experiments performed under free-field conditions
fairly straightforward.
Depending on the directionality of the radiating
antenna, the exposure area where the irradiated
subjects are placed is large, and the irradiation is
nearly uniform (±10 percent or less).
The principal disadvantages of free-field exposure
methods are:
• The facilities are costly and often require
extensive floor space.
• Very-high-power RF sources are needed to obtain
the necessary power density levels. Consequently,
many free-field facilities employed in bioeffects
research operate on either of two ISM frequency
Figure 3-16. EPA 2450-MHz anechoic chamber facility, or
2.45-GHz far-field exposure facility. Horn
antenna (top), temperature control chamber
(center), and one air duct (bottom left) are
visible in the shielded anechoic room (Blackman
or a/. 1975. Elder and Ali 1975).
3-26
-------
Figure 3-17. EPA 2450-MHz anechoic chamber facility: Diagram of the microwave exposure facility (Blackman eta/. 1975; Elder
and AH 1975)
Command Signal Power Command __
i
Microwave
Microwave Power Sense Power
Data
Acquisition
System
I
Controller Control and Sense Lines
Varian
Microwave
Generator
2450 MHz
3.0 kW CW
Microwave Power Sense
y
Parameter i^
Commands^ fm,mn r, Air In IX
Control ""j^
Package Air Out 1
Environmental '
—• Parameter ^_____^__
Sense '
I '
~w,,\
~ ' /
^ Animal /
^Exposure ^
Chamber^
Physiological Data
1
l^\
\
1
1
1
_l
Anechoic
Chamber
3 m Long
3 m Wide
4.5 m High
assignments used for microwave heating, 2450
MHz or 915 MHz, where high-power sources are
commercially available at relatively low cost. It is
for this reason, as well as the explosive growth in
the use of microwave sources at ISM frequencies
(e.g., microwave ovens and hyperthermia treat-
ment devices) and the resulting potential for
exposure of significant portions of the population,
that 2450 MHz has become an important
frequency for bioeffects research.
Free-field systems are an excellent simulation of
the idealized exposure concept visualized in many
protection standards, but these systems do not
represent the real-life exposure situation en-
countered by humans.
The whole-body-averaged SAP cannot be mea-
sured directly in a free-field situation. Reasonably
accurate estimates of the SAP can be made by
calorimetric measurements on animal carcasses.
(See Sec. 3.4, Dosimetric Methods.)
Georgia Institute of Technology developed several
such techniques. One employs the absorber-lined
horn antenna, which enables a subject to be placed
much closer to the horn aperture than is the case with
a conventional horn and yet to remain within the far-
field zone of the radiator, so that a source of lower
power can be used to create the same power density
at the irradiated subject. One of these absorber-lined
horns has been used for several years at the National
Institute of Environmental Health Sciences in
Research Triangle Park, N.C. (Figure 3-18). Another
technique involves the compact range (Figure 3-19),
which uses a feed horn to irradiate a large parabolic
reflector. The test subject is exposed in the collimated
beam region of the reflector. The advantage of this
system is that it creates a much larger test volume of
nearly uniform field intensity with associated
decrease in the anechoic facility size, as well as
reduced requirements for absorbing materials. The
compact-range technique is used at the Naval
Aerospace Medical Research facility in Pensacola,
Fla.
Various attempts have been made to modify
conventional free-field exposure methods to amelio-
rate the cost and space problems associated with
them. A study (Bassett et al. 1971) performed at the
As discussed earlier, a critical need in whole-body
exposure of animals is to expose large numbers of
animals. Consequently, in many experiments,
unrestrained animals have frequently been placed
3-27
-------
Figure 3-18. Diagram of absorber-lined horn (Bassett et al. 1971).
RF Absorbing
Material
Section A-A'
-•- A
26"
26"
L,
inside an anechoic chamber in a closely spaced
matrix for simultaneous exposure. This practice tends
to obviate the principal advantage of free-field
exposure methods, because the power density to
which the animal is exposed can no longer be
accurately defined due to RF-energy scatter from one
animal to another. The degree of scatter depends on
much the same factors as absorption (see Sec. 3.2.1)
and varies randomly as the animals constantly alter
their relative posture and orientation. Interanimal
scatter is most serious when the frequency of
exposure lies in the resonant and supraresonant
region. Several solutions to this problem have been
devised:
(a) sequential exposures of single animals in the
same free-field facility
(b) miniature anechoic chambers for exposing
animals individually
(c) separating the restrained animals so that they are
spaced one or more wavelengths apart
Figure 3-19. Diagram of a point-source compact range (Bassett et al. 1971).
Reflector
3-28
-------
The first solution is obviously costly and time-
consuming, and may not be acceptable in certain
critical biological experiments requiring all animals to
be exposed at exactly the same age or the same time
of day, etc. The second solution has been advanced by
Guy (1979) at the University of Washington in
Seattle. He has described a system of 16 miniature
anechoic chambers designed for chronic low-level (<
10 mW/cm2) exposure of rabbits and rodents at 2450
MHz; eight of these chambers are energized, and the
other eight serve as control chambers (Figure 3-20). A
similar chamber has been constructed at EPA (Figure
3-21). Such a system has, of course, the advantage of
ensuring total RF isolation between animals and,
although costly, it may be more economical in cost
and power requirements than is the conventional
anechoic chamber.
The third solution has been tried by a few workers and
appears to be a reasonable compromise between the
conflicting requirements of adequate isolation and
low cost. Oliva and Catravas (1977) have described a
method for simultaneously exposing 10 animals in a
conventional anechoic chamber with minimal field
interaction between animals (Figure 3-22). The
animal cages are located on the antenna beam's
three-dimensional contour of constant power
density, with cages separated by ~ 2.5 wavelengths
at 2450 MHz. The authors claim that the average
variation of power density from one cage location to
another does not exceed ±5 percent. The major
disadvantage of this technique is that its implementa-
tion may require a large exposure volume, which, in
turn, creates costly problems of ensuring satisfactory
environmental control. D'Andrea et al. (1979, 1980)
at the University of Utah have developed an alternate
method involving a monopole radiator on a vertical
ground plane. The animals are located next to the
ground plane on a circular locus that is centered at
the monopole (Figure 3-23). Each circular array
contains 10 animals that are separated by ~ 5.5
wavelengths at 2450MHz, and by 2.1 wavelengths at
915 MHz. This system offers the advantage of
reducing both space and RF-power requirements.
Furthermore, the presence of a ground plane makes
this system more representative of the real-life
exposure situation for humans. On the other hand,
the exposure characteristics of this system may not
be comparable to a conventional anechoic chamber
facility, so that caution is needed when data are
compared.
For situations involving the exposures of only one
subject at greatly increased power density values,
D'Andrea et al. (1977) and Hagmann and Gandhi
(1979) have discussed a modification of this system in
which a corner reflector is placed behind the
monopole. By placing the subject 1.5 wavelengths
from the corner point, one can get an SAR
enhancement of more than 20 times that obtained
without the reflector.
3.3.1.2 Enclosed Systems
Enclosed exposure systems are those in which the
EM fields are contained within a conducting
structure. They fall into two basic subcategories,
which are considered separately: (a) transmission-
line systems, and (b) cavity systems. The principal
advantages of enclosed systems are as follows:
• By suitable monitoring of the incident, reflected,
and transmitted power in the exposure system,
more accurate SAR estimates can be made for the
exposed subject than is possible in free-field
facilities. The accuracy in estimating SAR
depends in part on how much base-line power loss
there is for the unloaded system and to what
extent it is affected by the presence of the exposed
subject.
• The cost and space requirements of such a system
are usually lower than those for free-field
methods, depending on the number of identical
systems needed. Also, much smaller and less
expensive power sources will suffice to establish
the same field intensities.
• Better control of RF absorption in the irradiated
subject is possible.
The principal disadvantages are as follows:
• With the exception of TEM-mode transmission
lines (to be explained), the fields are complex and
not plane-wave equivalent, so that comparison
with free-field data is more difficult.
• With the exception of multimodal systems (also to
be explained), the exposure space available inside
such systems is limited. Although the available
space may be adquate for small animals such as
rodents, it may not be possible to fit a rabbit or
monkey in it. Thus, the variety of species that can
be employed in an existing facility of the enclosed
type is restricted.
• The field distribution within the exposure system
is rarely as uniform as that found in a free-field
facility. The field distribution is well defined for
single or dominant mode operation, but undefined
for multiple-mode operation.
Enclosed systems have been the preferred exposure
method for samples, specimens, in vitro preparations,
3-23
-------
Figure 3-20. Miniature anechoic chamber facility (Guy 1979).
Tapered Radiation Chamber
Front View E-Plane
32.4
cm
11.43cm square
Muffin Fan
NARDA
644 Horn
2.0 cm sq Horn
Mount Centering ^26.6 cm"
Strip (Wood)
1375cm.
Distance from Horn
to SPY-12 Tips
Door
.Styrofoam Fastener
Floor
(Top View)
60.9
cm
Typ.
FXR
S601B
Adapter
0.32 cm
Tapered Radiation Chamber
Side View H-Plane
33.6 j r—t-4cm
H
All Aluminum
Strips and Angles
Assembled with
0.32 cm Pop Rivets
0 95cm Hardboard
Plywood
Plywood Horn Mount
(with 2 Alignment
Centering Strips) /
Sits on Chamber /
Separation Point
90.4 cm
016cmX
2.54 cm Alum Strips/
0.32 cm (0.125 in)
Hardboard
Door
75.5 cm X 60.9 cm
92.7 cm
2.54 cm X 7.6 cm X
20.3 cm Styrofoam
Brace Bonded to
AN-77 With
Silastic
Adhesive
5.08 cm square
0.95 Plywood
40W Candelabra Lamps
T\
26.6cm 4 each mounted 4cm
'From Each Edge
\ 0.95 cm
Plywood
Plywood Parts
Glued & Nailed
0.32cm (0.375 in)
Hardboard
AN-77 Absorber
5.08 cm (2.0 in)
1.27 cm (0.5 in)
Aluminum Angle
Square Air
Intake Hole
a) Construction details of tapered exposure
chamber.
1.27 cm Plywood
Plywood
b) Construction details of tapered exposure
chamber.
/2 Scale
-R = 10.32
Weaved
Nylon Line
c) Construction details of cage for housing
rat in tapered exposure chamber.
3-30
-------
Figure 3-21. Photograph of tapered exposure chamber at EPA facility.
3-31
-------
Figure 3-22. Facility for simultaneous exposure of 10 animals with minimal inter-animal interaction (Oliva and Catravas 1977).
0 4 S 6
r- -1.5
Meters
Feet
0 1
Distance from Antenna
. 13 14 15 16 17 18 19
_0_ Locus of Equal Power
Density (calculated)
L_l Cage on Tall Pedestal
EZ] Cage on Medium Pedestal
•• Cage on Short Pedestal
r
a) Locus of equal power density in the H plane through
the axis of the transmitting antenna.
- -1.0
- -0.5
- 0
-+0.5
-+1.0
—1-1.5
Meters
0
Meters L_
4
I
5
Feet
Distance from Antenna
01 13 14 15 16 17 18 19
—•— Locus of Equal Power Density
I I Cage on Antenna Axis
|~~j Cage Intermediate Distance
— from Antenna Axis
Hi Ca9e Furthest from Antenna Axis
+3S
+1 S
-11
0)
r+1-0
-+0.5
- 0
-3
Feet
L-1.0
Meters
b) Locus of equal power density in the E plane through the
axis of the transmitting antenna.
• s-gSfca-^jfisH
,i"55SiMykjMsiiasr-
• • • ?.<• 9. t'--". '. .
c) Multiple-animal array for equal power density
microwave irradiation.
3-32
-------
Figure 3-23. Monopole-over-ground plane irradiation facility
(D'Andrea et at. 1979. 1980).
Ground
Plane
Monopole
Antenna
Styrofoam
Mounts &
Rat Cage
Walk-On
Eccosorb
Pyramidal
Eccosorb
a) Representation of the microwave-exposure chamber.
Left Chamber
Mean mW/cm2
5.42 ± .21
Right Chamber
Mean mW/cm2
4.85 ± .27
SAR -mW/g
1.23 ±.25
(n = 3)
b) Distribution of power densities measured at each rat's location
within the Plexiglas holding cages for both sides of the
microwave exposure chamber in the absence of the rats
(2450 MHz).
etc., since these materials are small enough to fit
easily inside such systems. Many experiments have
been described, too numerous to survey here, in
which various types of waveguide, TEM-mode lines,
and cavities have been used to irradiate such
preparations. In recent years, some enclosed-type
systems have been specifically designed for
whole-body irradiation of animals. They are discussed
here in more detail. Because of the need to define
accurately the field level to which the animal is
exposed, dominant-mode operation of these devices
has been preferred over multimode operation.
However, dominant-mode operation puts an upper
limit on the frequency of operation, depending on the
size of the system needed to expose an experimental
animal. For example, most of the dominant-mode
enclosed systems that have been used to expose rats
operate at frequencies below 1000 MHz; for mice,
which require a smaller exposure volume, single-
mode operation to ~ 3000 MHz is possible. Since
free-field methods of exposure are largely impractical
at these lower frequencies, as discussed earlier,
enclosed systems do provide experimenters with
virtually the only practical and economical method of
exposing animals in the HF, VHP, and lower UHF
segments of the RF spectrum. A few large-scale
systems have been built to operate in the dominant
mode at HF and lower VHF frequencies; they are large
enough to accommodate a group of animals within
the exposure area, and the animal-to-animal
interaction problem is minimized because exposures
are conducted in the subresonant region where
interanimal scatter is minimal. However, at higher
frequencies such methods become impractical, and it
becomes necessary to provide an identical exposure
system for each animal to be irradiated. Each
exposure device is fed from a single high-power
source by a power dividing network. One of the basic
electrical problems associated with any enclosed
exposure system is that, when loaded, there is
considerable reflection of RF energy from the load,
which propagates via feed lines back to the RF power
source. This characteristic creates particular
problems for multiple systems fed by a single power
source because, without sufficient isolation between
each exposure device, energy is continuously
reflected from one system into the others and causes
unwanted fluctuations in the RF energy incident to
each system. These problems can be solved by
installation of isolators in each feed line to prevent
the reflected energy from reaching the dividing
network and the RF power source. The two categories
of enclosed system are discussed separately.
Transmission lines—In these systems, an EM wave
propagates down the line from source to termination.
When the line is terminated in its characteristic
impedance, only the outwardly propagating wave
exists with no reflected wave present. (The
characteristic impedance is a basic electrical
parameter that is defined by the line's configuration
and dimensions.) However, if the line is terminated in
a short circuit or an open circuit, all the energy is then
reflected at the line's termination. The two systems of
traveling waves together create a standing wave that
possesses successive maxima of electric and
magnetic fields (E and H, respectively) spaced a
quarter of a wavelength apart. (This property is a
useful feature that has been used by some workers to
3-33
-------
expose specimens or samples to isolated E or H fields,
depending on the location along the line.) The
characteristics of a shorted or open transmission line
are similar to those of the resonant cavity, and are
discussed below.
Transmission-line devices can be subcategorized into
TEM-mode or waveguide. In TEM-mode lines-
coaxial air lines, parallel-plate (strip) lines, etc.—the
dominant mode of operation is a propagating TEM
mode, provided the line is properly terminated in its
characteristic impedance. In TEM-mode operation the
E- and H-field vectors are mutually orthogonal, and
they lie only in the plane transverse to the direction of
wave propagation. The resulting fields are virtually
identical to those of a plane wave, so that it is possible
to simulate free-space conditions inside such lines,
provided that the exposed subject does not occupy
more than about a third of the line's cross-sectional
area. (If the one-third restriction is exceeded, ground-
plane effects are observed.) Because of its circular
cross section, the coaxial air line has been used only
with fluid or precut solid samples; the primary
application has usually been in making dielectric
measurements. A sophisticated coaxial air-line
system, designed to expose cell cultures to high field
strengths, has been described by Guy (1977) (Figure
3-24). Parallel-plate systems consisting of a
conductor located over a ground plane or between
two ground planes are better suited to animal
exposures since they provide a rectangular volume
where animals can be exposed. D'Andreaefa/. (1976)
have described a simple parallel-plate system used in
the range 200 to 500 MHz (Figure 3-25). This system
is equivalent to a large-scale version of a microstrip
line with air dielectric. Capacitive-plate devices,
which are equivalent to a short length of parallel plate
that is terminated in an open circuit, have been used
for exposing in vitro preparations to isolated electric
fields. This type of simple device has been incorporated
in a unique HF-band (10- to 40-MHz) exposure
system developed by the National Bureau of
Standards (Figure 3-26). Termed a near-field
synthesizer, it is capable of separate E- and H-field
excitation, the latter generated by special loop
inductors (Greene 1976). By altering the spatial
position of the loop with respect to the E vector and by
changing the phase relationship between the signals
exciting the plates and the loop, one can simulate the
complex field environment existing in the near field of
an HF source. Two of these systems are being used at
present: one is at the U.S. Afr Force School of
Aerospace Medicine, Tex., and the other at the
National Institute of Occupational Safety and Health
laboratory in Cincinnati, Ohio.
Triple-plate lines, in which a conductor is mounted
between two ground planes, have been used by a few
workers. These lines have the advantage of allowing
for simultaneous irradiation of two animals while
maintaining good isolation between them. In a more
popular version of this system, the open sides of the
structure are closed off with two side plates so thai the
center plate is entirely surrounded by a rectangular
ground structure. Such lines are commercially
available in different sizes (from Instruments for
Industry, Inc., Farmingdale. N.Y.) and have, been
termed "Crawford cells" by the manufacturer, after
M.L. Crawford (1974) of the National Bureau of
Standards, Boulder, Colo., (also available from Narda
Microwave Corp., Plainview, N.Y.). This author
prefers the term "rectangular strip line." In addition,
a few large-scale facilities of this type have been built
for various specialized exposure applications at
relatively long (^ 3 m) wavelengths. The largest is at
the Defence Research Establishment in Ottawa,
Canada, and is being used to measure human RF
absorption in the HF band. A smaller facility has been
used at the U.S. Air Force School of Aerospace
Medicine for exposing infrahuman primates and
phantoms to 10- to 50-MHz radiation (Allen et al.
1976). The U.S. Environmental Protection Agency
has also built a Crawford-type structure (Figure 3-27)
for exposing 20 rats to 100-MHz radiation.
The second category of transmission-line devices,
waveguides, cannot support the propagation of a TEM
mode so that the incident radiation is inevitably more
complex than that in a TEM-mode line. However, the
lack of a center conductor means that more exposure
space is available in waveguides than in the
corresponding TEM line. Multiple systems that use
commercial waveguide systems have not been
applied much for animal whole-body irradiation
because of high cost. Hoe? a/. (1973) have described a
single, environmentally controlled system employing
a standard S-band rectangular waveguide that has
been used in studies of mice at 2450 MHz. Ho et al.
(1976) have also described a system of six waveguides
fed from a common 2450-MHz source that provides
simultaneous irradiation of six mice. Besides cost,
another problem associated with using standard
waveguides for whole-body irradiation is the high
mismatch condition created by the presence of an
animal in the waveguide. As discussed earlier, this
necessitates the use of costly isolation circuitry. This
problem has, to a certain extent, been eliminated in a
specialized waveguide system developed by Guy and
Chou (1976) at the University of Washington in
Seattle. Guy's system is specifically tailored for
chronic whole-body irradiation of rats for extended
periods of time with known and reproducible
dosimetry. It consists of a number of 20-cm (8-in)
diameter circular waveguides (Figure 3-28), eco-
nomically constructed from galvanized wire mesh
and short lengths of brass tubing, in which a
circularly polarized TEn dominate mode is excited at
915 MHz. Figure 3-29 is a photograph of this type of
facility. The use of circular polarization (see Sec. 3.1,
3-34
-------
Figure 3-24. Coaxial air-line system for high power exposures of cell cultures (Guy 1977).
First Surface
Mirror —
Current Sensing
Probe
Thermograph
Constant Temperature
Liquid Source & Pump
• Culture Sample Holder
Voltage Sensing Probe
Vector Voltmeter or
Network Analyzer
Digital Voltmeter
Temperature Monitor
Directional
/ Coupler
Feedback
Loop
Incident
Power
a) Complete system for exposing cell cultures to EM fields.
Outlet
r-,
3
ecm |
r-,
)
twi V 1 Stainless fitael
vattti& Brass
Cross-Linked Styrene
b) Cross-sectional view of assembled transmission-line cell-culture sample holder and
heat exchanger. (A section of the outer conductor is machined to 7.70-cm ID so a
7.71-cm diameter dielectric support can be firmly locked into place after being pressed
in while the conductor is heated.)
3-55
-------
Figure 3-25. Parallel-plate (microstrip) exposure system (D'Andrea et al 1976).
Figure 3-26. Block diagram of the complete RF near-field synthesizer showing all principal components including RF power
sources.
Balanced
Feed
to Parallel
Plates
Lower
Plate
RF Power
Ampl.
No 1
Doubler
Ampl
No 1
Driver
No 1
Driver
No. 2
Doubler
No 2
RF Power
Ampl.
No 2
Common i
Oscillator
3-36
-------
Figure 3-27. EPA 100-MHz rectangular strip line or
Crawford cell.
Electromagnetic Field Theory) has two major
advantages:
1) The wide variations in absorption due to constant
changes in the animal's orientation are partially
reduced so that the energy coupled to the animal
load remains relatively constant. Note that.
whereas in a linearly polarized free-field of perfect
field uniformity, the average SAR can vary by — 5-
8 dB (~50 percent) at or near resonance, in this
system, the average variation of SAR does not
exceed —0.4 dB (~8 percent), even though the
incident field uniformity is far from constant
2) The hybrid coupler used to establish the circular
polarization in the waveguide provides a way to
isolate reflected from incident energy. One
achieves the isolation by dumping most of the
unwanted reflected energy into a load connected
to the hybrid, rather than allowing it to return
through the power dividing network to the source.
This technique effectively reduces the mismatch
normally encountered with loaded waveguides
(mean voltage standing wave ratio of less than
1.5:1) and permits parallel operation of multiple
units with less isolation circuitry.
Guy .er a/. (1979) have described a modifiction of this
waveguide system such that it operates in a
multimode field configuration at 2450 MHz. Though it
is difficult to define quantitatively the incident energy
levels in these units because of the complexity of the
fields, the absorption characteristics have been well
defined for rats of varying weights. An extensive
system of 100 of the$e units has been installed at
Guy's laboratory (Guy et at. 1980a) for conducting a
chronic radiation study in which rats will be
continuously irradiated over a 3-year life span. This
Figure 3-28. Physical details of the exposure chamber of the circularly polarized 915-MHz waveguide facility (Quy and Chou
1976).
RG 58
Cable
: 40.25cm 35cm j
Aperture for
Food Dispenser
63 Square
Mesh
Shorting Plate
11.1cm
Mount
Bolt
•HH4 • . ' L '
±JJtJ.\|
^ 298cm j \
nq V
1.27cm Dia.
Tubing
7.23cm Long
20.32cm -t
Epoxy
Capsulate * x Hybrid
1.27cm Dia.
Tubing
3.8cm Long
2.5cm Long Section
8" Brass Tubing
3-37
-------
Figure 3-29. Exposure chamber with associated instrumentation for the 970-MHz circularly polarized waveguide facility at EPA.
study underlines a major advantage of Guy's
waveguide systems, animal subjects are able to live
continuously in their exposure system with minimal
disturbance to their normal living patterns and
without artifactual perturbation. Consequently, the
system is ideal for the kind of chronic, long-term
studies that are now being emphasized.
Cavities—The resonant cavity, which is the microwave
analog of the lumped-element tuned circuit, consists
of a cylindrical, rectangular, or square box with
conductive walls. By suitable means, a system of
standing waves may be excited within the cavity. By
adjusting the cavity dimensions, the system can be
made to resonate at the frequency of excitation, such
that intense field levels are created within the cavity.
The use of the resonant cavity as an exposure device
has both a major advantage and disadvantage. A
cavity system represents the most efficient way to
couple RF energy into a subject per watt of input
power; this coupling constitutes its principal
advantage. The primary disadvantage is that the field
structure within a resonant cavity is probably the
most complex to be found in any exposure device.
Although some researchers have argued that the
field structure within a resonant cavity, particularly
when operated multimodally, is a good simulation of
the complex multipath environment in which humans
are often exposed, it is unlikely that the human
exposure environment ever approaches this level of
complexity. For the reasons already discussed, the
field complexity existing within a cavity makes it
difficult to compare experimental data obtained in a
particular cavity with those obtained in free-field
exposures or even another cavity. Indeed, there are
some basic differences between a free-field exposure
system and a resonant cavity. For a resonant cavity
3-35
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that is empty (unloaded), or that contains a biological
load small in comparison to the cavity's volume
(minimal loading), the fields in the cavity are in a
standing-wave condition and do not propagate; the
energy within is only stored. When the loading is
greater (i.e., when the exposed subject occupies an
appreciable fraction of the cavity's volume) the fields
are hybrid, containing both stored and propagating
energy. Because the fields are in a standing-wave
pattern, minimally loaded cavities are useful for
simulating a quasi-static interaction in which object
size is small relative to wavelength (i.e., a long-
wavelength type exposure). This characteristic has
been used by Guy et al. (1976), who designed a large
rectangular cavity that could be excited either
separately or jointly in the TMno or TEioz modes at
frequencies of ~ 147 MHz (Figure 3-30). This system
has been used to study absorption distributions in
scaled-down phantom models of man independently
exposed to electric or magnetic fields, depending on
the mode of excitation. Single-mode circular cavities
have also been used by Edwards and Ho (1975) for
exposing the head of a monkey at 385 MHz. Guy and
Korbel (1972) have discussed the dosimetric aspects
of a rectangular cavity used to multiply expose rats at
500 MHz and have sought to emphasize some of the
problems associated with cavity exposure systems.
Recently, Spiegel et al. (1980b) described an
interesting variable-volume cavity that contains
movable walls such that the cavity can be tuned
across a wide frequency range. The system is capable
of simultaneously exciting two independent cavity
modes and can be used to synthesize complex EM
fields.
Multimodal cavities, such as microwave ovens, have
been used frequently for experimental purposes
because of ready availability and modest cost
(Justesen et al. 1971). Where ovens have been used,
they have been extensively modified to achieve the
experimenter's objectives. Multimodal cavities have
often been preferred over single-mode types because
of the larger exposure volume available and the more
uniform field distribution. The latter is achieved by a
mode stirrer that helps average out the field
variations within the cavity. The degree of field
uniformity achieved in these devices seems to
depend greatly on its design. Heynick et al. (1977)
have described a multimodal cubical cavity suitable
for irradiating nonhuman primates at 2.45 GHz
(Figure 3-31). Each unit possesses its own regulated
power source. Twelve of these units have been used
at SRI International, Menlo Park, Calif., for chronic
irradiation of a group of squirrel monkeys as part of an
EPA-sponsored project. Each cavity housed two
animals plus offspring.
3.3.1.3 Conclusions and Unresolved Issues
Diverse exposure methods are used in biological
effects experimentation, most of which differ
considerably in their field characteristics. Since each
has its own particular advantages and disadvantages,
the choice of which system to use has depended
on the application. For experiments involving whole-
body irradiation of animals, some kind of standardized
method of exposure on which most researchers can
agree is needed. Although such ideas have been
proposed and discussed in the past, they are difficult
Figure 3-30. VHF resonant cavity facility (Guy ef al. 1976)
Exposure Chamber
2.58m
a) Exposure of phantom scale model of man in a resonant cavity.
b) Block diagram of resonant cavity driving system.
3-39
-------
Figure 3-31. SRI multimodal cavity facility for primate irradiation (Heynick at al. 1977).
a) Microwave cavity with door open, showing mode
stirrer, iris, radiopaque windows, and waste-
collection tray.
to implement because many exposure requirements
are conflicting, and, therefore, no one exposure
system can satisfy all of the various requirements.
However, some agreement on standardization should
make experiments more readily replicable and effects
more readily confirmed. Further efforts are needed to
this end.
During the past decade, there has been significant
improvement in the exposure facilities available for
biological experimentation. Many of these facilities
have succeeded in overcoming the deficiencies
inherent in many of the older exposure devices.
Exposure systems specifically designed for chronic
irradiation studies must also be developed further,
particularly to reduce their cost without significant
sacrifice in performance.
Also seriously needed are further studies that
compare absorption and biological end points for
different forms of exposure. This problem can be
summarized as follows: For the same experiment
performed in different exposure systems involving
plane-wave, complex, or multi-path fields, are there
differences in biological outcomes even where the
same whole-body-averaged SAR is maintained
throughout?
b) Dielectric cage.
3.3.2 Animal Holders
Any experimental irradiation of nonanesthetized
animals requires use of some form of holder or
restrainer to keep the animal in a location of known
field strength or power density. For multiple animal
exposures, it is also necessary to keep the animals
separated from each other. From a dosimetric point of
view, the optimal exposure condition is one in which
the animal is constrained in one orientation and
posture. This way, both whole body and regional
dosimetry could be determined with satisfactory
precision. However, complete restraint of an animal
is considered by most biologists an excessive stress
and, therefore, unacceptable. Consequently, the
commonly accepted exposure environment represents
a reasonable compromise between these conflicting
demands: the holder is designed to restrain the
animal, allow it to change posture and orientation,
and also allow for a small degree of lateral and
vertical movement.
3.3.2.1 Perturbation by Restrainers
One of the important criteria in designing animal
holders is that they be constructed of materials that
3-40
-------
cause the least perturbation of incident fields
possible. What that means is that cages can be built
only from nonmetallic materials. Various types of
low-loss dielectric materials are available in rigid and
semirigid form, and have been the material of choice.
The most popular has been acrylic plastic (polymethyl
methacrylate), because of its optical transparency,
superior mechanical strength, and ease of machining.
Some experimental and analytical studies have been
performed to determine the degree to which these
materials perturb the incident field (Weil 1974; Lin et
al. 1977). These studies showed that, under certain
conditions, these materials can indeed cause
serious field perturbations, so that the real power
density of the field to which the animal is exposed is
not known precisely. Use of foamed polystyrene
instead of acrylic is a possible solution. Foamed
polystyrene has a relative permittivity value close to
unity and creates only minimal field perturbation.
However, two disadvantages are associated with
polystyrene materials: They are optically opaque, so
that animals cannot be observed in their cages; and
they are not strong and can be readily gnawed by
rodents. Coating the material with a substance to
which the rodents are averse, such as quinine, has
been tried by a few workers (Catravas 1976) to reduce
gnawing. However, this practice adds an unwanted
additional insult to the experimental subjects.
Nonetheless, foamed polystyrene is useful in studies
involving short-term exposures.
A more recent paper by Ho (1978) questioned the
significance of the incident-field perturbations
created by holders made of acrylic materials. In an
analytical study involving a two-dimensional model
that contained a cylinder of muscle-equivalent
material mounted concentrically inside an acrylic
cylinder. Ho showed that despite a significant
perturbation of the incident field in the empty holder,
there was relatively little perturbation in the whole-
body-averaged SAR and the SAR distribution inside
the muscle-equivalent cylinder when compared with
that which existed when no holder was present. Ho
concluded that large perturbations of the field created
by animal holders do not automatically create a
correspondingly large perturbation in the animal's
absorption rate because the presence of a mass of
lossy dielectric (i.e., the animal) tends greatly to damp
out the standing-wave patterns created by the acrylic
holder. Further experimental observations are
needed to confirm this conclusion.
As part of a behavioral investigation. Gage et al.
(1979) investigated the influence of two different
holders on the whole-body SAR of rats and mice at
2450 MHz. One holder was a cuboidal container
made of foamed polystyrene; the other was an acrylic
cylinder. They concluded that there was a significant
alteration of SAR values for both rats and mice due to
the presence of the acrylic cylinder when the animals
were oriented parallel to the E field. This effect was
considerably more pronounced in the mouse,
probably because 2450 MHz is a frequency close to
resonant absorption for the E-parallel orientation of
the mouse.
3.3.2.2 Feeding and Watering During Exposure
Experiments involving chronic, long-term RF
irradiation of animals usually require that some
arrangements for food and water be made during
irradiation. Provision of food does not present
difficulties if the standard form of dry food pellets fed
to laboratory animals is used, since these pellets
absorb little RF energy. However, providing drinking
water or liquid nutriment does present some
problems because water is a comparatively good
conductor and, therefore, absorbs energy. Two
methods of supplying water have been used; each
has problems.
In the first, the water reservoir is placed in the
exposure system with the animal. The major
disadvantage here is that, since the water supply is
located in a high-field-strength environment, it
absorbs RF energy and perturbs surrounding fields.
These factors create uncertainty in both dosimetric
and densitometric measurements. Furthermore, it is
conceivable that, if the field levels are intense
enough, the water temperture could rise until the
animal would refuse to drink. Consequently, this
approach is not recommended.
The second method involves placing the reservoir
outside the exposure system in a region of little or no
field strength, and supplying water to the animal via a
supply tube or pipe.This method is superior, but it too
has associated pitfalls which, without special
precautions, can introduce serious experimental
artifacts. As Guy and Chou (1976) have pointed out,
the water tube or pipe provides a conductive pathway
for microwave currents. When the animal attempts to
drink, a circuit is closed between the animal, which is
at high potential, and the water reservoir, which is at
zero or ground potential. RF currents then pass from
the animal to the watering system; because the
contact point area is small and involves sensitive
tissue, a high current density may exist in the
animal's tongue. Since the animal will find this
condition aversive, it will probably refuse to drink.
Therefore, the RF current flow through the water
supply system must be interrupted. Three methods of
interruption have been devised: (a) When the animal
interrupts a beam of light using a tongue-licking
operant, a small bolus of fluid is injected into the
animal's mouth (King et al. 1970); (b) the animal
holder is equipped with a small water trough which is
continuously supplied through a water drip system;
and (c) an RF-choke assembly is placed between the
animal and the water reservoir to effectively decouple
the animal from the water supply when drinking
(Figure 3-32). In the choke assembly design (applying
3-41
-------
Figure 3-32. Water-supply system for exposure chamber
(Guy and Chou 1976).
(3-13)
Metal
Walls
8 Ounce
Bottle
R, = 1.75cm
R, = .875
R3= .475
U = 1/2 (Co E2 + ,UoH2) = UE + UH
Exposure
Chamber
Wall
(Screen)
Contacting
Fingers
• Plastic
Cage Wall
4 mm
only to enclosed systems), water is supplied through
copper tubing that forms the center conductor of a
shorted quarter-wave section of a triaxial air line. To
prevent the animal from coming into contact with the
copper tubing, a short section of glass or acrylic
tubing is mounted at its tip. The choke assembly
effectively provides a high impedance at the point of
animal contact and thus reduces the RF current in the
watering system to near zero.
3.3.3 Densitometr/c Instrumentation
Densitometry is the measurement of RF-field
strength and is usually expressed in units of
equivalent plane-wave power denisty. Dosimetry is
the measurement of absorbed energy, or the rate of
energy absorption by some object in an RF field. In
this section, the relationships between the strength
or intensity of an RF field and a suitable and
measurable field variable are given. The question of
what constitutes a suitable variable has been
addressed (Bowman 1970). For a linearly polarized
plane-wave EM field in free space—and, for practical
purposes, in air—the following relationships exist
between the electric field, the magnetic field, the
power density, the electric energy density, and
the magnetic energy density:
(3-14)
(3-15)
(3-16)
= *„
H
(3-12)
where E = electric field, V/m
H = magnetic field, A/m
r7o = characteristic or intrinsic impedance of
free space, 377 Q
/t/0 = permeability of free space, H/m
c0 = permittivity of free space, F/m
W = power density, W/m2
U = total energy density, J/m3
UE = electric energy density, J/m3
UH = magnetic energy density, J/m3
The quantities /u0 and c0 are properties of the medium
and are scalar constants for free space. Equation 3-
1 2 therefore states that in free space the magnitudes
of E and H are related by a constant factor r)0. Equation
3-14 relates the power density W to individual field
components E and H for the basic plane wave.
Equation 3-15 is a general relationship for the total
energy density U of an RF field and defines the
individual electric- and magnetic-field energy densities
UE and UH.
The relationships between field variables for a plane
wave are simple, so that the measurement of any one
field parameter allows calculation of the others.
Although power density is a variable of interest in
biological effects studies, it is particularly difficult, if
not impossible, to measure directly because it is a
time-averaged vector cross product that, in general, is
not expressed as simply as Equation 3-14. However,
it may be indirectly evaluated for plane waves by
measurement of the E or H field, as indicated by
Equation 3-14. This measurement, when coverted to
units of power density (W/m2) by Equation 3-14, is
referred to as the "equivalent plane-wave power
density." Above 1 GHz, it is usually not necessary to
measure both the E and the H fields (Bowman 1 970),
whereas below ~ 300 MHz, the H field becomes
increasingly important, and an independent mea-
surement of H is necessary (Asian 1979; Lin et al.
1973).
However, power density is inappropriate in the
evaluation of near fields of antennas or fields near
reflecting surfaces because intense fields can exist in
these regions when the power density is low or even
zero. A plane wave normally incident on a conducting
surface can create standing waves with large E and H
values but very low power density. Since power
density is a measure of the power flow across a unit
area, the net power flow of a plane wave normally
incident on a conducting surface and reflecting back
3-42
-------
is zero (or small in practical cases), and hence the
power density is zero. The E and H fields in that case
would be in a standing-wave pattern with amplitudes
twice those of the fields of the incident wave.
In the near field of sources or for complex RF fields,
the E and H fields are not related by Equation 3-12;
however. Equation 3-15, which related the individual
E and H fields to their respective energy densities, is
always true. Therefore, measurements of both the E
and H fields are required to evaluate the total energy
density where Equation 3-12 does not apply.
Bowman (1970), Swicord (1971), and others have
described the desirable characteristics of an
instrument for quantifying hazardous EM fields. The
instrument and probe should (1) measure in terms of
energy density and respond only to the variable being
measured, (2) be small to permit a high degree of
spatial resolution and thus be useful in small
volumes, and (3) have an isotropic response and be
insensitive to field polarization. The probe should also
cause little scattering of the field and operate over a
broad frequency range. The instrument and probe
should be battery powered, lightweight, and rugged,
and should read either peak or average values and
have a dynamic range of at least 20 dB (one
hundredfold) without the need to change probes. The
readout instrument should be direct reading and free
from susceptibility to RF interference.
Many approaches have been used to develop field
probes that meet these criteria. The most successful
and enduring designs have centered around the thin-
film thermocouple or bolometer sensor/antenna and
the crystal detector/antenna. The first type of sensor is
a square-law-responding device that senses a
temperature change due to the absorption of energy.
The second type uses a semiconductor diode that
produces a voltage or current related to the strength
of a field variable. The diode can respond as either a
square-law detector or a linear detector, depending
on the region in which it is operating. Some
commercially available electric-field probes are
shown in Figure 3-33.
3.3.3.1 Electric-Field Probes
The NBS EDM-2 electric energy density meter
(Belsher 1975) was developed for accurate measure-
ment of occupational exposure to EM fields from 10 to
500 MHz. This probe uses three short orthogonal
dipoles terminated by crystal rectifiers to detect the
RF field, and produces an isotropic response within
±1 dB. The DC signal appearing on the diodes is
conducted to the meter's circuits through RF-
transparent high-resistance lines. The meter displays
electric energy density in units of microjoules per
cubic meter. Energy density was chosen as the field
variable to be displayed because of the ambiguity of
power density in the near field of radiating elements.
The meter has a dynamic range of 50dB in nine ranges
from 0.003 to 30 fjj/m3. Although the probe's
detector diodes are used in both the square-law and
linear regions, a square-law response is achieved
over most of the range by a varistor network. The
meter is calibrated at specific frequencies within the
FCC ISM bands at 13.56, 27.12, and40.68 MHz. The
frequency response is flat within ±1.0 dB over the 10-
to 500-MHz operating range. One of the improvements
in the EDM-2 device over previous designs is reduced
temperature-induced drift. The reduced drift is
achieved by loading of the dipole-detector diodes with
equivalent load diodes. This technique has reduced
the temperature response to < ±0.7 percent/°C in
the 15 to 35°C range. The field probe design provides
a rapid response time to permit observation of
the modulation of the field and the measurement of
peak values. The rise and fall times (10 to 90 percent
of the signal and 90 to 10 percent of the signal,
respectively) are both < 0.6 ms on the most sensitive
range.
A commercial version of the NBS electric-field probe
is marketed by Holaday lndustries(Edina, Minn.). This
field-strength meter (Model HI-3001) operates over
the frequency range 0.5 to 1000 MHz and is accurate
within ±1.0 dB over this range. The meter has an
isotropic response within ±1.0 dB and has peak-hold
and read circuitry to capture the highest reading
observed. The response time is 1.5 s. Measuring
range of the meter is 1 to 3160 V/m in six ranges on
an analog meter. An audible tone, with a pitch
proportional to the meter reading, is provided to
prevent operator overexposure in survey applications.
In 1980 the General Microwave Corporation (Farming-
dale, N.Y.) introduced the RAHAM Model 4A
radiation-hazard meter. This instrument is a
broadband crystal-detector design with a frequency
coverage of 200 kHz to 26 GHz, and a display
calibrated in units of equivalent plane-wave power
density that ranges from 0.001 to 20 mW/cm2. This
meter has an isotropic response, is battery powered,
and has a response time of 1.5 s.
For use in the near field, Rudge( 1970) constructed an
electric-field probe using two short crossed-dipole
antennas. This meter was designed to operate from
915 to 2450 MHz in proximity to RF emitters. The
probe detected the electric field in two perpendicular
planes, and was calibrated in power density terms.
Pudge carefully analyzed sources of error in the
design of near-field probes. His study included the
effects of field curvature and antenna backscatter,
particularly with regard to multiple coupling and
impedance variation, both of which affect the
calibration of the field probe. The major source of
scattering was the probe's antenna, particularly
when the lengths of the dipole wings were of the
order of one-fourth wavelength. The prototypal probe
achieved a dynamic range of 47 dB with a square-law
3-43
-------
Figure 3-33. Samples of commercially available survey meters for measuring RF electric-field strength. From left to right the units
shown are: The Narda Microwave Corporation Model 8315A meter with a Model 8321 isotropic probe: the General
Microwave Corporation Model 481A meter with a Model 81 probe; and the Holaday Industries, Inc., Model HI-3001
meter and probe.
response, by addition of fixed values of load
resistances at increasing power levels to keep the
detector diode operation in the square-law region.
Sensitivity was reported at 300 nW/cm2 with a probe
antenna of 8-mm overall dipole length.
Bassen et al. (1975) developed a miniature broadband
electric-field probe. Although the probe wasdesigned
for free-space operation, the ultimate goal was to
develop an implantable isotropic probe for biological
effects research (Bassen et al. 1977a). With 3-mm
dipole elements, the free-space probe achieved a
relatively flat frequency response over the range of
915 MHz to 10 GHz. After some refinements were
incorporated (Bassen 1977; Bassen et al. 1977b), the
probe was tested over a frequency range of 200 MHz
to 12 GHz. The improved version had a 30-dB
dynamic range with a 20-/uW/cm2 sensitivity,
isotropic response to ±2 dB, a detection bandwidth of
2 kHz, and a spatial resolution of ~ 3mm.
The requirement of small size was imposed on the
implantable-probe design to ensure minimal alteration
of the field when the probe is used relatively close to
sources and dielectric boundaries. At the same time,
the constraint of small dipole size has the further
advantage of extending the frequency response of the
probe into higher frequencies. With 3-mm dipoles,
theoretically, resonance should occur at 50 GHz. The
probe uses dipole elements terminated with three
zero-bias Schottky diodes for a maximal square-law
response, arranged in an 'T'-beam configuration.
High-impedance leads are connected to the diodes
and routed along the probe's body to an optical
telemeter. A fiber-optics cable then routes the
digitally encoded field-strength signal to a digital
receiver that is calibrated to display the equivalent
plane-wave power density. A commercial version of
the miniature field probe is marketed by Electronic
Instrumentation and Technology (Sterling, Va.).
An electric-field sensor (EPS) and readout system
capable of operating over the frequency range 10 kHz
to 200 MHz has been developed by Instruments for
Industry, Inc. (Farmingdale, N.Y.) and was described
by Ruggera (1976). The EFS-1, -2, and-3 are linearly
3-44
-------
polarized square-law electric field detectors with an
analog readout calibrated in volts per meter. The EFS-
1 is intended for CW fields, the EFS-2 for pulsed
fields, and the EFS-3 for both types of fields with the
addition of a peak-reading provision. The dynamic
range is 1 to 300 V/m with antennas of different
lengths. An optical transmitter is used when remote
readout is required, which eliminates field perturba-
tions introduced by metallic cable. An isotropic
monitor has also been designed (RHM series) that
essentially encloses three EPS-series sensors in one
box. Readings from each sensor can be summed (by
the square root of the sum of the squares of the field
strengths) to measure the total electric field, or a
particular sensor can be read directly when field
polarization is a variable of interest.
Another design of an electric-field probe uses thin-
film thermocouple arrays acting as both the dipole
antenna and the detection element. The dipole
elements are lossy; therefore, their temperature
increases proportionally with the square of the
tangential electric field. The dipole elements can be
thought of as the series connection of a large number
of tiny thermocouple dipoles. This detection method
provides true square-law response and produces
signals proportional to the average energy density of
the electric field in the measured volume.
The Narda Microwave Corporation (Plainview, N.Y.)
produces a wide selection of RF-radiation monitoring
instruments, such as the Model 8606 broadband
isotropic radiation monitor. This instrument uses
three orthogonal, thin-film thermocouple sensors that
respond to the square of the electric field. Two probes
are available that have the combined dynamic range
of 0.02 to 100 mW/cm2 over the frequency range 0.3
to 26 GHz. The probes have isotropic response within
±0.5 dB except when the electric field is aligned with
the handle axis. The General Microwave RAHAM
Model 3, another electric-field-sensitive meter
with thin-film thermocouple sensors, performs
comparably to the Narda 8606 system. The Narda
8100 series meters were designed earlier (Asian
1970) for measuring the leakage of microwave ovens,
dryers, and medical equipment, which operate at 915
and 2450 MHz. The probe used with the 8100 series
meters is not isotropic but must be oriented with the
probe handle perpendicular to the wavefront. Three
probes are used to measure across a dynamic range
of 0.02 to 200 mW/cm2. The probes contain two
orthogonal, thin-film vacuum-evaporated thermo-
couple elements that function both as antennas and
detectors. When the probes are used at 915 MHz, an
adapter is attached to the end of the probes, so that
the effective length of the dipoles is increased. This
increase in length compensates for the reduced
efficiency of the antenna at 915 MHz.
3.3.3.2 Magnetic-Field Probes
As discussed previously, measurement of only the
electric field for frequencies below — 300 MHz does
not fully characterize the hazard or heating potential
of an RF field, because the electric and magnetic
fields are not related by the free-space intrinsic
impedance at frequently encountered distances from
radiation sources. In the mid-1970's, NIOSH
supported an NBS effort to develop a magnetic-field
probe that would operate in the 10- to 300-MHz
band. Two probes were developed (Greene 1975a,b)
that consist of small single-turn, balanced loop
antennas 10 ancj 3.16 cm in diameter. The dynamic
ranges of the two probes are 0.5 to 5.0 A/m and 5.0
to 50 A/m, respectively. The probes are capable of
measuring the magnetic field within a few centi-
meters of an RF-radiation source, in the near field.
The loop antennas are constructed with two short
gaps; one gap is terminated with a silicon diode that
detects the induced RF voltage; the other gap is
terminated with a capacitor to bypass RF currents
without short-circuiting the DC output. The DC signal
is then transmitted over NBS-developed conducting
plastic lines to an electrometer voltmeter. One of the
inherent problems of loop antennas is that the
response is proportional to frequency, which makes
these antennas particularly sensitive to errors if
harmonics (integral multiples of the fundamental
frequency) are present in the field under study.
Greene also shows that both the electric-dipole
response of the loop and the partial-resonance effect
increase with frequency. An experimental method is
provided to minimize the error due to electric-field
sensitivity, and plots are provided for the two probes
to indicate worst-case measurement error vs.
frequency due to the electric-dipole response. The
self-resonant frequencies of the two loops were
computed to be 280 and 760 MHz for the 10- and
3.16-cm loops, respectively, and a correction curve
was provided to estimate the increase in response
due to this effect.
Asian (1976) reported the development of a
magnetic-field-radiation monitor that has a frequency
response within ±1.0 dB over the frequency range of
10 to 200 MHz. Two probes, the Narda Corporation
Models 8631 and 8633, are used to provide a full-
scale measurement range of 0.2 to 100 mW/cm2.
(Sensitivity extends to 20/vW/cm2 on the Model 8631
probe.) These probes have an isotropic response
(±0.5 dB) and accept all polarizations. Each probe has
three orthogonal coils; each coil has two turns. The
coils are terminated with thin-film thermocouple
elements. High-resistance lines are used to route the
DC signal to a preamplifier in the handle of the
shielded probe, and the preamplifier output is con-
nected via shielded cable to an indicating meter. To
achieve a partial solution to the problems of
frequency dependence of loop antennas, the coils
3-45
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were designed to be series resonant slightly below
the low-frequency end of the operating band. The
response of the coils increases at frequencies above
200 MHz, as the electric-dipole effect begins to
govern the response.
Magnetic-field probes of various designs were
reviewed by Ruggera (1976); many were commer-
cially available and others were experimental.
Ruggera described electric-field-shielded loops
constructed with semirigid coaxial transmission line
from 2 to 6 cm in diameter. Ruggera also described an
isotropic, electric-field-shielded, three-loop, ortho-
gonal, magnetic-field probe that has a cross-polariza-
tion rejectivity of ~ 20 dB from 40 kHz to 50 MHz.
Signals from the probe are recovered with terminated,
coaxial cables. In addition, the author described a
three-axis, magnetic-field-measuring instrument
developed by Southwest Research Institute. The
original design was plagued by cable-pickup
problems, which limited the usable frequency to 50
MHz. Refinements by the FDA Bureau of Radiological
Health (BRH) that incorporated the optical telemetry
systems (see Sec. 3.3.3.1) used on the BRH miniature
electric-field probe led to a flatter frequency response
over the extended frequency range of 150 kHz to 150
MHz.
In 1981 Holaday Industries introduced a new
magnetic-field probe for their 3000 series of field-
strength meters. The Model STH-01 probe has a
frequency response of 5 to 300 MHz within ±2 dB.
The uniformity of response improves to ±1 dB over
the range of 10 to 200 MHz. When used with the Hl-
3001 meter (Sec. 3.3.3.1), full-scale sensitivity of the
probe is 0.1 A2/m2 in the low range and 1.0 A/m2 in
the high range. The sensor consists of three
orthogonal loops terminated with detector diodes
that rectify the RF voltages induced in the loops. The
sensors can withstand an 800-percent overload
above the full-scale field strength without damage.
3-46
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3.4 Dosimetric Methods
James B. Kinn
Dosimetric methods are used to determine where
and how much energy is absorbed by a biological
target. Two areas are considered: (1) whole-body
dosimetry, dealing with the integrated or spatially
averaged SAR for the entire animal; and (2) regional
dosimetry, dealing with the SARs or internal field
strengths in a specific site of the biological target.
3.4.1 Whole-Body Dosimetry
Whole-body dosimetry is based on either a power
difference or a calorimetric method. The power-
difference method is limited to closed exposure
systems such as waveguides, TEM-mode trans-
mission cells, and coaxial air lines. In this method,
power meters are attached to the exposure systems
by directional couplers to measure the incident,
reflected, and transmitted power through a section of
the closed system containing the biological target.
The power absorbed by the biological target is then
measured by subtracting the values of the reflected
and transmitted power from the incident power. In
the case of exposure systems using live animals, the
values of those three measurements vary as the
animals move, because absorption is a function of
the animal's orientation relative to field polarization.
What is needed is a data-collection system that can
integrate the measured power difference and then
determine an average over a period of time, usually
the exposure duration (Christman et at. 1974; Ho and
Edwards 1977b). The advantage of this method is
that it provides on-line instantaneous measurements
of absorbed power. A disadvantage is that its
optimum application is in single-animal exposure;
simultaneous exposures of multiple animals in the
same closed system would result in average dose
rate values for the group, rather than for an
individual animal. A second disadvantage is that,
under exposure conditions where the RF energy
absorption rate is very low, it may be impossible to
measure the power absorption, because the
measurement error in the power meter exceeds the
computed power difference.
Calorimetric methods use the thermalization of the
absorbed power as a measure of SAR. Under the tacit
assumption that all the RF energy absorbed by a
biological target is converted to heat, the calorimetric
method measures the heat added to the target. The
approach is to irradiate an animal carcass with a
short exposure at high power to reduce heat loss
errors due to conduction and convection during the
exposure. The thermalized energy added to the
carcass is measured with the calorimeter. Calories
per unit time per unit mass are then converted to
W/kg, the SAR for the high incident power density.
The SAR for any other power density is then scaled
from this measured value in direct proportion to the
ratio of power densities. Three calorimetric methods
that have been used in whole body dosimetry are
gradient-layer calorimetry (Gandhi et al. 1979),
Dewar-flask calorimetry (Blackman and Black 1977),
and twin-well calorimetry (Hunt and Phillips 1972;
Kinn 1977). All three methods use a freshly killed
animal carcass that has been briefly exposed to high-
power RF fields and thus raised to a higher tempera-
ture. It has been assumed that the dielectric
properties of the carcass do not differ significantly
from those of a living animal.
The gradient-layer calorimeter measures the rate at
which heat passes from the heated animal through
the walls of the calorimeter to the room air. It is
accurate, but it takes several hours to make the
measurement.
The Dewar-flask calorimeter method uses the
difference between the average temperature of the
animal carcass before and after rapid heating with RF
radiation to determine the heating rate and thus the
dose rate. To determine the average temperature of
the animal carcass, it is placed (with a coupling fluid,
usually water) into a Dewar flask, and the equilibrium
temperature of the mixture is measured. From the
theory of mixtures and a knowledge of the average
specific heat capacity of the animal, the average
carcass temperature is determined. The average
temperature of the heated carcass is determined
similarly, and the SAR is computed. Although the
method is simple by design, a disadvantage is that a
long time is required to measure equilibrium
temperature. Furthermore, the average specific heat
capacity of the carcass must be known, and, because
the body's composition is complex, this capacity
cannot be precisely determined.
The twin-well calorimeter method uses pairs of
carcasses of equal mass. One carcass of a pair is
heated with RF radiation; the heated and unheated
carcasses are each placed in a well of the
calorimeter, and the calorimeter is allowed to return
to equilibrium. The twin-well calorimeter measures
the increment of heat introduced by the exposure.
The SAR is then calculated from the measured
caloric increase, carcass mass, and exposure time.
This method does not require the specific heat
capacity of the carcass but requires 4 to 16 h to make
a measurement. A recent improvement of the
method (Kinn et al. 1984) has reduced the measure-
ment time to 1 5 to 30 min and increased measure-
ment accuracy by control of the calorimeter with a
microprocessor system. This arrangement is the
same as the standard setup except that the
unexposed carcass is in contact with a heating
element (Figure 3-34). The microprocessor program
controls the rate at which heat is applied to the
unexposed carcass. Using the twin-well calorimeter
as a "thermal" balance, the program controls the
3-47
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heating rate so that equilibrium is established in as
short a time as possible. All of the power applied to
the heating element, and thus to the animal carcass,
is integrated and divided by the mass of the carcass to
determine theSAR. A 2-percent error due to heat lost
to the calorimeter walls has been measured using
electrically heated water bottles as animal substitutes.
3.4.2 Regional Dosimetry
Regional dosimetry is performed to determine either
the energy absorption rate or the field strength at a
specific location within an animal or tissue preparation.
The average field strength within the animal can be
measured directly or inferred from the SAR. Direct
measurement of field strength is made with an
implantable probe containing one or more miniature
diodes mounted on a dielectric substrate and attached
with high-resistance leads to a voltage-reading device
(Bassen et al. 1977b). The voltage across the diode is a
measure of the field strength at the diode, provided the
animal tissue material in which the probe is implanted
does not differ significantly in dieletric properties
from the material used in the calibration procedure
(Bassen 1977). The useful frequency range over
which such field strength measurements can be
made is 100 to 12,000 MHz. The reduced sensitivity
at lower frequencies and the greatly reduced field
strength in biologicaI targets at the higher f requencies
delineate the useful frequency range. Indirect
measurement of internal field strength is derived
from the SAR value. The heating rate is proportional
to the square of the electric-field strength.
Measurement of regional SAR can also be accom-
plished by temperature probes or by thermographic
imaging. Temperature probes are small (1-mm
diameter) and are designed to be implanted in the site
of interest without altering the EM field in that area
(Rozzell et al. 1974; Bowman 1976; Christensen
1977; Wickersheim and Alves 1982). An animal or
preparation is briefly exposed to RF fields of high
intensity, and the temperature rise is measured. The
rate of temperature rise, together with the amount of
heat loss, is then used to compute the SAR at a
specific site in an absorber, such as a rat brain.
The technique described above is a special case of
heating and cooling curve analysis, i.e., estimating
the initial rate when the rate of heating is much
higher than the rate of cooling. The analysis of the
complete heating and/or cooling curve is especially
useful in cases where the RF energy absorption is of
the same order of magnitude as the cooling rate of the
animal or preparation. In this procedure, the
temperature is recorded continuously during
exposure and/or after exposure until a steady state or
equilibrium temperature is reached. Analysis of
either curve yields the cooling rate, which is directly
related to the SAR. The heating curve also contains
Figure 3-34. Microprocessor-controlled twin-well
calorimeter.
the cooling rate that can be determined by the
appropriate analysis; therefore, the SAR can be
determined from either a heating or a cooling curve
(Allisera/. 1977).
Thermographic imaging also requires very high
power exposures. This method uses a thermographic
camera containing a mirror scanning system, a
liquid-nitrogen-cooled detector, and a data-collection
system usually interfaced to a minicomputer (Guy
1971; Guy et al. 1968,1977; Kantor and Cetas 1977).
The investigator prepares specimens by cutting a
frozen carcass into halves and supporting each half in
an RF-transparent medium such as urethane foam.
The surface of the cut plane is covered with either a
plastic film polyester "silk" screen material to hold
each half of the specimen in its foam support. The
"silk" screen material allows electrical contact
between the two halves when they are readjoined
during exposure. Unlike plastic film, which prevents
induced current from flowing across its surface, the
"silk" screen material allows current flow, and the
model may be placed in a complex field of unknown
polarization. The assembled specimen is allowed to
equilibrate to room temperature (25°C). Thermo-
graphic pictures are taken of the animal specimens at
3-48
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the plane of the cut before and after exposure, and the
SAP is computed from the point-to-point temperature
change during exposure. The SAR values are then
used to produce a contour plot of iso-SAR lines or
averaged values over a specific area.
Scaled-down or full size physical models made with
materials having dielectric properties similar to those
of biological tissues are also used to determine the
SAR distribution in a biological specimen, such as
man and small animals. Animal models have been
used for the investigator's convenience. Scaled
models of man (Guy et al. 1976; Gandhi et at. 1977)
have been used to simulate human exposures under
varying conditions. This procedure involves frequency
scaling, in which a combination of higher-frequency
radiation with a smaller-than-life-size model is used
to simulate the absorption characteristics of man
when exposed to lower-frequency radiation. The
technique also requires suitable scaling for the
dielectric parameters of the tissue-equivalent
materials used in the model. The validity of the
models used to date is open to some question,
because the physical "equivalent" model is filled with
a homogeneous material whose complex dielectric
constant is the estimated average for the whole body;
a more realistic model would attempt to simulate the
inhomogeneous tissue structure of the body. The
dielectric material normally used in human modeling
is gelled water whose conductivity has been adjusted
with sodium or potassium chloride. The model is
made in two halves, and the thermographic method
described above for animal specimens is used.
3.4.3 Unresolved Issues
Refinements are lacking for models of the in-
homogeneous tissue structure of man and animals,
and the equivalency of these models to the actual
biological target has not been validated. In simulta-
neous exposure of multiple animals, to what extent do
animal movements create uncertainty in the SAR
estimates? How much target separation is required
before this uncertainty falls within acceptable limits?
As research into RF-induced biological effects grows
more sophisticated and as the sites for many of the
reported effects—particularly those associated with
the nervous system—become better isolated and
defined, there will be an ever increasing need for
localized dosimetry of greatly improved spatial
resolution. Finally, although it is well understood that
RF energy is converted to heat in a biological target,
the question remains: Are there transient "field-
specific" effects not explicable by a temperature
change?
3-49
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Section 4
Effect of RF-Radiation Exposure on Body Temperature
4.1 Thermal Physiology
Christopher J. Gordon
4.1.1 Temperature Regulation
Almost all animal species, including vertebrates and
invertebrates, are capable of sensing and responding
to changes in environmental temperature. The ability
to maintain a constant body temperature independent
of ambient temperature, termed homeothermy, is
restricted to humans and other mammals, as well as
most birds. Reptiles, amphibians, fish, and inverte-
brates generally have a body temperature similar to
ambient temperature, and are thus termed poikilo-
therms (i.e., having changeable temperature). Many
poikilotherms use behavioral mechanisms (e.g., seek
shade or sunlight) to regulate their body temperature
against fluctuations in ambient temperature.
Homeotherms employ an array of physiological
mechanisms to control body temperature. Thermal
stimulation of the skin or sites within the body,
especially the central nervous system (CNS), leads to
the activation of heat-dissipating or heat-producing/
conserving effectors such as evaporation, vasomotor
tone, metabolism, and behavior.
Since the absorption of RF radiation can lead to an
increase in tissue temperature, the bioeffects from
RF-radiation exposure at these thermal levels may be
a principal manifestation of a homeothermic
response to rising tissue temperature rather than a
direct RF-radiation effect (i.e., athermal effect) in a
biological system. Thus, it is important to have a
detailed assessment of the characteristics of
thermoregulation in animals and man. This section is
divided into two major parts. First, the structure and
physiology of the thermoregulatory system of
humans and commonly used experimental mammals
are discussed in enough detail to a How the reader to
interpret the second division of the section, the
specific effects of RF radiation on the activity of the
thermoregulatory system. The major conclusions of
this section are:
• Thermoregulatory effectors such as vasomotor
tone, metabolism, evaporative water loss, and
behavior are activated during exposure to RF
radiation.
• Many effectors are activated in the absence of any
measurable change in deep-body temperature
during RF-radiation exposure.
• The SAR required to increase activity of a
thermoregulatory effector or raise body tempera-
ture generally decreases with increasing body
mass of the exposed species.
• Thermoregulatory effectors employed by home-
otherms during RF-radiation exposure at levels
that produce heat stress are similar to the
response during exposure to high ambient
temperature.
4.1.1.1 Effect of Temperature on Biological
Systems
Below the point of protein denaturation at about 42 to
45°C, temperature has a direct effect on the rate of
biochemical reactions and thus affects the rate of
physiologic processes. The effect of temperature on
biological reactions is described by the Qioparameter,
a dimensionless number equal to the change in the
reaction rate for a 10°C change in temperature:
Qio=-
10/(T2-T,)
Ri
or log Qio = (10/T2 - Ti) (log R2 - log Ri)
where Ri = reaction rate at Ti
R2 = reaction rate at T2
T = temperature, °C
Thus, a Qio of 2 means that the reaction rate doubles
with a 10°C increase in temperature, a Qio of 3
means a tripling of the rate, and so forth. For
biological reactions, the Qio generally ranges
between 2 and 3. In many biological systems the Qio
is temperature dependent; thus, Ti and T2 must be
specified in the calculation of
The activity of poikilotherms is dictated by the
prevailing environmental temperature. At low
temperatures enzymatic activity is decreased,
causing reduced muscle. activity, active transport, etc.
Hence, poikilotherms generally have a narrow range
of ambient temperature (~ 20 to 40°C) where normal
life functions can take place. On the other hand, many
homeotherms, by maintaining a relatively constant
body temperature, can function normally at ambient
4-1
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temperatures far below 20°C and occasionally above
40°C. Of course, to maintain a constant body
temperature at extremely high and low ambient
temperatures requires additional metabolic energy.
These metabolic demands can be attenuated through
activation of behavioral mechanisms (e.g., for
humans, by the addition or removal of clothing at low
and high temperatures, respectively).
4.1.1.2 Heat Balance
For body temperature to remain constant, heat loss
must equal heat gain. If heat gain exceeds heat loss,
body temperature increases, and if heat loss exceeds
heat gain, body temperature decreases.
Heat exchange between the body and the environ-
ment takes place by the principal mechanisms of
conduction (including convection), radiation, and
evaporation. Normally, each of these represents heat
loss from the body. However, if air temperature
exceeds the surface temperature of the body, there
is a net exchange of heat into the body by conduction.
Infrared radiation from external sources may also
result in a net transfer of heat from the environment
to the body.
The variables for heat loss can be incorporated into a
simple equation, patterned after the first law of
thermodynamics, which relates metabolic heat
production to whole-body heat loss (Bligh and
Johnson 1973):
M=±K±C±R±E±S
where M = metabolic heat production (always positive)
K = conductive heat transfer (+ for loss)
C=convective heat transfer (+ for loss)
R = radiative heat transfer (+ for loss)
E = evaporative heat transfer (+ for loss; gene-
rally always positive)
S = heat storage by body (+ for increase)
M may include heat produced in the body during
work, as well as heat produced by absorption of RF
radiation. Dimensions of each term in the heat
balance equation are usually normalized with respect
to heat transfer per unit surface area per unit time or
heat transfer per unit body mass per unit time (e.g.,
W/m2 or W/kg, respectively).
The three avenues of heat exchange depend on a
number of external factors, the most important of
which is temperature. As ambient temperature (Ta)
increases, heat loss by radiation, convection, and
conduction decreases, leaving evaporative heat loss
as the primary avenue for heat loss. When body
temperature is constant, S = 0, and M=K+C + R + E.
4.1.1.3 Autonomic and Behavioral Mechanisms
of Temperature Regulation
The neural regulation of body temperature is depicted
in a simple scheme in Figure 4-1. Thermal receptors
located on the periphery and deep in the body
transduce temperature into nerve impulses which
are relayed to the anterior hypothalamus and preoptic
area (POAH), the primary site in the CNS for the
integration of temperature information. A relatively
high percentage of the POAH neurons are sensitive to
changes in temperature (e.g., POAH and/or skin
temperature). Activity from the peripheral and deep-
Figure 4-1. Simple neural model of thermoregulation in a mammal for predicting the motor responses to short-term (i.e., hourly)
changes in ambient and/or body temperature. Activation of the warm-sensitive pathway leads to an increase in heat
dissipatory mechanisms, whereas activation of the cold-sensitive pathway leads to an increase in heat-generating/
retaining mechanisms. This information is taken from several models proposed by Hammel (1968) and Hensel (1973).
Trigeminal Nucleus
Spinal Cord Thalamus
. Warm *•
Peripheral
Cutaneous Receptors
Deep Body
Warm and Cold
Receptors y
Sensory
Inputs
Preoptic/Anterior Hypothalamus
', CNS Cold-Sensitive Neuron ,'
Motor
Outputs
I
Heat Dissipation
• Peripheral Vasodilation
• Panting/Sweating
• Behavioral Selection of a
Cooler Environment
Heat Generation/Retention
• Peripheral Vasoconstriction
• Shivering Thermogenesis
• Nonshivering Thermogenesis
• Behavioral Selection of a
Warmer Environment
4-2
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body thermal receptors is integrated within the POAH
and other CNS sites. Electrophysiological studies
have shown that neurons in the POAH are approxi-
mately 10 times more sensitive to changes in POAH
temperature than to changes in Ta (Reaves 1977).
Specific areas in the CNS generate appropriate
signals to drive thermoregulatory effectors that either
raise or lower heat loss or increase heat production to
maintain core and skin temperatures at their
regulated (i.e., set point) levels.
There is a complex interaction of systems in the body
that are, in some part, responsible for the regulation
of body temperature. Werner (1980) developed a
schematic of the major components of the thermore-
gulatory system that is useful in explaining, in
general terms, the physiological and behavioral
mechanisms of temperature regulation (Figure 4-2A).
The complex systems portrayed in Figure4-2A can be
grouped into four principal parts: sensory system,
control system, effector system, and passive system
(Figure 4-2B). Simply stated, heat exchange between
the environment and the passive system causes
changes in temperature that are detected by the
sensory system and are then integrated in the
controller system for generating appropriate motor
signals to the effector system, which then counteracts
the influence of environmental heat exchange.
However, each system is relatively complex; Figure 4-
2A shows that the temperature regulatory system
operates through the utilization of a variety of
physiological systems to achieve a regulated body
temperature.
The sensory and control systems are very important
but are only briefly described here (see above),
because few studies on the bioeffects of RF radiation
have been directed toward these components of
thermoregulation. For review of sensory studies in
humans, see Sec. 5.6.5. The main thrust of work has
leaned toward effects on the effector and passive
systems; thus, the basic characteristics of effector
control and regulation of the passive system, body
and skin temperatures, will receive primary attention.
4.1.1.4 Metabolism
The effects of changing Ta on tissue blood flow,
cardiac output, and evaporation impart additional
metabolic demands on a homeothermic species,
thereby increasing its basal metabolic rate (BMR).
Because measurement of BMR in experimental
animals is generally not feasible, resting metabolic
rate is a parameter commonly used to assess
thermoregulatory function of homeotherms.
The resting metabolic rate of a homeotherm normally
exhibits three major phases as a function of Ta (cf.
Figures 4-6, 4-7, and 4-10). There is typically a range
of Ta's where metabolism is at a minimal, stable level
(close or equal to the BMR). This range of T.'s is
identified as the thermoneutral zone (TNZ). In the TNZ
the body temperature of a homeotherm at rest can be
kept constant by controlling the amount of passive
heat loss through adjustments in thermal conduc-
tance. When Ta increases above the TNZ, the rates of
metabolic heat production and evaporative heat loss
increase because excess body heat must be dissi-
pated actively rather than passively (e.g., sweating,
increase in ventilatory rate). Metabolism also in-
creases because of the "Qio effect" of rising temper-
ature on metabolism (Sec. 4.1.1.1). The Ta where
metabolism begins to increase with rising T. is
defined as the upper critical temperature (UCT). As Ta
decreases below the TNZ, metabolism increases as a
result of activation of thermogenic physiological
processes to maintain a constant body temperature
(e.g., shivering). The Ta at the low end of the TNZ
where metabolism increases is defined as the lower
critical temperature (LCT).
Ideally, at all Ta's equal to and below the LCT, a
homeotherm has reduced heat loss to the minimum
through vasoconstriction of blood vessels in the skin.
Therefore, whole-body thermal conductance, which
relates to the ease at which heat is lost from the body,
is as low as physically possible. AsTa increases above
the LCT, more blood is shunted to the peripheral
vessels, and whole-body thermal conductance
increases.
Minimal whole-body thermal conductance is rather
simple to calculate and has been reported for a
multitude of avian and mammalian species with a
body mass less than 10 kg (Aschoff 1981). In an
idealistic situation, decreasing Ta below the LCT is
associated with a linear increase in metabolic rate.
Under these conditions, metabolic rate can be
calculated with a linear equation derived from the
principles of Newton's law of cooling which relates
the heat loss of a warm object placed in a cold
environment (Kleiber 1972):
MR = C(Tb - Ta)
where MR = metabolic rate, W/kg
C=whole-body thermal conductance,
W/kg/°C
Tb = body temperature, °C
Ta = ambient temperature, °C
Solving for C when Ta is below the homeotherm's
LCT,
r=
Tb-Ta
This equation is commonly used in thermal
physiological studies of relatively small homeotherms.
Above the LCT, thermal conductance begins to
increase as the animal's metabolic rate stabilizes and
Ta approaches body temperature. Above the UCT,
thermal conductance takes a sharp increase because
of the combined increase in metabolism, along with a
4-3
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Figure 4-2A. Current view of the principal systems employed in the regulation of body temperature (from Werner 1980).
Receptors
Controller
Effectors
Behavior
(Nutrition, Action,
Clothing, Change
of Environment
/
ferent i
\
Environmental
Temperature
I Velocity i
Receptors
Passive System
Effectors
4-4
-------
Figure 4-2B. Overall relationship of the sensory, controller, effector, and passive system components of the thermoregulatory
system. Note that the overall structure of Figure 4-2A is retained (modified from Werner 1980).
Receptors
Peripheral
and Deep-Body
Warm and
Cold Sensors
Controllers
Integration of Temperature
Information in CMS
Passive System
Skin and Core Temperature
Effectors
• Behavior,
• Vasomotor Tone,
• Metabolism,
• Evaporative
Heat Loss
Environmental
Heat Flow
further reduction of the ambient-body-temperature
gradient.
There is an inverse correlation between minimal
thermal conductance and body mass (Figure 4-3). In
general, the thermal conductance of a 10,000-g
homeotherm is 10 times less than that of a 100-g
species (Scholander et al. 1950). Simply stated, for a
given decrease in Ta, to maintain a normal body
temperature a small homeotherm must elevate heat
production (W/kg) much higher compared to a larger
homeotherm. The relationship also implies that at a
given Ta the rate of passive heat loss (W/kg) increases
with decreasing body mass.
In studies on the thermal physiology of humans and
other primates, thermal conductance is often
calculated as follows:
K=MR-E
Tre - TSk
where K = tissue thermal conductance, W/mV°C
MR = metabolic rate, W/m2
E = respiratory evaporative heat loss, W/m2
_Tr=rectal temperature, °C
T»k =mean skin temperature, °C
This value of conductance is commonly called tissue
thermal conductance. The numerator includes all
heat produced from metabolism minus the heat lost
through respiration. The lower the gradient between
rectal and mean skin temperature, the greater the
peripheral blood flow and the higher the value of
tissue thermal conductance. For example, total skin
blood flow in humans ranges from 150to 200ml/min
in a cool environment, to as high as 2000ml/min in a
hot environment (Bullard 1971).
4.1.1.5 Cardiovascular and Vasomotor
Responses
The thermoregulatory system is a unique control
system in that it has no specific organ or tissue
devoted solely to thermoregulation. (Sweat glands
may be an exception.) The cardiovascular system is a
primary example of a thermoregulatory effector
which is perhaps more critical to other bodily
functions (e.g., tissue perfusion). Heat transfer from
the deep body to the skin and thence to the
environment would be nil if it were not for the
enhanced convective transfer of heat via blood flow
by the cardiovascular system.
Blood flow to the skin is a crucial mechanism of
thermoregulation. In humans the rate of blood flow to
the fingers ranges from 0.5 to 1.0 ml/min/100 ml of
tissue during maximal vasoconstriction, to 80 to 90
ml/min/100 ml of tissue during maximal vasodilation
(Burton 1939). This tremendous adjustment in
peripheral blood flow allows for a five- or sixfold
change in tissue thermal conductance (Hardy et al.
1941). Blood flow from the deep body to the skin
allows for dissipation of internal heat loads accrued
during exercise. In hot environments, raising the skin
blood flow increases skin temperature, which
reduces the temperature gradient between the air
and skin and so lessens overall heat gain from the
environment. In extremely cold conditions, blood flow
to the skin prevents cold-induced tissue damage
(such as frostbite).
Decreasing Ta below the thermoneutral zone (see
Sec. 4.1.1.6) also results in an elevation in heart rate
and cardiac output, which is a response to the need
for more oxygen in skeletal muscle and other tissues
that are metabolically more active at lower Ta's. When
4-5
-------
Figure 4-3. Effect of body mass on whole-body thermal conductance of various mammals (data modified from Aschoff 1981).
1.0
u
o
0>
CD
S
O
u
fa
I
0.1
0.01
«™ I
i inn
I i i i 11 ill r i -i mm -
c_
LOG, = LOG 0.18-0.52 LOG,
0.01
0.1
1.0
Body Mass, kg
10
100
Ta increases above the thermoneutral zone the
increase in metabolism, along with the shunting of
more blood to the skin, increases the requirement for
a greater cardiac output.
The rat is often used in a variety of thermophysiologi-
cal studies. The tail of the rat is the principal site for
the control of nonevaporative heat exchange. At Ta's
between 27 to 30°C there is an abrupt increase in
tail blood flow (Figure 4-4A). Below these Ta's blood
flow to the tail is minimal. For comparison, the blood
flow versus skin temperature in the hand, foot, and
forearm of a human is shown in Figure 4-4B. The
overall response pattern is similar for the two species,
but the flow rates differ substantially, with the rat
having a much higher rate of blood flow at given
temperatures above 27°C.
4.1.1.6 Evaporation
Evaporation of water from the skin and respiratory
tract is a major avenue of heat loss in homeotherms at
high TB'S. Approximately 2426 joules (580 calories) of
heat are lost from the body in the evaporation of 1 g of
water. Insensible water loss, the water lost by
diffusion through the skin and expired during
ventilation but excluding sweating, occurs at all
times, provided the relative humidity is below 100
percent. In the rat, a nonpanting and nonsweating
homeotherm, up to 50 percent of evaporative water
loss occurs through insensible water loss through the
skin (Tennent 1946).
Typically, as Ta increases above the upper critical
temperature (approximately 30 to 32°C for many
species), homeotherms undergo an active increase in
evaporative heat loss (EHL). Below this T. EHL is
relatively stable and amounts to roughly 25 percent of
the total heat loss. As Tfl increases the temperature
gradient between the skin and air decreases, which
reduces the rate of the heat loss by conductance,
convection, and radiation. Thus, EHL is a crucial
avenue of heat dissipation in homeotherms at
relatively high Ta's above the thermoneutral zone.
The major avenues of active evaporative water loss
are sweating and panting. Humans and many other
primates sweat to dissipate heat by evaporation (Sec.
4.1.1.9). The dog, cat, and rabbit have few sweat
glands and dissipate heat evaporatively by panting.
Rodents neither pant nor sweat when heat stressed
but increase their ventilatory rate, and subsequently,
increase pulmocutaneous water loss. Rodents also
apply saliva to their fur to enhance evaporative heat
loss. Denervating saliva glands in rats reduces their
tolerance to heat exposure (Strieker and Hainsworth
1971).
4.1.1.7 Thermoregulatory Behavior
Heretofore, the principal autonomic thermoregulatory
responses, metabolism (heat generation), blood flow,
and evaporation, have been discussed. Thermoregul-
atory behavior is another important effector which
animals and humans use to regulate the body
4-6
-------
Figure 4-4. Blood flow vs. skin temperature. (A) Tail blood flow vs. tail skin temperature in three different rats. Notice the abrupt
rise in blood flow at temperatures of 27 to 30°C (data from Rand ttal. 1965). (B) Blood flow in a human hand. foot, and
forearm vs. temperature of the water in which the limb is immersed (skin temperature equals water temperature) (data
from Thauer 1963).
50
40
E
8
I 30
20
10
30
25
20
15
10
• Hand
• Foot
« Forearm
15
20
25
30
35
Temperature,
10
20
30
40
50
temperature in response to changes inTa. Changes in
behavior require less metabolic energy compared to
changes in activity of autonomic effectors; thus,
behavioral responses normally take precedence over
autonomic responses (Adair 1976; Gordon 1983a). For
example, when placed in a temperature gradient
(Ogilvie and Stinson 1966) adult mice will select a
temperature of approximately 31 °C (Figure 4-5). This
is a thermoneutral Ta where the animals maintain
normal body temperature without increasing
metabolic rate or evaporative heat loss. Very young
mice select notably warmer temperatures in a
gradient because their metabolic capacity is not fully
developed compared to the adult. A wide variety of
species can be trained to bar-press for heat or cold
reinforcements and thereby select a comfortable Ta
(Satinoff and Hendersen 1977).
All organisms display subtle thermoregulatory
behaviors in the absence of complex experimental
apparatus. For example, in the cold, groups of rodents
huddle together to minimize heat loss. Mice build
dense, thick nests in the cold and thin-walled nests in
the heat. Solitary animals adjust their posture to
control heat loss. For example, in a very hot
environment the rabbit extends its limbs in a
sprawled position to maximize the surface-area-to-
volume ratio, whereas in a cold environment it
withdraws its limbs under the body and assumes a
ball shape to minimize the rate of passive heat loss.
Humans vary clothing in accordance with Ta.
4.1.1.8 Autonomic Thermoregulatory Responses
vs. Ambient Temperature
Because the absorption of RF radiation may activate
thermoregulatory mechanisms similar to those that
occur during an increase in Ta, it is of importance to
show in this section the effect of Ta on the activity of
autonomic effectors. In Figures 4-6 and 4-7 the rectal
temperature, evaporative heat loss, tissue thermal
conductance, and metabolic rate are plotted as
functions of Ta for the dog and rhesus monkey. (For
data on humans, see Sec. 4.1.1.9). These thermo-
regulatory profiles were selected from the literature
because they demonstrate not only basic thermo-
4-7
-------
Figure 4-5. Effect of age on the preferred ambient temperature
of mice (data from Ogilvie and Stinson 1966).
38.0
o
°. 36.0
34.0
a
32.0
M
30.0
28.0
10 20 30 40 50 60 70 80 90
Age, days
Figure 4-6. Effect of T. on evaporation (Etoi), conductance (K)
rate (M), and rectal temperature (!„) of dogs
acclimatized to summer and winter (data from
Sugano 1981.
\
5
E
x
E
x
o
o
S
60
50
40
30
6
5
4
3
2
1
0
30
20
10
0
39
38
Dog
37
• Summer
O Winter
18 20 22 24 26 28
Ambient Temperature, °C
4-8
30 32
Figure 4-7. Effect of T. on evaporation (E10i). conductance (K)
metabolic rate (M). and rectal temperature (T,.) of
the rhesus monkey under unanesthetized and
ketamine-anesthetized conditions (data from
Hunter «f«/. 1981).
E
x
o
o
£
X
X
I
80
Rhesus Monkey
70-
60-
50-
40-
30
50-
40-
30-
20-
10-
0-
50-
40-
30
ui 20-
10-
0-
40
y 39-
O
^ 38
37-
36
• Unanesthetized
O Ketamine
14 16 18 20 22 24 26 28 30 32 34 36 38 40
Ambient Temperature, °C
regulatory effector activity as a function of T,, but also
the effect of anesthesia and seasonal acclimatization
on thermal responsiveness.
In the dog (Figure 4-6), seasonal acclimatization has a
tremendous effect on the thermoregulatory profile
(Sugano 1981). For example, summer-acclimatized
dogs (mean Ta = 25.3°C) have a UCTof 29°C, whereas
winter-acclimatized dogs (mean Ta = 3.1°C) have a
UCT of 22°C. At warm T»'s the winter-acclimatized
dogs have a higher rate of metabolism and
evaporation. These differences in thermoregulatory
profiles in the dog may prove to be helpful in
understanding the metabolic and evaporative
response of other mammals to RF-radiation exposure.
-------
The effect of ketamine anesthesia on the thermoreg-
ulatory response in rhesus monkeys is shown in
Figure 4-7. These data are presented because many
RF-bioeffects studies are done with anesthetized
animals. The anesthetized monkeys have a reduced
thermal conductance and depression in heat loss at
the high Ta (38°C), which contributes to an elevated
rectal temperature compared with unanesthetized
animals. Note the linear relation between Ta and Tre in
the anesthetized monkey. This and other studies on
the effects of anesthesia on thermoregulation
indicate a general depression in the ability of the
animal to defend its body temperature against heat
stress or cold stress. Anesthetized animals exposed
to RF radiation are likely to also be more susceptible to
RF heating depending on the prevailing Ta(Sec. 4.1 .3).
4.1 .1 .9 Thermal Physiology of Humans
In view of the paucity of studies on human physiology
during RF-radiation exposure, this section deals
primarily with the responses of laboratory mammals.
One must be cautious in relating measured biological
effects in experimental mammals to man because the
thermal physiology of humans and other mammals
differs substantially in certain aspects.
The human body has an inner core with a temperature
of approximately 37°C and an outer shell with a
variable temperature (Figure 4-8). The normal
strategy of the human thermoregulatory system is to
have a well-controlled inner-core temperature at the
expense of a fluctuating shell temperature. Circadian
rhythms cause core temperature to oscillate daily
with an overall amplitude of approximately ± 1°C
(Hardy and Bard 1 974).
Generally, about two-thirds of the body mass is
assumed to be at the core temperature and one-third
is at the skin temperature. This assumption may be in
error because of shifts in the relative size of the core
and peripheral shell. The average body temperature
(Tb) can be calculated as:
Tb = 0.33Tsk + 0.67 T,e
where TSk is the average skin temperature collected
over a variety of sites on the surface of the body, and
Tre is rectal temperature.
The average body temperature is a useful variable
because it allows one to calculate the rate of heat
storage (S) in watts:
Figure 4-8. Temperature distributions in the human body at
T.'s of 20 and 35°C (data from Aschoff and Wever
1958).
S =
= c
m
where Tb
andTb2 = initial and final average-body
temperatures, respectively, during
the specified time (t, seconds)
c- specific heat of the body tissues
(-3.48 kJ/kg/°C)
m = mass (kg)
20°C
35°C
The calculation of rate of heat storage from average
body temperature is useful because the dimensions
for the rate of heat storage are the same as that used
in RF-radiation dosimetry (W or W/kg). For example,
humans placed in a very hot environment (Ta = 55°C,
vapor pressure =15 torr) for 2 h undergo a more than
1 °C rise in rectal temperature and an increase in heat
storage from 2.1 to 6.5kJ/kg, or a heat storage rate of
0.6 W/kg. At a slightly cooler but more humid
environment (Ta = 48°C, vapor pressure = 34 torr) the
change in heat storage over 80 min was 2.0 to 6.5
kJ/kg, or a heat storage rate ,of 0.94 W/kg. These
heat storage rates were associated with large
increases in plasma cortisol and the feeling of
discomfort (Follenius et a/. 1982).
A major difference between humans and most
experimental mammals is the ability to secrete sweat
on the skin. Under resting, thermoneutral conditions
there is a certain amount of insensible EWL through
the skin, which accounts for about 8 W of heat.
Approximately 25 percent of the total metabolic heat
at rest is lost through evaporation. Raising Ta causes
a tremendous increase in the amount of heat lost by
4-9
-------
evaporation. The partitioning of heat loss at various
Ta's in humans is listed in Table 4-1.
Sweating in man and certain other homeotherms may
be evoked by heating the skin or thermally sensitive
sites in the nervous system (Figures 4-9A.B). It is
interesting to compare the relatively high threshold of
sweating at low vs. high skin temperatures (Figure 4-
9B). This comparison may be relevant to some deep
Figure 4-9. Effect of skin temperature on sweating: (A) Effect
of increasing skin temperature on sweating from
the forearms of a human (data from Elizondo
1973); (B) effect of skin temperature on the
threshold internal cranial temperature for activa-
tion of sweating in humans (data from Benzinger
1969).
Table 4-1. Partitioning of Heat Loss in Humans as a Function
of Ambient Temperature under Still Air Conditions
c
E
E
u
o>
ID
W
0.15-
400
300-
200 H
100-
Skin Temperatures. °C
39, 38, 37, 36, 35. 34, 33
33 32 31 30 29
—• Skin Temperatures, °C
Ambient
Temperature
(°C)
25
30
35
Radiation. IR
(%)
67
41
4
Convection
(%)
10
33
6
Evaporation
(%)
23
26
90
Data derived from Hardy era/. (1941 land compiled by Folk (1974)
penetrating frequencies of RF radiation that heat
predominantly the inner tissues and organs without
first substantially warming the skin. Such responses
may affect the organism's ability to respond to RF
heating.
The effect of Ta on the steady-state rate of heat
production, heat loss, evaporative water loss, thermal
conductance, and rectal and skin temperature of
nude adult men and women is shown in Figure 4-10.
Sweating is activated at Ta's of 30 to 32°C. For both
sexes, thermal conductance increases at a Ta of 28°C,
which is indicative of an increase in skin blood flow.
The thermoneutral zone is quite narrow: the upper
and lower critical temperatures are approximately 32
and 30°C, respectively. At warm Ta's women have a
*
Figure 4-10. Effect of calorimeter temperature (x-axit) on rectal
and skin temperature, heat loss, heat production,
evaporation, and thermal conductance in men
and women (data from Hardy at al. 1941).
W/m2
g/m2 • h
W/m2 • °C
36.4 36.8 37.2 37.6
Cranial Internal Temperature. °C
24 26 28 30 32 34
Calorimeter Temperature, °C
4-10
-------
steeper thermal conductance response, which
perhaps indicates increased ability to shunt blood to
the skin compared to males.
It is important to understand the thermoregulatory
responses of humans during exercise and fever, since
these represent two cases where internal temperature
can increase without rising ambient or skin
temperature and, in this respect, may appear similar
to that of RF heating at certain frequencies. However,
as will be demonstrated, thermoregulation during
exercise and fever may differ substantially from
thermoregulation during RF exposure.
Humans are well adapted to dissipate excess heat
loads accrued from exercise. Examples of thermoreg-
ulatory responses during two levels of exercise on a
bicycle ergometer are shown in Figure 4-11. A work
load of 40 W causes an increase in metabolism from
1.5 to 4.2 W/kg and a concomitant 0.34°C rise in
tympanic temperature. The temperature of the
tympanic membrane in the ear is considered to be a
good indicator of the internal temperature of the
head. A 90-W work load increased metabolism to 7.0
W/kg and raised tympanic temperature by 0.96°C.
The rise in metabolism from pedaling the ergometer
and the heat load normalized to time and mass from
RF-radiation exposure have the same dimension
(W/kg), albeit the two forms of heat loading may not
always evoke the same physiologic effects. However,
measuring the rise in body temperature, evaporation,
and other physiological parameters during an
exercise-induced heat load may aid our understanding
Figure 4-11. Effect of exercise on heat loss, metabolic rate,
and tympanic temperature of humans (data from
Chappuis et al. 1976).
Ambient Temperature = 30°C
Rest T Work at 40 WJWork at 90 W~T Recovery
0 20 40 60 80 100 120 140
Time, min
of the human response to RF radiation. It is clear from
the data in Figure 4-11 that healthy humans can
tolerate exercise-induced metabolic heat loads of 7.0
W/kg without significantly stressing the thermoreg-
ulatory system. However, it remains to be shown
whether humans can tolerate RF-induced heat loads
of the same magnitude under similar ambient
conditions.
Fever can be distinguished from forced hyperthermia
in that the former represents a regulated increase in
body temperature whereas forced hyperthermia can
be defined as an increased thermal load on the
organism (Stitt 1979; Gordon 1983d). The process of
pyrogenesis can be described in three major steps, as
shown in Figure 4-12: (i) a hypothermia state where
the reference or set-point temperature (in the POAH)
has been raised above body temperature as a result of
the introduction of a pyrogenic agent, so that the
animal generates and conserves heat to raise body
temperature to the new reference temperature; (ii) a
febrile state where body temperature is regulated at
the new reference temperature; and (iii) a hyper-
thermic state where the influence of the pyrogen is
removed, so that body temperature is now higher
than the reference temperature and heat-dissipating
mechanisms are employed to reduce body tempera-
ture to the original normothermic level (Bligh 1973).
The thermoregulatory state of a homeotherm
exposed to RF radiation is similar to the hyperthermic
stage of fever only when body temperature is above
the normal set-point temperature of 37°C. Otherwise,
the thermoregulatory responses of fever and RF-
radiation exposure are radically different. Fever
entails a regulated change in body temperature,
whereas during RF-radiation exposure the organism
activates heat-dissipating effectors in an attempt to
maintain normal body temperature.
4.1.1.10 Mechanisms of Heat Gain During RF-
Radiation Exposure
The coupling of RF energy into irradiated biological
subjects exposed to RF radiation was discussed in
detail in Sec. 3.2, RF-Field Interactions with
Biological Systems. To introduce the following
material, some of the important features of that
discussion are reiterated and summarized here.
The penetration of RF energy into biological tissues is
dependent on the wavelength of the incident energy.
Longer wavelengths can penetrate deeply into living
tissues, but the shorter wavelengths found in the
microwave region of the spectrum cannot penetrate
deeply. For example, at 2450 MHz (wavelength of
12.5 cm) the RF energy is largely absorbed within
approximately the first 2 to 3 cm of muscle tissue,
assuming that the RF radiation is incident on an
object that is large in comparison to this wavelength
(such as a human). Similarly, RF energy of still higher
frequencies (i.e., in the millimeter wave region of the
4-11
-------
Figure 4-12. Relationship between body temperature (TB) and set point (!„,) during pyrogenesis; (A) before the onset of fever; (B)
during the rising phase of the fever; (C) during a maintained fever (heat loss and heat gain are balanced); (D) during the
subsiding phase, and (E) after the return to normal body temperature (data from Bligh 1973).
Normothermic
at Normal Tb
Hypothermia
Normothermic
at Raised TD
Hyperthermic
Normothermic
at Normal Tb
T..,
RF spectrum) does not penetrate more than 1 to 2 mm
and will be absorbed primarily in the skin.
This difference in penetration poses a major problem
for comparing the effects of RF radiation of various
wavelengths on thermoregulatory function in various
species. For example, when a 20-g mouse or a 70-kg
man is exposed to RF radiation of millimeter-size
wavelengths or to infrared (IR) radiation, the energy is
deposited in the first 1 to 2 mm of the skin in a
basically similar fashion. However, at 2450 MHz a
mouse is compa rable in size to the wavelength so that
a resonant absorption condition exists and results in
efficient energy coupling with deep penetration and
nonuniform internal energy deposition. On the other
hand, when a human is exposed to the same 2450-
MHz radiation, the energy will be deposited
peripherally within a few centimeters of the body's
surface in the area facing the radiation source.
interaction takes place at this frequency (Sec. 3.2).
The coupling of RF energy into the animal is less than
optimal (i.e., the coupling is of intermediate
efficiency), and most of the energy is peripherally
deposited, although less so for the rat than for the
man. If the same interspecies comparison were to be
performed under conditions in which the RF-
radiation coupling is optimal (i.e., the resonant
absorption case), then the results would probably be
very different (i.e., the power density values needed
for a 1 °C elevation in rectal temperature may well be
significantly reduced). Telf and Harlen (1979) have
Figure 4-13. Power densities at 2450 MHz necessary to raise
the rectal temperature by 1 °C in 60 min for the
rat. squirrel monkey, and rhesus monkey (de
Lorge 1979). T. ranged from 22.5 to 24°C.
Notwithstanding these problems, some attempts
have been made to compare thermoregulation in
different species when subjected to RF radiation of
the same frequency. For example, de Lorge (1979)
compared the power density at 2450 MHz that
induced a 1 °C elevation in the rectal temperature of
rats, squirrel monkeys, and rhesus monkeys. Using a
semi-log plot of power density vs. body mass (Figure
4-13), de Lorge extrapolated the data on rats and
sub-human primates to a 70-kg man. He predicted that
a value of 92 mW/cm2 is needed to raise the rectal
temperature of man by 1°C at 2450 MHz. This
comparison is probably acceptable because, for the
four species considered, a supraresonant kind of RF
E
i
120
100
80
60
40
20
0
i i i nun IT
_ Y = 24.88 Log X + 45.82
r = 0.975
0.1
Rhesus
Monkey
11111
1.0 10
Body Weight, kg
100
4-12
-------
indicated that if a human were exposed to 2450 MHz
at a power density of approximately 90 mW/cm2,
irreversible local peripheral tissue damage may occur
without an appreciable rise in body temperature.
When there are supraresonant-type interactions, the
absorption coefficient is roughly constant and is
~ 0.5. Under these conditions, the RF-energy absorption
depends only on the geometric cross-sectional area
of the exposed animal. Assuming a spherical shape of
radius r for the animal, it can be shown that the cross-
sectional area-to-volume ratio is proportional to r23
(Sec. 4.1.4.1). This means that the area-to-volume
ratio, as well as the area-to-mass ratio, decreases as
animal size increases. Consequently, at a given
power density, the absorbed energy per unit of body
mass (i.e., whole-body-averaged specific absorption
rate, SAR) decreases with increasing size. This
general rule of thumb is valid only for interaction
conditions of the supraresonant type and for
resonant- and subresonant-type conditions.
4.1.2. Effect of RF-Radiation on
Thermophysiological Effectors
4.1.2.1 Vasomotor Control
Interest during the early 1940's in using short-wave
diathermy (13 to 43 MHz) as a therapeutic agent
prompted research into the effect of RF radiation in
producing localized changes in peripheral blood flow.
Near-field diathermic application with capacitance
plates (SAR not determined) was shown to produce a
more than twofold increase in blood flow of an
exposed limb of a dog (Wakim et al. 1948) and of a
human (Abramson et al. 1957). Using the 133Xe
clearance technique, McNiven and Wyner (1976)
found that localized exposure to 2450 MHz caused
nearly a fourfold increase in blood flow of the vastus
lateralis muscle (femoral) in humans. Using local
diathermy application to the human thigh (915 MHz)
Lehmann et al. (1978) found that at a muscle
temperature of 43 to 45°C, blood flow to the muscle
increased, which caused a reduction in muscle
temperature. Although it was not possible to
determine the SAR, these studies are important
because they contain some of the few data
concerning RF effects on blood flow in humans.
RF-radiation-induced increases in peripheral blood
flow can be attributed to a direct effect of heat on the
caliber of arterioles, or to an indirect, neurally
induced vasodilation via the activation of peripheral
and deep-body thermal receptors .(Sec. 4; 1.1.5). The
increase in femoral blood flow during RF-radiation
exposure (2450 MHz and 27.3 MHz) is similar in dogs
with intact and denervated limbs (Siems et al. 1948).
Hence, RF radiation can directly affect peripheral
vascular resistance; however, the fact that this
response occurs in the denervated limbs does not
preclude a neural response to RF radiation under
normal circumstances.
Gordon (1983b) recorded the tail skin temperature of
mice exposed to 2450 MHz in a waveguide. As in rats,
the tail of the mouse is a principal site of
nonevaporative heat exchange (Sec. 4.1.1.5). Heat
loss from the tail is proportional to the difference
between tail skin temperature and Ta. At a Ta of 25°C
an SAR of 11.5 W/kg was sufficient to promote
vasodilation in the tail. It was shown that the
vasodilation response was sensitive to the rate of
heating (i.e., SAR). The integrated vasomotor
response (°C • s) was normalized to the absorbed heat
load (J/g) to yield a skin temperature index (°C • s •
g/J). A doubling of the SAR leads to more than a
twofold increase in the skin temperature index
(Figure 4-14). These data indicate that the mouse
responds not only to the total amount of energy (heat)
absorbed from RF radiation but also the rate at which
the energy is absorbed.
Phillips ef al. (1975b) measured tail skin temperature
in the restrained rat immediately after exposure for
30 min to 2450 MHz at SARs of 0,4.5, 6.5, and 11.1
W/kg. At a Taof 24°C an SAR of 4.5 W/kg resulted in
a 1.5°C increase in tail skin temperature. This was
associated with a 0.5°C increase in colonic
temperature. Higher SARs caused larger increases in
colonic temperature with minor additional increments
in skin temperature.
Adair and Adams (1980a) found that RF-radiation
exposure in the squirrel monkey at 2450 MHz and 8 to
10 mW/cm2 (SAR = 1.5 W/kg) at a Ta of 26°C
promoted vasodilation in the tail without any change
in rectal temperature. Furthermore, it was shown
that an equivalent power density from an infrared
heat source, which has a much shorter wavelength
and is absorbed on the skin surface, was ineffective in
promoting vasodilation.
Exposing the squirrel monkey to RF radiation
promotes vasomotor responses similar to direct
heating of the preoptic area/anterior hypothalamus,
an extremely thermally sensitive area of the
brainstem considered to be an integrative center for
the control of body temperature (Sec. 4.1.1.3). The
conclusion was that RF-induced vasodilation was
caused by the activation of warmth-sensitive neural
sites in and/or outside the CMS, which in turn affect
the central neural control of heat-dissipating motor
outputs, including the dilation of the peripheral
vasculature (Adair and Adams 1980a).
4.1.2.2 Evaporative Heat Loss
Gordon (1982a) measured whole-body evaporative
water loss (EWL) in mice exposed in a waveguide to
2450 MHz over a 90-min exposure period at a Taof
20°C (Figure 4-15A). EWL remained stable up to an
SAR of 29 W/kg. Above 29 W/kg EWL increased
abruptly. In the same animal EWL was measured at a
Ta of 20, 25, 30, 33, and 35°C (Figure 4-15B).
4-13
-------
Figure 4-14. Examples of change in tail skin temperature (AT*) in restrained mice exposed to 2450 MHz at 25°C and specific
absorption rate (SAR) of 10.6 W/kg (A) and 20.0 W/fcg (B). Note that the absorbed heat load (J/g) is similar in both
cases (data from Gordon 1983b).
< °
c/j 0
10
20
Time, min
30
-
1 1
6.4 J-g"
i i
i i i i i
i i i i i
-
1
6.0 J-s
1
1 1 1 1 1
. -
1 I 1 1 1
40 0
10 20
Time, min
30
Between 20 and 30°C EWL remained at the same
level as observed at SARs of 0 to 29 W/kg. EWL
increased significantly at Ta's of 33 and 35°C. The
mouse increased EWL at an SAR of 29 W/kg and at a
T» of 20°C and at TB's of 30 to 33°C at an SAR of 0
W/kg. These data allow one to relate the effects of RF
exposure and Ta on the activation of a thermoregula-
tory effector (EWL). Heat-stressed rodents can
actively increase EWL by raising their ventilatory
frequency (e.g.. Hart 1971) and by applying saliva to
the fur (Strieker and Hainsworth 1971). These two
mechanisms are no doubt responsible for the rise in
EWL which occurred in mice exposed to SARs above
29 W/kg or above a Ta of 30°C.
Michaelson et al. (1961) demonstrated the importance
of evaporative cooling in the thermoregulatory
response of dogs to high-intensity RF exposure (100
or 165 mW/cm2 at 2790 MHz). During exposure dogs
will pant to increase EWL. If the animal is dehydrated
its rectal temperture reaches a critical level much
faster than in hydrated dogs. With exposures lasting 4
h (165 mW/cm2, SAR unknown) the dogs lose body
mass while hematocrit increases, which indicates a
depletion of body water.
The rate of heating, or SAR, is also a critical factor
in the control of EWL. Gordon (1982c) exposed mice
to 2450-MHz radiation in a waveguide for brief
periods of time while continuously monitoring EWL at
a T. of 30°C. EWL was converted to evaporative heat
loss (EHL) by assuming that 1.0 g of evaporated water
-was equal to a heat loss of 2426 joules. After an
episode of exposing the mice, total EHL normalized to
body mass in dimensions of J/g was calculated. The
total heat load absorbed from RF exposure was
calculated by integrating SAR over time, which yields
the dimension of J/g. The open-loop gain (OLG) of
EHL was calculated by dividing the integrated EHL
response by the RF heat load. The OLG EHL, a
dimensionless number, describes the sensitivity of
the control of evaporative water loss (Gordon 1982b).
4-14
-------
Figure 4-15. Evaporative water loss (EWL) of mice exposed to
2460 MHz for 90 min: (A) Relationship between
EWL and SAR of mice exposed at a T. of 20°C; (B)
effect of T. on EWL of mice (data from Gordon
1982a).
1 \ 1 1 1 1 1
0 10 20 30 40
Specific Absorption Rate, W kg'1
25 30
Ambient Temperature, °C
35
At a Ta of 30°C the OL.GEHL increased nearly three-
fold by doubling SAR. Thus, the mice responded not
only to the absorbed heat load but also to the rate the
heat load was absorbed. This finding is important
because it indicates that biological sensitivity can be
defined not only in terms of a dose perse (i.e., J/g) but
also in terms of the dose rate (i.e., J/(g-s)). A similar
pattern was observed when skin temperature of mice
was measured during 2450-MHz exposure (Sec.
4.1.2.1).
Using the same methods as described above, Gordon
and White (1982) exposed mice to whole-body heat
loads of 12 to 13 J/g by exposure to 2450 MHz at
SARs of 19, 68, or 194 W/kg while recording the
OL.GEHL. The OL.GEHL at a Ta of 32.5°C displayed a
saturation at an SAR of approximately 160 W/kg. The
large change in OL.GEHL over an order of magnitude
change in SAR demonstrated a high degree of rate
sensitivity at a low range of SARs.
Adair (1981) measured the rate of sweating from the
foot of squirrel monkeys exposed to 2450 MHz at a T.
of 33°C (just below the monkey's upper critical
temperature). Sweating was activated consistently
with 10-min exposures at power densities of 6 to 8
mW/cm2 (SAR - 1.1 W/kg) (Figure 4-16). Lowering
Ta led to an increase in the threshold SAR for activating
sweating and a decrease in the sensitivity of sweating
(i.e. A sweating/A power density).
4.1.2.3 Metabolism
When a homeotherm is exposed to a Ta below its lower
critical temperature it must increase metabolism
above the basal level to maintain a normal deep-body
temperature (Sec. 4.1.1.4). If a homeotherm is
exposed to RF radiation at a Ta below its thermoneutral
zone one would expect a decrease in metabolic rate
as the animal substitutes RF heat for metabolic heat.
On the other hand, RF exposure at a TB above the
upper critical temperature of the thermoneutral zone
should lead to an increase in metabolic rate as the RF
radiation causes additional heat stress to the animal.
Ho and Edwards (1977b) exposed mice to 2450 MHz
at a Ta of 24°C in a waveguide while recording
metabolic rate by indirect calorimetry (i.e., oxygen
consumption). They found a decrease in metabolic
Figure 4-16. Change in the rate of sweating from the foot of a
squirrel monkey exposed for 10 min to 2460
MHz. The parameter is ambient temperature.
Data are from Adair (1981).
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4-15
-------
rate when SAR for a 30-min exposure exceeded 10to
23 W/kg. In another study (Ho and Edwards 1979)
mice were exposed to 2450 MHz at Ta's of 20, 24,30,
and 35°C. Exposure at SARs greater than 10 W/kg at
T.'s of 20 and 24°C caused depressions in metabolic
rate. However, the decrease in metabolic rate never
reached the level of the sham irradiated group
maintained at a Ta of 30°C (i.e., thermoneutral
temperature for the mouse). At a TBof 35°C metabolic
rate increased during microwave exposure.
Phillips et a/. (1975b) measured oxygen consumption
and carbon dioxide production in rats immediately
after being exposed to 2450 MHz for 30 min at SARs
of 0 to 11.1 W/kg at a Ta of 24°C. Oxygen
consumption was not affected at an SAR of 4.5 W/kg.
At SARs of 6.5 and 11.1 W/kg oxygen consumption
decreased and did not recover for at least 300 min
following microwave exposure (Figure 4-17). Carbon
dioxide production followed a pattern similar to that of
oxygen consumption.
Adair and Adams (1982a) recorded metabolic rate at
TB'S of 15, 20, or 25°C in restrained squirrel monkeys
exposed to 2450 MHz in an anechoic chamber.
Reductions in metabolic rate were achieved with 10-
min exposures at power densities of 4 to 6 mW/cm2
(SAR = 0.6 to 0.9 W/kg). In a 10-min exposure period
the metabolic response was vigorous with a nearly
2.5-W/kg decrease in metabolic rate for a 1.0-W/kg
increase in SAR. However, with prolonged exposure
(90 min) metabolic rate adapted to a level where there
was an approximate 1:1 substitiution of microwave
energy for metabolic energy.
To summarize briefly, the metabolic rate of three
species has been measured at a Ta below the
Figure 4-17. Oxygen consumption and carbon dioxide produc-
tion of rats immediately after a 30-min exposure
to 2450 M Hz at a T. of 24°C (data from Phillips ft
•/. 1975b).
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thermoneutral zone during exposure to 2450 MHz.
For the 0.032-kg mouse at a Ta of 24°C, metabolic
rate is reduced reliably when SAR exceeds 10 to 12
W/kg; for the 0.43-kg rat at a Ta of 24°C, metabolic
rate is reduced at an SAR of 6.1 W/kg; and for the 1.0-
kg squirrel monkey at a Ta of 20°C, metabolic rate is
reduced at an SAR of 0.9 W/kg.
4.1.2.4 Thermoregulatory Behavior
Artificially raising the temperature of the hypothalamus
(Cabanac and Dib 1983; Gale eta/. 1970), spinal cord
(Carlisle and Ingram 1973), and rectum (Adair 1971)
will activate behavioral thermoregulatory responses
leading to a reduction in the preferred Ta. These
changes in behavior can be initiated before there is a
change in skin temperature. Hence, it is not surprising
to find that deeply penetrating RF radiation can
similarly affect behavioral thermoregulation as does
local, artificial warming of thermosensitive areas
described above.
Gordon (1983c) measured thermoregulatory behavior
of unrestrained CBA/J mice in a combined wave-
guide-temperature gradient system during exposure to
2450 MHz. Without microwave exposure, the mice
selected a preferred ambient temperature (PTA) of
31.5°C. The mice did not select a lower PTA until SAR
exceeded 5.3 W/kg. After a 1 -h exposure at 18 W/kg,
the mice selected a PTA that was 9.5°C cooler than
during the sham treatment. Then, 30 min after the
termination of RF exposure, the mice returned to the
warm end (~ 30°C) of the temperature gradient.
Using a waveguide-temperature gradient system
similar to that described above, Gordon (1983a)
measured PTA and ventilatory frequency of BALB/c
mice during exposure for 60 min to 2450 MHz. The
mice did not select a cooler PTA until SAR exceeded
7.0 W/kg. At an SAR of 25 W/kg the mice selected
the coolest part of the temperature gradient (19°C).
There were slight increases in ventilatory frequency
at 20.5 W/kg when the mice could behaviorally select
a cooler PTA. However, if the mice were forced (while
unrestrained) to remain at their normal PTA of 31 °C,
ventilatory frequency increased significantly at SARs
of 9.6 W/kg and above (Figure 4-18). Thus, mice will
preferentially activate a behavioral thermoregulatory
response (selecting a cool PTA) rather than activate
an autonomic effector (ventilatory frequency) during
RF exposure.
Stern et a/. (1979) trained rats to bar press for
infrared heat in the cold and then exposed them to
2450-MHz RF radiation for 15-min periods. They
found a decrease in the rate of bar pressing at a power
density of 5 mW/cm2 (SAR = 1.0 W/kg) compared to
bar-pressing activity at 0 mW/cm2. This power
density, as well as exposure to 10 and 20 mW/cm2,
did not produce any increase in rectal temperture
under similar environmental conditions (Ta = 5°C, fur
of rat clipped from body). Thus, behavioral thermoreg-
4-16
-------
Figure 4-18. Ventilatory frequency and preferred T. of mice
during exposure to 2450 MHz inside a waveguide-
temperature gradient system. Responses without
temperature gradient were measured in mice
exposed to RF radiation at their preferred T. of
31 °C. Data are from Gordon (1983a).
Ventilatory Frequency, breaths/min
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ulation was offset by RF-radiation exposure in the
absence of a change in rectal temperature.
Adair and Adams (1980b) trained squirrel monkeys to
control their Ta while being exposed for 10 min-
periods to 2450 MHz in an anechoic chamber.
Without microwave exposure the monkeys selected
a Ta of approximately 35 to 36°C. Power densities
below 6 to 8 mW/cm2 (SAR -1.1 W/kg) had no effect
on the controlled Ta. Increasing power density above
6 to 8 mW/cm2 led to a decrease in the controlled Ta
(Figure 4-19). For example, at an exposure level of 22
mW/cm2 (SAR ~ 3.2 W/kg), preferred Ta was
reduced by 5°C while rectal temperature remained
constant. Exposure to infrared radiation at the same
power densities as RF exposure elicited no change in
thermoregulatory behavior.
Using a similar experimental apparatus, Adair and
Adams (1982b) exposed squirrel monkeys to 2450
MHz for 5 to 150 min while observing changes in
thermoregulatory behavior. Exposure to 4 mW/cm2
{SAR ~ 0.6 W/kg) had no effect on controlled Ta no
matter how long the exposure lasted. Exposure to 10
and 20 mW/cm2 (SAR ~ 1.5 and 3.0 W/kg) resulted
in a lowering of the controlled Ta by 1.5 and 3.0°C,
respectively. With few exceptions, the duration of RF-
radiation exposure had no significant effect on the
controlled TB.
Postural adjustments in an RF field can be used to
modify energy absorption, as well as the rate of heat
loss, resulting from an RF-radiation heat load.
Although rectal temperature was not measured, this
behavior may still be viewed as a form of behavioral
thermoregulation (Sec. 4.1.1.7). Monahan and Ho
(1977) exposed mice to 2450 MHz inside a waveguide
while measuring SAR. They found that at sufficiently
high intensities the mice would reduce their
absorption of RF power, presumably by postural
adjustments. For example, at a Ta of 30°C the percent
power absorbed did not decrease until SAR equalled
or exceeded 25.8 W/kg. At a Ta of 20°C, changes in
RF absorption were not seen until SAR equalled or
exceeded 43.6 W/kg.
Gage et al. (1979) monitored the orientation of mice
and rats exposed to 2450 MHz for 1 h in the far field at
a power density of 15 mW/cm2. Depending on the
type of animal cage, by reorienting their position in
the RF field, mice could change their SAR by a ratio of
1:1.2 to 1:2. However, because of their large size
relative to the RF wavelength, the rats could not
change SAR by reorientation. AtTa's of 22 and 28°C,
exposure for 1 h elicited no significant change in
orientation for the mouse or rat (maximum SAR ~ 3.6
W/kg for rat and 11.1 W/kg for mouse). The lack of
effect in mice may be due to the relatively low
intensity of exposure. Monahan and Ho (1977) did not
observe a change in absorption until SAR equalled
25.8 W/kg at a Ta of 30°C. The lack of effect in the rat
is probably due to the inability of this species to
Figure 4-19. Mean T. selected by one squirrel monkey exposed
to 2450-MHz RF radiation (data from Adair and
Adams 1980b).
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4-17
-------
reduce SAR regardless of orientation in the far field at
2450 MHz.
4.1.2.5 Endocrine Systems
The thyroid and adrenal glands are two principal
endocrine glands that are highly sensitive to thermal
stimulation from RF radiation, as well as to other
sources of thermal stimuli. For example, reducing Ta
or direct cooling of the preoptic/anterior hypothalamic
area (POAH) leads to an increase in the serum level of
thyroid-stimulating hormone (TSH) and thyroxine
(Gale 1973). Prolonged exposure to heat or cold leads
to hypertrophy of the adrenal cortex, along with
increased secretion of glucocorticoids. Local heating
of the POAH leads to a rise or fall (species dependent)
in glucocorticoids and a rise in serum levels of
antidiuretic hormone. Hence, thermally sensitive
neurons in the POAH and perhaps other sites in the
CNS mediate some control over the thyroid gland,
pituitary gland, and the cortex of the adrenal gland
(Gale 1973).
Parker (1973) exposed rats to 2450 MHz at 0 and 15
mW/cm2 for du rations of 4,16, or 60 h at a Ta of 22°C.
Plasma-bound iodine (PBI) and thyroxine in the serum
were significantly reduced at 15 mW/cm2 for the 60-
h exposure (SAR ~ 5 W/kg, assuming a conversion
factor of 0.3 W/kg per mW/cm2; Durney et al. 1978).
These parameters were not affected at 10, 20, or 25
mW/cm2 for the 16-h exposures. Lu et al. (1981)
found a decrease in serum TSH in the rat following
exposure to 2450 MHz for 1 h at 10mW/cm2 at a Taof
24°C (SAR = 2.5 W/kg). The changes in serum
thyrotropin were significantly correlated with RF-
radiation effects on body temperature. Lu era/. (1977)
found decreases in serum thyroxine in rats after
exposure to 2450 MHz at 20 mW/cm2 for 4 or 8 h at a
Ta of 24°C (SAR = 5 W/kg). There was a transitory
stimulation of thyroid function in rats exposed for 1 h
to 1 mW/cm2 (SAR = 0.25 W/kg).
Lu et al. (1977) found an increase in serum
corticosteroid levels in rats exposed to 2450 MHz at
20 mW/cm2 for 8 h (SAR = 5 W/kg). Lotz and
Michaelson (1978) found a positive correlation
between serum corticosterone and cotonic tempera-
ture in rats exposed to 2450 MHz for 30,60, or 120 m in
at a Ta of 24°C. This relationship has also been
reported in humans exposed to extreme ambient heat
stress (Follenius et al. 1982; see Sec. 4.1.10). No
significant increases in plasma corticosterone for the
30- and 60-min exposures were observed below
power densities of 50 mW/cm2 (SAR ~ 8.0 W/kg).
However, the 120-min exposure elicited a significant
increase in plasma corticosterone at a power density
of 20 mW/cm2 (SAR ~ 3.2 W/kg). Lu et al. (1981)
found a significant increase in plasma corticosterone
in rats exposed to 2450 MHz for 1 h at 50 mW/cm2
(SAR -10.5 W/kg) and for 4 h at40mW/cm2(SAR ~
8.4 W/kg).
Many of the above data indicate an accumulative
thermal effect of RF-radiation exposure on the activity
of the endocrine systems. The general trend is that
longer exposure times are needed to elicit significant
changes if) hormone levels as SAR is reduced. In
addition, the RF-radiation-induced activation of
thyroid and adrenal cortical systems is intimately
related to RF-radiation effects on body temperature.
In general, hormone levels in the blood increase or
decrease in unison with significant changes in core
temperature. RF-radiation effects on the endocrine
system are addressed in more detail in Sec. 5.7.1.
4.1.3 Body Temperature Regulation During RF-
Radiation Exposure
Referring to the heat balance equation in Sec.
4.1.1.2, it can be seen that when heat gain (from
metabolism or RF-radiation exposure) exceeds heat
loss there will be positive heat storage and,
consequently, an increase in average body tempera-
ture. Note the use of the term "average body
temperature," meaning the average temperature of
all tissues in the body (Sec. 4.1.10). Changes in the
average body temperature represent imbalances
between heat gain and heat loss that cannot always
be detected by measuring rectal temperature alone.
For example, rectal temperature may remain fixed
while subcutaneous temperature increases and
results in an increase in the average body tempera-
ture.
In a steady-state condition during RF-radiation
exposure, if the thermoregulatory effectors described
above (blood flow, evaporation, and behavior) cannot
dissipate the RF heat load, then the average body
temperature will rise. If we assume that during
temperature regulation deep-body temperature (e.g.,
rectal, colonic, or core) should be regulated within a
restricted range (see Glossary), in a first approximation,
it can then be sard that when the core temperature
rises above the normal mean temperature by at least
one standard deviation (defined as hyperthermia by
Bligh and Johnson 1973) the regulatory system is no
longer capable of maintaining the regulated variable,
core temperature, within normal limits. However, this
conservative view of defining the characteristics of
the regulatory system may need to be compromised
because of peculiarities of temperature regulation
during RF-radiation exposure (see below).
Principal factors that influence the ability of a species
to thermoregulate (i.e., maintain core temperature
within one standard deviation of the normal mean
level) during RF exposure are (i) species characteristics,
(ii) degree of restraint, (iii) wake-sleep state (including
anesthesia), (iv) ambient temperature, (v) relative
humidity, and (vi) air velocity. Certain species are
better able to maintain a constant body temperature
in warm environments than others. For example, in
hot desert conditions a rodent weighing 100 g would
4-18
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have to dissipate 15 percent of its body weight in
water per hour to thermoregulate, whereas a 70-kg
man need only evaporate 1 to 2 percent per hour.
Since a water loss of 10 to 20 percent per hour is
lethal, small rodents in the desert burrow in the earth
to avoid the heat during the day, whereas relatively
large homeotherms, such as the human, can survive
direct exposure from the desert heat (Schmidt-
Nielsen 1964). Based on these examples one would
predict tremendous species differences in thermo-
regulatory capacity during RF-radiation exposure.
However, there are problems in relating ambient heat
stress to RF-radiation heat stress (Sec. 4.1.4.3).
Restraint has a large impact on the ability to
thermoregulate. Restrained animals have a reduced
thermoregulatory capacity (e.g., Frankel 1959). The
effect of anesthesia on thermoregulatory capacity
at different ambient temperatures has already been
discussed (Sec. 4.1.1.8). Generally, anesthetics
reduce the ability of homeotherms to defend body
temperature in the heat and cold.
Ambient temperature (TJ, relative humidity (RH), and
air velocity (V) affect the capacity of homeotherms to
thermoregulate. As Ta increases, the temperature
gradient between the skin and air is reduced, thereby
causing a reduction in passive, nonevaporative heat
loss. Thus, with increasing T«, homeotherms rely
more on evaporative heat loss to balance heat gain
and heat loss. The efficiency to evaporate is
dependent on the partial pressure of water in the air
(which is, of course, related to RH). The ability to
evaporate water from a surface is reduced as the
partial pressure of water of the surrounding air
increases.
4.1.3.1 Mouse
CD-1 mice exposed 100minto2450MHz(farfield)at
28mW/cm2(SAR~22.2W/kg)atTa = 20°CandRH =
50 percent underwent a 0.8°C increase in rectal
temperature, when compared to the post-treatment
shams (Berman et al. 1978). AJ mice restrained in a
waveguide and exposed for several minutes to 2450
MHz at a Ta of 32.5°C (dry air) underwent an abrupt
increase in colonic temperature at SARs of 20 to 205
W/kg (Gordon and White 1982). The rate of body
heating was 0.021 °C/min per W/kg increase in SAR.
Gordon (1982d) exposed hypothermic (body temper-
ture equalled 17 to 30°C) CD-1 and AJ mice to very
intense 2450-MHz radiation inside a waveguide at
SARs of 200 to 1800 W/kg. The resultant warming
rate of colonic temperature of the restrained mice
ranged from 0.05 to 0.65°C/s. Provided that body
temperature did not exceed the lethal limit (~43°C)
the mice could survive any warming rate up to
0.65°C/s. Thus, the rate of warming does not affect
the tissue per se. but it does have a large impact on
the degree of activation of thermoregulatory effectors
(Sees. 4.1.2.1 and 4.1.2.2).
Smialowicz et al. (1981b) used a unique form of
hypothermia as an assay for detecting the thermal
effects of low level RF-radiation exposure. Below the
thermoneutral zone, mice injected intraperitoneally
with 5-hydroxytryptamine (5-HT) became hypothermic,
the decrease in body temperature being inversely
related to Ta (Figure 4-20). The 5-HT-induced
hypothermia was attenuated in a dose-related
response by exposure to 2450-MHz radiation at 1 to
10 mW/cm2. The linear regression of colonic
temperature after 5-HT vs. Ta calculates to a slope of
0.30°C colonic temperature/°C Ta. Plotting the 5-HT
colonic temperature against power density yields a
slope of 0.15°C colonic temperature/1.0 mW/cm2.
Dividing the Ta response by the RF-radiation
response, we obtain
Figure 4-20. Effects of 6-HT injection* on mice (data from
Smialowicz »t al. 1981 b). (a) Linear regression of
colonic temperature after an intraperitoneal injec-
tion of 5-HT at various T.'s. The drop in body
temperature increases with decreasing T.. (b)
Linear regression of 5-HT-induced hypothermia
for various power densities at 2450 MHz. Similar
to ambient temperature, the magnitude of hypo-
thermia is less with an increasing power density.
38
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4-19
-------
030 °C colonic temp
1.0°C ambient temp _ ,.,, , ,„_
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0 15 °C colonic temp
1.0 mW/cm2
That is, for the mouse a 2-mW/cm2 increase in the
power density (2450 MHz) is equivalent to a 1°C
increase in TB when tested at a T, of 22°C. This study
is one of the very first attempts to relate ambient
temperature and RF-radiation exposure.
4.1.3.2 Hamster
Berman et al. (1982) exposed Syrian (Golden)
hamsters to 2450-MHz (CW, far field) at a 22°C Ta and
50-percent RH. The change in rectal temperature
before and after 100 min of exposure was -0.8°C ±
0.4 at 0 mW/cm2, -0.4°C ± 0.5 at 20 mW/cm2 (SAR
~ 6 W/kg), and + 0.8°C ± 0.7 at 30 mW/cm2 (SAR
~ 9 W/kg). Considering just the rectal temperatures at
the end of RF-radiation exposure, an SAR of 9 W/kg
induced a temperature of 39.8°C, compared with
38°C for the controls.
4.1.3.3 Rat
A majority of the data on temperature regulation
during RF exposure has been collected from rats.
Phillips et al. (1975b) measured colonic temperature
in restrained rats immediately after they were
exposed to 2450 MHz at a Ta of 24°C for 30 min.
Colonic temperature was elevated by 0.6°C and
0.7°C immediately after exposure to 4.5 and 6.5
W/kg, respectively. Immediately after exposure to
11.1 W/kg, core temperature was 1.7°C above the
control group. Within 30 min after RF-radiation
exposure the colonic temperature of all exposed
groups had returned to the unexposed level.
However, during the course of recovery (over 5 h) the
colonic temperature of the exposed animals
undershot the control group. For example, the colonic .
temperature of the 11.1 -W/kg group was nearly 1 °C
below the controls 2 h after the termination of RF-
radiation exposure.
Several investigators have measured rectal or colonic
temperature of unrestrained rats following RF-
radiation exposure. Berman era/. (1981) exposed rats
to 2450 MHz for 100 min (Ta = 22°C, RH =50 percent)
at a power density of 28 mW/cm2 (SAR —4.2 W/kg)
and found colonic temperature to increase from 38.2
to 40.3°C. Berman and Carter (1984) exposed
unrestrained rats to 2450-MHz RF radiation for 100
min (Ta = 22°C, RH = 50 percent) to 40 mW/cm2 (SAR
~ 6.0 W/kg) and found an increase in colonic
temperature from 37.6 to 39.6°C. Lotz and Michaelson
(1978) found a significant increase in colonic
temperature (0.27°C) of unrestrained rats following a
30-min exposure to 2450 MHz at a power density of
13 mW/cm2 (SAR -2.1 W/kg) at a Taof 24°CandRH
of 40 to 60 percent. Increasing the duration and
power density led to a further increase in colonic
temperature. From the same laboratory, Lu et al.
(1977) found a 0.7°C increase in colonic temperature
after 120 min of exposure to 2450 MHz (Ta=24°C. RH
= 40 to 60 percent) at a power density of 20 mW/cm2
(SAR — 5.0 W/kg). Under similar environmental
conditions, Lu et al. (1981) found a significant (0.5°C)
increase in colonic temperature after 60 min of
exposure to 2450 MHz at a power density of 20
mW/cm2 (SAR - 4.2 W/kg).
D'Andrea et al. (1977) found a significant rise in
colonic temperature (~ 0.04°C/min) in unrestrained
rats (Ta = 21 °C, RH = 27 percent) exposed to 600 MHz
for 55 min at a power density of 10 mW/cm2 but not
at 7.5 mW/cm2 (SAR ~ 7.5 and 5.7 W/kg,
respectively). In the same study, rats were exposed to
RF frequencies of 400, 500, 600, and 700 MHz at a
power density of 20 mW/cm2 while the rate of
increase of colonic temperature was measured. A
frequency of 600 MHz was found to have the greatest
thermal effect. Changing frequency in 100-MHz
increments above or below this point resulted in
lower rates of warming. Thus, 600 MHz appears to be
the resonant frequency for the rat (body weight — 350
g). The Radiofrequency Radiation Dosimetry Handbook
(Durney et al. 1978) also predicts 600 MHz to be
resonant for the rat, as based on a prolate spheroid
model.
Phillips et al. (1973) assessed the effects of repeated
RF-radiation exposure on metabolic rate and on skin
(tail) and colonic temperature immediately after a 30-
min exposure to 2450 MHz at an SAR of 11.1 W/kg.
One group of rats was exposed for 10 days to 30
min/day of 2450 MHz (11.1 W/kg). The control group
was subjected to 9 sham exposures followed by a 30-
min exposure to 2450 MHz on the 10th day. The
group that was exposed every day showed acclimation
to RF-radiation exposure. For example, the group
exposed only once to RF radiation had a 3.9°C
elevation in colonic temperature, whereas the group
exposed to RF radiation on 10 consecutive trials had a
temperature elevation of 3.1 °C. Skin temperature
and colonic temperature followed similar patterns.
Both rat groups had similar depressions in metabolic
rate following exposure. This study shows that rats
can apparently acclimate to repeated exposures of
2450 MHz. Acclimation to RF-radiation exposure
appears to enhance heat-dissipatory mechanisms,
since the acclimated group had a lower body
temperature following exposure.
The variability in temperature regulation of rats
reported in the above studies is of interest. At 2450
MHz Berman et al. (1981) found a 2.1°C rise in
colonic temperature after 100 min of exposure at 4.2
W/kg, whereas Lu et al. (1977), using similar
environmental conditions, found that a 120-min
exposure to 5.0 W/kg led to only a 0.7°C increase in
colonic temperature. D'Andrea et al. (1977) did not
4-20
-------
observe significant colonic warming at 600 MHz until
SAR equalled 7.5 W/kg. The variation in methodology
(e.g., airflow, degree of restraint, animal training)
used at different laboratories appears to have a large
impact on the results of temperature regulation
during RF-radiation exposure.
4.1.3.4 Rabbit and Dog
Ely and Goldman (1956) exposed restrained rats,
rabbits, and dogs to 2884-MHz (PW) radiation A
rectal thermistor probe was connected in a closed-
loop feedback to the RF generator such that the
average power for maintaining rectal temperature at
a given level could be constantly delivered to the
animal. They found for each species that a power
density of ~ 25 mW/cm2 was required to maintain
rectal temperature 1 °C above normal. At this power
density the estimated SAR was 5.0 W/kg for the 0.2-
kg rat, 1.6 W/kg for the 4.0-kg rabbit, and 0.9 W/kg
for the 10-kg dog. This SAR value for a 1°C risemthe
temperature of the rat is similar to the data obtained
at 2450 MHz that have been reported more recently
by other investigators. (See citations above.) It should
be noted that the metallic temperature probe may
have affected the measurement of rectal temperature
in the rat (Ely and Goldman 1956).
Michaelson et al. (1961) exposed confined dogs to
2790 MHz (PW) while recording rectal temperature
at a Ta of 23 to 41 °C. Exposure for 1 to 2 h at power
densities of 100 or 165 mW/cm2 (SAR ~ 3.7 to 6.1
W/kg) caused elevations in rectal temperature of
approximately 1.5°C at a Ta of 22°C. The change in
rectal temperature with time had three principal
phases (Figure 4-21): (I) during the first 25 min of
exposure the rectal temperature rose rapidly, with the
dogs increasing their ventilatory frequency (panting);
(II) for the next ~ 40 min rectal -temperature was
relatively constant at the hyperthermic level; and (III)
after approximately 1 h of exposure there was a
breakdown in the capacity of the dogs to dissipate
heat, and rectal temperature increased rapidly,
approaching lethal limits. Anesthetizing the dogs
with pentobarbital sodium or chlorpromazine greatly
reduced the capacity to maintain body temperature
during RF-radiation exposure. (See also Ely et al.
1964).
The response of RF-exposed dogs to have a relatively
constant but hyperthermic body temperature (Phase
II; see Figure 4-21) might suggest that the animals are
thermoregulating normally since rectal temperature
is maintained at a steady level below lethal limits.
However, as discussed at the beginning of this
section, when core temperature exceeds the normal
mean by more than 1 standard deviation, the animal
is classified as hyperthermic. Conservatively, one can
view any increase in body temperature that occurs
during Phase II as a failure to maintain normal body
temperature; however, the rise in body temperature
may also be viewed as a response of the dog to better
Figure 4-21. Example of the triphatic rectal temperature
response of a dog exposed to 2790-MHz RF
radiation at a power density of 165 mW/cm2
(data from Michaelson ft al. 1961).
• Initial Heating
• Increased
Respiratory Rate
• Decreased Depth
• Panting
• Thermal Equilibrium
• Breakdown
in Thermal
Equilibrium
• Collapse
43
42 -I
165 mW/cm2 2790MHz
I II
15 25 35 45 55 65 75 85
Time, min
survive the thermal effect of RF-radiation exposure.
For exa mple, if the average body temperature of a 10-
kg dog is allowed to rise by 2°C, a considerable
amount of water is saved that would normally be used
to dissipate the additional heat. The water savings
would be calculated as:
Water saved (g) =(ATb)
-------
of power density at 2450 MHz to achieve a 1 °C rise in
rectal temperature of the rat, squirrel monkey, and
rhesus monkey and the logarithm of body mass (cf.
Figure 4-13). The approximate SAR was 5.8 W/kgfor
the rat, 2.5 to 4.5 W/kg for the squirrel monkey, and
4.7 W/kg for the rhesus monkey (Ta = 22.5 to 24°C).
Adair and Adams (1982b) found very slight increases
in rectal temperature of squirrel monkeys exposed to
2450 MHz at SARs from 1.5 to 3.0 W/kg (initial Ta -
35°C). However, in these experiments the monkeys
could control their Ta. The animals appeared to
counter the rise in core temperature by selecting a
cooler Ta.
Lotz and Podgorski (1982) recorded rectal temperature
in restrained rhesus monkeys exposed for 8 h to 1290
MHz at power densities of 0, 20,28, and 38 mW/cm2
(SAR ~ 0 to 4.1 W/kg) at a Ta of 24°C and RH of 55
percent. Rectal temperature increased an average
0.5°C at 2.1 W/kg, 0.7°C at 3.0 W/kg, and 1.7°C at
4.1 W/kg. It is of interest to compare these results to
that of the de Lorge (1979) experiment with monkeys
working for food at a frequency of 2450MHz. At 2450
MHz and a Ta of 24°C, a 1 °C rise in recta I temperature
of the rhesus monkey was observed at an SAR of ~
4.7 W/kg (de Lorge), compared with a 1.7°C rise
when exposed to 1290 MHz at 4.1 W/kg (Lotz and
Podgorski).
Lotz (1982) compared the effects of 225-MHz (near
resonance) and 1290-MHz (supraresonance) RF-
radiation exposure on the rectal temperature of
rhesus monkeys at a Ta of 24°C. Monkeys were
generally exposed for 4 h at either frequency. At 1290
MHz a 0.5 to 0.6°C rise in rectai temperature was
achieved at a power density of 28 mW/cm2 (3.0
W/kg). During exposure to 225 MHz, a similar rise in
rectal temperature was achieved at a power density
of only 2.5 mW/cm2 (1.2 W/kg). Thus, as the
frequency approached resonance the efficacy to raise
rectal temperature of the rhesus monkey improved.
Overall, for the rhesus monkey at 2450 MHz, rectal
temperature rose 0.21 °C per W/kg increase in SAR; at
1290 MHz the conversion factor was 0.24 to 0.41 °C
per W/kg; and at 225 MHz the conversion factor was
0.45 to 0.78°C per W/kg increase in SAR. It was
estimated that the rhesus mo'nkey could not
thermoregulate within reasonable limits (42°C rectal
temperature) for longer than 1 h at an SAR of 2.4
W/kg at a frequency of 225 MHz.
4.1.3.6 Lethality
Heretofore this section has discussed the following
points: (i) relatively low levels of RF-radiation
exposure lead to the activation of thermoregulatory
effectors such as peripheral vasodilation, evaporation,
metabolism (decrease), and behavior (selection of a
cool Ta), which together increase heat loss from the
body to the environment; and (ii) as the level of RF-
radiation exposure exceeds the capability of the
species to dissipate the RF heat load, heat gain
exceeds heat loss, and there is a rise in average body
temperature. If the exposure reaches the level
whereby body temperature cannot be controlled, then
thermal death will occur. Therefore, it is appropriate
to review briefly the levels of RF-radiation exposure
that cause thermal death.
In general, the lethal core temperature of homeo-
therms is approximately 6°C above the average
normal core temperature (Table 4-2). These data are
derived from work done at high Ta's, not RF-radiation
exposure. The information is provided only to
familiarize the reader with the general upper limits of
body temperature of homeotherms.
Table 4-2. Approximate Normal and Lethal Core Tempera-
ture* of Some Bird* and Mammals*
Animal
Marsupials
Euthenan mammals
Man
Birds, nonpasserine
Birds, passerine
Normal Core
Temperature
<°C)
35-36
36-38
37
39-40
40-41
Lethal Core
Temperature
(°C)
40-41
42-44
43
46
47
'Compiled by Schmidt-Nielsen (1979).
Rugh et al. (1974) measured lethality in mice exposed
to 2450 MHz in a waveguide for various durations up to
5 min. The forward or incident power into the
waveguide was 7.37 W. Assuming an average
absorption efficiency of 42 percent (Ho and Edwards
1977), the estimated SAR was approximately 99
W/kg. The lethal dose, calculated in dimensions of
J/g body mass, was measured at various air
temperatures (15 to 40°C) and relative humidities(25
to 70 percent). The temperature-humidity index(THI)
was used to assess the influence of the interaction
between temperature and relative humidity on
lethality (THI = 1.41T + 0.1 RH + 30.6). The lethal dose
at 2450 MHz varied from 20 to 77 J/g and was
inversely related to THI (Figure 4-22).
In a similar experimental protocol Rugh (1976b)
measured the lethal dose of RF radiation and the final
rectal temperature at the time of death in mice
exposed to 2450 MHz. The average lethal dose for 1 -
month-old weanlings, 2-month-old animals, and
adults more than 12 months of age was approximately
40 to 45 J/g. The mean rectal temperatures at the
time of depth for male and female mice of all ages was
46.6°C; however, in isolated cases, body temperature
rose as high as 50°C before death occurred. The
average lethal temperature is substantially higher
compared to previous reports (Table 4.2).
4.1.4 Effect of Body Size on Thermoregulatory
Sensitivity to RF Radiation
Few data exist on the whole-body thermoregulatory
effects of RF-radiation exposure in humans. Detailed
4-22
-------
Figure 4-22. Effect of an increasing THI on the lethal dose of
RF radiation (2450 MHz) in mice (data from Rugh
«tal. 1974).
100
60 70 80 90 100
Temperature-Humidity Index (THI)
information on the dose response of humans to whole-
body RF-radiation exposure may never be collected.
Thus, we must rely on data collected on laboratory
mammals.
Extrapolation of RF-radiation effects in laboratory
mammals to humans has been attempted (Michaelson
and Schwan 1973; de Lorge 1979; Ely et at. 1964). A
degree of uncertainty exists in predicting the
response of humans to RF-radiation exposure by
extrapolation from the known bioeffects data
collected in laboratory mammals. An obvious
disadvantage to such extrapolations is the large
difference in body size between experimental
mammals and adult humans. For example, the mass
of a laboratory rodent or a primate is 1.0 to 3.4 orders of
magnitude smaller than the mass of a human
(assuming an average adult male human body weight
of 70 kg).
In many respects, the thermoregulatory physiologic
processes of laboratory mammals and humans differ
markedly. A prime example is the physiologic
mechanism of heat dissipation during thermal stress.
At high Ta's, primates rely principally on sweating to
dissipate excess body heat, whereas rodents are
unable to sweat but can dissipate heat through
insensible evaporative water loss from the skin and
respiratory tract (Sec. 4.1.1.6). Primates commonly
used for RF-radiation experiments, such as squirrel
monkeys (which sweat only on feet and hands) and
rhesus monkeys sweat when subjected to heat
stress, but these mammals are considerably smaller
than humans (~ 1 and 5 kg, respectively). Hence,
physiologic data collected on laboratory primates
during RF-radiation exposure may aid in predicting
human responses, but the dose-response differences
between humans and primates may be very large.
Computer models of the human response to RF-
radiation exposure are useful for estimating the
probable magnitude of the threshold SAR capable of
activating physiologic responses (Sec. 4.2). Modelers
attempt to compensate for the problems mentioned
above by using appropriate physiologic responses of
adult humans to heat stress, for which abundant data
exist, to calculate human responses to RF-radiation
exposure. The physiologic responses incorporated
into the computer models are those of humans
exposed to high Ta's and/or exercise, but not to RF-
radiation. Thus, these models can be used to
calculate a dose-response relationship to RF-
radiation exposure if the physiologic responses are
the same as those of humans subjected to natural
forms of heat stress (e.g., exercise and/or radiant or
convective heat). However, the similarity of response
between RF-radiation exposure and heat stress from
exercise or exposure to high Ta's is currently under
debate because of the uniqueness of RF-energy
absorption.
The purpose of this section is to demonstrate that a
comparative analysis of the bioeffects of RF-radiation
exposure on laboratory mammals may be useful in
predicting SAR thresholds for exposed humans, if the
effe'ct is assumed to be due only to heating of tissue.
Heretofore, data on the physiologic and behavioral
effects of RF-radiation exposure have been presented
for various laboratory mammals with body masses
ranging from 0.02 to 7.0 kg, the largest body mass
being 350 times greater than the smallest. If a
relationship exists between an animal's mass and its
sensitivity to thermalizing levels of RF-radiation, then
an analysis of the known physiologic effects and their
corresponding threshold SARs over such a wide span
in body mass should allow a reliable extrapolation to a
body mass of 70 kg. This would be an extrapolation of
only a tenfold increase in mass and could give an
estimation of SAR thresholds for humans.
4.1.4.1 Effect of Body Mass on Thermal
Physiology of Mammals
An animal's weight, mass, and volume are propor-
tional to the cube of its radial dimension, whereas its
total surface area is proportional to the square of its
radial dimension (for discussion, see Schmidt-
Nielsen 1975). Thus, an animal's total surface area
increases by approximately the 0.67 power with
increasing body mass. Also, the surface area.mass
ratio decreases logarithmically with increasing body
mass. A regression line based on mammalian body
mass vs. surface area/body mass has a slope of -0.33
(Figure 4-23).
The importance of the surface area:mass ratio in the
physiology of homeothermic animals can be
illustrated by comparing the metabolism of two
species with large differences in body mass, such as a
70-kg human and a 0.03-kg mouse. In Figure 4-23,
4-23
-------
Figure 4-23. Relationship between the surface area:body mass ratio and the body mass of various mammals (data from Altman and
Dittmer 1972). The solid line represents the same relationship for a sphere of density 1.0.
1.0-
Mice
-------
Figure 4-24. Relation between metabolic rate and body mass of mammals (data from Schmidt-Nielsen 1975). All measurements
were made on resting animals under thermoneutral conditions.
IOC-
(D
tr
.2
"o
10-
1 -
Mice
\
Squirrels
Rats
Dogs •
Sheep
Humans
0.001
I
0.01
I
0.1
I
1.0
10.0
I
100.0
Body Mass, kg
larger mammal. The 72-percent increase in a human
represents slightly less than a doubling of metabolic
rate.
The relation between body mass and percent
increase in heat loss necessary to maintain
normothermic temperature during exposure to RF
radiation at SARs of 0.1, 0.4, and 1-.OW/kg is shown
in Figure 4-25. An SAR of 0.4 W/kg represents the
recently suggested exposure guideline recommended
by ANSI (1982). Because of the logarithmic
relationship between surface area and body mass,
the percent heat loss increases exponentially with
body mass.
Data from exercise physiology research provide
valuable insight into the influences of body mass on
the threshold percent heat loss necessary for
activating a physiologic response. In a comparative
analysis of these data, Taylor (1977) calculated
the maximum rate of passive heat, or nonevaporative
heat, which mammals can dissipate as a function of
body mass. An inverse relationship was shown to
exist between body mass and magnitude of
nonevaporative heat loss (Figure 4-26). For example,
a 0.02-kg animal can dissipate 9 times its metabolic
heat production with nonevaporative heat loss,
whereas a 100-kg animal can dissipate only 4.5 times
its metabolic heat production (assuming a 20°C
gradient between body and ambient temperature). If
an increase in evaporative heat loss is used as a
biological end point, the total heat loss of 0.02-kg
animal would have to exceed 90 W/kg before it was
observed, whereas that of a 100-kg species would
have to exceed only 6 W/kg. Of course, the thermal
load from exercise and RF-radiation exposure cannot
always be equated physically or physiologically.
However, Taylor's analysis is presented here to show
that because of surface area:body mass relationships,
a small mammal can passively dissipate heat at a far
greater rate than a larger mammal.
Ambient temperature is critical in determining a
homeotherm's sensitivity to a heat load. For example,
at a Ta of 20°C, humans exercising at a work load of
40 W experience a 2.5-W/kg increase in heat
production (and loss) and a slight elevation in
evaporative heat loss. However, when the same work
is performed at 30°C, the increase in evaporative heat
loss is 5 times the magnitude of heat loss at 20°C
(Sec. 4.1.1.6).
It would not be surprising to find, given the above
analysis, that relatively high SARs are required to
promote a thermoregulatory response in small
experimental animals. Figure 4-27 is a plot of the
SARs necessary to either activate a thermoregulatory
effector or raise body temperature in the mouse,
hamster, rat, squirrel monkey, and rhesus monkey.
The data points essentially represent all the data
discussed in Sees. 4.1.1.1, 4.1.2, and 4.1.3. The data
include SARs required to raise skin temperature.
4-25
-------
Figure 4-25.
Relation between mass and percent increase in
whole-body heat loss necessary to maintain
normothermia in mammals exposed to RF radi-
ation at SARs of 0.1. 0.4. and 1.0 W/kg. The
calculations are based on the assumption of
resting metabolic rate at a thermoneutral T., as in
Figure 4-24. Percent heat loss was calculated as
[SAR/fSAR + metabolic rate)] X 100.
80-
10
CO
= 40-
0.01
Figure 4-26.
0.1 1.0 10
Body Mass, kg
100
Effect of body mass on the maximum rate of
nonevaporative heat loss relative to resting metab-
olism in mammals during exercise at a T. of 20°C
(data from Taylor 1977). The calculations are
based on the assumption that thermal conduc-
tance is a constant 1 cal (cm2 • h • °C)~'.
10
2 5
0.1
1.0 10
Body Mass, kg
4-26
100
1000
Figure 4-27. Relationship between SAR and T. on the activa-
tion of various thermoregulatory effectors and
elevation in body temperature in the mouse,
hamster, rat, squirrel monkey, and rhesus monkey
exposed to RF radiation. Data points represent
those discussed in Sees. 4.1.2 and 4.1.3. Expla-
nation of code: B—threshold for change in
preferred T., BT—elevated colonic temperature
(0.3 to 2°C), C—elevated serum corticoids,
EWL—threshold for increasing evaporative water
loss, MR—threshold for lowering metabolic rate,
P—threshold for altering posture, PVMT—thres-
hold for altering peripheral vasomotor tone (i.e.,
vasodilation), and VF—threshold for elevating
ventilatory frequency. Note logarithmic scale of
abscissa. RF—radiation frequency was 2450 MHz
for all species except rhesus monkey (1290 and
225 MHz).
o
o
eg
i
0>
h-
c
.2
1
30
20
40
30
20
10
40
30
20
10
40
30
20
10
40
30
20
10-
Mouse B B pVMT P
VF •• .\'EWLD
MR BTV -P
MR
Hamster
BT
BT T^MR
B BT
Squirrel Monkey B
MR
Rhesus Monkey
BT BT BT.BT
C
0.1 1.0 10 10C
SAR, W/kg
elevate evaporative water loss, lower metabolic rate,
alter behavioral temperature regulation, and raise
deep-body temperature by 0.3 to 2.0°C. The data are
also plotted as a function of the Ta at which the
thermoregulatory parameters were mesured. A trend
is evident in Figure 4-27, despite the variations in Ta
and RF frequency; that is, the SAR required to activate
a thermoregulatory effector or raise body temperature
decreases with increasing mass of the species.
The lowest SAR shown in Figure 4-27 at which body
temperature of rhesus monkeys was elevated (Lotz
1982) is important because exposure occurred at a
near-resonant frequency of 225 MHz. Resonant
exposure, in which the energy is deposited very deep
in the body, may be a worst-case situation. Similar
SARs at a supraresonant frequency of 1290 MHz
caused less severe rises in body temperature of the
rhesus monkey. The mouse body temperature data in
-------
Figure 4-27 were also collected at a near-resonant
frequency (2450 MHz). For a 0.03-kg mouse exposed
to resonant RF radiation at a Ta of 22°C, an SAR of 22
W/kg was required to raise the body temperature 0.5
to 1 °C. For a comparable temperature rise in a 4-kg
rhesus monkey at a Ta of 24°C, an SAR of only 1.2
W/kg was required. Assuming that large species
follow a pattern similar to that of small species, an
animal having 17 times the mass of the rhesus
monkey (e.g., 70 kg, the mass of an adult human)
exposed to a resonant RF radiation would be expected
to undergo a similar rise in temperature at an SAR
less than 1.0 W/kg.
4.1.4.3 Relating Heat Stress from RF-Radiation
and Ambient Temperature Exposure
To some, there is a paradox in the hypothesis of the
foregoing discussion concerning an inverse relation-
ship that exists between body mass and the threshold
SAR for activation of a thermoregulatory response.
As mentioned earlier (Sec. 4.1.1.6), humans are well
adapted to warm environments and are able to
survive high Ta's much longer than smaller
homeotherms such as rodents, rabbits, and infra-
human primates. There is an abundance of research
on the functioning of humans in hot environments
(Dill et a/. 1964; Hardy and Bard 1974). However, one
must be very careful in relating the adaptability of
humans to survive high Ta's to that of thermoregulating
during RF-radiation exposure.
The problem with such a comparison is that the data
on human thermoregulation in hot environments are
reported intermsofTa(°C), relative humidity (percent),
wind velocity (m/s), etc. In the study of RF radiation
the whole-body dose rate is commonly measured in
W/kg. The dimensions °C and W/kg have no
relationship to each other. Simply stated, an RF-
radiation field represents a heat source (i.e., M
increases in the heat balance equation; see Sec.
4.1.1). On the other hand, increasing Ta does not
represent a heat source (provided Ta is less than Tre)
but rather impedes the dissipation of metabolic heat
(i.e., raising Ta lowers K, C, and R in the heat balance
equation). One can be misled by a prediction of an
animal's response to a W/kg dose rate if the
prediction is based only on the animal's response to
ambient conditions. For example, in Sec. 4.1.1.9 it
was shown that a human exposed to a very hot
environment of 55°C Ta underwent a positive change
in the rate of heat storage of 0.6 W/kg. A small rodent
could not possibly survive this Ta exposure for very
long, mainly because its surface area/mass ratio is so
much larger than the human that the rodent will heat
at a tremendously faster rate. On the other hand, the
small rodent, because of the surface area/mass
relation, can tolerate a much larger dose rate of RF
energy (W/kg). A mouse with a body mass of 30 g has
a metabolic rate of 10 W/kg, which is more than 16
times greater than the increase in the rate of heat
storage of the human exposed to a Ta of 55°C.
Another way of viewing this problem is to look at the
change in heat production during exercise. The
maximal increment in metabolism of mammals with a
mass of 0.018 to 25 kg is approximately 7 times
greater than the basal metabolic rate (Hart 1971).
Well-trained athletes can endure 10 times the basal
metabolic rate. This implies that the 0.03-kg mouse
can endure an overall increase of approximately 50
W/kg, which is 3 times greater than the maximal
increase of a well-trained athlete (~ 15 W/kg). Thus,
it is apparent that heat tolerance measured in °C (Ta)
is not a valid indication of tolerance in terms of the
rate of tissue energy absorption by the whole body
(W/kg). The relationship in Figure 4-27 only affirms
this deduction. Small homeotherms generally have
much higher threshold SARs than larger species
during exposure to RF radiation.
4.1.5 Unresolved Issues
At least three major issues in thermal physiology
remain unresolved: (i) the effect of various thermal
environments (exogenous or endogenous) encount-
ered by most human beings that might affect their
sensitivity to RF-radiation exposure, (ii) the validity of
extrapolating the known bioeffects data in laboratory
animals to humans, and (iii) the effect of RF-radiation
frequency on thermoregulation. These issues are
discussed below.
(i) Elevating Ta above thermoneutrality places a
greater strain on the capacity of the thermoregulatory
system to dissipate body heat. In such a situation an
organism's normal thermoregulatory response to RF
radiation is compromised. Most of the data concerning
RF-radiation effects on thermoregulation have been
collected in experiments with animals at a Ta below
their thermoneutral zone. At a Ta below the
thermoneutral zone the thermoregulatory system has
a substantial capacity to dissipate the RF heat load. At
Ta's above the thermoneutral zone homeotherms rely
mostly on evaporation to dissipate heat. One can
visualize the potentially stressful situation of a
human exposed to 0.4 W/kg, or ~ 25 percent of the
resting metabolic rate, at a Ta of 35°C(96°F). At this Ta,
at least 90 percent of the heat lost is dissipated by
evaporation (Sec. 4.1.1.9). Assuming that a human
must evaporate 1 g of water for each 2426 J
dissipated, in an environment of a Taof 35°C in which
the human is absorbing 0.4 W/kg RF radiation, the
amount of evaporative water loss would increase by
— 25 g/h -m2 over the base-line level of 50 g/h-m2. If
the exposure took place at a Ta below the thermoneu-
tral zone, most RF heat could be dissipated by
radiation and convection or by lowering metabolic
rate.
Either hot and dry or warm and humid environments
are commonly encountered by much of the human
4-27
-------
population during the summer. In addition to these
ambient heat loads, one must consider altered thermal
states created by exercise and fever. These conditions
raise body temperature, which makes the effects of RF
radiation on thermoregulation more apparent than in
the nonworking or afebrile subject. Overall, combina-
tions of abiotic factors (ambient temperature, relative
humidity, solar radiation, "wind chill," and insulation)
and biotic factors (fever, exercise, and the presence of
medication or pathological conditions that impair
thermoregulation) clearly make predicting the
thermoregulatory capacity of a human population
a very difficult task.
(ii) Can the thermoregulatory data collected in
laboratory animals be used to predict how human
beings might respond to RF-radiation exposure? In
Sec. 4.1.4 a discussion is presented of how body
mass influences the sensitivity of homeotherms to
thermalizing levels of RF radiation. On this basis it
may be possible to extrapolate the known bioeffects
data of laboratory mammals to humans. However, it
should be noted that this concept of extrapolation is
not universally accepted in the scientific community.
For example, Adair et a/. (1983) were strongly critical of
the attempt by Gordon (1982a) to extrapolate the
known bioeffects data from laboratory mammals to
humans based on body mass. It was stated by Adair et
al. (1983) "Since we understand the thermoregulatory
responses of man far better than the responses of
any other species, and can quantify them more
accurately, it is clear that no relation as that depicted in
Fig. 5 (i.e., the graph showing an inverse relation as
between body mass and threshold SAR) of Gordon
(1982a)can possibly exist." Accordng to Adair, in the
area of thermoregulation it is impossible at this time
to extrapolate from animals to humans (E.R. Adair,
personal communication).
However, Gordon (1983e) countered these criticisms
by stating that our understanding of human
thermoregulatory physiology is based on research of
exposure to conventional heat sources (e.g., high Ta,
infrared heat, and exercise), not to whole-body RF-
radiation exposure. Thus, in the study of the effects of
RF radiation on thermoregulation we understand the
thermoregulatory responses of laboratory animals far
better than those of human beings (Gordon 1983e).
Because nearly all research in the study of RF
radiation has been performed on inf rahuman species,
it is essential to have a means of extrapolating the
animal data to humans. The use of body mass as an
independent parameter for scaling the bioeffects of
RF radiation may be useful.
(iii) Because of the nonuniformity of RF-energy
deposition, the frequency of RF radiation (at a given
SAR) has a large impact on the thermoregulatory
system. Resonant frequencies appear to be a worst-
case situation (e.g., see discussion on primates in
Sec. 4.1.2). Average whole-body SAR perse may not
adequately define the potential thermal effect of RF-
radiation exposure because the frequency relative to
the size of the animal (that is, infraresonant,
supraresonant, or resonant) must be considered in
evaluating the thermoregulatory effects of RF
radiation.
4-28
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4.2 Numerical Modeling of
Thermoregulatory Systems in Man
Ronald J. Spiegel
This section reviews the models for calculating the
thermal response of human beings exposed to RF
fields. From this review the following generalizations
can be drawn:
• The models predict that an exposure to a plane-
wave field at 80 MHz (the whole-body resonant
frequency for the adult human) will produce the
highest temperatures in the legs.
• An exposure to a plane-wave field at 200 MHz
(partial-body resonance in the arms) produces the
highest temperatures in the arms.
• Elevated temperatures tend to occur where the
localized SARs are the largest.
• Higher localized temperatures are produced at
whole-body resonance because the body absorbs
more energy from the incident field.
The limitations of the numerical models are
discussed in Sec. 4.2.4, Unresolved Issues.
4.2.1 Heat-Transfer Models
It is important to develop accurate mathematical
models to predict the absorption of electromagnetic
energy and the thermal response of biological
subjects. Mathematical modeling can provide a
method for gaining qualitative and quantitative
information that may be valuable in explaining and
understanding many of the effects measured in
experimental animals. More important, experimenta-
tion on human subjects is often unethical. Thus, to
extrapolate RF-field results in experimental animals
to equivalent effects in man, one must know
thoroughly the dosimetry for both species. This
knowledge can be achieved by the application of a
sophisticated and realistic numerical simulation of the
energy absorption and subsequent thermal response
of subjects exposed to RF fields.
Several investigators have developed mathematical
models to calculate the thermal response of the
human body when it is subjected to different environ-
mental conditions or levels of exercise. The same basic
approach can be taken to develop a model to simulate
the thermal response to RF radiation. However, this
model must take into account that RF fields deposit
energy nonuniforrnly in the human. The simple one-
dimensional heat transfer models used in the past do
not accurately simulate this condition. However, a
short review of these previous attempts to model man
in one dimension provides a good background for
developing a more general model.
One of the earliest attempts at modeling the human
body was made by Pennes (1948), who developed a
cylindrical model of a human limb. This model was
first used to simulate the human forearm but was
later applied to the general case of limbs. The
following factors were included in this model: (1)
radial conduction, (2) metabolic heat generation, (3)
convection to the blood, and (4) environmental
exchange by convection, radiation, and evaporation.
Machle and Hatch (1947) introduced the concept of a
core-and-shell model by comparing measured values
of rectal and skin temperatures representing the core
and shell temperatures used in the model. Empirical
correlations for radiation, convection, and evaporation
were experimentally developed for inclusion in this
model. A modification by Kerslake and Waddell
(1958) extended the model to include the case of
complete skin wetness due to sweating.
Wyndham and Atkins (1960) further extended the
core-and-shell model by introducing several concen-
tric cylinders representing the various body layers.
This model used a finite-difference technique to solve
a set of resulting first-order differential equations by
an analog computer.
A more rigorous analytical approach was taken by
Hardy (1949), who applied the laws of thermodyna-
mics and heat transfer to the human system. This
analysis included radiant exchange with the
environment, thermal conduction through concentric
cylinders, natural and forced convection, and
evaporation from the skin and lungs. The analysis
was accompanied by experimental verification of
several of the calculated responses.
Wissler (1961, 1964) modified the models of Pennes
and Wyndham and Atkins and combined them to
obtain a model of the entire human body. This model
sub-divided the body into six elements: head, torso,
two arms, and two legs. Each of these elements was
assumed to have the following: (1) a uniformly
distributed metabolic heat generation, (2) a uniformly
distributed blood supply, (3) a composition of
homogeneous materials, and (4) a geometry of
isotropic cylinders. The effects of heat loss through
the respiratory system and countercurrent heat
exchange between the arteries and veins were also
included.
In contrast to the models based on concentric
cylinders, Crosbie era/. (1963) used an infinite-slab
model to represent an element of the body. These
investigators argued that the physics and physiology
of the human system could be better understood if
based on this configuration and that many uncertain-
ties in previous analyses could be clarified. This
model was programmed on an analog computer and
verified by experimental observation.
Smith and James (1964) developed another analog
model to study thermal stress in man. This model had
the following characteristics: (1) metabolic heat
production in the working muscles, (2) muscles
insulated by a layer of subcutaneous tissue, (3) blood
4-23
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flow from the muscles to the skin, and (4) blood flow
between various elements of the body and heart. This
model considered radial conduction through three
concentric cylinders and countercurrent exchange
between the arteries and veins, and it was verified
experimentally.
The next major effort at modeling the entire human
body was made by Stolwijk and associates at the John
B. Pierce Foundation Laboratory. The initial effort by
Stolwijk and Hardy (1966) was a model composed of
three cylindrical segments, one each for the head,
trunk, and extremities. The trunk was divided into
three concentric layers: skin, muscle, and core. The
head and extremities were divided into two
concentric layers: skin and core. In this work, the
concept of the body being composed of a controlled
system and a controlling system was suggested.
These investigators also did a rigorous review to
determine accurate thermal properties of the
constituents of the human body. This model was then
programmed for analysis by an analog computer and
compared to experimentally developed parameters.
The 1966 Stolwijk-Hardy model was expanded
(Stolwijk and Cunningham 1968; Stolwijk 1969,
1971; Stolwijk and Hardy 1977) to include six
segments: head, trunk, arms, hands, legs, and feet.
All these segments were composed of four layers:
skin, fat, muscle, and core. The geometry of each was
cylindrical except for the head, which was spherical.
This model was programmed for analysis by a digital
computer and included high metabolic heat production,
sweating, blood flow to all layers, and convective and
radiant exchange with the environment. Stolwijk's
model is one of the most comprehensive programs to
date, and has been used to investigate a variety of
heat stress situations. For example, for better
understanding of the effect of local hyperthermia,
heat has been deposited in local areas such as the
brain (Stolwijk 1980). In addition, several investigators
have adapted it to special cases; e.g., Montgomery
(1972; 1974a,b; 1975) used the model to study the
effects of man immersed in water.
Gordon et al. (1976) extended and improved the basic
ideas formulated by Stolwijk (1971) and Wissler
(1964) to model the human temperature regulatory
response after exposure in a cold environment. This
model characterized the human body as 14 cylindrical
and spherical segments with a cold exposure control
system. The control of metabolism, skin blood flow,
and muscle blood flow was achieved by feedback
controller signals consisting of the head core
temperature, mean skin temperature, and mean skin
heat flux. The heat flux control signal was not
included in previous models, but the results of this
study indicate that it is important when modeling the
human thermoregulatory response in cold environ-
ments.
4.2.2 RF-Radiation/ Heat-Transfer Models
As discussed earlier, there exist reasonably realistic
RF-energy deposition models (Sec. 3.2.3, Analytical
and Numerical RF Electromagnetic Interaction
Models) and heat transfer models (see above
discussion) for the human body. However, few
attempts have been made to combine the two models
to predict the body's thermal response under
exposure to RF fields. Inone study, Emery era/. (1976)
determined the thermal effects of a uniform
deposition of RF energy for a one-dimensional model
of heat conduction. Although this model may yield
realistic values for whole-body temperatures, the
heating pattern produced by nonuniform deposition of
energy may deviate substantially from that produced
by uniform absorption; this deviation may occur if
various parts of the body (head, arms, legs, etc.)
selectively absorb energy from the incident field
because of whole- and partial-body resonance. In
another study, Guy et al. (1978) used thermographic
determinations of the distribution of RF energy in
phantom models of man, which were subsequently
used to provide input for Emery's one-dimensional
thermal model. This method certainly accounted for
the nonuniformity in the RF-energy deposition, but it
apparently did not account for heat flow along the
major axis of the body. This factor is important,
because the primary nonuniformity in the RF-energy
deposition will occur along the body's major axis,
since the body is much longer than it is thick. Thus,
this model will tend to overestimate the temperature
profile in the body because the model allows heat
flow to occur only from the core to the skin. In reality,
as a result of localized RF-energy deposition, heat
flow must also occur along the major length of the
body.
The most general attempt to date has been the work
of Spiegel et al. (1 979, 1 980a), who have used block
models to calculate the RF-energy deposition in the
body with a two-dimensional extension of Stolwijk's
model to determine the resulting thermal response of
the body. This model allows heat flow from the core to
the skin as well as along the major axis of the body.
The authors used a transient heat conduction model
with internal heat generation and heat dissipation.
The internal heat generation is caused by metabolism
and absorption of RF energy. The internal dissipation
is caused by convective exchange with the cardiovas-
cular system and a combined convective and radiant
exchange with the surrounding environment at the
surface of the skin. The equation simulating the
response is, therefore,
pc
9t
where p= tissue density
c= tissue specific heat
T = local tissue temperature
4-30
-------
t=time
V=tissue volume
k=tissue thermal conductivity
OEM = electromagnetic energy deposition
QM = metabolic heat generation
QE = evaporative heat dissipation in the skin
QR = respiratory heat loss in the lungs
To solve Equation 4-1, the body is divided into several
finite elements and this relationship is applied to each
element or node. The body is represented by 15
segments, with each segment subdivided into 4
concentric layers — core, muscle, fat, and skin. The
head is modeled by a sphere; the neck, hands, and
feet are approximated as single cylindrical segments;
the arms and legs are each divided into four
cylindrical segments, and the trunk is divided into
three cylindricl segments. The radius and length of
each of these cylindrical segments are based on
dimensions for a standard man (Diffrient et al. 1974).
Calculations of heat capacitance, thermal conductance,
and density are based on the type of tissue, the
surface area, and the volume for each segment and
layer.
In this model, the time and spatial derivatives are
represented by finite difference approximations, and
the resulting system of equations is solved by an
iterative procedure in which the initial temperatures
are used to compute the temperatures a short time
later. These new temperatures are then used to
compute the temperatures at the new time and so on
until thermal steady-state conditions are reached.
Figure 4-28 shows the relationship of the various
thermal conductances for a typical segment that
includes four nodes in the finite element analysis.
Each lumped conductance represents heat exchange
with the other nodes. The quantities KC and KA
represent the radial and axial conductances,
respectively, the values of which are determined by
layer and segment geometry and by tissue thermal
conductivity (Carslaw and Jaeger 1959). Heat
exchange between the skin and surrounding
environment by convection and radiation is repre-
sented by the quantity H, which is determined in the
standard engineering manner as described by
Stolwijk (1971). The BF terms designate the amount
of heat exchanged by each node and the central blood
pool, and are a function of blood flow. Blood flow rates
to all segments, except the skin, are set to basal
values (Stolwijk 1971). The skin-blood flow rate is
controlled by vasodilatation, which is a function of the
temperature difference between the local skin
temperature and the skin set-point temperature, as
well as the difference in temperature between the
hypothalamic temperature and its set-point tempera-
ture. It is believed that all tissues respond to local
temperatures in excess of 40°C by an increase in
blood flow. However, the literature does not appear to
provide enough information to include this response
for all 100 compartments of the model.
The other heat exchange modes shown in Figure 4-
28 include metabolic heat production QM; heat loss
by sweat evaporation on the skin QE; respiratory heat
loss in the lungs QR; and electromagnetic heat input
OEM. The respiratory loss is determined according to
Stolwijk, and the model assumes that the expired air
has come to thermal equilibrium with the upper trunk
Figure 4-28. Block diagram for one segment of the thermal model.
OEM
QR
QM
KA
OEM
QM
OEM
OEM
CORE
BF
M
KA
MUSCLE
KA
BF
n
HS/NA/-
QE
QM
KA
FAT
KC
•'WV-
QM
KA
SKIN
KA
Central
Blood
Pool
BF
KA
KA
4-31
-------
core temperature and is saturated. This term enters
the equation for thermal balance (Equation 4-1) only
at the node that represents the core of the upper trunk
segment. Several mathematical models have been
proposed to calculate the heat lost by sweating
(Emery et al. 1976). All are empirical and attempt a
best fit to experimental data for various conditions,
such as for a sedentary subject or for various levels of
exercise. This model is based on the detailed work of
Stolwijk (Stolwijk 1971, Stolwijk and Hardy 1977).
Evaporation basically is controlled by the sweating
rate. As with the rate of blood flow, the term that
simulates sweating is a function both of the
temperature difference between the local skin
temperature and the skin set-point temperature and of
the difference between the hypothalamic temperature
and its set-point temperature. The body develops its
own source of heat as a result of metabolic heat
production QM. For a sedentary subject, this value
can be at the basal level or can be accelerated by
shivering. Shivering is initiated when the body is
subjected to a low ambient temperature (< 28°C for a
nude subject) and experiences a chill. Since the air
temperature for this study is always in excess of 28°C,
the effects of shivering and vasoconstriction are not
included in the analysis. The RF energy input term
OEM is calculated by a block model comprised of 180
cubical cells of various sizes (Hagmann et al. 1979a).
4.2.3 Numerical Results
To illustrate the model used by Spiegel et al. (1980a),
Table 4-3 shows the resulting steady-state tempera-
ture distribution in a resting, nude, 70-kg, 170-cm-
high man in a thermally neutral environment (air
temperature = 30°C; relative humidity = 30 percent)
exposed to a plane wave at 80 and 200 MHz. The
electric field vector is oriented parallel to the major
axis of the body (i.e., E polarization). Whole-body
resonance occurs for the 80-MHz field, and partial-
body resonance occurs in the arms for the 200-MHz
field. For the 80-MHz case, an incident power density
of 10 mW/cm2 is used (SAR = 2.25 W/kg). For the
200-MHz field, incident power densities are 10 and
32.5 mW/cm2 (SARs = 0.58 and 1.9 W/kg,
respectively). As mentioned above, the RF-energy
deposition term OEM is inserted into Equation 4-1 in
a manner prescribed by the 180-cell model.
The distribution of temperatures is quite different in the
two cases. For the 80-MHz field, a thermal hot spot
(a temperature of around 41.6°C) is generated in the
lower thigh; for the 200-MHz field the hot spot tends
to occur in the arms. In addition, for the 200-MHz
case there is an elevated temperature (40.6°C) in the
neck. Another difference is that the hot spot occurs
for an incident power density of 10 mW/cm2 for the
80-MHz field, whereas 32.5 mW/cm2 was required
to produce a hot spot for the 200-MHz case. This
difference occurs because the whole-body SAR is at
least four times greater for the 80-MHz field.
Table 4-3. Steady-State Temperatures (°C) ina Human Body
After Exposure to 80- and 200-MHz RF Fields
80 MHz 200 MHz
10mW/cm*
Segment
Head
Neck
Upper
trunk
Middle
trunk
Lower
trunk
Upper
humerus
Lower
Humerus
Upper
forearm
Lower
forearm
Hand
Upper
thigh
Lower
thigh
Upper
calf
Lower
calf
Foot
No.
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
Muscle
36.3
38.3
37.7
38.8
38.9
34.5
34.6
34.4
34.0
36.4
39.5
40.3
39.9
38.4
36.4
Core
37.4
38.9
37.3
37.5
37.8
35.9
36.0
35.7
35.0
36.6
40.3
41.6
41.2
40.0
36.8
10mW/cm2
Muscle
36.1
37.7
36.9
37.2
37.1
35.3
36.9
36.3
35.1
36.0
35.7
35.5
35.7
35.5
35.6
Core
37.0
38.2
36.9
37.0
37.0
36.5
38.0
37.5
36.1
36.2
37.0
36.7
36.9
36.4
35.8
32.5 mW/cm?
Muscle
37.0
40.6
37.6
39.3
38.4
37.0
41.2
39.8
36.9
36.4
35.8
35.7
36.7
36.7
35.9
Core
37.2
40.6
37.1
37.2
37.2
38.4
42.9
41.4
384
36.6
37.1
37.0
37.9
37.9
36.1
As another useful method to present the data. Figure
4-29 graphically shows the time it takes to obtain a
hot spot for a given level of incident power density
level for the two frequency conditions. The production
of a hot spot can be viewed in terms of a strength-
duration model; for example, Figure 4-29 shows that
the time required to create a hot spot in the lower
thigh for an 80-MHz field takes only a few minutes at
50 mW/cm2, but at 10 mW/cm2 it will take an hour or
more of exposure. In addition, different minimum
levels of power density are required to produce hot
spots at various body locations. For instance, the
rectal temperature profile has an asymptote at a level
just above 35 mW/cm2, but the lower-thigh core
temperature asymptote occurs around 10 mW/cm2.
For 200-MHz radiation, the lower humerus core
temperature was considered, and the intensity-
duration curve for this case is shown by the dashed
curve.
Based on these results the most critical temperature
elevations evidently occur at whole-body resonant
frequencies, as might be expected. In fact, the rise in
temperature is sufficient to produce a hot spot
(41.6°C) in the legs for an incident power density of
10 mW/cm2. The increased blood-flow response
(based on the calculated results) for tissue tempera-
tures in excess of 40°C was not included in the model.
Therefore, the model most likely overestimates the
magnitude of the temperature rise in the thigh.
4-32
-------
Figure 4-29. Incident power density vs. exposure duration to
obtain a hot spot (41.6°C).
100
90
80
70
60
50
40
30
20
10
0
——— Exposure at 80 MHz
— ~— Exposure at 200 MHz
Lower Thigh Core Temperature
50 100 150
Exposure Duration, min
200
4.2.4 Unresolved Issues
Although the combined RF-heat-transfer model
reported here is realistic enough to predict gross
effects and trends, the model could be further refined.
The most obvious refinement is the extension of the
two-dimensional heat transfer model to a three-
dimension! simulation. Although this extension is
numerically straightforward, problems might arise in
computer storage requirements and in the computa-
tional time needed to generate the heating patterns.
In addition, altered tissue blood flowfor temperatures
in excess of approximately 40°C has not been
implemented in the model. This modification would
be simple, but its implementation would require
experimentation to quantify the altered blood flow
rates.
Another problem is that little is known about the
effects of RF energy on the predominant heat-
dissipating mechanisms of sweating and vasodilata-
tion. Although the empirical models yield results that
compare well with experimental measurements from
a human subject placed in a room at a controlled
temperature and relative humidity, it is certainly open
to question whether good agreement between
measured and calculated results would likewise be
obtained when the thermal load is caused by an RF
field. This problem could be resolved by experimental
verification of the model with animal models.
4-33
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-------
Section 5
Biological Effects of RF Radiation
5.1 Cellular and Subcellular Effects
John W. Allis
The investigation of RF-radiation effects on cellular
and subcelluar systems is principally an attempt to
elucidate specific biochemical mechanisms for
the interaction of the radiation with macroscopic
biological systems. This approach takes advantage of
the relative simplicity of in vitro systems, the ability to
control variables, the rapid and economical way with
which results may be obtained, and the perceived
ease of mechanistic interpretation of the results. In
practice, however, these advantages are not always
realized.
The divisions between molecular, subcellular, and
cellular systems are somewhat arbitrary, but for
convenience, results presented in this section will be
discussed in this format, illustrated in Table 5-1.
When investigating molecular and subcellular
systems, one normally looks at a single key structure
or function where, one hopes, all other variables may
be held constant. In these cases, thorough under-
standing of the end point under study allows the
investigator to interpret results more easily in terms
of a detailed biochemical mechanism. For instance, if
a change in the kinetics of an enzyme-catalyzed
reaction is found, the type of inhibition can be
determined, the particular molecules involved can be
identified, and a hypothesis for the effect can be
constructed.
In some experiments on intact cells, these conditions
can also be approached. An example of this is sodium
(Na+) and potassium (K+) transport across the red-
blood-cell (RBC) membrane. The RBCs limited
metabolic activity is geared primarily to performing its
main function of transporting oxygen from lungs to
tissue. In this case, ion transport across the
membrane is I inked to the mode of energy production
in the cell and to very little else, and studies on this
system are relatively simple to interpret.
Experiments on most living cells are complicated by
complex biochemical systems, many of which have
multiple or alternate pathways. Rather than isolated
functional changes, broad end points such as growth
or ^genetic changes are often assayed. Here, the
investigator tries to use "biological amplification"
where, for example, the cell's growth is highly
sensitive to disruptions of a critical but unspecified
metabolic step, or where a mutant appears that must
reproduce over several generations before sufficient
numbers are present to be measurable. The
investigator also recognizes that the redundancies in
a complex system like a living cell may negate any
efforts to detect the putative effect.
This inherent complexity makes it difficult to ascribe a
detailed biochemical mechanism to effects found.
Such effects must be viewed as a starting point from
which a mechanism may eventually be deduced. On
the other hand, effects on cells can also be used to
Table 5-1. Classification of Cellular and Subcellular Experiments
Classification
Type of System Studied
Examples of
Experimental Measures
Molecular
Molecular
Subcellular
organelles
Subcellular
organelles
Subcellular
organelles
Cellular
Cellular
Cellular
" Purified enzyme preparations
Purified DNA preparations
Membrane-bound enzymes
Cell membranes, phospholipid
vesicles
Isolated mitochondria
Red blood cells
Bacteria
Isolated neurons
Enzyme activity, bind-
ing to small molecules
DNA melting
Enzyme activity
Infrared, Raman spectra
Mitochondrial function
Ion transport
Growth, survival,
infectivity
Neuronal firing,
membrane potential
5-1
-------
rationalize or interpret—perhaps even predict—
effects in the intact animal.
Dosimetry for in vitro systems presents problems to
the researcher that are in many respects unique to
the study of RF-radiation interactions. In general,
average SAR in the sample is relatively easy to
measure and has become the standard dose-rate
measurement in this research area. The most
convenient methods are thermal measurements, i.e.,
analysis of heating and/or cooling data (Allis et al.
1977), and electrical measurements, where forward,
transmitted, and reflected power are recorded in a
closed exposure system. (See Sec. 3.4.) Thermal
measurements have become much more convenient
and accurate since the development of temperature
probes that do not perturb the RF field. A third
commonly used dosimetric method is calculation of
SAR based on incident power or power density. This
approach is less satisfactory than the methods
mentioned above because simplifying assumptions
must normally be made to model the exposure
geometry. In this section on cellular and subcellular
systems, the SAR given for each study is the average
for the sample unless otherwise noted.
In most in vitro as well as in vivo exposures, the
distribution of absorbed energy in the sample is not
constant throughout the sample. Most researchers in
the field recognize this fact, and the standard
approach for treating the problem is to stir or agitate
the solution if possible. Normally this is an effective
way to eliminate thermal gradients produced by
inhomogeneous absorption patterns. When stirring is
not possible, and occasionally even when it is,
potentially serious problems arise because the end
points measured for in vitro systems are often very
sensitive to temperature, inhomogeneities in
temperature within the sample can give misleading
results (Livingston et al. 1979, for example). The
potential for this problem exists in some of the work
discussed later in this section.
Because of temperature sensitivity of biological end
points measured in many in vitro systems, researchers
are generally careful about maintaining temperature
control of the exposed sample and matching it to the
control or sham-exposed sample. Two methods are
normally used. In one, the researcher establishes a
steady-state temperature in the presence of the RF
radiation and then begins the assay. In this case, the
exposed sample is cooled to (or experiences an
ambient temperature) below the temperature at
which the assay is conducted, with the RF energy
making up the temperature difference. The sham or
control sample is matched to the steady-state
temperature and remains at thermal equilibrium with
its surroundings. Because the exposed sample is at a
higher temperature than its surroundings, a
temperature gradient necessarily exists in the RF-
exposed sample that does not exist in the control. The
magnitude of the gradient depends on the energy
absorbed from the field and the sample geometry.
Among the more conventional methods of heating,
infrared exposure mimics most closely the heating
patterns for in vitro samples exposed to RF radiation.
The second method of temperature control often used
is to allow the temperature of the exposed sample to
rise during exposure and then to mimic the rise in
the control sample by applying conventional heating
techniques. This method has the same difficulty with
a gradient in the exposed sample as just described;
also, it is difficult to match precisely the kinetics of the
temperature rise due to exposure to RF radiation
using conventional techniques. However, properly
designed experimental apparatus and good techniques
can significantly reduce the difficulty.
One must also recognize that generally in vitro
systems are primarily made up of a solvent medium in
which the cells or subcellular systems are suspended.
Temperature probes are macroscopic and necessarily
measure the temperature of the solvent, whereas the
measurement desired is that of the temperature
experienced by the cell, or by the immediate
environment about the subcellular systems. On the
other hand, a more detailed analysis of the thermal
properties of a sample, and more precise and
accurate data, can be obtained from in vitro systems
than can be achieved with in vivo experimentation.
The foregoing discussion has presented the major
problems with dosimetry for in vitro systems. In
general, however, these problems are less severe
than those encountered with in vivo work. The
investigation of mechanisms of interaction of RF
radiation with biological systems is critical to a basic
understanding of the biological effects and is best
accomplished using in vitro techniques. If careful
attention is paid to dosimetry and if the difficulties
presented here are addressed, dosimetry need not be
a principal concern in the interpretation of the
experimental results.
The general conclusions that can be made at this time
concerning the effects of RF radiation on cellular and
subcellular systems are:
• No consistent biological effects have been
demonstrated for molecular or subcellular
systems exposed in vitro that can be attributed to
RF-specific interactions.
- • No consistent effects have been demonstrated on
growth and colony-forming ability of single cells
that can be attributed to RF-specific interactions.
• There is an indication that sodium and potassium
ion transport across red blood cell membranes can
be affected by exposure in vitro to RF radiation in a
manner different from generalized heating.
• The electrophysiological properties of single cells,
especially the firing rate of neurons in isolated
5-2
-------
preparations, may be affected by RF radiation in a
manner different from generalized heating.
5.1.1 Effects on Molecular Systems
To obtain insights into possible direct interactive
mechanism(s) of microwave radiation at the
molecular level, several investigators have attempted
to measure changes in biologically important
macromolecules exposed in vitro (Table 5-2). Enzyme
kinetics studies form a majority of the reports, but a
few examine changes in macromolecular structure.
In sum, these reports do not demonstrate consistent
effects on molecular systems exposed in vitro to RF
radiation that can be attributed to RF-specific
interactions.
In one study of macromolecular structure, Hamrick
(1973) measured DNA melting curves after exposure
of calf thymus DNA to 2.45-GHz (CW) radiation for 16
h (SAR = 67 W/kg) and at dose rates to 160 W/kg for 1
h. Temperature was controlled during all exposures,
usually at 37°C, but for some experiments it was
maintained at 40, 45, and 50°C. The intent of the
study was to determine whether microwaves
disrupted hydrogen bonding between the DNA
strands of the double helix and thus affected the
melting curve. The assay was carried out after
exposure. In one experiment the investigators
preserved any disruption of hydrogen bonding
between the strands by performing the microwave
exposure with formaldehyde in the buffer. However,
all melting curves were virtually identical to those of
unexposed, temperature-matched controls.
In another report concerning macromolecular
structure (Allis 1975), the protein bovine serum
albumin (BSA) was exposed to 1.70- and 2.45-GHz
(CW) radiation (SARs ranging from 30 to 100 W/kg).
The author recognized that structural changes due to
microwave exposure may be reversible. In this study,
he attacked the problem by developing an exposure
apparatus in which ultraviolet (UV) and visible
spectrophotometric measurements could be per-
formed during exposure. The difference in UV
absorption between the exposed and unexposed
samples was measured directly by a double-beam
spectrophotometer. Differences of this type reflect
small changes in the surroundings of certain UV-
absorbing amino acids and, in this case, could be
interpreted as changes in the structure of the protein.
The temperature of the exposed samples was
controlled during exposure, and it was matched by
the temperature of the control sample. Temperatures
ranged from 24 to 32°C, depending on the SAR value.
Spectra were measured immediately upon beginning
exposure, and again 30 min later with continuous
exposure. The study results showed that no changes
in the UV spectrum could be found over a variety of
structural states of protein, so that structural changes
due to microwave exposure could not be inferred.
The ability of microwave radia~tion to alter enzyme
activity has been studied by several workers.
Measurements were performed during microwave
exposure by two groups, each using spectrophoto-
metric measures of enzyme activity. Ward et at.
Table 6-2. Summary of Studies Concerning RF-Radiation Effects on Molecular Systems
Exposure Conditions
End Point Measured/
Effects
No change in UV difference
spectra measured over pH range
2.5-5.5
UV spectra and binding constants
for mononucleotides showed no
difference from controls
Experimental
System
BSA-
Ribonuclease
Frequency
(GHz)
1.70(CW)
2.45 (CW)
1.70ICW)
2.45 (CW)
Duration
(min)
30
30
Exposure
Facility
(type)
Waveguide
Waveguide
SAR
(W/kg)
30-100
39
Reference
Allis (1975)
Allis et a/. (1976)
No change in enzyme activity
No difference in melting curves
Inactivation of enzyme; probably
temperature inhomogeneity effect
at very high doses
Glucose-6 phosphate
dehydrogenase;
adenylate kinase; NADPH
cytochrome C reductase
DNA
2.45 (CW) 5
Waveguide 42
2.45 (CW)
Horseradish peroxidase 2.45 (CW)
Heat inactivation of enzymes
found at highest SAR (T = 50 °C)
corresponded closely 'o heat-
treated controls
60.
960
5, 10,
20, 30,
40
4.5,
18.5
Far field
Waveguide
67.
160
62,500-
375,000
Glucose-6-phosphate 2.8 (PW)
dehydrogenase; lactate
dehydrogenase; acid
phosphatase; alkaline
phosphatase
Heat inactivation of enzyme found Lactate dehydrogenase 3.0 (CW) 20
at SARs > 165 W/kg
Waveguide -200-500
Ward era/. (1975)
Hamrick (1973)
Henderson et al. (1975)
Belkhode et al.
(1974a,b)
Waveguide 33-960 Bini et al. (1978)
"BSA = bovine serum albumin.
5-3
-------
(1975) examined three enzymes (glucose-6-phosphate
dehydrogenase, adenylate kinase, and NADPH-
cytochrome c reductase) exposed to 2.45-GHz (CW)
radiation (SAR = 42 W/kg). All exposed and control
samples were maintained at 25°C. Exposure durations
were ~ 5 min, during which the enzyme activity was
measured. No differences between exposed and
control samples were found. Bini et al. (1978)
followed the activity of lactate dehydrogenase
exposed to 3.0-GHz (CW) radiation (SARs between 33
and 960 W/kg). They demonstrated that the changes
found in the enzyme activity were entirely consistent
with calculations of thermal inactivation of the
enzyme at the temperatures attained. The sample
exposed at 33 W/kg was not different from the
unexposed control; all other exposures (SARs ranging
from 165 to 960 W/kg) showed evidence of enzyme
inactivation.
Belkhode et al. (1974a,b) reported the effect of 2.8
GHz square-wave modulated (1-kHz) radiation on
four enzymes: glucose-6-phosphate dehydrogenase,
lactate dehydrogenase, acid phosphatase, and
alkaline phosphatase. Enzyme preparations were
analyzed after exposures (SARs ~ 200 to 500 W/kg
on average). Exposures were conducted at 37, 46.7,
and 49.7°C; enzyme activities were compared to the
activity of sham-exposed samples at the same
temperatures. Activities of the exposed enzymes at
each temperature were indistinguishable from the
shams.
Henderson et al. (1975) reported a change in enzyme
activity that was interpreted as an indicator of direct
interaction on the enzyme by microwaves. In this
experiment, horseradish peroxidase was subjected to
2.45-GHz (CW) radiation (SARs between 62,500 and
375,000 W/kg) with the sample-exposed in a tube
(4.7-mm ID) that protruded through a waveguide. The
sample tube was surrounded by a concentric cooling
jacket, through which an organic coolant was
pumped continuously to maintain the temperature at
25°C. Thermocouples were placed in the sample tube
so that the sample temperature could be monitored
from positions just outside the waveguide. The total
volume of the exposed sample was —0.8 ml. A marked
decrease in enzyme activity was found at 62,500
W/kg after 30 min of exposure, and at 187,500 W/kg
after 20 min of exposure, even though the temperature
was reported never to exceed 35°C. It is possible that
the very high fields present .at these SARs could
produce field-specific effects. However, it appears
likely that very high local heating occurred in the
sample that was responsible for enzyme inactivation.
This likelihood is substantiated by the work of
Harrison et al. (1980), who performed liquid-crystal
thermography under similar exposure conditions.
Temperature rises of as much as 0.3°C were recorded
within a micropipette suspended in a waveguide and
cooled with water circulating through the waveguide.
5-4
Henderson et al. (1975) exposed their samples at 5 to
10 times the levels used by Harrison et al.; also, the
latter researchers used water as a coolant, which
would attenuate the energy reaching the sample
much more strongly than would the organic solvent
used by Henderson et al. A study by Livingston et al.
(1979) graphically illustrates the effect of temperature
gradients during microwave exposure.
The binding of small substrate-like molecules to the
enzyme ribonuclease was studied to determine
whether the binding relationship between an enzyme
and substrate could be affected by microwaves (Allis
et al. 1976). In this work, UV-absorption spectra were
measured during exposure to 1.70- and 2.45-GHz
(CW) radiation (SAR =39 W/kg). Measurements were
performed immediately upon beginning irradiation
and after 30 min of exposure. Neither structural
changes in the enzyme-substrate complex nor
changes in the binding constants were found.
5.1.2 Effects on Subcellular Organelles
There has been relatively little research on the effects
of microwave radiation on subcellular organelles
(Table 5-3). The reports included in this document
range from work with phospholipid bilayers (i.e.,
synthetic analogs of cell membranes) to experiments
on intact mitochondria, the energy-producing system
in eukaryotic (e.g., mammalian) cells. Most of the
work to be discussed here has not demonstrated
effects of microwave exposure at dose rates ranging
from 1 to 430 W/kg. Two reports that have indicated
an effect do not meet all criteria for inclusion here and
are therefore discussed with other reports that
present unresolved issues.
Two reports describe work with enzymes bound to
biological membranes. The study by Ward et al.
(1975), discussed above, focused on the enzyme
NADPH-cytochrome c reductase, which is loosely
bound to the membrane of the endoplasmicreticulum
of rat liver cells. Allis and Fromme (1979) studied
adenosine triphosphatase (ATPase) in RBC mem-
branes and cytochrome oxidase in the inner
mitochondrial membrane of rat liver cells. The latter
two enzymes are thought to be integral parts of
membranes. Conditions of the exposure were
identical for all three enzymes in that the essay was
performed spectrophotometrically during exposure to
microwaves. In the latter study the dose rate was 26
W/kg, and the 2.45-GHz radiation was sinusoidally
modulated at 16, 30, 90, and 120 Hz. Enzyme activity
was not measurably affected by these exposures; a
10- to 15-percent change in enzyme activity would
have been required to detect a reliable microwave
effect.
Ismailov (1977) investigated the infrared (IR)
absorption spectra of proteins in RBC membranes
exposed to 1.009-GHz fields (SARs up to 45 W/kg)
and maintained at 25°C. The samples were exposed
-------
for 30 min in aqueous suspension in a stripline and
were then dried to a thin film to obtain the IR spectra.
No change in cr-helix or /3-sheet content of
the membrane proteins was noted. However, when
D2O (heavy water) was added to the suspension
before beginning exposure, application of microwaves
was found to increase the degree to which strongly
bound amide hydrogens were exchanged. This effect
was pronounced at SAR =45 W/kg but disappeared
when the SAR was below 10 W/kg. The increase in
accessibility of the poorly exchangeable amide
hydrogens indicates that the microwaves disturb the
relationship of the protein to its neighboring
membrane lipid.
IR spectra of Escherichia coli after exposure to
microwaves were also measured (Corelli et al. 1977).
After 12 h of exposure to 3.2-GHz (CW) radiation (SAR
= 20 W/kg), £. coli were dried to a film, and spectra
were measured in the protein and nucleic acid
absorption regions. No differences were found. These
results are comparable with those of Ismailov (1977),
which indicated no changes, but they do not address
the conditions for which Ismailov did report effects.
The functional properties of the microtubule
assembly system extracted from rabbit brain cells
were studied after exposure to 3.1-GHz fields by
Paulsson et al. (1977). The binding of the drug
colchicine to the microtubule precursor protein
tubulin was measured after exposure to PW
microwaves for 15 min at average dose rates of 112
and 243 W/kg (pulse-repetition rate of 200 Hz, pulse
duration of 1.4 /js). Colchicine normally blocks the
formation of microtubules, which halts cell division.
The normal assembly of microtubules from tubulin
exposed for 10 min to PW microwaves, as above, at
430 W/kg was also studied. No noticeable effect on
either process was found. The data indicate that a
change of about 15 percent in the colchicine binding
and about 10 percent in the microtubule assembly
measurement would have been noted. Paulsson eta/.
also studied the migration of proteins within the axonal
membrane of the rabbit's vagus nerve. In this case the
samples were exposed for 24 h (the SAR estimated
from their data was 10 to 100 W/kg) at a pulse-
repetition rate (PRR) of 100 Hz and a pulse duration 1.4
/js. The distribution of tritium-labeled protein in the
axonal membrane was found to be the same in
exposed and control samples. A difference of > 20
percent would have been required for detection in this
experiment.
Two papers (Elder and AM 1975; Elder et al. 1976)
present results of exposure of rat liver mitochondria
to microwave radiation. Both papers examine oxygen
utilization by measuring respiratory activity (e.g.,
respiratory control ratio, ADP to oxygen ratio) under
Table 5-3. Summary of Studies Concerning RF-Radiation Effects on Subcellular Systems
Exposure Conditions
End Point Measured/
Effects
Exposure
Experimental Frequency Duration Facility SAR
System (GHz) (min) (type) (W/kg) Reference
Increase in exchange of strongly
bound amide hydrogens in membrane
protein measured by IRt spectra
for SAR > 10 W/kg, no change in
cr-helix or /3-sheet content of
proteins
No change in activity of membrane
bound enzymes measured
spectrophotometrically
No change in activity of membrane-
bound enzyme measured spectro-
photometrically
RBC membrane* 1.0 (CW)
30
Stripline 5-45
RBC membrane.
mitochondrial
inner membrane
Endoplasmic
reticulum
2.45 (SWH) 10
2.45 (CW)
Waveguide
Waveguide
26
42
Ismailov (1977)
Allis and Fromme (1979)
Vvardef a/. (1975)
No difference in respiratory
activity
No difference in respiratory
activity
No change in formation of
microtubules
No change in migration of proteins
within axonal membrane
No changes in IR spectra of
proteins and nucleic acids in
E. coli exposed before drying
Mitochondria
Mitochondria
Tubulin
(rabbit brain)
Vagus nerve cell
Dried film of
E. co/i cells
2.45 (CW)
2-4 (Swept)
3.4 (CW)
3.1 (PW)
3.1 (PW)
3.2 (CW)
30 to
210
10
15
24 h
8, 10,
11 h
Anechoic
chamber
far field
Coaxial
airline
Far field
Far field
Waveguide
17.5,
87.5
1.6-2.3
41
112-430
-10-100
20
Elder and Ali (1975)
Elder et al. (1976)
Paulsson et al. (1977)
Paulsson et al. (1 977}
Corelli era/. (1977)
*RBC = Red blood cell.
tIR = Infrared.
#SW = Sine-wave modulated.
5-5
-------
various conditions. These parameters are functional
indications of the energy production system in
eukaryotic cells. The earlier paper tested mitochondria
kept at 0°C, or inactive state, during exposure in the
far field at 2.45 GHz. The mitochondria! functions
were examined after exposure in the active state at
2^°^ CFxnosures for periods up to 3.5 h were
conducted at SARs of 17.5 and 87.5 W/kg.) No
rhsoooc; jn mi*ochondrial activity were seen. In the
laiLi paper, the disadvantage of exposing inactive
mitochondria was overcome by use of a novel flow-
through system that coupled a coaxial airline and an
oxygen electrode. The mitochondria! suspension was
cycled continuously between the airline, where
exposure was accomplished, and the oxygen
electrode. Samples were exposed to 2.45-, 3.0-, and
3.4-GHz (CW) radiation (SAR = 41 W/kg) and also to
radiation at swept frequencies between 2 and 4 GHz
(SARs from 1.6 to 2.3 W/kg). As in the earlier work,
no effects of microwave exposure were detected
under any condition. In general, a five-percent
change would have been sufficient for detection.
Other workers have presented data on microwave
exposure of mitochondria, either in a form too
incomplete for inclusion or in oral presentations.
Their findings do not differ from those described here.
5.1.3 Effects on Single Cells
Effects on single cells have been investigated by
several researchers (Table 5-4). Most of the work
discussed in this section falls into three classes:
studies of ion transport into or out of red blood cells,
growth or colony-forming ability of various lines of
cells, and responses of single neurons exposed to RF
radiation. In the ion transport studies two papers have
demonstrated effects, but one of them has not been
replicated despite two attempts. Only one of the
reports involving cell growth reported an effect,
but sample heating may have been responsible for the
result. The potentially most significant effect is that of
the response of neurons. Two papers from one labora-
tory are discussed in this section, and a third report
from a second laboratory is discussed under Unre-
solved Issues (Sec. 5.1.4). All show very similar results
for the firing rate of neurons exposed to RF radiation. In
sum, for cellular systems, effects have been found
that may prove significant and should provide leads
for elucidating a new mechanism of action. However,
at present, these effects require additional documen-
tation.
Transport and related properties of RBC membranes
have been studied by five groups. In each case Na+ or
K+ transport was used as an end point. In the RBC,
active (or energy requiring) Na* and K* transport
across the membrane is by the enzyme Na+-K+
ATPase (the same enzyme discussed in Sec. 5.1.2,
Effects on Subcellular Organelles), and passive
transport is through channels in the membrane.
Ismailov (1971) exposed human RBCs to 1.0-GHz (CW)
microwaves at 45 W/kg and found an increased
efflux of K* and a concomitant increased influx of Na*.
The Na+ influx was twice as large, ion per ion, as the
K* efflux. Exposures were carried out in a coaxial
stripline for 30 min, with analysis of the ion content of
the supernatant performed afterwards. These results
indicate either a reversal of the normal action of the
Na+-K+ ATPase, or an inhibition of the enzyme,
which permitted ion leakage across the membrane to
change the NaVK* ratio. Hamrick and Zinkl (1975)
and Peterson et at. (1979) have performed similar
experiments by exposing RBC's at 2.45 GHz in the far
field (SAR's were 3 to 57 W/kg, and ~ 200 W/kg,
respectively). Neither study found a difference
between the K+ efflux from microwave-exposed
RBC's and conventionally heated RBCs with similar
histories of temperature elevation, although Peterson
et al. did find a difference between unexposed rabbit
cells maintained at 25°C compared with those
maintained at 37°C. This difference did not occur
with human cells. Ismailov also used temperature
controls but did not describe the solution parameters
for the cell suspensions. Under certain conditions of
chemical concentration, it is possible to reverse the
Na+-K* ATPase; however, Ismailov's controls
behaved normally, which wou.ld indicate that
chemical concentrations in the controls were not
unusual. The origin of the discrepancy between these
studies is not clear.
Hamrick and Zinkl (1975) and Peterson et al. (1979)
measured other end points as well. The former looked
at osmotic fragility of the RBC's and concluded that
there was no difference. The latter paper gives data
on hemoglobin release from RBC's, an indicator of
membrane fragility. Again, no differences were found
between irradiated and heat-treated RBCs; however,
as for K+ efflux, the unexposed rabbit cells released
less hemoglobin at 25°C than at 37°C.
Liu et al. (1979) also studied K+ efflux, hemoglobin
release, and osmotic fragility in red blood cells.
Exposure to RF radiation was conducted in a
waveguide system at frequencies of 2.45, 3.00, and
3.95 GHz. A 1.2-cm-diameter polystyrene tube
containing a 0.6-ml suspension of RBCs was inserted
through the center of the waveguide with the long
axis of the tube parallel to the electric field.
Temperature was measured before and after
exposure by insertion of a thermistor. The temperature
of the exposed sample was allowed to rise, and heat-
treated controls were placed in a water bath at the
temperature equivalent to the maximum exposure
temperature. Time of treatment was the same for
exposed and heat-treated samples. No statistically
significant differences were found between exposed
and heat-treated samples in any of the measurements
performed. Experiments included exposure of rabbit
RBCs at SARs of 22 to 200 W/kg (equilavent to 5.2 to
22°C rise in temperature); ouabain treatment of the
5-6
-------
rabbit RBCs to block the Na*-K* ATPase; and a
comparative study of rabbit, human, and dog RBCs
exposed at 3.00 GHz and an SAR of 173 W/kg.
In a separate paper, Ismailov (1978) reported
increases in the electrophoretic mobility of human
RBCs exposed under conditions identical to those in
his previously discussed study. The electrophoretic
mobility was measured at 10-mm intervals after
cessation of exposure. The mobility was found to peak
30 min after exposure and to return to base line ~ 60
min after exposure. The peak mobility decreased with
shorter exposure durations (30, 15, 8, and 4 min).
Also, the mobility change decreased as a function of
dose rate and disappeared altogether between 5 and
10 W/kg. Although a change in the counter-ion
distribution around the cell and possible conforma-
tional changes in the membrane proteins were
discussed or suggested as possible causes, it
remained unclear why these phenomena peaked 30
min after exposure.
Passive ion transport was examined by Olcerst et al.
(1980) after they exposed rabbit RBCs to 2.45-GHz
(CW) radiation (SARs at 100, 190, and 390 W/kg).
The cells were treated wth ouabain to inhibit active
transport of Na+ and K* by Na*-K* ATPase, the
important enzyme discussed previously in several
papers. Exposures took place in a waveguide system
in which the sample was placed parallel to the E-field
in a cylindrical tube. An organic coolant of low
dielectric constant was circulated around the sample
Table 5-4. Summary of Studies Concerning RF-Radiation Effects on Single Cells
Exposure Conditions
End Point Measured/
Effects
Increase in RBC electrophoretic
mobility 30 min post-exposure
(SAR > 10 W/kg)
Increase in K* efflux and Na* influx
K* transport no different from
heat-treated controls; no change
in osmotic fragility
K' transport no different from
controls at corresponding
temperatures; no difference in
hemoglobin release
Experimental
System
RBC*
RBC
RBC
RBC
Frequency
(GHz)
1 .0 (CW)
1 .0 (CW)
2.45 (CW)
2.45 (CW)
Duration
(min)
4.8,
15, 30
30
60, 120,
1 80, 240
45
Exposure
Facility
(type)
Stripline
Stripline
Monopole
far field
Anechoic
chamber
far field
SAR
(W/kg)
5-45
45
3-57
200
Reference
Ismailov (1 978)
Ismailov (1971)
Hamrick and Zinkl (1975)
Peterson et al. ( 1 979)
Passive transport of Na* and Rb*
increased at transition temperature
No significant changes in K* efflux,
hemoglobin release, or osmotic
fragility
Rapid response in change of firing
rate of pacemaker neurons which
does not correlate with tempera-
ture changes in minority of trials
No change in growth or CFUt of
exposed cultures
No change in growth, CPU, of vari-
ous strains of exposed cultures
under several growth conditions
No change in survival curves
(measuring CPU) of exposed
cultures
Growth rate slowed; morphological
changes found
No change in light emission of
photoactive bacterium
No effect on colony-forming
ability
Temporary decrease in virulence
(> 6 h) of bacteria for its host
cells; recovery within 24 h at
37 °C
RBC
RBC
2.45 (CW)
2.45 (CW)
3.00 (CW)
3.95 (CW)
60 Waveguide 100,190 Olcerst et al. (1980)
390
20.180 Waveguide 22-200 Liu et al. (1979)
Isolated neuron 1.5,2.45 3
from Aplysia (CW and PW)
E. co/i
P. aeruginosa
E. coli
2.45 (CW)
2.45 (CW)
720
240
E. coli 2 45 1
B. subtilis spores
Chinese hamster 2 45 (CW) 20
lung cells, V79
P. tischeri 2.6-3.0 (CW) -22
Stripline
Par field
Anechoic
chamber
far field
Microwave
oven
1-100 Wachtel et al. (1975);
Seaman and Wachtel
(1978)
29-320 Hamrick and Butler
(1973)
0.0075- Blackman et al. (1975)
75
—400 Goldblith and Wang
(1967)
E. coli
2.6-4.0 (CW) 8 h
A. tumefaciens 10 (CW) 30,60,
230
Waveguide
Waveguide
Waveguide
Cavity
1059
660 to
5300
29
-1
Chen and Lin (197£
Barber (1962)
Corelli et al. (1 977)
Moore et al. (1979)
*RBC = Red blood cell.
tCFU = Colony forming unit.
5-7
-------
in a larger concentric cylinder to maintain the
temperature of the sample under exposure. The SARs
were computed from readings of forward and reflected
power. The RBCs were pre-incubated with radioactive
Na+ or Rb+. (The latter is a K+ substitute.) Samples
were exposed or heat-treated for 1 h, and the
suspending medium was analyzed for radioactivity.
Graphs of the logarithm of the efflux vs. inverse
temperature were identical except at three transition
temperatures, where the slope of these plots changes
sharply (Figure 5-1). At these points, the exposed
samples exhibited considerably higher efflux than the
heated samples; however, no consistent difference
between exposure levels could be established. These
results imply that the cell membrane structures
responsible for passive ion transport are sensitive to
microwave exposure at temperatures at which
transitions between two states are taking place.
Living cells depend on closely regulated ion
concentrations for many processes, and serious
disruption of these balances could be lethal. It should
be noted that none of the previously discussed
studies of Na+or K+transport in RBCs were conducted
at the temperatures at which transitions were found in
this report.
Many studies focus on a major function of a cellular
species as a generalized end point. The reasoning for
this approach is that if microwaves disrupt an
important metabolic step, the result will be a decline
in the ability of the cell to perform its major function.
As mentioned earlier, this reasoning assumes that no
compensating mechanism will operate. A broad
spectrum of such end points has been investigated for
cells exposed in vitro. Some of them are discussed
elsewhere: phagocytosis and bfastic transformation in
lymphocytes in Sec. 5.2, Hematologicandlmmunologic
Effects; and the induction of the antibiotic colicin,
along with point mutations in single cells, in Sec. 5.8,
Genetics and Mutagenesis.
Perhaps the ultimate test of a cell's functional ability
is growth and survival. Several workers have
concentrated on this end point and have investigated
the frequency range between 1 and 4 GHz. In general,
the results have proved negative. Far-field exposures
were conducted (Hamrick and Butler 1973; Blackman
etal. 1975)onseveralstrainsormutantsof£. co//and
on Pseudomonas aeruginosa. Samples were exposed
in T-flasks or petri dishes, principally to 2.45-GHz
(CW) radiation. Growth was measured by assays of
colony-forming units (CFUs). In both experiments the
duration of exposure was sufficiently long (12 and 4
h) for the average cell to divide at least once.
Blackman et al. examined several growth conditions
such as lag, log and stationary phases of growth, rich
and minimal media, and a "normal" as well as a
mutant amino-acid-requiring strain. In each case, no
differences between the exposed samples and
temperature-matched control samples were found.
Hamrick's SARs ranged from 29 to 320 W/kg with
Figure 5-1.
Arrhanius plot of Na* efflux. Unirradiated tempera-
ature controls are represented by open symbols;
irradiated samples are represented by darkened
symbols. Specific absorption rates are expressed
as watts per kilogram (e = 100. •= 190, A = 390).
Control samples had an average standard error of
0.98 percent. Irradiated samples had an average
standard error of 4 percent (Olcerst et al. 1980).
39.3
29.8
Temperature, °C
20.9 12.5
3.2
3.6
power densities of 60 to 600 mW/cm2, and
Blackman's from 0.0075 to 75 W/kg with power
densities of 0.005 to 50 mW/cm2.
Corelli et al. (1977) exposed f. coli at the end of a
waveguide to microwaves swept from 2.6 to 4.0 GHz
for 8 h at a dose rate of 29 W/kg. No effect of the
microwave exposure was found on colony-forming
ability of the bacteria. Goldblith and Wang (1967)
exposed E. coli and Bacillus subtil is spores in a
microwave oven at 2.45 GHz for periods to 1 min(SAR
estimated at 400 W/kg). In this case, microwave
irradiation and conventional heating were found to
have identical effects on survival.
Chen and Lin (1978) exposed Chinese hamster lung
cells, V79, in a waveguide fitted with a micropipette
that contained the cell suspension. Temperature was
regulated by circulation of cooling water through the
waveguide around the micropipette. Samples were
exposed to 2450-MHz (CW) radiation for 20 min, and
the cells were allowed to grow in cultures for 12 days
after exposure. The exposed cells were observed to
divide at a lower rate and to exhibit a fibroblastic type
5-8
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of growth, in contrast with the controls. These cells
were exposed at 400 mW/cm2 (SAR = 1059 W/kg)
under conditions similar to those in which Harrison et
al. (1980) found temperature elevations in the sample
that were as much as 0.3°C higher than the cells in
the cooling bath. Chen and Lin (1978) state that
temperature-treated controls at 38°C (1 °C higher than
the coolant temperature during microwave exposure)
did not display the changes observed in the
microwave-exposed cells. However, it is not entirely
clear whether the changes in the microwave-treated
cells were caused by elevated temperatures within
the micropipette.
The emission of light by a photoactive bacterium,
Photobacterium fischeri, has been used as the end
point of one study (Barber 1962), where the bacterial
suspension was circulated through a waveguide.
The bacteria were undergoing exposure in the
waveguide for approximately half the time during a
typical 43-min experiment. Bacteria were exposed at
several -frequencies between 2.6 and 3.0 GHz; the
assay was performed 24 h later. In spite of extremely
high dose rates, 660 to 5300 W/kg, there were no
differences between microwave-irradiated and
conventionally heated samples that received parallel
treatment.
In the single experiment conducted at 10-GHz
frequency, a transient effect was found in the
virulence of Agrobacterium tumefaciens towards its
normal hosts, potato and turnip disks (Moore et al.
1979). This bacterium produces a plasmid, which it
injects into the host cells and which is responsible for
turning these cells into uncontrolled tumor cells. In
this experiment, a suspension of A. tumefaciens was
exposed in a petri dish for 30, 60, and 230 min. The
longer exposures produced a decrease of virulence
near 60 percent with no essential change in the
number of viable cells. The effect was unchanged 6 h
post-exposure, but virulence returned to normal 23 h
post-exposure when the bacteria were maintained at
27°C. An additional experiment, in which treated and
untreated cells were added to the host simultaneously,
indicated that the exposed cells were able to compete
effectively with untreated cells for binding sites on
the host cells. The treated bacteria -were always
maintained at or below 27°C during irradiation. From
the temperature data in the paper, a dose rate of ~ 1
W/kg and power density of 0.58 mW/cm2 can be
estimated. A possible explanation for this effect,
which was not offered by the original authors, is that
the plasmid DNA of the A. tumefaciens was
incorporated into the major DNA of the bacteria during
microwave exposure, preventing injection into the
host. Normal growth may have subsequently allowed
the plasmid to return to its original state and activity.
In two papers, Wachtel and co-workers (Seaman and
Wachtel 1978, Wachtel et al. 1975) have examined the
effects of microwave irradiation on the firing rate of
isolated neurons from the marine gastropod Aplysia.
Neurons were exposed in a stripline to 1.5- and 2.45-
GHzfCW and PW) fields (0.5- to 10-//S duration, 1000
to 15,000 pulses/s). The firing rate of pacemaker
neurons and the burst rate of bursting cells were
measured during microwave exposure at dose rates
between 1 and 100 W/kg. Glass capillary electrodes
filled with 0.5 M KCI were used to inject current
and measure the firing rate of the cells. The
electrodes had artifactual DC potentials of less than 1
mV and currents of less than 10 pA during exposure;
these values were judged by the authors to be too
small to affect the performance of the cells. In the
majority of cases, the firing rate of pacemaker cells
increased with an increase in temperature, and
decreased with a decrease in temperature. In a
minority of cases, 13 percent, for the pacemaker cells, the
microwave irradiation reversed the normal change
in firing rate; i.e., the rate decreased or stopped with a
microwave-induced increase in temperature. The
authors were able to detect slow and rapid
components. The slow component, occuring in 30 to
60 s, was correlated with the slow rise of temperature
associated with exposure. The rapid component,
occurring within 1 s, appeared to correlate with the
presence of the microwave field. The rapid component
was always found to be a decrease in firing rate in the
presence of the field and was never produced by
convective heating. Similar but more variable effects
were found for the bursting cells. The threshold for
the slow component was ~ 7 W/kg, but in one case
the rapid component was found at an SAR as low as 1
W/kg. For all cases in which effects were found, the
firing rates returned to normal when the radiation
was terminated and when the temperature was
returned to normal. The authors hypothesized that at
a dose rate of ~ 1 W/kg, conversion of 0.1 percent of
the microwave energy into a polarizing current
density across the cell membrane would be sufficient
to affect the firing rate of pacemaker neurons.
5.1.4 Unresolved Issues
Several issues remain unresolved in the area of
cellular and subcellular effects of microwave
radiation. Nearly all of the relevant research is
concentrated in a narrow frequency band, between
1.0 and 4.0 GHz. No acceptable studies have been
reported for a large portion of the frequency spectrum
of concern, 0.5 MHz to 100 GHz.
An active area of research at present is concerned
with the role of structured water in the cell. Questions
such as how much water in a cell is structured to a
greater degree than "bulk" water, and whether this
structure plays an important role in cell metabolism,
are as yet unanswered. Three monographs (Alfsen
and Berteaud 1976; Drost-Hansen and Clegg 1979;
Grant eta/. 1978) summarize knowledge in this area.
Experiments attempting to establish the presence
and extent of structured water within biological
5-9
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systems are described, and the dielectric data
indicating a possible frequency range for the
structured-water resonance are presented. According
to the limited information now available, RF radiation
is most effective in modifying the state of structured
water at frequencies below 1 GHz (Grant etal. 1978,
pp. 160-165). As yet no experiments have been
conducted that define whether absorption of RF
energy by structured water leads to a measurable
change in a biological system.
Three of the reports discussed in Sec. 5.1.3, Effects
on Single Cells, also raise questions. The explanation
offered by Ismailov (1978) for the change in
electrophoretic mobility of exposed RBCs is specula-
tive and does not account for the peaking of the
phenomenon 30 min post-exposure. These results
must be considered an effect of unknown origin until
more information is available. The results of
experiments by Moore et al. (1979), in which the
virulence of A. tumefaciens was decreased for more
than 6 h after exposure to microwave radiation,
suggest reversible functional changes in the
organism. In this case, the implications for cellular
function after microwave exposure would be broad.
However, no other worker has noted a similar effect
with other single-cell organisms, and this experiment
has not been independently confirmed. Therefore, its
significance is unknown at this time.
The results of Wachtel and co-workers (Seaman and
Wachtel 1978; Wachtel et al. 1975) are potentially
highly significant because they indicate the possibility
of a direct interaction between the microwave field
and the functioning of the pacemaker neuron (i.e., the
rapid effect). Three other workers have obtained
supportive results. The documentation in these
reports is not sufficiently complete for inclusion in the
preceding sections, but they bear mentioning here.
Yamaura and Chichibu (1967) found results strikingly
similar to those of Wachtel in ganglia of crayfish and
prawn exposed at 11 GHz. The regular firing rate of
the ganglia decreased rapidly during microwave
exposure, rebounded to a higher than normal rate
when the radiation was removed, and then returned
to normal. Temperature controls showed only an
increased firing rate as the temperature was
increased. The authors stated that the SAR was ~
100 W/kg but did not describe the method of
measurement.
Arber (1976) found a hyperpolarization of the resting
potential of giant neurons of the mollusk Helix
pomatia during exposure to 2.45-GHz(CW) radiation.
In this experiment, the ganglion was isolated and
mounted in a stripline. The cell potential was
measured, as in Wachtel's experiment, by insertion of
microelectrodes into the neuron. Exposure to
microwaves (SAR near 15 W/kg) for 1 h produced a 5-
to 10-percent increase in resting potential, followed
by a stabilization or slight additional increase over 1 h
post-exposure. This result is presumably caused by a
change in the Na+-K+ balance in the cell. When Arber
treated the cells with ouabain (post-exposure), which
inhibits Na*-K* ATPase, he found that part of the
hyperpolarization could be accounted for by the
action of this enzyme under the influence of
microwaves. The remainder was attributed to
changes in passive ion transport.
Pickard and Barsoum (1981) have recently presented
results in which single cells from Chara braunii and
Nitella flexilis, plants from the family Characeae,
exhibited a large step increase in voltage when
exposed to 0.1 - to 5-MHz (PW) radiation (pulses were
of 250-ms duration, pulse interval was 6.3 s). These
authors also found a fast and slow component. The
slow component correlated with a temperature rise in
the sample; the fast component was frequency
dependent and disappeared abruptly at ~ 10 MHz.
The authors suggest that the fast component was
produced by rectification of the oscillating electric
field by the cell membrane. The fast component
disappeared into noise at ~ 667 V/m and may have
been an effect of intense fields.
The results of these four studies indicate a possibility
of a direct microwave interaction with the electric
potential across the cellular membrane of all living
cells. This kind of interaction would have broad
significance in the functioning of all cells and, in
particular, cells of the nervous system.
Additional studies have been conducted recently that
have not yet been sufficiently documented to include
in the previous sections. However, because of their
potential importance, they are discussed here. The
first two reports concern microwave effects on
phospholipid bilayers, whereas the third is concerned
with changes in growth of the yeast Saccharomyces
cerevisiae exposed at frequencies between 41 and 42
GHz.
Tyazhelov et al. (1979a) have exposed a phospholipid
membrane formed between two chambers containing
solutions of NaCI or KCI. An antibiotic that forms
pores through the membrane was added to facilitate
passage of Na+ or K+. Conductance was measured
across the membrane while 4-s pulses of 900-MHz
radiation were delivered at between 125 and 280
V/m (field strength in the aqueous medium). The
results showed a change in conductance under
exposure that is consistent with temperature rises of
12°C, but the temperature of the NaCI or KCI
solutions did not vary by more than 0.5°C. However,
insufficient information concerning the exposure
system makes it difficult to judge whether serious
inhomogeneities in energy deposition, and thus
similar inhomogeneities in the temperature distribu-
tion, were likely. One cannot estimate an SAR from
the information presented.
5-10
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Sheridan et al. (1979) have presented at meetings,
but so far have not published, results of Raman
spectroscopy of single- and multilamellar phospholipid
vesicles exposed to 2.45-GHz (CW) radiation. No
change was found in the Raman bands of single-
layered vesicles. In contrast, the data for multilamellar
vesicles indicate that the hydrocarbon tails of the
phospholipids were undergoing a temperature-
dependent phase transition at a point at which the
bulk temperature was too low for the transition to
have begun. The change was reported to be
equivalent to a temperature difference of ~ 2°C at an
exposure of 25 mW/cm2. The bulk temperature of the
sample in these experiments was measured by a
unique method. Small ruby crystals were suspended
in the sample, and the shifts in the Raman bands of
the crystal were measured and compared with
calibration curves. This appears to be an accurate
method for temperature determination. The origin of
this effect is unknown, but if a similar effect were
found in naturally occurring membranes, it could
have an impact on the functioning of the biological
membrane.
Keilmann and co-workers (Grundler et al. 1977;
Keilmann 1978; Grundler and Keilmann 1980) have
demonstrated that S. cerevisiae exhibits an enhanced
or inhibited growth rate when exposed at certain
closely spaced frequencies between 41.60 and 41.80
GHz. For instance, they found a 10- to 15-percent
increase in growth rate at 41.64 and 41.68 GHz, and a
20-percent decrease at 41.66 GHz. The experiments
were conducted with a unique waveguide termination
that was dipped into a suspension of yeast cells. In a
typical experiment, 24 W was dissipated in the yeast-
cell suspension, and the authors estimated a
maximum exposure intensity of about 10 mW/cm2.
However, because of the unusual nature of the
waveguide termination and the high attenuation of
high-frequency radiation by aqueous samples, SAR
values cannot be determined. Sample temperature
was monitored and was within 0.5°C of the desired
32°C. Equivalent temperature controls were per-
formed, and the authors believe that changes of the
observed magnitude could not be purely temperature
effects. This contention appears reasonable, since
the growth rate both increased and decreased at the
same levels of incident energy but at different
exposure frequencies. The decrease is difficult to
explain, based on the authors' reports of no
observable temperature rise. However, if a localized
temperature > 37°C (> 5°C above the controlled
temperature) were attained close to the waveguide
termination, then the decrease could be explained
solely on the basis of temperature. There are scanty
reports from the Soviet literature that present results
similar to those of Keilmann and co-workers. These
studies are important because they are suggestive of
a specific interaction mechanism between RF
radiation and a biological system.
In summary, the available literature on cellular and
subcellular effects of microwaves does not yet
definitely establish whether effects unrelated to
elevation of temperature exist at dose rates on the
order of 1 W/kg. Several investigators have reported
effects, but a majority have not found effects
unrelated to temperature variations. In some cases,
the results conflict. In other cases, the effects found
are equivocal. Effects of elevated temperature may
not be clearly eliminated, or, as in the case of
neuronal firing rate, the change in the rate may occur
only in a minority of cases (Seaman and Wachtel
1978). The question of microwave-induced tempera-
ture rises must always be carefully considered when
one is dealing with the biological effects of exposure
to microwave radiation. In cellular systems, a
principal effect is to increase the rates of all
biochemical reactions, including the rate at which
denaturation of proteins and DNA occurs (Lehninger
1975), at which bases are removed from DNA(Lindahl
and Nyberg 1974), and at which mutations occur in
DNA (Bingham et al. 1976). When temperature is
raised to a certain level, often ~ 43°C, cell functions
become so disrupted that the cell's capacity to repair
the damage is exceeded and the cell dies. The effect of
a rapid heating rate is less clear. Some disruption of
cefl function may be expected from a rapid
temperature rise, even if the critical temperature
(e.g., 43°C) has not been reached. Whether this
disruption is fully reversible has not been well docu-
mented. RF-radiation exposure can produce such
high heating rates, especially from high-peak, low-
average power pulses. Effect of nonuniform heat
deposition is probably the most difficult aspect to
account for when one is evaluating the effects of
exposure of RF radiation.
The effects presented in this section are sufficiently
well established to warrant continued concern and
effort. The effects of microwave radiation on the
electrical properties of the cell are potentially the
most significant. Four separate experiments have
demonstrated these effects. All cells use the electrical
potential across the cell membrane in their life
functions, and perhaps the most important cells are
those of the nervous system. Microwave effects have
been found in the functioning of the nervous system
and in behavior, as will be discussed in the following
sections.
At this time, nearly all the effects documented for
cellular and subcellular systems are observed in
intact cells. This finding could imply that a living cell is
required for the necessary interaction with microwave
radiation to occur; or, it may be that the right
questions are not being asked about the subcellular
level, perhaps because the levels of understanding
and instrumentation capabilities are as yet too
limited. Although the primary mechanism(s) of
interaction other than heating the water medium
5-11
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have not yet been defined, some useful directions are
indicated by the results reviewed here. One might
also conclude that some of the effects noted at the
cellular level, particularly the changes in nerve cell
function, may be correlated with effects at higher
levels of organization.
5-12
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5.2 Hematologic and Immunologic
Effects
Ralph J. Smialowicz
Over the years, a considerable number of reports has
appeared in the literature dealing with the effects of
RF radiation on the hematologic and immunologic
systems of animals. For the most part, the responsible
investigators have been motivated by a concern for
the possible adverse health effects of exposure to RF
radiation. Studies in which animals have been
exposed at various frequencies and intensities have
shown inconsistent changes in elements of both
biological systems. In some instances, a thermal
burden to the exposed animal has been credited with
the observed changes, whereas in others, a
"nonthermal" (i.e., lack of measurable elevation of
temperature) or direct (i.e., athermal or field-specific
effect) interaction of RF radiation with the blood and
blood-forming systems has been suggested as the
causative mechanism for the observed effects. In any
case, the final interpretation of RF-induced changes
must consider many variables that affect the
interaction of RF radiation with the biological entity.
As has been noted previously, variables such as body
shape and mass, radiation frequency, duration of
exposure, field intensity, specific absorption rate,
energy distribution, orientation of the body in the field,
ambient environmental conditions, area of the body
exposed, and field modulation may all influence the
final results. Variability of response among species
and strains as well as between sexes must also be
considered.
been examined, the effects have proven to be
transient.
• Some of the reported effects of RF radiation on the
hematologic and immune systems are similar to
those (a) resulting from a stress response involving
the hypothalamic-hypophyseal-adrenal axis, or(b)
following administration of glucocorticoids.
• Several reports show an association between RF-
induced thermal loading or increased core
temperature and hematologic and immunologic
changes. Conversely, there is a lack of convincing
evidence for a direct interaction of RF radiation
with hematologic and immunologic systems in the
absence of some form of thermal involvement.
• That an increase in rectal temperature is not
observed after exposure to RF radiation does not
preclude a thermal interaction that the animal is
able to compensate for and control.
• There is presently no convincing evidence from
animal studies for adverse alterations in the
hematopoietic or immune systems at RF-radiation
intensities comparable to average environmental
levels, i.e., 0.01 to 0.1 /uW/cm2 in the frequency
range of 54 to 900 MHz, which encompasses the
resonant frequencies for human beings.
For convenience, this section is divided into two
general topics: hematologic effects and immunologic
effects. These two topics are further subdivided into
reviews of studies in which cellular components of
these systems have been exposed in vitro and of
studies dealing with in vivo exposures to RF radiation.
This section critically reviews the reported effects of
RF radiation on the hematologic and immunologic
systems of laboratory animals. On the whole, direct
comparisons between many of these studies are
difficult to make because of differences in species, in
exposure parameters, and in the biological end points
examined. Furthermore, as mentioned above, the
reported responses are inconsistent and highly
variable, with general trends in the data not readily
apparent. Nevertheless, from this review the
following generalizations may be fo/mulated:
• Partial or whole-body exposure of animals to RF
radiation may lead to a variety of changes in the
hematologic and immunologic systems. Depending
upon the exposure conditions, species, and
parameters measured, the changes may be
stimulatory or suppressive.
• Transient changes in peripheral blood composition,
possibly caused by redistribution of blood cells
and hemoconcentration, have been reported.
• In those cases where the reversibility of RF
radiation effects on the immune system have
5.2.1 Hematology
Hematology is the study of the anatomy, physiology,
and pathology of the blood and blood-forming tissues.
The hematopoietic system is comprised of a variety of
cells and cell products. In fetal life, the production of
blood cells occurs in the liver, spleen, and bone
marrow. After birth this function is limited largely to
the bone marrow, which produces red cells
(erythrocytes), white cells (neutrophilic, eosinophilic,
and basophilic granulocytes; lymphocytes; and
monocytes), and platelets. Each of these cell types
performs specific functions that are essential to life.
For example, mature erythrocytes transport Oz and
C02 to and from tissues, granulocytes and monocytes
phagocytize invading microorganisms, and lympho-
cytes are involved in immune responses. These
functional cells are all descendants of progenitors
(stem cells) that reside within the bone marrow.
Blood-cell formation consists of two essential
processes, proliferation and differentiation; bone
marrow progenitor cells proliferate and differentiate
into red and white cells. As the process of
differentiation progresses, the capacity for cellular
proliferation decreases. Impairment of either of these
5-13
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processes may lead to dysfunctions in the hematologic
system that may be life threatening.
5.2.1.1 In Vivo Studies
A paucity of information on the health effects of RF-
radiation exposure from clinical and epidemiological
studies has led to studies of effects on the
hematologic systems of laboratory animals (Table 5-
5). Many of the early investigations on the blood-
forming system of laboratory animals employed
power densities of 10 mW/cm2 and higher. For
example, Deichmann et al. (1964) reported significant
leukocytosis, lymphocytosis, and neutrophilia in rats
following 7 h of exposure to 24,000-MHz (PW)
microwaves at an average power density of 20
mW/cm2 (SAR estimated at 3 W/kg). One week
following exposure, peripheral blood values returned
to normal. Rats exposed for 3 h at 10 mW/cm2
displayed the same changes and returned to normal
after 2 days (SAR estimated at 1.5 W/kg). Increases
in circulating erythrocytes, hemoglobin concentration,
and hematocrit were observed in two of three strains
of rats (Osborne-Mendel and CFN) exposed to
24,000-MHz fields at 10 or 20 mW/cm2. However, in
Fischer rats exposed under the same conditions,
there was a reduction in the number of circulating
erythrocytes and a reduction in hematocrit and
hemoglobin concentration. These differences in
Fischer rats are difficult to reconcile in light of the
hematologic responses to thermal loads displayed by
the Osborne-Mendel and CFN rats. In another
experiment, Deichmann et al. (1963) exposed two
dogs to 24,000-MHz (PW) fields at an average power
density of 24 mW/cm2 (SAR estimated at 1 W/kg).
One dog was exposed for 20 months, 6.7 h/day, 5
days/week; the second dog was exposed for 20
months, 16.5 h/day, 4 days/week. No significant
changes were observed in blood volume, hematocrit,
hemoglobin, erythrocytes, total and differential
leukocytes, blood cholesterol, or protein-bound
iodine. The only finding attributed to the exposure
was a slight loss of body mass.
Kitsovskaya (1964) exposed rats to 3000-MHz (PW)
radiation at 10, 40, or 100 mW/cm2 for various
periods of time (SAR estimated at 2, 8, and 20 W/kg,
respectively). No changes were found in rats exposed
at 10 mW/cm2; at 40 and 100 mW/cm2, however, the
absolute number of peripheral blood erythrocytes,
total leukocytes, and lymphocytes decreased, and
granulocytes increased. These blood changes did not
return to normal until several months after cessation
of exposure.
The apparent discrepancy between the results of
Deichmann et al. (1964) and Kitsovskaya (1964) may
be partially explained by the work of Michaelson era/.
(1964). These investigators reported that the
hematopoietic effects of 2800- and 1280-MHz (PW)
fields depend on the frequency, intensity, and
duration of exposure. For example, dogs exposed to
2800-MHz fields showed a marked decrease in
circulating lymphocytes and eosinophils after 6 h at
100 mW/cm2 (SAR estimated at 4 W/kg). This
exposure resulted in a 1 °C mean increase of rectal
temperature. Neutrophils remained slightly increased
at 24 h; eosinophils and lymphocyte values returned
to normal levels. After a 2-h exposure at 165
mW/cm2 to 28,000-MHz fields (SAR estimated at 6
W/kg), there was a slight leukopenia, neutropenia,
and definite hemoconcentration. These changes
were accompanied by a rectal temperature rise of
1.7°C. Eosinopenia was still evident 24 h after this
exposure. Changes in leukocyte counts were more
apparent following exposure of dogs to 1280-MHz
(PW) fields or to 200-MHz (CW) radiation. After
exposure of dogs at 1280 MHz for 6 h at 100 mW/cm2
(SAR estimated at 4.5 W/kg), a leukocytosis and
neutrophilia were observed. After 24 h the neutrophil
level was still increased above pre-exposure levels.
Lymphocyte and eosinophil values were slightly
depressed following exposure, but at 24 h they were
slightly higher than initial values. A 6-h exposure to
200-MHz (CW) fields at 165 mW/cm2 (SAR estimated
at 25 W/kg) caused a marked increase in neutrophils
and a slight decrease in lymphocytes. After 24 h this
trend was more evident. Michaelson et al. (1964)
suggested that the results indicated a stress response
of the exposed animals in the hypothalamic and/or
adrenal axis that was brought about by a thermal
stimulation from RF-radiation exposure.
Spalding et al. (1971) exposed mice to 800-MHz fields
at an average power density of 43 mW/cm2 (SAR
estimated at 10.7 W/kg) for 2 h/day, 5 days/week,
for a total of 35 weeks. These investigators found no
changes in blood erythrocytes, leukocytes, hematocrit,
or hemoglobin concentrations. It is interesting that
these investigators did not detect changes in the
peripheral blood picture of exposed mice, despite the
thermal burden that was being placed orr these
animals. Failure to detect changes may have been
due to the animal's ability, over the prolonged period
of exposure, to adapt to the RF-induced thermal load.
Four mice died from "thermal effects" following the
33rd and 34th RF-radiation exposures.
Effects produced at levels at or below 10 mW/cm2
(SAR estimated at 0.5 to 2.0 W/kg) have also been
reported. For example, Baranski (1971, 1972a,b)
exposed guinea pigs and rabbits to 3000-MHz (CW
and PW) microwaves at an average power density of
3.5 mW/cm2 (SAR estimated at 0.5 W/kg) for 3
months, 3 h daily. At this power level, the body
temperature of the animals was not elevated.
Observations were made of increases in absolute
lymphocyte counts in peripheral blood, abnormalities
in nuclear structure, and mitosis in the erythroblastic
cell series in the bone marrow and in lymphoid cells in
lymph nodes and spleen. No changes were observed
5-14
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Table 5-5. Summary of Studies Concerning Hematologic Effects of RF-Radiation Exposure*
Exposure Conditions
Effects
Increased: WBC. lymphs, PMN,
RBC. Hct, and Hgb
No change
No change
Decreased: RBC, WBC and lymphs
Increased: PMN
Decreased: lymphs and eosin
Decreased: WBC, PMN, and eosin
Decreased: WBC, lymphs, and eosin
Increased: PMN
Decreased: lymphs
Increased: PMN
No change
Increased: lymphs and mitotic
index of lymphoid cells
Increased: RBC, Hct, and Hgb
No change
Increased: eosmophils
Increased: WBC, CPU
Decreased: 59Fe uptake
Accelerated recovery following
x-irradiation; increased
erythropoiesis and myelopoiesis
Accelerated recovery from
x-irradiation
Increased: PMN and RBC
Decreased: lymphs
Accelerated recovery from
x-irradiation
Increased: lymphs
Decreased: PMN
(Not reproduced consistently)
No change
No change
No change
Decreased: Hct, WBC, and lymphs
No change
Decreased: lymphs
Increased: PMN
Decrease in CPU for erythroid
and granulocyte-macrophage series
Reduction in CPU granulocyte-
macrophage precursors exposed
in vitro
Species
Rat
Dog
Rat
Dog
Mouse
Guinea pig
Rat
Rat
Rabbit
Mouse
Mouse
Dog
Chinese
hamster
Rat
(Perinatal
exposure)
Rat
(Perinatal
exposure)
Rat
(Perinatal
exposure)
Quail egg
Rat
(young)
Mouse
Mouse
Mouse
Mouse
Frequency
(MHz)
24.000 (PW)
24,000 (PW)
3,000 (PW)
2.800 (PW)
2.800 (PW)
1,280(PW)
200 (CW)
800
3.000 (CW or
PW)
2,400 (CW)
2,400 (CW)
2.450 (CW)
2,450 (CW)
2,450 (CW)
2.800 (PW)
2,450 (CW)
425 (CW)
2,450 (CW)
100(CW)
2.450 (CW)
2,736 (PW)
2,450 (CW)
26 (CW)
2,450 (CW)
2,450 (CW)
Intensity
(mW/cm2)
10
20
24
10
40
100
100
165
100
165
43
3.5
10
5
10
100
100
100
60
10
5
46
30
24.4
30
8610
15
60-1000
Duration
(days x min)
1 x 180
1 x420
400 x 400-900
21 6 x 60
20x15
6x5
1 x360
1 x 1 20
1 x360
1 x360
175 x 120
120 x 180
30 x 1 20
90x60
180 x 1380
1 x5
1 x5
1 x3600
1 x30
47 x 240
57 x 240
57 x 240
1 x 1440
35 x 240
22x30
9x30
1 x 15
SAR
(W/kg)
3.0t
1t
2t
8t
20t
4t
6t
4.5t
25t
12.9t
0.5t
2t
It
1.5
70t
70t
4t
28t
3-7
1-5
2-3
14
5-25t
22
13t
10
120-2000
References
Deichmann et al. (1964)
Deichmann et at. (1963)
Kitsovskaya (1964)
Michaelson et at. ( 1 964)
Spalding et a/. (1971)
Baranski(1971 and 1972a)
Djordjevic and Kolak (1973)
Djordjevic et at. (1977)
McReeefa/. (1980a)
Rotkovska and Vacek (1 975)
Rotkovska and Vacek (1 977)
Michaelson et at. (1963)
Lappenbusch era/. (1973)
Smialowicz et at. (1982)
Smialowicz et al. (1979a)
Smialowicz et al. (1981 a)
Hamrick and McRee (1975)
Pazderova-Vejlupkova and
Josifko(1979)
Smialowicz et al. (1979b)
Liburdy (1977)
Huang and Mold (1980)
Lin et al. (1979b)
*WBC = white blood cell, PMN =polymorphonuclear leukocytes, RBC = red blood cell, Hct =hematocrit, Hgb = hemoglobin, andCFU colony-
forming unit.
tSAR estimated.
5-75
-------
in the granulocytic series in peripheral blood. Shifts in
peripheral blood cells were found to correlate with
changes in the cellularity of the spleen and lymph
nodes. An increase in the mitotic index and in the
percentage of cells incorporating 3H-thymidine was
observed in the spleen and lymph nodes of exposed
animals.
Djordjevic and Kolak (1973) exposed Vats to 2400-
MHz (CW) fields at 10 mW/cm2 (SAP estimated at 2
W/kg) 2 h/day for 10 to 30 days. Body temperature in
rats exposed under these conditions increased by 1 °C
within the first 30 min of exposure and remained at
this level throughout the exposure period. Hematocrit,
hemoglobin concentration, and circulating erythro-
cytes increased during the 30-day exposure.
Fluctuations in the various leukocyte populations
were also observed. The authors suggested these
changes were caused by the thermal effect of
microwaves. In a more recent study, Djordjevic et al.
(1977) found no significant difference in any of
several hematologic end points for rats exposed to
2400-MHz (CW) microwaves at 5 mW/cm2 (SAR
estimated at 1 W/kg) for 1 h/day during a 90-day
period.
Recently, McRee et al. (1980a) reported significant
decreases in eosinophils and a lowering of albumin
and calcium in blood from rabbits immediately
following chronic exposure to 2450-MHz fields. In
this study, rabbits were exposed 23 h daily for 180
consecutive days to 2450-MHz (CW) radiation at a
power density of 10 mW/cm2 (SAR = 1.5 W/kg). No
change in hematologic parameters was observed 30
days after termination of exposure (i.e., depression in
eosinophils seen immediately following exposure
had normalized); however, a significant decrease in
albumin/total globulin ratio was observed in the blood
of exposed rabbits at this time. The authors contend
that, because only 3 of the 41 blood-chemistry
parameters measured immediately after exposure
were significantly different (p <0.05), and because
this observation is close to that expected by chance,
further validation of these changes is warranted.
Rotkovska and Vacek (1975) reported changes in
hematopoietic cell populations of mice following a
single 5-min exposure to 2450-MHz (CW) radiation at
an intensity of 100 mW/cm2 (SAR estimated at 70
W/kg). The response of microwave-exposed mice
was compared with that of mice placed in a warm-air
chamber at an ambient temperature of. 43°C for 5
min. Both treatments caused a rise in rectal
temperature > 2°C. A leukocvtosis occurred in mice
under both conditions; however, the time course for
the leukocvtosis and the response of hematopoietic
stem cells differed between the two treatments.
Following RF-radiation exposure, a decrease in the
total cell volume of the bone marrow and spleen was
observed, and the number of hematopoietic stem cells
in bone marrow and spleen, as measured by the
colony-forming unit (CFU) assay, increased. Incorpor-
ation of 59Fe in the spleen decreased 24 h after RF-
radiation exposure. On the other hand, the exposure
to heat caused a decrease in the CFU's in bone
marrow and spleen and an increase in the percentage
of 59Fe incorporation. Rotkovska and Vacek concluded
that the different effects of RF radiation and
externally applied heat on the hematopoietic stem
cells indicate that biological effects caused by high
intensities of RF radiation may not necessarily be
related only to increases in internal temperature. They
indicated that their results suggest a possible
"direct" effect. This study is significant because it
demonstrates a marked difference in the kinetic
response of the hematopoietic system to two forms of
heat stress. Consequently, these differences must be
considered in the interpretation of RF-radiation-
induced changes in the hematopoietic system.
Subsequently, Rotkovska and Vacek (1977) studied
the effect of microwaves on the recovery of
hematopoietic tissue following exposure to x-
irradiation. Mice exposed to X rays at 300 to 750 rads
were then exposed to 2450-MHz (CW) microwaves
for 5 min at 100 mW/cm2 {SAR estimated at 70
W/kg). The combined treatment resulted in an
accelerated recovery of hematopoietic tissue, a
heightened erythropoiesis and myelopoiesis, and an
increased survival rate compared with x-irradiated
mice. The increase in the number of endogenous
hematopoietic colonies in the spleens of the x-
irradiated mice after microwave exposure supports
Rotkovska and Vacek's earlier (1975) observation of
an elevation in the number of stem cells in the
spleens of intact mice after microwave exposure
alone. These investigators suggested that RF
radiation may influence the mechanisms that
activate the pool of stem cells, either by improving the
repair of sublet ha I radiation damage or by increasing
the proliferative capacity of stem cells that survive x-
irradiation. The authors concluded that this accelera-
tion of the processes of repairing radiation damage in
hematopoietic cells after thermogenic doses of RF
radiation depended on the stage of intracellular repair
at the time of RF-radiation exposure. In earlier work,
Michaelson et al. (1963) reported that simultaneous
exposure to X rays and microwaves (2800 MHz, PW
modulated, 100 mW/cm2, SAR estimated at 4 W/kg)
caused an accelerated recovery of the hematopoietic
function in dogs. Thomson et al. (1965) reported that
pretreatment of mice with RF radiation (2800 MHz,
PW modulated, 100 mW/cm2, SAR estimated at 70
W/kg) reduced the mortality after x-irradiation (800
rads). The 30-day lethality was 40 to 55 percent
among mice given single or multiple RF treatment
prior to x-irradiation, compared with 76 percent
lethality in mice not pretreated with RF radiation.
Exposure of Chinese hamsters to RF radiation (2450
MHz, CW, 60 mW/cm2, SAR estimated at 28 W/kg,
for 30 min) 5 min after X irradiation (725 to 950 rads)
B-16
-------
significantly increased the X-ray LD|8 dose compared
with exposure of animals to X rays only or with
exposure to RF radiation before irradiation (Lappen-
busch et at. 1973). Lappenbusch et al. reported that
the radio-protective effect of RF radiation appears to
be associated with a delayed decrease in the number
of circulating white blood cells, reduced period of
decreased cell density, and complete replenishment
of white blood cells within 30 days following the dual
treatment. Exposure to RF radiation either alone or
combined with X-ray exposure increased the relative
number of neutrophils, reduced the relative number
of lymphocytes, and slightly increased the number of
circulating red blood cells. On the other hand,
animals exposed first to RF radiation and then to X
rays demonstrated a more severe leukocyte picture
than hamsters x-irradiated only; in these animals,
leukocyte counts decreased faster, and the animals
developed leukopenia.
The effect of exposure to RF radiation on circulating
blood cells of developing rats has been studied by
Smialowicz et al. (1979a, 1982). Rats were exposed
pre- and postnatally to 425-MHz (CW) fields at 10
mW/cm2, 4 h daily up to 41 days. Because the
animals were growing, SARs ranged from 3 to 7
W/kg. No consistent changes in blood values were
observed in exposed compared to sham-irradiated
control rats (Smialowicz et al. 1982). Rats exposed
under the same regimen but to 2450-MHz (CW) fields
at 5 mW/cm2 (SAR estimated at 1 to 5 W/kg) also
showed no difference in circulating erythrocyte
count, leukocyte and differential counts, or hematocrit
and hemoglobin concentration compared with sham-
irradiated controls (Smialowicz et al. 1979a). Rats
exposed to 100-MHz fields at 46 mW/cm2 (SAR
estimated at 2 to 3 W/kg) pre- and post-natally as
above showed no change in blood parameters
compared with controls (Smialowicz et al. 1981 a).
Pazderova-Vejlupkova and Josifko (1979) reported
decreases in the hematocrits, number of leukocytes,
and absolute numbers of lymphocytes in young rats
exposed to 2736-MHz (PW, 395 Hz, 2.6-fJs pulse
width) microwaves at 24.4 mW/cm2 for 7 weeks (5
days/week, 4 h/day). The means of body mass of rats
at the beginning and at the end of the 7-week
exposure period was 65 and 350 g, respectively (SAR
estimated at 5 to 25 W/kg). These changes
disappeared within 10 weeks after termination of
exposure. The activity of alkaline phosphatase in
neutrophils increased during the first week of
irradiation but decreased transiently after the
irradiation. In a similar experiment by the same
authors (data not given), in which adult rats were
exposed for 14 weeks to 3000-MHz (PW, 300 Hz, 2.5-
fjs pulse width) microwaves at 1 mW/cm2 (SAR
estimated at 0.2 W/kg), no difference was observed
in hematologic parameters between exposed and
Control rats.
Hamrick and McRee (1975) examined the effect of RF
radiation on developing birds. Quail eggs were
exposed for 24 h during the second day of incubation
to 2450-MHz (CW) fields at 30 mW/cm2 (SAR = 14
mW/g). At 24 to 36 h after hatching, quail chicks
were examined for gross deformities, changes in organ
weight, and hematologic changes. No significant
effects due to RF exposure were detected.
In another study, Smialowicz et al. (1979b) exposed
mice to 2450-MHz (CW) fields at 30 mW/cm2 (SAR =
22 W/kg) for 30 min on 22 consecutive days. These
mice showed no significant difference in circulating-
erythrocyte count, leukocyte and differential counts,
or hematocrit and hemoglobin concentration
compared with sham-irradiated controls. In this
experiment, mice were maintained in an environ-
mental chamber in which temperature, humidity, and
air flow were continuously controlled. Under the
conditions of this study, the RF radiation did not
significantly elevate rectal temperatures of exposed
mice. In contrast, when mice were exposed to
thermogenic levels (2 to 4°C rise in rectal temperature)
of 26-MHz (CW) radiation, 8610 mW/cm2 (SAR
estimated at 13 W/kg), a decrease in the number of
circulating lymphocytes and an increase in circulating
neutrophils was observed immediately after exposure
(Liburdy 1977). These mice were held in a chamber
that lacked a continuous turnover of air. Liburdy
(1977) reported that this shift reached its peak 3 h
after exposure. The number of circulating lymphocytes
and neutrophils was reported to return to normal,
pre-exposure levels 55 to 96 h after exposure. On the
other hand, mice exposed at high ambient tempera-
tures (79°C) in a vented, dry-air oven showed an
increased number of circulating lymphocytes and
neutrophils for a 12-h period after exposure. The
response of circulating leukocytes to exogenous
thermal loading thus depends on the means by which
the body is heated. These results are similar to those
reported by Rotkovska and Vacek (1977) and indicate
that the heating properties of RF radiation differ from
those of conventional modes of tissue heating.
Recently Huang and Mold (1980) reported that bone
marrow (cultured in vitro) from mice exposed to 2450-
MHz (CW) fields at 15 mW/cm2 (SAR = 10 W/kg) for
30 min on 9 consecutive days had significantly fewer
(p < 0.05) CFUs of both the erythroid and granulocyte-
macrophage series. No data were presented on the
peripheral blood counts of any of these blood cells
that would confirm or expand the information
gathered in the CFU assay.
5.2.1.2 In Vitro Studies
Lin et al. (1979b) reported a reduction in the number
of CFU's (granulocyte and macrophage precursor
cells) formed by bone marrow cells exposed in vitrolo
2450-MHz fields at 60 to 1000 mW/cm2 (SARs at
120 to 2000 W/kg). This reduction in colony
5-77
-------
formation was reported to be dose dependent and
occurred without a significant rise in the temperature
of the cell suspension. The authors indicate that their
results point to a direct effect of microwave radiation
on these hematopoietic precursor cells. Although
these results are interesting, the in situ application
of fields as intense as those required to produce the
observed effects would certainly cause gross thermal
injury to the tissue.
In summary, levels of RF radiation that cause an
increase in body temperature elicit changes in the
hematopoietic system that can for the most part be
ascribed to a thermal stress response. Changes in the
blood of animals exposed to RF radiation at intensities
below those that cause an increase in core
temperature suggest a similar stress-response
mechanism. The failure to record an increase in core
temperature does not preclude the possibility that the
animal is compensating for the added thermal energy
by thermoregulatory mechanisms. Indeed, lack of a
temperature change indicates that thermoregulation
is operating. The response elicited by RF-radiation-
induced heating, however, appears to differ from that
of conventional heating because of the differing
internal heating patterns of this form of radiation.
5.2.2 Immunology
The immune system is comprised of myriad
mechanical, cellular, and humoral components that
act as the body's defense against various pathogenic
microorganisms, viruses, and neoplasias. The
immune system is divided into the humoral element,
i.e., antibodies and complement, and the cellular
elements, which are composed of the lymphoid and
phagocytic cells. The cellular elements of the immune
system are also part of the hematologic system. The
phagocytic cells responsible for engulfing and
digesting certain microorganisms are the neutrophils
or polymorphonuclear leukocytes (PMNs) and the
monocytes or macrophages. In the presence of
antibodies and complement, neutrophils are aided in
engulfing and digesting invading organisms. The
monocyte is also a phagocytic cell. Monocytes move
into an area in which an infection has begun and then
differentiate into macrophages. Macrophages can be
"activated" to kill certain microorganisms (e.g.,
intracellular, facultative bacteria such asMycobacteria
tuberculosis and Listeria monocytogenes, viruses,
and fungi) through the interaction of certain
subpopulations of lymphocytes, such as the T
lymphocytes.
The other cellular components of the immune system
are the lymphocytes. These cells are broadly divided
into two groups, the B lymphocytes and the T
lymphocytes. Although these cells are similar
morphologically, they are different functionally; Band
T lymphocytes can be distinguished by the presence
of unique antigens or receptors on their membrane
surface. Both T and B lymphocytes are believed to
originate in the bone marrow and then to proceed
through various stages of development and differen-
tiation, maturing into functional cells of the immune
system.
The B lymphocyte, or bursa-equivalent lymphocyte, is
responsible for humoral immune responses. The B
lymphocytes, after appropriate stimulation by
antigens, proliferate and undergo morphological
changes and develop into plasma cells that actively
synthesize and secrete antibodies.
The T lymphocyte, or thymus lymphocyte, is
processed through the thymus after leaving the bone
marrow. Classically cell-mediated or T-lymphocyte
responses include protection against viruses, fungi,
and several bacteria. T lymphocytes are also involved
in reactions such as delayed hypersensitivity or
contact hypersensitivity and rejection of tumors and
foreign tissues such as transplants (allografts). Cell-
mediated reactions are so named because these
reactions, which operate by specifically sensitized T
lymphocytes, can be transferred by these cells to
normal animals. B-lymphocyte-mediated humoral
responses, in contrast, are transferable by serum.
The recent availability of monoclonal antibodies has
made the typing of lymphocyte subpopulations
possible on a routine basis. Various functional
categories of T cells can be recognized: "helper"
(inducer/amplifier) T cells, "suppressor" T cells,
"cytotoxic" T cells, and NK (natural killer) cells.
Immature thymocytes may be identified by surface
antigens distinct from mature peripheral T cells.
Cellular interactions between the various T-cell
subtypes and other immunocompetent cells are vital
to the modulation of the immune response. Because
of their pivotal role in enhancing antigen-mediated
immune responses, disorders involving T-cell
subsets may result in immunodeficiency syndromes
involving either cell-mediated or humoral immunity.
Each element of the immune system—the T and B
lymphocytes and macrophages—plays a cooperative
role in defending the host against infection and
disease. A-delicate balance exists to prevent the
immune system from reacting to its own tissues so
that autoimmune reactions are avoided. The
alteration or dysfunction of any of these elements
may lessen the host's ability to combat infection or
may lead to autoimmune disease. However, because
of adaptability and redundancy in the immune
system, the host can generally survive subtle
perturbations. Consequently, although subtle effects
on the immune system may be generated by physical
5-18
-------
or chemical agents, all such effects may not lead to
clinically significant immune dysfunctions.
5.2.2.1 In Vivo Studies
A summary of in vivo studies concerning immunologic
effects of RF-radiation exposure is presented in
Table 5-6.
Effects on adult animals—One of the most consistently
found RF-radiation-induced changes in the hemato-
poietic system is the increase in lymphocyte
formation and activity following exposure of animals
of several species to RF radiation at various
frequencies (Baranski 1971, 1972a,b; Czerski 1975).
There have been several studies of the effects of RF
radiation on lymphocytes and the immune system. In
a study reported by Czerski (1975), mice were
exposed 2 h daily to 2950-MHz (PW modulated)
microwaves at 0.5 mW/cm2 (SAR estimated at 0.5
W/kg) for 6 to 12 weeks. After 6 weeks, there was a
large increase in the relative number of lymphoblasts
in the lymph nodes of exposed mice. In another series
Table 5-6. Summary of Studies Concerning Immunologic Effects (In Vivo) of RF-Radiation Exposure
Exposure Conditions
Effects-
Frequency
Species (MHz)
Intensity
(mW/cm2)
Duration
(days x min)
SAR
(W/kg)
References
Increase in lymphoblasts in
lymph nodes and increased
response to SRBC
Increase in "spontaneous"
lymphoblast transformation
of cultured lymphocytes
Increase in lymphoblasts in
spleen and lymphoid tissue
Increased transformation of
unstimulated cultured lymphocyte
and decreased mitosis in PHA-
stimulated lymphocyte cultures
Transient decrease and increased
response of cultured lymphocytes
to PHA. Con A, and LPS
Increased mitosis of PHA-
stimulated lymphocytes
Increase in CR* Fc*. and Ig*
spleen cells. Increased response
to B-cell mitogens. Decrease
in primary response to SRBC
Increase in CR* and Fc*, spleen
cells
Increase in CR" spleen cells.
strain specificity
Increase in CR* spleen cells
Increased lethality to endotoxin
Increase in response of
cultured lymphocytes to T-
and B-cell mitogens
No change
No change
Increase in T and B
lymphocytes in spleen
Decrease in DTH
Reduction of lymphocyte
traffic from lung to spleen
Decrease in NK activity, increase
in macrophage phagocytosis
Decrease in NK activity
Increase in macrophage viricidal
capacity
Decreased response to PWM
No change
Decrease in tumor development
Mouse
Rabbit
Mouse
Mouse
Mouse
Mouse
2950 (PW) 0.5
2950 (PW)
3105 (PW)
42 x 120
0.5t
24-48x120 0.8t
Chinese 2450 (CW) 5.15,30
hamster or 45
2450 (CW) 5 or 15
Rhesus 10-27(PW) 1320
monkey
Mouse 2450 (CW) —
2450 (CW) —
2450 (CW) —
6-8700
5x 15
1-17x30
2t
2.3, 6.9,
13.8 or
20.7
3.6 or 10
1 x 30 0.4-2.0t
1 or 3x30 14
1 x 15
1 x 30
1 x 30
11.8
5
10-19
Mouse
Mouse
Rat
Mouse
Rat
Mouse
Mouse
Mouse
Hamster
Hamster
Rabbit
Quail
Mouse
2450 (CW)
2450 (CW)
2450 (CW)
425 (CW)
2450 (CW)
100(CW)
26 (CW)
2600 (CW)
2450 (CW)
2450 (CW)
2450 (CW)
2450 (CW)
2450 (CW)
2450 (CW)
40
20, 30
5
10
5-35
46
800
5 or 25
30
25
25
10
5
(near-field
application)
1 x30
1 x 1 20
57 x 240
47 x 240
(Perinatal exp)
1-22 x 15 or 30
57 x 240
1 x 15 or
10x 15
1 x 60
2 or 9 x 90
1 x 60
1 x60
180 x 1380
12 x 1440
11-14 day of
gestation or
11-14 & 19-45
x20
28
12, 18
1-5
3-7
4-25
2-3
5.6t
3.8 or 19
21
13
13
1.5
4.03
35
Czerski (1975)
Czerski (1975)
Mnoetal. (1974)
Huang eta/. (1977)
Huang and Mold (1980)
Prince et al. (1972)
Wiktor-Jedrzejczak et al.
(1977a, b, c)
Sulekera/. (1980)
Schlagel el al. (1980)
Smialowicz et al. (1981C)
Riddle et al. (1982)
Smialowicz ef al. (1979a, 1982)
Smialowicz et al. (1979b)
Smialowicz et al. (1981b)
Liburdy(1979)
Liburdy(1980)
Smialowicz et al. (1983)
Yang et al. (1983)
Rama Rao et al. (1983)
McReeetal. (1980a)
Hamrick et al. (1977)
Preskorn et al. (1978)
5-19
-------
Table 5-6. (Continued)
Exposure Conditions
Effects*
Decreased granulocytic response
Tumor regression and increase in
antitumor antibodies and anti-BSA
Tumor inhibition and immune
stimulation
Increased tumoricidal activity
in lymphocytes and macrophages
Tumor regression
Increase in lung cancer
colonies and inhibition of
contact sensitivity to
oxazolone
Decrease in response to BSA
Species
Rabbit
Rabbit
Rat
Mouse
Mouse
Mouse
Rabbit
Frequency
(MHz)
3000 (CW)
13.56
2450 (CW)
1356
3000 (CW)
2450 (CW)
1356
Intensity
(mW/cm2)
3
(near-field
application)
200W
600-900
40
50
(near-field
application
Duration
(days x min)
42 to 84 x 360
1 x 10-15
3 or 6 x 45
1 x 5
1-14x 120
4, 7, 10 or
14 x 120
3x60
SAR
(W/kg)
0.5
(local
hyperthermia)
(local
hyperthermia)
(local
hyperthermia)
28t
36t
(local
hyperthermia)
References
Szmigielski et al. (1975)
Shah and Dickson (1978b)
Szmigielski era/. (1978) '
Marmor et al. (1977)
Szmigielski et al. (1977)
Roszkowski et al. (1980)
Shah and Dickson (1978a)
*SRBC = sheep red blood cells, PHA = phytohemagglutinin. Con A
immunoglobulin positive, Fc* = Fc portion of immunoglobulin. DTH =
tSAR estimated.
= concanavalin A, LPS = lipopolysaccharide, CR* = complement-receptor positive, Ig* =
delayed-type hypersensitivity, PWM -pokeweed mitogen, BSA = bovine serum albumim.
of experiments (Czerski 1975), rabbits were exposed
2 h/day, 6 days/week for 6 months to 2950-MHz
(PW) microwaves at 5 mW/cm2 (SAR estimated at 0.8
W/kg). After culturing for 7 days in vitro, peripheral
blood lymphocytes from these animals were found to
undergo an increase in "spontaneous lymphoblastoid
transformation." Maximal increases occurred after 1
to 2 months of exposure; the transformation rate then
returned to base line and rose again 1 month after an
irradiation had been terminated. Miro et al. (1974)
continuously exposed mice to 3105-MHz (PW)
microwaves over a 145-h period at an average power
density of 2 mW/cm2 {SAR estimated at 2 W/kg). No
description was given of how animals were fed or
watered. An increase in lymphoblastic cells in the
spleen and lymphoid areas of exposed mice was
observed. A somewhat similar response was
observed (Huang et al. 1977) in lymphocytes cultured
from Chinese hamsters that were exposed to 2450-
MHz (CW) microwaves for 15 min on 5 consecutive
days at 5 mW/cm2 (SAR = 2.3 W/kg) without a
detectable rise of rectal temperature. Increased
transformation to lymphoblastoid forms in the
absence of mitogens was maximal in cultures from
hamsters exposed at 30 mW/cm2 (SAR = 13.8 W/kg).
Irradiation at this power density caused a 0.9°C rise
in rectal temperature of exposed hamsters. Mitosis of
lymphocytes cultured in the presence of the mitogen
phytohemagglutinin (PHA), however, was depressed
in cells obtained from hamsters exposed at 5,15, 30,
or 45 mW/cm2. These effects were reported to be
transient and reversible; control levels were again
observed after 5 to 10 days (Huang et al. 1977).
More recently, Huang and Mold (1980) reported an
oscillating response of spleen cells to PHA,
concanavalin A (Con A), and lipopolysaccharide (LPS)
from mice exposed to 2450-MHz fields at 15
mW/cm2 (SAR = 10 W/kg) for 30 min. Mitogen
responsiveness decreased significantly after 2 days
of exposure, returned to normal after 4 days of
exposure, and was significantly increased for all
mitogens after 9 days of irradiation. Responsiveness
to mitogens tended to return to normal or to fall to
subnormal levels after 17 days of exposure. In
contrast, when mice were exposed at 5 mW/cm2 for
30 min on 5 consecutive days, a significant increase
in the response to LPS was observed, whereas no
change was observed in LPS responsiveness to
exposure at 15 mW/cm2 for 5 days. When macro-
phages were removed from spleen-cell suspensions
of mice irradiated at 15 mW/cm2 for 9 days, the
responsiveness to LPS was greater than the already
increased spleen-cell responsiveness without macro-
phage removal. However, addition of macrophages
from the RF-irradiated mice to spleen-cell cultures
from nonirradiated mice caused a significant
decrease in responsiveness to LPS. The authors
suggest that macrophage activation (macrophages
from irradiated mice displayed increased spreading
and increased phagocytosis of latex particles in vitro)
by microwaves may be responsible for inhibiting LPS
responsiveness.
Prince et al. (1972) reported the opposite effect in
rhesus monkeys. These investigators found an
enhanced mitotic response of peripheral blood
lymphocytes stimulated in vitro with PHA from
monkeys 3 days following a 30-min exposure to 10.5-
MHz (PW) radiation at 1320mW/cm2 (SAR estimated
at 0.4 W/kg). Enhancement of mitosis of cultured
lymphocytes from monkeys similarly exposed to
19.27- and 26.6-MHz were also reported. Also
reported were increases in circulating lymphocytes
that ranged from 4 to 47 percent above pre-exposure
levels. At a frequency of 26.6 MHz (SAR estimated at
5-20
-------
2 W/kg), the rectal temperature of monkeys following
exposure was reported to increase by 2.5°C above pre-
exposure levels.
The particular susceptibilities of lymphocytes to RF
radiation have led to an examination of the effects of
this form of radiation on the immune response. For
example, Czerski (1975) reported that mice exposed
for 6 weeks to 2950-MHz (PW) microwaves at 0.5
mW/cm2 (SAR estimated at 0.5 W/kg) had signifi-
cantly greater numbers of antibody-producing cells
and higher serum antibody tilers following immuni-
zation with sheep red blood cells (SRBCs). Interestingly,
mice that were exposed for 12 weeks did not show
this increased responsiveness. This return to normal
responsiveness may have resulted from the animal's
ability to adapt to the RF exposure after 12 weeks.
More recently, Wiktor-Jedrzejczak et al. (1977a,b,c)
exposed mice in a rectangular waveguide to 2450-
MHz radiation for 30 min at an average dose rate near
14 W/kg. At 3, 6, 9, and 12 days after a single or
multiple exposures, mice were tested for (1) the
relative frequency of T and B splenic lymphocytes, (2)
the functional capacity of spleen cells to respond toT-
and B-cell-specific mitogens, and (3) the ability to
respond to SRBCs (a T-dependent antigen) or
dinitrophenyl-lysine-Ficoll (DNP-lys-Ficoll, a T-
independent antigen). A single 30-min exposure
induced a significant increase in the proportion of
complement-receptor-positive (CR*) lymphocytes in
mouse spleens that peaked 6 days after exposure.
This effect was further enhanced by repeated (three)
exposures, which also produced a significant
increase in the proportion of immunoglobufin-positive
(Ig*) spleen cells (Wiktor-Jedrzejczak 1977a). A
significant increase in the proportion of Fc-receptor-
positive (FcR*) cells in the spleens was also observed
7 days after a single 30-min exposure (SAR = 13.7
W/kg). However, no change in the number of lg+ cells
in spleens of these mice was observed (Wiktor-
Jedrzejczak 1977c). The type and combination of
surface receptors (CR, Ig, Fc) expressed on splenic B
cells represent different maturational stages in B-
cell development. Wiktor-Jedrzejczak era/. (1977a,b,c)
were unable to demonstrate any change in the total
number of theta-antigen-positive (0*) T cells in the
spleens of mice following a single or multiple exposure
to 2450-MHz microwaves. No change was detected in
the in vitro spleen-cell response to stimulation by the
T-cell-specific mitogens PHA and Con A or by
pokeweed mitogen (PWM), which stimulates both T
and B cells (Wiktor-Jedrzejczak et al. 1977a).
However, the response to the B-cell-specific
mitogens lipopolysaccharide (LPS), polyinosinic
polycytidylic acid (Poly I C), and purified protein
derivative (PPD) of tuberculin was significantly
increased over controls following a single exposure.
These results clearly correlate with the observed
changes in the proportion of cells bearing different
surface markers. Wiktor-Jedrzejczak et al. (1977a)
noted that RF irradiation did not stimulate lymphoid-
cell proliferation per se but rather appeared to act as a
polyclonal B-cell activator, which led to an early
maturation of noncommitted B cells. They also found a
significant decrease in the primary immune response
to SRBCs, a thymus-dependent antigen, in mice that
had been immunized just prior to the first exposure to
RF radiation. They suggested that this decreased
response may result from the nonspecific stimulation
of some cells by RF radiation to mature before they
are activated by antigen (SRBCs), so that the
proportion of unresponsive cells was increased.
Recently, Sulek et al. (1980) corroborated this
increase in CR+ and Fc* spleen cells in mice 6 days
following a 30-min exposure to 2450-MHz fields
(average SAR = 12 W/kg). The kinetics for increased
frequency of CR* cells in the spleens of irradiated
mice showed an initial increase 3 days following
exposure that persisted for 5 to 6 days and then
returned to normal within 9 to 10 days. The authors
determined the threshold for this effect by varying the
time of exposure with a constant forward power (0.6
W), or by maintaining a constant time of exposure
while varying the forward power (0.1 to 0.78 W). It
was shown that a minimum of a single 15-min
exposure (11.8 W/kg) or a single 30-min exposure (5
W/kg) caused significant increases in CR* cells 3 or 6
days after exposure. The effect of absorption of
multiple subthreshold quantities of microwaves was
found to be cumulative only if the exposures occurred
within 1 h of one another. The increase in CR+ cells
was found at dose rates ranging from 10 to 18 W/kg
for mice within a weight range of 18 to 25 g. The
rectal temperature of exposed mice was found to be
elevated no more than 0.6°C above that of sham-
irradiated mice. No change in 0* (T lymphocytes) cells
was observed. In contrast, Huang and Mold (1980)
reported a significant increase in 6* cells but no
change in B cells (Ig*) of mice exposed to 2450-MHz
fields at 15 mW/cm2 (SAR at 10 W/kg) for 30 min on
9 consecutive days.
Smialowicz et al. (1979b) exposed BALB/c mice (H-
2d) to 2450-MHz (CW) fields under far-field conditions
for 15 or 30 min daily for periods to 22 consecutive
days at power densities from 5 to 35 mW/cm2 (SARs
at 4 to 25 W/kg). Splenic lymphocyte function was
assayed by the in vitro mitogen-stimulated response
as measured by 3H-thymidine incorporation after
culture in the presence of T (PHA, Con A, PWM) or B
(LPS, PWM, PPD) mitogens. The proportions of T (0*)
and B (CR*) splenic cells and the primary immune
response of mice to SRBCs were also studied. No
difference in the response to mitogens or to SRBCs or
in the frequency of T or B cells in spleens was
observed in RF-irradiated compared with sham-
irradiated mice.
Subsequent to the report by Smialowicz et al.
(1979b), Schlagel et al. (1980) reported that
5-21
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sensitivity to RF-induced CFT cell increases was
under genetic control. Mice that were responsive*
were found to be of the H-2k haplotype (i.e., CBA/J),
while other mouse strains of the H-2", H-2b, H-2d(i.e.,
BALB/c) and H-1'5 haplotypes did not display
increased CR+ cells following RF exposure. The age of
thp mice was also found to be critical for expression
of increase CR* cells following 2450-MHz (SAR = 14
W/krO RF-radiation exposure. Mice less than 12
wt -o uid did not respond.
In light of the findings by Schlagel et al. (1980) that
indicated that RF-induced increases in CR+cells were
under genetic control, Smialowicz et al. (1981c) re-
examined the effect of RF radiation on CR* cells in
CBA/J mice (H-2k). Increases in the frequency of CR+
spleen cells of CBA/J mice 6 days following a single,
2450-MHz exposure (SAR =28 W/kg), under far-field
conditions in an anechoic chamber, were reported by
Smialowicz et al. (1981c). This increase in CR+ cells
was observed only in 16-week-old mice and not in
younger mice, a result similar to that reported by
Schlagel et al. (1980). However, unlike the results of
Schlage et al. (1980), an increase in CR* cells was
accompanied by a significant decrease in the number
of nucleated cells in the spleens of these mice that
were obviously under thermal stress. No increase in
CFT cells was observed in mice irradiated at SAR
values of 10,14, or21 W/kg, SARs at which Schlagel
et al. (1980) observed effects. Smialowicz et al.
(1981c> concluded that the age and strain of the
mouse, the RF-exposure characteristics (waveguide
vs. far field), and the environmental conditions are all
sources of variation that affect CR+ cell appearance.
Evidence that exposure of mice to far-field 2450-MHz
RF radiation at an SAR > 12 W/kg is thermogenic
was provided by Riddle et al. (1982). Mice were
injected with various doses of lipopolysaccharide
(LPS) and exposed to 2450-MHz CW RF radiation, and
the 50-percent lethal dose (LDSO) of LPS was
determined. A significant decrease in the LPS LD5o
dose was observed at SAR values of 12 and 18 W/kg.
High ambient temperature (37°C) also potentiated
the lethal effect of endotoxin, indicating that RF
heating was responsible for the observed effect. The
SAR values used in this study were comparable to
those used in studies by Wiktor-Jedrzejczak et al.
(1977a,b,c), Schlagel et al. (1980), and Sulek et al.
(1980) in which augmented CR* spleen cells were
observed. This further supports the hypothesis that
increases in CR* spleen cells following RF exposure
may be due to an RF-induced thermal response.
Further evidence for an RF-induced thermal
mechanism in spleen cell changes comes from
Liburdy (1979), who reported that changes in splenic
lymphocyte populations similar to those observed by
Wiktor-Jedrzejczak et al. (1977a,b,c) can be produced
by exposure of mice to thermogenic levels of 26-MHz
radiation. When mice were exposed to 26 MHz at an
intensity (800 mW/cm2, SAR at 5.6 W/kg) that
produced a 2 to 3°C rise in rectal temperature, a
relative increase in splenic T and B lymphocytes was
observed. Similar responses (i.e., increase in T and B
cells) were induced following administration of the
synthetic glucocorticoid methyl prednisolone sodium
succinate. These results indicate that these RF-
radiation-induced changes might represent some
form of stress. It is difficult to understand how a 2 to
3°C rise in rectal temperature would occur in mice
irradiated for 15 min at an SAR of 5.6 W/kg. A
possible explanation is that these mice were
restrained in perforated acrylic cages and held in an
exposure chamber in which the air was not circulated
during this period of irradiation.
In examining further possible mechanism(s) for the
shift in lymphocyte populations in the spleens of mice
exposed to RF radiation, Liburdy (1980) examined
the circulation of lymphocytes in microwave-exposed
mice. Mice injected with 51Cr-labeled syngeneic
spleen cells were exposed for 1 h at either 5 or 25
mW/cm2 to 2600-MHz fields (SAR at 3.8 and 19
W/kg, respectively). Controls included sham-
irradiated mice, mice held in a 63°C warm-air oven
for 1 h, and mice injected with methyl prednisolone
sodium succinate. The distribution of injected cells
was determined for the lung, liver, spleen, and bone
marrow at 1, 6, and 24 h after exposure. Exposures at
25 mW/cm2 caused a 2.0°C increase in core
temperature. This regimen led to a 37-percent
reduction in lymphocytes leaving the lung and migra-
ting to the spleen. Also, a threefold increase in spleen
lymphocytes entering the bone marrow occurred in
this group of mice. A similar pattern of lymphocyte
circulation was observed in the steroid-treated group.
No change in lymphocyte traffic was observed in mice
of the 5-mW/cm2 or warm-air groups. Liburdy (1980)
concluded that these results suggest that steroid
release associated with thermal stress and attempts
by the animal to thermoregulate during exposure to
RF radiation are responsible for effects on the
immune system.
More recently, further evidence for an association
between RF-induced thermal stress and effects on
the immune system has been reported. Thermogenic
doses of RF radiation were found to suppress the
natural killer (NX) cell activity of mice (Smialowicz et
al. 1983). Exposure of CBA/J mice to 2450-MHz (CW)
RF radiation at an SAR of 21 W/kg for 90 min on 2 or 9
days caused a significant reduction splenic NK
activity as determined using in vitro or in vivo assays.
No effect on NK activity was observed at SAR values
of 3.5 or 10.5 W/kg. NK activity returned to normal
levels within 24 h following the last exposure at 21
W/kg. Treatment of mice with hydrocortisone also
caused suppression of NK cell activity measured in
vitro and in vivo. Paradoxically, a concomitant
increase in macrophage phagocytic ability was
5-22
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observed in mice exposed to RF radiation at an SAR of
21 W/kg. These results were essentially in
agreement with work reported by Yang et a/. (1983)
and Rama Rao et al. (1983). Yang er al. (1983)
reported that a single, 2450-MHz exposure of
hamsters at an SAR of 13 W/kg caused a significant
suppression of splenic NK activity that returned to
normal levels by 8 h. This exposure also caused a 2.0
to 3.5°C increase in colonic temperatures, as well as
elevated serum glucocorticosteroid levels. Exposure
of mice at 8 W/kg caused no demonstrable effect on
NK cell activity. In another study Rama Rao et al.
(1983) reported that exposure of hamsters to
thermogenic levels (13 W/kg) of 2450-MHz RF
radiation resulted in activation of peritoneal
macrophages. Macrophages from irradiated hamsters
were found to be significantly more viricidal to
vaccinia virus as compared to that from sham-
irradiated hamsters. In all of these studies (Smialowicz
etal. 1983; Yang era/. 1983, Ra mo Rao era/. 1983) a
strong association exists between RF-radiation-
induced immune system effects and RF-induced
thermal stress.
Effects on young animals—RF-radiation effects on the
development of the immune response have been
studied. Smialowicz etal. (1979a) exposed rats on day
6 of gestation through 41 days of age to 2450-MHz
(CW) fields at 5 mW/cm2 (SAR at 1 to 5 W/kg). The
young animals absorbed microwaves at a higher rate
(5 W/kg) than the adults (1 W/kg). In this study the
exposed rats had lymphocytes that responded to a
significantly greater extent than those from control
animals following in vitro stimulation by T- or B-cell
mitogens. A similar increase in lymphocyte respon-
siveness was seen in another study in which rats
were exposed pre- and postnatally to 425-MHz
radiation (SAR at 3 to 7 W/kg, with the neonates
absorbing at the latter SAR) for periods to 41 days
post part urn (Smialowicz er al. 1982). However,
lymphocytes from rats exposed perinatally to 100-
MHz fields at 46 mW/cm2 (SAR at 2 to 3 W/kg)
showed no change in mitogenic responsiveness
(Smialowicz er al. 1981b). The results of the two
former studies indicate that long-term exposure of
developing (especially neonatal) rats to RF radiation
at absorption levels higher than those achieved in the
latter study may give rise to increased responsiveness
of cultured lymphocytes. These results are similar to
other reported changes in mammalian lymphocyte
responsiveness following RF-radiation exposure
(Czerski 1975; Prince er al. 1972; Wiktor-Jedrzejczak
er al. 1977a,b,c). Increases in lymphocyte activity can
also be elicited by conventional heating (Roberts
1979). Although the benefits are not known
concerning this increased responsiveness to
mitogens by lymphocytes from animals exposed
perinatally to RF radiation, a recent report by Preskorn
er al. (1978) indicates that irradiation at this time
during development may be beneficial for increased
immunosurveillance against tumors. These investi-
gators exposed mice to 2450-MHz fields (SAR = 35
W/kg) for 20 min either on days 11 through 14 of
gestation, or on days 19 through 45 postpartum, or
during both periods. On the 16th day postpartum, all
mice were implanted with a lymphoreticular cell
sarcoma. Mice irradiated in utero only (colonic
temperature increase of 2.2°C in dams) showed a
lower incidence of tumors (13 percent vs. 46 percent
for sham-irradiated mice) 93 days postpartum In
mice irradiated in utero and postnatally, tumors
initially developed at a lower rate compared with
controls; however, after 2.5 months, no difference
was observed in tumor incidence between groups. At
the end of 4 months, the tumor incidence in irradiated
mice was slightly greater than controls (46 vs. 40
percent, respectively). An interesting finding,
however, was that both tumor-bearing and tumor-
free animals that had been irradiated only in utero
lived longer on the average than their respective
controls. This result is somewhat similar to that
reported by Prausnitz and Susskind (1962), who
found that mice briefly irradiated hundreds of times
by a highly thermogenic level of RF radiation survived
longer than controls.
McRee er al. (1980a) reported that 30'days after
termination of a 6-month 23-h daily irradiation to
2450-MHz fields (SAR = 1.5 W/kg) spleen cells from
rabbits showed a decreased responsiveness to PWM.
Decreased responsiveness to PHA and Con A by these
spleen cells was also reported, but responses to PHA
and Con A were not statistically different from those
of controls. Although these results are interesting,
they are not conclusive and are of questionable value,
because only four exposed and four sham-irradiated
rabbits were employed. Also, both irradiated and
sham-irradiated rabbits were transported from one
laboratory to another (University of Washington to the
National Institute of Environmental Health Sciences
in Research Triangle Park, N.C.) between the
termination of RF exposure and spleen-cell assay.
Hamrick er al. (1977) examined the avian humoral-
immune response in Japanese quail exposed to RF
radiation during embryogenesis. Fertile quail eggs
were continuously exposed to 2450-MHz (CW)
radiation at 5 mW/cm2 (SAR = 4.03 W/kg)
throughout the first 12 days of development. At 5 weeks
of age, quail were immunized with SRBCs, and the
levels of anti-SRBC antibodies were determined. No
difference was observed in the antibody liters of
exposed and sham-exposed quails. The masses of the
bursa of Fabricius (site of B-cell production in birds)
and spleen were not altered significantly by exposure
to RF radiation.
Effects on phagocytosis—RF-radiation-induced
effects on phagocytic leukocytes of animals have
been reported by Szmigielski er al. (1975). Rabbits
were exposed to 3000-MHz fields for 6 h daily for 6 to
5-25
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12 weeks at 3 mW/cm2 (SAR estimated at 0.5 W/kg).
After the last exposure to RF radiation, rabbits were
infected with an intravenous injection of virulent
Staphylococcus aureus. At periods before and after
infection, functional tests of granulopoiesis were
performed. The investigators reported a decreased
production of mature granulocytes in infected, RF-
radiation-exposed rabbits, which was manifested as
a more serious illness in these animals.
Summary—Exposure of laboratory animals to RF
radiation can lead to changes in the functional
integrity of lymphocytes. These cells play an
important role in the immune-defense system of man
and animals. The significance of the changes caused
by RF radiation is difficult to interpret. Although some
studies indicate that RF radiation causes an
increased responsiveness, of lymphocytes (Czerski
1975; Smialowicz et al. 1979a, 1982; Prince et al.
1972; Wiktor-Jedrzejczak et al. 1977a,b,c) and a
potentiation of the immune response to antigen
(Czerski 1975), others indicate a depression in
responsiveness (Huang et al. 1977; Wiktor-Jedrzej-
czak et al. 1977a; Liburdy 1979; Szmigielski et al.
1975). In most cases these alterations can be
attributed to a stress response, since qualitatively
similar but quantitatively more pronounced changes
are observed at obviously stressful thermogenic
levels of RF radiation (Huang ef al. 1977; Huang and
Mold 1980; Prince era/. 1972; Liburdy 1979; Riddle et
al. 1982; Smialowicz eta/. 1981 b) or after administra-
tion of glucocorticoids or detection of increased levels
of glucocorticoids (Liburdy 1979; Smialowicz et al.
1983; Rama Rao et al. 1983; Yang et al. 1983). It is
well known that stress alters physiological systems
that regulate immunological function. Both immuno-
suppression and immunoehancement have been
observed to result from stress (Monjan 1981; Blecha
et al. 1982; Bradley and Michel! 1981; Palmbald
1981; Rogers and Matossian-Rogers 1982), which is
not inconsistent with the reported effects of RF
radiation on the immune system. However, stress-
induced modulation of the immune system is still
imperfectly understood. Recent data suggest that the
mechanisms by which stress affects the immune
system are more complex than previously recognized
and that, in addition to adrenal-dependent pheno-
mena, adrenal-independent effects, which are as yet
poorly understood, may be operative (Keller et al.
1983). The role of stress as a possible mediator of
observed RF effects on the immune system remains
speculative, although useful heuristically, at the
present time. Critical experiments (especially, with
careful consideration of other environmental
stressors and proper controls—i.e., adrenalectomized
animals) examining the relationship between stress
and RF-radiation effects have yet to be done.
Effects caused by RF-induced hyperthermia—
Alterations in the immune system can be produced by
RF-radiation-induced hyperthermia. Whole-body
microwave-induced hyperthermia has been reported
to serve a therapeutic role either alone (LeVeen et al.
1976) or in combination with ionizing radiation
(Nelson and Holt 1978). In many cases, the direct
destruction of malignant tissues by RF-radiation-
induced heating is the ultimate goal. However, in
some cases, hyperthermia has led to changes in the
immune response. For example. Shah and Dickson
(1978b) reported that following local heating of VX2
(carcinoma) tumor-bearing rabbits by a 13.56-MHz
field, tumor regression and host cure were observed
in 70 percent of the rabbits. Intratumoral temperatures
of 47 to 50°C were achieved within 30 min. Along
with tumor regression, cell-mediated immunity—as
measured by skin reactivity to tumor extract and
dinitrochlorobenzene—markedly increased. A hund-
redfold increase in serum levels of antitumor
antibody and increased response to the antigen
bovine serum albumin (BSA) were also observed. In
contrast, whole-body hyperthermia led to temporary
reduction of tumor growth, followed by a return to an
exponential increase in tumor volume and rapid
death of the rabbit. This course of events following
whole-body hyperthermia was accompanied by
abrogation of the enhanced cellular and humoral
immune responsiveness, observed following local
RF-induced heating.
Szmigielski ef al. (1978) reported that local heating
(43°C) of the Guerin epithelioma in Wistar rats by
2450-MHz (CW) radiation inhibited tumors and
stimulated the immune reaction against the tumor.
Other immune reactions stimulated by this treatment
were the antibody response to BSA, high reactivity of
spleen lymphocytes to the mitogen PHA, and
increased serum lysozyme levels as a measure of
macrophage activity. Tumor-specific reactions
observed were increased cytotoxicity of spleen cells
and peritoneal macrophages to cultured tumor cells.
Similar results were reported by Marmor etal. (1977),
who exposed tumors in mice to focal 1356-MHz
radiation. The EMT-6 tumor was found to be
extremely sensitive to RF heating. The cure rate was a
function of temperature and duration of exposure. A
5-min exposure at 44°C reduced the tumors by
almost 50 percent. To determine the effectiveness of
RF-induced heating on tumor regression, tumor-cell
survival was studied by the treatment of EMT-6
tumors in situ. Cell inactivation by RF-radiation-
induced heating was similar to that for heating by a
hot water bath. The results indicated that direct cell
killing could not account for the observed cures, and
these investigators suggested that hyperthermia (RF
or convection-induced) may stimulate a tumor-
directed immune response.
Szmigielski et al. (1977) exposed mice bearing
transplanted sarcoma-180 tumors to 3000-MHz
radiation, 2 h daily on the 1 st through 14th day after
transplantation, whole-body at 40 mW/cm2 (SAR
5-24
-------
estimated at 28 W/kg). This exposure led to a 3 to4°C
increase in rectal temperature and resulted in a
reduction of tumor mass by ~40 percent, a reduction
enhanced when microwave hyperthermia was
combined with Colcemide, Streptolysin S, or both.
Colcemide enhances the inhibiting effect of hyper-
thermia on proliferation of cells//; v/fro(Szmigielski et
al. 1976), and Streptolysin S is an antineoplastic
agent. Szmigielski et al. (1978) suggested that
immunostimulation is important in the complex
inhibition of tumor growth by increased temperature.
Although many investigators see local and systemic
hyperthermia as a possible cancer treatment, either
alone or in combination with drugs or ionizing
radiation, there is evidence that hyperthermia may
enhance the dissemination of certain cancers and
abrogate the immune response. For example,
Roszkowski et al. (1980) reported that exposure of
mice to 2450-MHz radiation at 50 mW/cm2 for 4, 7,
10, or 14 days, 2 h daily (SAR estimated at 36 W/kg)
caused an increased number of lung-cancer colonies
and an inhibition of contact sensitivity to oxazolone (a
measure of T-lymphocyte activity) with increased
duration of hyperthermia. Shah and Dickson(1978a)
exposed normal rabbits either to RF-radiation-
induced (13.56 MHz) or to watercuff-local hyperther-
mia of thigh muscles, which are maintained at 42°C
for 1 h on 3 consecutive days. No alteration in the
response to dinitrochlorobenzene challenge was
observed. However, the humoral immune response to
BSA was significantly depressed. This response was
independent of the method and degree of heating.
The results indicate that B lymphocytes might be
more susceptible to hyperthermic damage than are T
lymphocytes.
The above results indicate that if the applied
microwaves are of sufficient intensity to cause heating
of tissue or of the whole animal, changes in the
immune system will follow. With heating to any
extent, the hypothalamic-hypophyseal-adrenal axis
plays a major role in the responses elicited. It is well
known that endogenous or exogenous adrenal
glucocorticoid hormones affect the immune response.
In addition, heat alone may affect immune function.
For example, heat has been shown to affect the
response of mitogens in vitro (Ashman and Nahmias
1978; Roberts and Steigbigel 1977; Smith et al. 1978;
Gutman and Chang 1982), which suggests that
elevation of temperature per se may mediate some
of the observed RF-radiation-induced changes. But
what of the RF-induced responses reported in the
absence of measurable temperature increases or at
rates of energy absorption well below that of the
resting or basal metabolic rate? Observed changes
in the immune response under these conditions are
more difficult to explain on a thermal-stress basis,
primarily because of a lack of sensitive techniques to
detect subtle stress responses. However, no increase
of rectal temperature after exposure to RF radiation
does not mean that the animal might not compensate
for added thermal energy by thermoregulatory
mechanisms. RF radiation may also cause focal
heating (thermal "hot spots") in organs critical to the
immune response.
5.2.2.2 In Vitro Studies
Among the studies in this area (Table 5-7), several
have involved attempts to determine if in vitro
exposure of lymphocytes to RF radiation leads to
"direct" changes in the metabolic or functional state
of these cells. In an early study, Stodolnik-Baranski
(1967) exposed human lymphocytes in culture to
3000-MHz (PW) microwaves at 7 or 14 mW/cm2.
Some lymphocytes were irradiated 4 h/day at 7
mW/cm2 for 3 to 5 days, while those exposed at 14
mW/cm2 were irradiated 15 min daily for 3 to 5 days.
After 5 days in culture, the microwave-exposed cells
were found to have undergone a fivefold increase in
lymphoblastoid transformation compared with
controls. Czerski (1975) attempted without success to
repeat this experiment. But, in a more recent study,
Baranslki and Czerski (1976) reported that exposure of
human lymphocytes to 10,000-MHz fields at power
densities between 5 and 15 mW/cm2 could induce
lymphoblastoid transformation (SAR not given). At
power densities below 5 mW/cm2, this effect was not
observed, whereas at power levels above 20
mW/cm2, cell viability decreased. The induction of
blastic transformation depended on termination of
irradiation (5 to 15 mW/cm2) at the moment when the
temperature of the medium reached 38°C. These
results indicate that the microwave-induced blastic
transformation might be caused by a thermal
mechanism.
Similar increases in the lymphoproliferative response
of cells exposed to temperatures > 37°C have been
reported. As mentioned. Ashman and Nahmias
(1978) reported that human lymphocytes, when
cultured at 39°C with the mitogens PHA or Con A,
showed an enhancement and earlier onset of 3H-
thymidine incorporation compared with cultures
incubated at 37°C. In a similar study, Roberts and
Steigbigel (1977) reported that the in vitro human
lymphocyte response to PHA and the common
antigen streptokinase-streptodornase was enhanced
at 38.5°C relative to 37°C. Smith et al. (1978)
reported that the in vitro response of human
lymphocytes to PHA, Con A, PWM, and allogeneic
lymphocytes was markedly enhanced by culture at
40°C compared with 37°C. These studies demonstrate
the need to monitor and to control the temperature of
cultures exposed to RF radiation. Without adequate
temperature data, it is virtually impossible to accept in
vitro effects as due to RF radiation itself.
The proliferative response of lymphocytes exposed in
vitro to RF radiation appears to be related to culture
5-25
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Table 5-7. Summary of Studies Concerning Immunologic Effects (In Vitro) of RF-Radiation Exposure*
Exposure Conditions
Effects
Increased blastogenesis of
exposed lymphocytes in vitro
Increased blastogenesis
No change in mitogen
response to PHA, Con A
orLPS
No change in mitogen
response to PHA
No change in viability
or growth
Decreased macrophage
phagocytosis
Liberation of intracellular
hydrolytic enzymes and
increased death
Species
Human
lymphocytes
Human
lymphocytes
Mouse spleen
cells
Rat blood
lymphocytes
Human
lymphoblast
cell lines
(Daudi and
HSB:)
Mouse
macrophage
Rabbit
granulocytes
Frequency
(MHz)
3.000 (PW)
10.000
2,450 (CW)
2.450 (CW)
2,450 (CW)
2,450 (CW)
3,000 (CW)
Intensity
(mW/cm2)
7
14
5-15
10
5. 10 or 20
10-500
50
1 or 5
Duration
(days x min)
3-5 x 240
3-5x15
Observed effect
only when culture
temperature ap-
proached 38 °C
1 x60, 120, or
240
1 x240, 1440,
or 2640
1 x 15
1 x30
1x15. 30,
or 60
SAR
(W/kg)
t
t
19
0.7, 1.4
or 2.8
25-1200
15 J/min
t
References
Stodolnik-Baranska (1967)
Baranski and Czerski (1 976)
Smialowicz (1976)
Hamrick and Fox (1 977)
Lin and Peterson (1 977)
Mayers and Habeshaw (1 973)
Szmigielski (1975)
*PHA = phytohemagglutinin, Con A = concanavalin A, and LPS = lipopolysaccharide.
tUnable to calculate SAR.
temperature. Smialowicz (1976) exposed murine
splenic lymphocytes to 2450-MHz (CW) radiation for
1, 3, or 4 h at 10 mW/cm2 (SAR = 19 W/kg).
Immediately after irradiation the temperature of the
exposed cultures did not differ significantly from that
of controls, and cell viability was unchanged. These
cells were then cultured for 72 h in the presence of T-
or B-cell mitogens, and the proliferative response
was measured by 3H-thymidine incorporation. No
difference was found in the blastogenic response of
microwave-exposed and sham-exposed spleen cells
to any of the mitogens employed. In a similar
experiment, Hamrick and Fox (1977) exposed rat
lymphocytes to 2450-MHz (CW) radiation for 4, 24, or
44 h at 5,10, or 20 mW/cm2 (SARs at 0.7,1.4, or 2.8
W/kg, respectively). The transformation of unstimu-
lated or PHA-stimulated lymphocytes was measured
with 3H-thymidine. No significant differences were
found in the proliferative capacity of lymphocytes
from exposed and control cultures. The effects of RF
radiation on the growth and viability of cultured
human lymphoblasts was studied by Lin and Peterson
(1977). Human lymphoblasts (cell lines Daudi and
HSB2) were exposed to 2450-MHz (CW)radiation in a
waveguide for 15 min at incident power densities of
10 to 500 mW/cm2; the corresponding SARs were 25
to 1200 W/kg. No temperature increase was
observed, even at the highest power density in the
capillary tube that held the cell suspension in the
waveguide. No change was observed in the viability
or growth of microwave-exposed lymphoblasts
compared with controls. These studies provide
further evidence that no change in lymphocyte
activity occurs following RF-radiation exposure in
vitro when proper control of culture temperature is
achieved.
In vitro exposure of macrophages to 2450-MHz fields
has been reported by Mayers and Habeshaw (1973) to
depress phagocytosis. Monolayer cultures of mouse
peritoneal macrophages were perfused with suspen-
sions of human erythrocytes while being exposed to
2450-MHz radiation at 50 mW/cm2. The rate of
energy absorption in the sample was 15 J/min. The
phagocytic index of exposed cultures was significantly
lower than that of the control after a 3*0-min
exposure. Macrophage phagocytic activity returned
to normal levels if RF irradiation was discontinued.
During irradiation, a 2.5°C temperature increase was
observed; however, the final temperature in the
culture vessel in any given experiment reportedly did
not exceed 36.2°C. The investigators concluded that
the observed depression of phagocytosis in the
irradiated cultures was not thermally induced. The
2.5°C rise in temperature during irradiation,
according to the authors, would have been expected to
enhance rather than depress phagocytosis, since it is
optimal at 38.5°C. The mechanism by which the
observed effect occurs is not known; however,
heating effects are difficult to dismiss because of an
observed 2.5°C rise in culture temperature. Although
the temperature of the suspension medium did not
exceed 36.2°C, thermal gradients of much higher
temperature would be expected at the macrophage-
glass interface.
5-25
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An RF-induced effect on granulocyte integrity and
viability was reported by Szmigielski (1975). Rabbit
granulocytes were exposed in vitro to 3000-MHz
(CW) radiation at 1 or 5 mW/cm2 (SAR not given) for
15, 30, or 60 min. Cultures exposed at 5 mW/cm2 for
30 to 60 min showed increased numbers of dead cells
as demonstrated by an increase in nigrosine staining
and an enhanced liberation of lysosomal enzymes.
Exposure at 1 mW/cm2 did not cause increased cell
death but did lead to a partial liberation of hydrolase
enzymes. No change was observed in the temperature
of the irradiated cultures. The liberation of acid
phosphatase and lysozyme from granulocytes was
observed in cell suspensions exposed at 1 or 5
mW/cm2; both suspensions exhibited a time- and
dose-dependent response.
In summary, exposure of laboratory animals to RF
radiation may lead to changes in the functional
integrity of leukocytes, which play important roles in
the immune-defense system. The significance of the
changes caused by RF radiation is difficult to interpret,
since many observed effects are transient and
reversible. Furthermore, some studies indicate that
RF radiation causes immunopotentiation, whereas
others indicate immunosuppression. In many cases
the observed alterations in the immune system can
be attributed to thermal stress, because qualitatively
similar but quantitatively greater changes are
observed at obviously stressful (highly thermalizing)
levels of RF radiation or following the administration
of glucocorticoids. A possible explanation for the
immunomodulating effects of RF radiation arises
from the timing of the meausrements of immune
responsiveness after an animal is subjected to stress.
For example, corticoid-induced impairment of
immune responsiveness is commonly followed by
homeostatic recovery, then subsequent overcom-
pensation, which may be associated with immunoen-
hancement.
As for reports in which measurable elevations of
temperature from RF-radiation-induced heating are
not detected, a possible role by RF-radiation-induced
thermogenesis cannot be dismissed. The failure to
detect a measurable increase in tissue or core
temperature in RF-irradiated experimental animals
through the use of conventional techniques indicates
that the animal was able to compensate for the added
energy. The role that thermoregulating mechanisms
play in affecting the immune response needs further
study. There is at present no convincing evidence for
a direct effect of RF radiation on the immune system in
the absence of a thermal (heating) effect.
5.2.3. Unresolved Issues
Several issues relating to the effects of RF radiation
on the hematologic and immunologic systems remain
unresolved. Perhaps the most perplexing question is
what to make of the many Soviet reports on these
systems. In most cases these reports lack sufficient
technical detail for adequate critical assessment of
reported results. Alterations in the hematopoietic and
immunologic systems have been reported in animals
exposed to RF radiation at and below 10 mW/cm2 over
periods of weeks to months. Nevertheless, no
convincing evidence has been presented to demon-
strate a direct effect of RF radiation in the absence of
thermal involvement; well-defined and planned,
chronic (months to years), low-level (< 1 mW/cm2)
studies have not been carried out to investigate Soviet
claims of possible immune alterations including
induction of autoimmune reactions following chronic
exposure. Investigations of the possible hematologic
•and immunologic effects of PW vs. CW irradiation
have not been undertaken in response to the claims
by Eastern European investigators that PW modulation
is more effective than CW irradiation in causing
alterations in these systems.
Investigations are lacking that would define possible
synergistic effects of other agents or drugs with RF
radiation on the hematopoietic and/or immune
systems. RF radiation (at hyperthermic doses) has
been shown to provide a protective effect against
damage by ionizing radiation to the hematologic
system. Although this is a beneficial effect of RF
radiation, it is not known whether the combination of
drugs or other physical agents with RF radiation is
detrimental.
Another issue is based on the recent work of
Szmigielski et a/. (1980, 1982) who described the
increased incidence of cancer development in mice
exposed chronically to 2450-MHz (CW) fields. After
exposing the animals for several months at either 5 or
15 mW/cm2 (SAR = 2 to 3 and 6 to 9 W/kg,
respectively), these investigators reported an
increased incidence of spontaneously arising mammary
tumors in C3H/HeA mice and increased skin tumors
in BALB/c mice whose skin was painted with 3,4-
benzopyrene. These workers also reported that
chronic stress (i.e., overcrowding of mice) produced
an acceleration in tumor development comparable to
that found in mice irradiated at 5 mW/cm2, with still
greater acceleration in tumor development in mice
exposed at 15 mW/cm2. These results suggest that
RF radiation at 15 mW/cm2 was more stressful (i.e.,
via thermal-induced stress) than at 5 mW/cm2.
Szmigielski era/. (1982) suggest that the acceleration
in tumor development in mice irradiated at 15
mW/cm2 may be due to local thermal effects or RF-
induced "hot" spots. Acceleration of cancer
development in these mice was suggested by
Szmigielski et a/, to be accompanied by a lowering of
natural antineoplastic resistance, in particular effects
on immunocompetent cells. These investigators
conclude that the effects on immunocompetent cells
may be due to a direct interaction of RF radiation with
the immune system or via a stress response. Based
5-27
-------
on the results obtained from other laboratories (Rama
Rao et a/. 1983; Yang etal. 1983; Liburdy 1977,1979,
1980; Smialowicz et al. 1981, 1983; Smialowicz
1979; Riley 1981), as well as the results in the
Szmigielski et al. (1980, 1982) studies with mice
stressed by overcrowding, it appears that the latter
hypothesis (i.e., RF-radiation stress-induced effects)
is the most plausible explanation. Nevertheless, this
effect warrants corroboration because of its potential
significance. Studies should be undertaken that
strive to determine the threshold for RF-radiation-
induced accelerated tumor growth. Strict control of
both the RF-exposure parameters and ambient
environmental parameters is essential in any future
studies. Several species should be employed to
determine whether this phenomenon occurs across
species.
5-28
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5.3 Reproductive Effects
Ezra Herman
This section on the reproductive effects of RF
radiation is organized into three categories:
Teratology (5.3.1), where the treatment is adminis-
tered to the pregnant dam and observations are then
made on the embryo, fetus, neonate, or older
offspring; Reproductive Efficiency (5.3.2), where the
end point of the experiment occurs in the primary and
secondary sex organs of the parent; and Testes
(5.3.3), where testicular morphology and function of
testes are examined for alterations.
RF radiation has been examined intensively for its
potential reproductive effects for a variety of reasons:
(1) many reproductive toxicologic tests can be carried
out in a simple and inexpensive experimental design
after insult by RF radiation, (2) the laboratory
techniques used are conventionally acceptable as
toxicologic assays, and (3) detrimental reproductive
changes carry not only an emotional impact but have
potential for early and long-term consequences of a
serious nature.
5.3.7 Teratology
The science of teratology and its underlying principles
must be kept in mind if we are to make judgments on
the potential of RF radiation for teratologic manifesta-
tions. Wilson (1973) has developed general principles
of teratogenesis. These principles are rephrased here
to familiarize the reader with the guidelines one
should keep in mind when evaluating the available
literature, so that their relevance to RF radiation
teratologic investigations may be more easily
understood.
(1) Susceptibility to RF radiation teratogenesis
depends on species, strain, and stage of
development at the time of exposure.
(2) There are four indications of abnormal develop-
ment: death, malformation, retarded growth, and
deficient function.
(3) These indications increase in incidence and
degree with increasing dosage.
Teratology was initially confined to the study of birth
malformations, monstrosities, and serious deviations
from normal. As teratology has matured into a branch
of toxicology, included now in teratology are toxic
manifestations in the fetus with lesser symptoms
than gross morphologic changes. Such fetotoxic
symptoms may be decreased fetal or birth weight, as
well as changes in function observed well after birth.
In this discussion, the terms "teratogenesis" or
"terata" refer to gross morphologic or monstrous
changes. Subteratogenic doses are those just below
teratogenic doses and are not expected to cause
terata. Fetotoxic symptoms include body-weight
changes without terata. Functional changes are
fetotoxic symptoms not readily apparent in the fetus,
or even at birth, but are often seen later as postnatal
maturation occurs. This discussion posits that the list
of possible deviations caused in the conceptus is an
order of decreasing degree of severity (death >
malformation > growth retardation > functional
changes). The significance of any laboratory animal
or system as a model of human exposure may not be
universally accepted among scientists.
An attempt is made to derive from available data three
aspects of teratologic toxicology of RF radiation: the
presence of a teratologic effect, the generalization of
that effect across species, and the dose-response
character of that effect. From the evidence presented,
we believe that the reader will agree with the
following statements:
(1) RF radiation can cause teratogenesis in all the
mammalian species studied adequately so far if
sufficiently high power densities or SARs are
obtained.
(2) Reduced fetal weight seems to occur consistently
in rodents exposed gestationally to teratogenic
doses of RF radiation, or to doses somewhat
smaller than those which cause death or
malformation.
(3) There is evidence that gestational exposure toRF
radiation may cause functional changes later in
life.
5.3.1.1 Nonmammalian Models
The potential for human teratology is usually sought
in mammalian models. But other models that are
lower on the phylogenetic scale or cell-culture
models are also often informative. Workers at the
Bureau of Radiological Health of the Food and Drug
Administration have used an insect to demonstrate the
reproductive alterations due to RF radiation. Pay era/.
(1978) examined the egg production of female fruit
flies (Drosophila melanogaster) in response to RF
radiation. Using a 2450-MHz waveguide exposure
system housed in an environmentally controlled
chamber (24°C, 50 percent relative humidity), these
workers determined the survival rate of D. melano-
gaster pupae at SARs ranging from 400 to 800W/kg.
Approximately 70 percent of the pupae did not survive
a 10-min exposure when the rate of energy
absorption was 640 W/kg; the temperature of the
agar surface on which the pupae rested was45°C. If
pupae were incubated instead in a 44°C environment
without RF radiation, the death rate was less severe
(50 percent).
The potential for RF-radiation-induced teratology in.
birds has been examined by use of the fetal form of
5-25
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birds, the egg, as a model. This is a reasonably
popular model since use of bird eggs is more
economical than use of mammals. Study of the bird
egg can provide insight into fetal effects independent
of maternal influence. The egg is an object that can be
placed in almost any desired position by the
experimenter; it will remain there, a distinct
advantage over free-ranging mammals. The egg is
symmetrical externally and so lends itself more easily
to estimates of local and total absorption of RF energy.
In theory, mammalian models have no advantage
over avian models in the study of teratogenic
potential of RF radiation because concepts of
organogenesis apply equally to avian and mammalian
fetuses. It would be a mistake to dismiss the
considerable research on the teratologic effects of RF
radiation in birds' eggs because the avian egg is
poikilothermic and the mammal's egg is homeother-
mic. The mammalian conceptus is also poikilothermic;
it has little, if any, control of its own temperature
since it is entirely surrounded by placenta! fluids. It
can dissipate thermal energy only by radiating into
surrounding maternal tissues because its capacity to
rid itself of thermal energy depends entirely on the
gradient between itself and surrounding tissues. If
the temperature of the mammalian conceptus tissue
is increased because of RF-radiation absorption, it
also must radiate that absorbed energy into its
surroundings (dam), just as the egg in similar
exposure conditions must radiate energy into the air
of its incubator. If air or maternal temperatures are
detrimentally high, then the loss of thermal energy
from the egg or mammalian fetus is affected similarly.
Carpenter et al. (1960a) have studied RF radiation as
an inducer of cataracts. These investigators have also
likened the growth in the lens to the process of
embryonic development and growth, where prolifera-
tion and differentiation take place concurrently. To
further understanding of the RF-radiation-induced
effects that appear in the lens, Carpenter et al.
performed experiments on the egg of the domestic
chicken. They irradiated almost 500 chick embryos at
the 48-h stage and examined the eggs 48 h after
irradiation, scoring incidences of survival and
structural abnormalities. The irradiation was
conducted in an anechoic chamber at 2450 MHz and
at power densities of 200, 280, and 400 mW/cm2.
Estimates of SARs for these power densities are 70,
98, and 140 W/kg, respectively (Durney eta/. 1978).
Power densities were determined by calorimetry with
a saline-filled egg. The exposure durations ranged
from 1 to 15 min. The eggs were incubated at 39°C air
temperature before, during, and after irradiation.
However, the temperatures of the eggs are not
mentioned in the report. At the 96th hour of
development, all eggs were opened, and the embryos
were removed, fixed, stained, and examined as
whole-mounts.
Experimental results relevant to this section are
presented in Table 3 of the Carpenter et al. 1960a
publication. We have used the data in that table to
calculate the relative summed incidences of dead and
abnormal 96-h egg embryos for each experimental
group (power density: time) and present the
incidences in Figure 5-2.
The teratologic end points observed by Carpenter et
al. (1960a) were death and abnormal morphology,
which can be viewed as a continuum of the same
effect, interference with the normal processes of
development. When abnormal structure is so severe
as to interfere greatly with the continuation of
development, the embryo cannot develop or maintain
sufficiently normal structural and physiologic
systems. The relationships between these systems
collapse and the embryo dies. As stated earlier,
indications of abnormal development increase in
incidence and degree as the dosage increases. One
mechanism for the increase in death is that as the
dosage increases, more embryos undergo more
changes in more systems, which results in more
deaths.
Figure 5-2 contains three curves, one for each group
of eggs exposed at dose rates of 140, 98, or 70 W/kg
for varying durations. The data are plotted against the
summed relative incidence of affected (dead or
morphologically abnormal) eggs. The slopes of the
curves are steep, so that small increases in the
exposure duration cause disproportionate increases
of effect. For example, the incidence in the group
exposed for 4 min at 140 W/kg was 9 percent. An
increase of only 30 s in exposure time caused a
ninefold increase (80 percent) in incidence. An
additional characteristic of these slopes is the
disproportionate spacing of the three curves along
the axis of exposure duration.
Figure 5-2. Summed incidence of abnormal and nonviable
chick embryo eggs (percent of total) exposed to
2450-MHz radiation for varying durations at 70.
98. or 140 W/kg (from data in Carpenter et •/.
1960a).
1 2 3 4 5 6 7 8 9 1011 121314
Duration of Exposure, minutes
15
5-30
-------
Studies of RF radiation effects in the Japanese quail
have been conducted exclusively by workers at the
National Institute of Environmental Health Sciences.
In their first attempt to induce terata in the quail egg,
Hamrick and McRee (1975) exposed fertilized eggs in
an anechoic chamber to 2450-MHz (CW) fields,
producing an SAR of 14 W/kg in the egg. The eggs
were exposed for 24 h beginning 2 days after laying,
then were returned to their incubators until 24 to 36 h
after hatching. Several experimental replications
occurred; the sample numbers were 102 in
the control group and 110 in the RF-irradiated group.
After hatching, observations were made of cellular
elements of blood and of selected organ weights. No
significant differences between the two groups were
seen in hatchability, blood cell parameters, body
weights, or organ weights.
The same authors also reported a similarly designed
experiment on Japanese quail eggs, in which the
eggs were exposed during the first 12 days of
development at SARs of 4.03 W/kg (McRee and
Hamrick 1977). As before, the eggs were allowed to
hatch and were than examined for teratologic
alterations and blood-cell parameters. When the
experiment was conducted at an environmental
temperature of 35.5°C, there were no significant
changes in body weights, organ weights, or blood-cell
parameters.
The authors also demonstrated the importance of
ambient temperature in experiments in which RF
radiation is the agent under investigation. Absorption
of RF radiation energy produces increased tempera-
ture. In most studies of reproductive effects reviewed
in this document, fields were at sufficiently high
power densities to cause significant depositions of
energy. Temperatures in the animal subjects were
usually increased by 0.5°C or more. Therefore, the
ambient temperature in which the subject is
maintained or treated can be a significant determinant
of a resulting trend.
Levels of ambient temperature can be especially
relevant to experimental subjects that have no
significant thermoregulatory capability. For example,
the report by McRee and Hamrick (1977) included the
results of an experiment in which Japanese quail
eggs were in an environment at a temperature only
slightly higher (+1.5°C) than in the experiment
discussed above (35.5°C) The authors began their
study at an ambient temperature of 37°C because
that is the temperature at which quail eggs are
conventionally incubated. But this ambient tempera-
ture, with the addition of a 4 W/kg SAR, was
sufficient to cause a 93 percent death rate of the
fertilized eggs. The eggs that were irradiated at the
same SAR, but at an ambient temperature lower by
1.5°C, sustained only a 42 percent death rate. The
results of this seemingly slight (1.5°C) increase in
incubation temperature during RF irradiation shows
that for this poikilothermic model, the quail egg, the
temperature at which the egg is maintained during
experimentation is critical.
5.3.1.2 Mammalian Models
Morphologic teratology—The mouse is commonly
used in the determination of the teratogenic potential
of toxic agents and also appears to be a useful model
for determining the teratogenic potential of RF
radiation. The mouse's size is conducive to this kind of
experimentation because the apparent resonance of
mice is 2450 MHz, a frequency at which irradiation
equipment is commonly and economically available.
Rugh er al. (1974, 1975) conducted several
experiments on the mouse at 2450 MHz with a
waveguide exposure system to expose individual
pregnant CF1 mice at air temperature of 25°C and 50
percent relative humidity. All mice were exposed
once on the 8th day of pregnancy to CW fields at 2450
MHz for 2 to 5 min at a forward power that delivered a
measured average energy dose ranging from 2.45 to
8 cal/g; there were no control or sham-irradiated
mice in this study.
These and a few other authors have reported dose
parameters in calories or Joules per gram, which we
have converted to the SAR unit (W/kg) used in this
document. Each of the texts of the two papers by Rugh
et al. (1974, 1975) refers the reader to the other for
more detailed methodology, but neither adequately
describes exposure factors to convert accurately the
dose values to dose rate (SAR). Our best solution was
to convert to a range. The range of doses given by
Rugh et al. is 10.3 to 33.5 J/g delivered over 2 to 5
min. The four possible combinations (Table 5-8) of
two extremes of dose (10.3 and 33.5 J/g) and two
extremes for exposure duration (2 and 5 min) result in
SARs ranging from 34 to 280 W/kg for this study. The
most probable range of values is 85 W/kg (10.3 J/g
for 2 min) to 112 W/kg (33.5 J/g for 5 min).
The authors clearly demonstrated the teratogenicity
of RF radiation in mice, especially the potential for
death and generation of anomalies. By determining
the energy dose in each pregnant mouse, and
Table 6-8.
Average Dose
(J/g)
103
10.3
33.5
33.5
Conversion of J/g to W/kg*
Exposure Duration
(min)
5
2
5
2
SAR
(W/kg)
34
85
112
280
*W/kg = J/g x 1000 -r seconds (data from Rugh et al. 1974.1975).
5-31
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because varying doses were absorbed during the 2 to
5 min of exposure, the effect observed in each litter
could be assigned to a definite whole-body average
dose. These are the strong points in the Rugh et al.
studies.
Rugh et al. (1974, 1975) showed that resorption of
fetuses is a characteristic response to RF-radiation
exposure. Resorptions appeared at a dose rate of
approximately 85 W/kg. Both the incidence of
resorptions within litters and the incidence of litters
with resorptions increased as the average dose
increased. Near the maximum dose (33.5 J/g,
approximately 110 W/kg) almost all the litters were
affected. Even at 25 J/g, there were litters with 100
percent resorption rates.
Anomalies "...were various, but the one used for this
study, and which occurred most frequently, was
exencephaly (brain hernia)..." The report also
included data on resorptions, dead, and stunted
fetuses. In lieu of numerical data, the incidences of
brain hernia (also termed encephalocele, exencephaly,
or cranioschisis) are given by the authors in one
figure. Data, as percentage of affected liners, were
grouped into cells 8.4 J/g in width that ranged from
10.9 to 35.9 J/g. Approximately 30 percent of the
litters given an average dose of 15 J/g (approximately
90 W/kg) had fetuses with brain hernias. Of those
litters given an average dose of 31.8 J/g (estimated
as 109 W/kg) almost all contained fetuses with some
form of brain herniation.
Though sham, cage-control, or historical control
value for the incidence of brain hernia in this mouse
strain (CF1) is not given, the authors state "...since
this aberration rarely if ever occurs without trauma, it
is significant when even a single exencephaly
occurs." However, one report of the incidence of
spontaneous brain hernia in CF1 mice showed an
occurrence of 11 exencephalic litters in a total of 90,
approximately 12 percent of litters (Flynn 1968).
Apparently, spontaneous incidences of anomalies
are quite variable.
A report by Rugh and McManaway (1977) included
data on mice exposed once for 4 min to 2450-MHz RF
radiation (SAR = 100 to 114 W/kg) on days 0 to 11 (10
mice per day). In this group of mice (we cannot
differentiate these data from those reported in Rugh
et al. 1975 and Rugh 1976a,b) are uneven incidences
of stunted fetuses (irradiated on day 4 of gestation)
and death (irradiated on day 3, 8, or 10 of gestation).
Rugh considers small fetuses as stunted and believes
that this is a teratologic symptom.
Rugh's experiments included using a single, but high
field intensity for a very short time (i.e., 4 min on the
8th day of gestation). A longer period (100 min daily)
was used by Berman et al. (1978) in the exposure of
pregnant CD1 mice to 2450-MHz CW fields at power
densities of 0 to 28 mW/cm2 in an anechoic chamber.
Between 15 and 25 mice were irradiated simultane-
ously, each in a small ventilated container. Mean
rectal temperature was 38.2°C at the end of exposure
to the highest power density (28 mW/cm2). SARs
were determined by twin-well calorimetry and
averaged 2.0 W/kg at 3.4 mW/cm2, 8.1 W/kg at
approximately 14 mW/cm2, and 22 W/kg at 28
mW/cm2.
This study incorporated the examination of several
variables of fetal response to toxic agents. Values
were tabulated by power density for pregnancy rates,
incidences of live and dead fetuses, live fetal weights,
and incidences of anomalies. Values were expressed
that used the litter as the experimental unit. This is a
conservative approach in experiments in which the
potential fetal toxicity of an agent is determined
(Atkinson 1975). Berman eta/. (1978)also "corrected"
the mean fetal weight of each litter by a factor
representing the potential influence that litter size
had upon fetal weight. The technique is also endorsed
by Atkinson, because it allows greater confidence in
the interpretation of data.
The study by Berman et al. (1978) demonstrated that
daily exposure to 2450-MHz fields at intensities
producing an SAR of 22 W/kg during the entire
period of organogenesis caused a 10-percent
decrease in body weight of mouse fetuses. The
practical significance of this result is difficult to
determine without experimental confirmation of the
permanency or lack of reversibility of the smaller fetal
weight. Until it can be shown that the effect is
permanent (stunting) or temporary (delayed growth),
the effect remains hygienically unresolved. The effect
will have more practical significance if it can be
shown that stunting is the result.
Berman et al. (1978) also reported on the incidences
of anomalies. There did not appear to be a significant
increase of individual or total anomalies at any SAR.
The C3H-HeJ strain of mouse was used by
Chernovetz et al. (1975) in an attempt to determine
the effects of fetal irradiation with 2450-MHz RF
radiation. Pregnant mice were irradiated in a
multimodal cavity for 10 min on the 11th, 12th, 13th,
or 14th day of gestation at an SAR (determined by
calorimetry) of 38 W/kg with or without the
administration of cortisone, or given cortisone without
irradiation. The fetuses were examined near term
(near the end of the gestation period) without any
difference seen between the RF-irradiated and the
sham-irradiated groups of fetuses. The variables
observed in these fetuses related to the morphologic
and the lethal aspects of the RF irradiation. Fetal body
weights were not observed in these animals.
The scientific reports on the teratologic potential of
RF radiation in the rat represent the major fraction of
5-32
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rodent work. Perhaps the main reason is that many of
the studies that have looked for morphologic changes
have also included functional teratology as one of the
end points. For that kind of study, especially
behavioral studies, the rat appears to be preferred
over the mouse.
Chernovetz has probably published most on the
teratologic potential of microwaves in the rat. She
reported (Chernovetz et al. 1977) the results of
exposures of pregnant rats to 2450-MHz fields in a
multimodal cavity (most likely the same device used
to irradiate mice in experiments discussed above in
Chernovetz et al. 1975) at an SAR calculated by
calorimetry of approximately 31 W/kg. Exposures
were conducted during 1 of 7 days, from the 10th
through 16th day of gestation, and the fetuses were
examined on the 19th day of gestation. Each single
exposure lasted 20 min. The experiment included a
total of 74 time-bred female rats, each assigned to 1
of 7 days of gestation and to 1 of 3 treatment groups
(RF-irradiated, infrared-irradiated, or sham-irradiated).
The result is an experimental design with 21 different
cells into which 74 rats were distributed.
By the end of the 20-min exposure period, the mean
rectal temperature in the surviving pregnant rats was
42°C. Of the original group of 30 bred females that
were used in the RF-irradiation group, 7 (or 23
percent) died; none died in the sham-irradiated group.
Therefore, the application of 2450-MHz RF radiation
to bred rats for this duration at this SAR was lethal for
a significant portion of the animals involved.
No numerical data on the gross teratologic conse-
quences of this RF irradiation were given in the paper.
However, comments were made in the text regarding
the lack of any structural abnormalities. The number
of resorptions was significantly higher (approximately
6 times) in the RF-irradiated than in the sham-
irradiated fetuses, especially in the dams that had
been irradiated on the 11th day of gestation. Fetal
weights were also altered by the irradiation regimen;
there was a small but statistically significant
decrease in fetal weight. The alterations seen in the
fetuses, in this case decreased fetal weights and
death (in the form of resorptions), reflect the
teratogenic potential of RF radiation'exposure in the
rat. These fetal alterations were found from RF-
radiation exposure regimens where rectal temperatures
in the dam rose above 40°C.
Chernovetz et al. (1979) reported on the effect of
2450-MHz RF radiation in pregnant rats, this time at
SARs of 0, 14, or 28 W/kg. The same multimodal
cavity was used, through which air at 22 ± 1.5°C
flowed at 0.75 m/s. Pairs of bred female rats were
exposed for a 20-min period on the 8th, 10th, 12th, or
14th day of gestation and then were examined on the
18th day of gestation. With cage controls added to
each of these cells, the complete experimental design
used 4 different days of treatment and 4 treatments
(cage control, 0 W/kg [shams], 14 W/kg, and 28
W/kg), and 6 bred females per cell, for a total of 72
bred females. Those rats irradiated at 28 W/kg
developed rectal temperatures of approximately
42°C, temperatures that were similar to the authors'
previous experiments in which bred female rats were
dosed at 31 W/kg. The rats irradiated at 14 W/kg had
a mean peak rectal temperature near 40°C.
The values used by the authors in the statistical
analyses were individual fetal values, not litter mean
values. At the higher SAR level (28 W/kg), only ~ 10
percent below the sublethal level used in their
previous report, the authors did not demonstrate
lethality in the dams due to RF-radiation exposure.
The 20-min exposure period at other levels of SAR
produced no gross morphologic alterations in the
fetuses or any severely edematous fetuses; there
were also no statistically significant changes in
resorption rates.
The results of fetal weights are most interesting. In
the previous study (Chernovetz et al. 1977), the
authors reported that exposure for 20 min at
approximately 31 W/kg on odd-numbered days of
gestation produced a significant decrease in fetal
weight. In the 1979 study, a similar result was also
obtained from exposure at 14 W/kg on even-
numbered days (12 and 14), or 28 W/kg on the 8th
day of gestation. Unexpectedly, exposure at 28 W/kg
on the 12th or 14th day produced an increased body
weight. The unexpected increased body weight is an
interesting observation, especially when it is viewed
against the decreased fetal body weight documented
in the same authors' previous paper and other reports
of RF-radiation-induced fetal alterations in rats and
mice.
Berman et al. (1981) were not able to elicit any
fetotoxic or teratologic responses (body weight;
numbers alive and dead; external, visceral, or skeletal
morphology) in fetal rats irradiated daily (100
min/day) during gestation, even with a large number
of litters. The dams were exposed to 2450-MHz
radiation at power densitites of 0 or 28 mW/cm2 (4.2
W/kg). These conditions caused a mean rectal
temperature of 40.3°C by the end of the 100-min
exposure.
Kaplan (1981) did not find differences in the survival
of squirrel monkeys up to 10 months of age after daily
in utero and postnatal exposures to 2450-MHz in
multimodal cavities. Pregnant squirrel monkeys were
irradiated for 3 h daily, beginning in the first
trimester; after birth, the daily irradiation of the dams
and their young were continued, and from 6 to 10
months of age only the young monkey was irradiated.
The SAR was determined by calorimetry to be 3.4
W/kg. In 21 irradiated and 22 sham live-born,
differences were not seen in sex ratio, the number
dead by 10 months of age, or in the mean age at
death. Postmortem examinations did not reveal any
5-33
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tendency to specific causes for death. The results of
this study did not confirm the results of suspected
increased lethality in squirrel monkeys from a
previous study (Kaplan el al. 1982).
Functional teratology—Functional teratology is a
branch of reproductive toxicology that has allowed
increasingly greater insight into the toxicology of
environmental agents. The field contains a wide
variety of specialists who examine the functional
capacity of neonatal or growing animals after in utero
exposure. Except for the following discussion of
viability and of body weight, assays of functional
teratogenesis after in utero exposure to RF radiation
are discussed in the section dealing with each
relevant discipline.
The survival rate of fetuses can be used as an
indicator of immediate effects on the fetus. The rate of
survival of neonatal, infant, or older off-spring can be
also used as an indicator of delayed alterations in
functional capacity long after insult during the fetal
stage. For example, Kaplan et al. (1982) reported a
study of the postnatal effects of in utero exposure (at
dose rates to 3.4 W/kg) to 2.45-GHz RF radiation in
squirrel monkeys. One effect the authors observed
was an increase in neonatal deaths. However, after a
more intensive examination, Kaplan (1981) did not
demonstrate any change in death rate and could not
confirm the results of the study done earlier (but
reported later).
A simple test to determine whether RF irradiation in
utero would alter the survival of mice after birth was
conducted by Rugh (1976a). In this experiment,
pregnant CF1 mice were exposed on the 9th, 12th, or
16th day of gestation to a regimen of approximately 4
min of irradiation at 2450 MHz, which resulted in a
mean dose of ~ 25 J/g (104 W/kg). The survivors of
this sublethal exposure were allowed to give birth and
their young to mature to 2 months of age. At that time,
the offspring were again irradiated in the same device
until each one was dead. The time-to-kill and the
mean dose-to-kill was determined as a measure of
the radiosensitivity of the offspring irradiated
originally as fetuses. In this waveguide system,
measurement of absorbed dose was monitored by
power meters and calculated by the difference of for-
ward power, transmitted power, and reflected power.
While the subject in the waveguide was alive, the
values of transmitted and reflected powers were
constantly changing. When the subject died, these
values became constant. At the time of death, the
rectal temperatures of these mice, measured just
after the waveguide was opened, ranged from 40 to
51°C.
Because of body weight differences in the sexes at 2
months of age, the analyses were carried out by sex.
Time-to-kill was shortened in males irradiated
originally during the 12th or 16th day of gestation.
The males irradiated originally on the 12th day of
gestation had a lower mean dose-to-kill. Therefore,
Rugh (1976a) has shown that RF irradiation on select
days in utero can alter later (sometimes much later)
effects of re-irradiation with microwaves.
As noted, one effect observed commonly in fetuses
exposed to RF radiation is decreased body weight.
There are difficulties associated with interpreting
altered fetal weight as an indicator of toxicity,
especially when the permanency of decreased fetal
weight (delayed growth vs. stunting) is not yet
determined. But Rugh (1976a) gives evidence that
mice irradiated as fetuses weigh less at 2 months of
age. In that study, the mean weights of 2-month-old
male offspring of dams irradiated during the 9th,
12th, or 16th day of gestation were all lower than
concurrent sham-irradiated males (p < 0.05).
Females irradiated during the 16th day of gestation
were also smaller than their controls (p <0.05), but
not females from the 8th or 12th day groups. These
results are evidence of. a permanent change
(stunting) in mice caused by RF irradiation.
Chernovetz et al. (1975) carried out an experiment to
observe alterations in functional capabilities after in
utero irradiation. Pregnant mice were exposed once
during the 14th day of gestation at an SAR of 38
W/kg, and the offspring were examined until
weaning for survival. The RF-irradiated and sham-
irradiated groups each contained 15 dams. The
statistical analyses, done by litters, show that there
was a slight (approximately 12 percent) increase in
the survival rate of the RF-irradiated litters as
compared to the sham-irradiated controls.
Some experimental protocols continue irradiation past
birth. In one example of chronic adminsitration at 2450
MHz, reported by Smialowicz et al. (1979a), pregnant
rats were irradiated daily for 4 h/day at a power
density of 4 mW/cm2 from the 6th day of gestation to
term; irradiation of the offspring continued fftrough
40 days of age. The SARs were determined by twin-
well calorimetry for several ages of the animals.
Pregnant rats weighing 300 to 350g had a mean SAR
of 0.7 W/kg; offspring 1 to 5 days of age and 6 to 10 g
in weight absorbed approximately 4.7 W/kg. There
was no significant difference between the mean body
weights of the males (female offspring were not used
in this experiment) in the 12 sham-irradiated litters
when compared to the mean body weights of the
males in the 12 RF-irradiated litters.
Shore et al. (1977) reported decreased body weight and
decreased brain weight in postnatal rats exposed in
utero to 2450-MHz RF radiation. In this experiment,
pregnant rats were exposed at an average power
density of 10 mW/cm2 (SAR estimated, from Durney
et al. 1978, to be 2.2 W/kg) for 5 h per day repeatedly
on days 3 through 19 of gestation. Rats were allowed
to deliver naturally and were observed frequently
thereafter. Rats were grouped by E- or H-field
orientation during exposures; only the 3-day-old
5-34
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offspring that had been exposed parallel to the E-field
were significantly different, having lowered body and
brain weights. We cannot easily explain this
preferential decrement on the basis of either age or
orientation during exposure except that the data were
repeatedly analyzed using unadjusted r-tests. Our
expectation is that there is no significant difference
due to orientation in wholebody SAR in rats at this
frequency (Gage et al. 1979).
In experiments conducted by Michaelson et al.
(1978), some apsects of functional teratology of RF
radiation were explored in Long-Evans rats. In these
experiments, rats were exposed to 2450-MHz RF
radiation at power densities of 10 mW/cm2 for 1 h
on the 9th and 16th day of gestation, or 40 mW/cm2
for 2 h on the 9th, 13th, 16th, or 20th day of gestation.
According to data based on water-calorimetry, an
exposure at 40 mW/cm2 produced an SAR of
approximately 10 W/kg and approximately 2.5 W/kg
at 10 mW/cm2. Exposure at 40 mW/cm2 caused an
increase in the mean of rectal temperature of
approximately 1 to2°C over that of the sham-exposed
animals. The exposure at 10 mW/cm2 (2.5 W/kg) on
the 9th or 16th day of gestation caused a significant
increase (approximately 0.5 to 1 °C) in temperature of
dams at the 16th day of gestation. There were no
statistical differences in the sizes of litters as a
consequence of exposure during gestation. There
also appeared to be no difference in the growth rates
up to 21 days of age of the rat pups that were exposed
to RF radiation as compared with shams, nor in their
relative brain weights.
At the symposium where Michaelson described his
work, Johnson et al. (1978) reported on a study, then
in progress, on the functional teratologic effects in
rats exposed to 918 MHz for 20 h per day for 1 9 days
of gestation at a power density of 5 mW/cm2. The
experiment is especially interesting because it was
conducted at a frequency close to the resonance of
the experimental subject (rat) and because it is the
only reported study conducted with almost continuous
exposure. The SAR in this study is approximately 2.5
W/kg, determined by calculations from thermographic
scans. The eight RF-irradiated and eight sham-
irradiated bred dams were maintained in the
waveguide exposure apparatus under environmental
conditions of 22°C, 45 percent relative humidity, and
ad libitum access to rat chow and water. The
exposure was begun on the first day of pregnancy, the
day on which the copulatory plug was first seen. In
this experiment, the dams remained in individual
waveguides or sham condition until day 20 of
gestation, at which time they were removed and
placed in delivery cages. At 4 days of age, the litters
were culled to four males and four females per litter,
which were then observed through 91 days of age.
There appeared to be no differences in the litter
means for the number of pups born or for number
dead during the first day after birth. There were no
pups in any of these litters (including RF-irradiated,
sham-irradiated, and cage-controls) with any visible
physical defects. Body weights at birth, at 28 days of
age, and at 91 days were analyzed for significant
differences on an individual pup basis. The only
statistically significant differences in body weights
were found between the RF-irradiated and cage-
control females at 28 days of age. A difference also
existed in males at 91 days of age, when the RF-
irradiated and the sham-irradiated males weighed
less than the cage-control males.
Another parameter of development used as an assay
of functional teratology in this study was the age at
•eye-opening. The phenomenon of eye-opening is a
little-understood but frequently used indicator of
developmental maturation. There appeared to be a
significant shift to earlier eye-opening in animals
exposed to RF radiation during gestation, and this
maturation was earlier by approximately 1 day.
Jensh reported a series of experiments designed to
examine pre- and postnatally the effects of 915-MHz,
2450-MHz, and 6-GHz irradiation of rat fetuses
(Jensh et al. 1979; Jensh 1979,1980). These studies
included irradiation up to 8 h daily during most of
gestation with power densities not sufficient to cause
increased core temperatures (915 MHz, 10mW/cm2,
2 W/kg; 2450 MHz, 20 mW/cm2,3 W/kg; 6 GHz, 35
mW/cm2, 3.5 W/kg; SAR estimates from Durney et
al. 1978, p. 96). Offspring were examined pre- and
post part urn in a complex series of observations
meant to locate behavioral or morphological
alterations. None was noted.
In lieu of any other workable hypothesis supportable
by experimental data, the most plausible available
theory that can account for RF radiation effects is
that, upon absorption, microwaves deposit energy
that is converted to thermal energy. There remain
differences among theories that attribute individual
effects to a general input of energy, or the heating of
local (hot-spot) areas, or some more subtle contribu-
tion of microwaves not characteristic of conventional
methods of heating animals with infrared radiation,
convective heating, or immersion in water or oil
baths.
Comparisons between RF heating and infrared or
convective heating have been conducted in the study
of hyperthermia as a teratogenic agent. Edwards is a
frequently cited investigator of the effects of
hyperthermia on the development of mammals. His
extensive work on this agent as a cause of congenital
malformations is perhaps best summarized in one of
his reviews (Edwards 1974), which describes his
experiments on the teratologic manifestations of
hyperthermia in the guinea pig. The guinea pig is an
unusual laboratory animal in its long gestational
development, approximately 65 days. During the
latter two thirds of gestation in the guinea pig, the
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unborn offspring is in a stage of development similar
to that which occurs after birth in the mouse and the
rat. A long gestation period does not in itself prevent
use of the guinea pig as a model for teratogenesis. But
as far as teratologic experimental methodology is
concerned, the administration of the agent at 40 or 50
days of gestational age in the guinea pig has no
equivalent in rodent fetuses; this stage of develop-
ment occurs postpartum in mice and rats.
Studies of the teratogenic potential of conventionally
induced hyperthermia in almost all the species used
show some general changes that can be seen in RF-
radiation-treated animals as well. The symptom of
hyperthermia, whether induced by RF radiation or
otherwise, causes varied anomalies (such as kinked
tail, microphthalmia, exencephalia, cleft palate,
general edema). This is evidence that hyperthermia is
a general teratogen. Perhaps the only case where RF-
radiation-induced and conventionally induced
teratogenesis is not the same is in the development of
smaller brain weights in fetuses heated by non-RF-
radiation-heating agents. Except for Shore et al.
(1977), perhaps the literature in RF-radiation-
induced teratogenesis has not been sufficiently
developed to show this effect of decreased brain
weight.
Conventionally induced hyperthermia, like RF-
radiation hyperthermia, appears to affect most
species if sufficient energy is applied and proper
timing of the agent is obtained. A sufficiency is
usually manifested by a rise in maternal rectal
temperature, usually over 40°C, but often in a range
of 41 to 43 or even 44°C. At these temperatures, the
teratogenic potential of heat applied by conventional
means or by RF radiation does not appear to show any
significant differences. The authors of one study
attempted to differentiate teratogenic effects of
microwaves from the more conventional methods of
heating (in this case, infrared irradiation). Chernovetz
et al. (1977) exposed pregnant rats to 2450-MHz
fields at an SAR of approximately 31 W/kg, or to
infrared radiation. The rectal temperatures of the RF-
irradiated and the infrared-irradiated groups were
similar (approximately 42°C). The results of the
exposures showed little difference in effects due to
infrared heating or RF-radiation heating.
The symptom of decreased body weight of fetuses is a
general developmental effect. This response to
microwaves is commonly seen in experiments, even
those experiments that have not otherwise demon-
strated specific morphologic changes (e.g., O'Connor
1980). Body weight changes alone have also been
seen in mice fetuses at temperatures <40°C (Berman
et al. 1978).
Body temperatures reported in the above studies
were those of the dam, usually measured in the dam's
large intestine. Measurements of fetal temperatures
after RF-irradiation have not been reported. A report
by Morishima et al. (1975) provides some under-
standing of the physiologic changes that occur in the
fetus as a result of conventionally induced hyperther-
mia. Morishima et al. used pregnant baboons and
simultaneously monitored temperature and physio-
logic changes in the dam and the fetus during
hyperthermia. The temperatures in these dams were
raised to 41 to 42°C by infrared lamps and warming
pads. While the pregnant dam was maintained in an
analgesic state using nitrous oxide inhalation
anesthesia and intravenous succinylcholine chloride
infusions, thermistors and catheters were placed at
comparable positions in the dam and the fetus. Two
groups of animals were used: one group was kept at
38°C; the temperature of the other was allowed to
elevate gradually to 41 or 42°C. At the more normal
temperature, 38°C, there was a slight (0.5°C) but
steady increment in the temperature of the fetus over
that of the dam. When the temperature was
increased to 40°C in the dam, the fetal temperature
rose accordingly and remained 0.75°C higher than
the dam's temperature. The hyperthermia produced
increased uterine activity and some acidosis in the
dam, and a profound acidosis and hypoxia in the
fetus. If conditions comparable to those seen in the
baboon are also seen in the mouse, then we might
expect the mouse fetus to have temperatures greater
than that of its dam.
That the teratogenic potential of RF radiation might
depend only on the deposition of energy as heat was
shown experimentally by Rugh and McManaway
(1976). They exposed pregnant mice to highly
teratogenic (high incidence of fetal death) levels of RF
radiation with and without pentobarbital anesthetic.
The mice exposed during anesthesia had normal
rectal temperatures and normal incidences of fetal
death. Therefore, the anesthetic protected against
the primary temperature effect of the radiation by
reducing "...the body temperature to a degree
equivalent to the rise in temperature expected from
the conditions used." This result is clear evidence
that the increased fetal abnormalities are strongly, if
not solely, associated with increased maternal
temperature.
Further evidence for a direct relationship between
fetal effects and hyperthermia induced by RF
radiation is shown in several reports (Dietzel and
Kern 1970; Dietzel et al. 1972; Dietzel 1975). In these
experiments, groups of pregnant rats were subjected
to 27-MHz radiation to raise rectal temperature to
42°C. From these data, the thresholds for increased
malformation rates appear to be between core
temperatures of 39.0%. maintained for 5 min and
40.5°C for 10 min.
Observed teratological effects are summarized in
Table 5-9.
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Table 5-9. Summary of Studies Concerning Teratologic Effects of RF-Radiation Exposure
Exposure Conditions*
Effects
30% survival of pupae
Embryonic LDso
Decreased postnatal survival
Teratogenesis
No change in teratogenesis
Increased postnatal survival
Maternal lethality, resorptions,
decreased fetal weight
Decreased fetal weight
No change post-hatching: hatchability.
hemogram, body or organ weights
No change
No change
No change
Teratogenesis
No change
No change
No change
No change
No change
Decreased body and brain weight
Species
D. melanogaster
Chicken
Mouse
Mouse
Mouse
Mouse
Rat
Mouse
Japanese quail
Rat
Rat
Mouse
Japanese quail
Rat
Rat
Squirrel monkey
Rat
Rat
Rat
Intensity
(mW/cm2)
200
280
400
28
40
3. 4-14
5
28
10-35
5
10
Duration
(days x min)
1 x 10
1 x 12
1 x7
1 x4
1 x4
1 x2-5
1 x 10
1 x 10
1 x20
12x100
1 x 1440
1 x20
1 x120
12x100
12
Many x 240
12x100
Many x 180
Many
19x1200
16x300
SARt
(W/kg)
640
70
98
140
104
85-112
38
38
31
22
14
14
10
2-8
4
0.7-4.7
4.2
3.4
1-3.5
2.5
2.2
Reference
Payers/. (1978)
Carpenter et al. (1960a)
Rugh(1976a)
Rugh eta/. (1974, 1975)
Chernovetz et al. (1975)
Chernovetz et al. (1975)
Chernovetz et al. (1977)
Berman et at. (1978)
Hamrick and McRee (1 975)
Chernovetz et al. (1979)
Michaelson et al. (1978)
Berman et al. (1978)
McRee and Hamrick (1977)
Smialowicz et al. (1979a)
Berman et al. (1981)
Kaplan (1981)
Jensh et al. (1979)
Jensh (1979, 1980)
Johnson et al. (1978)
Shore et al. (1977)
"Frequency used was 2450 MHz. except for Jensh (914, 2450, and 6000 MHz), and Johnson et al. 1978 (918 MHz).
tFrom report or estimated from Durney et al. (1978)
5.3.2 Reproductive Efficiency
This section discusses aspects of reproduction where
the conceptus is not "insulted" directly by the agent,
although the fetus may be involved in demonstrating
the effect. Generally, reproductive efficiency is the
capacity of the dam or sire to effect conception and to
bear and rear offspring. Changes in this capacity
might be due to alterations in behavior, physiology, or
morphology. For example, reproduction efficiency
might be affected by changes in maternal cyclical
hormone secretions. Tests for reproductive efficiency
are not conducted as frequently as those for
teratologic effects, usually because the male and
female reproductive systems require considerable
alteration by a toxic agent to cause significant fetal
wastage or increased reproductive efficiency. The
testes as factors in reproductive efficiency are
discussed separately in the next section.
We have previously discussed the effects of 2450-
MHz RF radiation on D. melanogaster reported by Pay
et al. (1978). The fruit flies that were the subjects of
that study were irradiated before production of ova.
The SAR used in the study ranged from 400 to 800
W/kg. Reproductive efficiency, in this case the
production of eggs, was significantly reduced in both
conventionally heated and RF-irradiated females as
compared with the shams. But there appeared to be
no significant difference in the production of ova from
females exposed to RF radiation compared with those
exposed to the conventional source of thermal
energy.
The egg production of chickens can also be used to
provide an index of reproductive efficiency or
reproductive wastage. A single intense exposure of
day-old chicks was made in the experiment reported
by Davidson et al. (1976). In one of four experiments
they describe the reproductive efficiency of 28-week-
old hens that had been irradiated as chicks on day 1 of
age for 4.5 s at a power density of 800 W/cm in a
multimodal cavity. The estimated SAR was 2770
W/kg. No differences appeared between the control
group and the irradiated group in the production of
eggs during 100 days of laying. The authors also
stated that a dose rate of 2500 W/kg for 9 s at 2450
MHz is a lethal dose in day-old chicks and that 42
percent of the chicks dosed for 6 s at 2810 W/kg died.
The animals that survived were unconscious for upto
5 min. The day-old chicks had approximately the
same sublethal SAR (2770 W/kg for 4.5 s) used in the
examination for latent reproductive effects, but there
were no deaths that could be directly attributed to the
RF-radiation exposure. From these experiments, it is
concluded that the massive doses of this experimental
regimen left no latent alterations in reproductive
efficiency.
Rugh et al. (1975) reported an experiment in which
they examined differences in average lethal dose of
RF radiation (2450 MHz) during the estrous cycle of
CF1 mice. The weights of the mice ranged from 29 to
31 g. There was a prior 20-min acclimation to the
waveguide exposure chamber, and environmental
conditions were 23.5°C, 50 percent relative humidity,
and an airflow of 38 liters/min (0.38 km/h). There
5-37
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was a significant decrease in the average lethal dose
for females in estrus as compared to the average
lethal dose for those in diestrus (P < 0.01). The
forward power was 8.24 W. This experiment shows
that changes brought about during the reproductive
cycle can affect radiosensitivity.
In summary, it appears that the efficiency of the
female reproductive system is not easily altered. Only
irradiation at extremely high dose rates has made
changes in reproductive patterns. Small alterations
from normal values, though detectable by modern
scientific and statistical methodology, do not seem
able to sway the general outcome of the reproductive
cycle. Observed reproductive effects are summarized
in Table 5-10.
5.3.3 Testes
Considerable scientific work has been done to
determine effects of RF radiation on the testes. The
testes are so placed anatomically that they can be
conveniently irradiated without irradiation of the
remainder of the body. Tests for testicular function
are also conducted easily. Quantitative changes in
sperm concentration can be conveniently assessed
by repeatable laboratory techniques. It is known that
when the mammalian testes, which have a normal
temperature of 33 to 35°C, are heated to temperatures
approaching abdominal temperature (37-38°C),
sterility can occur. Sterility consequent to high
testicular temperatures can be viewed as a purposeful
contraceptive agent or as an unintended toxic agent.
Table 5-10. Summary of Studies Concerning Reproductive
Effects of RF-Radiation Exposure
Exposure Conditions'
Effects
Decreased ova
production
No change in egg
production
Lethality changes
with estrous cycle
Species
D
melanogaster
Callus
Mouse
Duration SAR
Idav x mm) (W kg)
40O-80O
1 x 0 08 2770
Reference
Pay ft al (1978)
Davidson et al
(1976)
Rugh et al (1975
"Frequency has 2450 MHz in all cases
A report by Muraca et al. (1976) describes the results
of irradiation of rat testicles with 2450-MHz
radiation. Each animal was anesthetized, placed in an
anechoic chamber, then irradiated in a free field at a
power density of 80 mW/cm2. The SAR for adult rats
was 16 W/kg (Durney et al. 1978).
In the experiment, the authors irradiated rat testes to
produce increases of mtratesticular temperature to
36, 38, 40, and 42°C; the testes were then
maintained at these temperatures. The technique of
irradiation included implantation of a thermistor into
one testis of the anesthetized male, with the
temperature of that testis acting as the control of the
on-off-on sequence of the RF irradiator. Both testicles
were irradiated until the temperature of the testes
was within ±0.5°C of the levels mentioned above.
The duration of each irradiation at a power density of
80 mW/cm2 varied from 10 to > 70 min. The animals
were irradiated once or repeatedly during 5 consecutive
days. Five days after the treatment endedr the
animals were killed and their bodies were infused
with solutions to preserve the testis that was not
"invaded" by the thermistor. The microscopic
appearance of the testicular tissue was categorized
as follows: apparently normal; appearance of early
inflammatory or degenerative changes in the
spermatogenic epithelium without well-developed
necrosis; or severe degeneration of the majority of
seminiferous tubules with coagulated cellular
elements.
When male rats were exposed once (80 mW/cm2;'
2450 MHz; 10 to 73 min; temperature of the testis
maintained at 40°C), no significant change was
observed in the incidence of apparently abnormal
testicular tissue. After a single exposure of 10 min,
during which the temperature of the testis was
allowed to reach 42°C, the number of animals that
had some abnormal changes tripled. Multiple (five)
exposures, even where the temperature reached only
36°C for 60 min, caused all the testes to have some
changes in the spermatogenic epithelium. When
temperatures were allowed to reach 40°C in the
testes for repeated short periods (10 to 27 min, five
times), severe degeneration in the spermatic tubules
was seen in all the testicular samples.
This study points to two important factors of irradia-
tion of the testes with 2450-MHz RF radiation: that a
minimum temperature (>40°C) must be reached in
an acute exposure, and that repetitive treatments are
much more effective than single ones. These two
factors also interplay, so that an acute temperature
excursion, even as high as 40°C for over 70 min, is not
as deleterious as a lower temperature (36°C) reached
repeatedly (five times).
Fahim et al. (1975) conducted an experiment to
compare the contraceptive capability of microwaves
with that of other methods of heating. The authors
used male Sprague-Dawley rats (Holtzman strain)
and irradiated them with 2450-MHz radiation (from a
diathermy unit of maximum output of 100 W) during
pentobarbital anesthesia. The applicator of the
diathermy unit was 7.5 cm from the testicles of the rat
and provided near-field exposures that do not allow a
good estimate of the associated SAR. By varying the
power output of the unit and by varying the exposure
time from 1 to 1 5 min, the authors developed four
subgroups of animals: those in which testicular
temperature reached 65°C for 5 min, 45°Cfor 15 min,
and 39°C for 1 or 5 min. The males were allowed to
mate with normal females 24 h after treatment, and
every 5 days thereafter until pregnancy was observed
in the females. 'The endpoint for fertility was the
amount of time required for every surviving male in
the treatment group to impregnate a female." Later,
5-38
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the sexual organs were weighed, and histological
examinations were made of the testes and secondary
sex organs.
Raising the temperature of the testes to 65°C for 5
min or to 45°C for 15 min caused complete infertility
in the males for 10 months. When these testes were
examined histologically, there was no observable
spermatogenesis. When the temperature was raised
to only 39°C, 70 percent of the males retained normal
breeding capability, whereas the remaining 30 per-
cent recovered their fertility within 2 wk. Histological
sections indicated normal spermatogenesis. There
appeared to be no differences in testicular weights or
secondary sex-organ weights, even in the group
(45°C, 15 min) that was sterile 10 months after the
RF-radiation exposure had ended.
This experiment demonstrates that a temperature of
45°C caused by RF-radiation exposure must be
attained in the rat testes to produce permanent
sterility. Temperatures that ranged to 39°C, some-
what above rectal temperature, for only a short period
(5 min) were not effective and produced only
temporary, if any, infertility. Along with the
permanent sterility induced by the high temperatures
(minimum of 45°C), there was damage to the tubules
and a lack of spermatogenesis.
Sterility can occur in rats following RF-radiation
exposure. At high temperatures, epithelial and
tubular structures of the testes can be damaged
permanently. At lower temperatures (approximately
normal body temperature) for short durations, the
temperature in the testicles due to RF-radiation
exposure resulted in temporary sterility. This last
condition implies that the spermatogenic cells
themselves are not damaged permanently. The rat's
spermatogenic cycle has a duration of about 10
weeks, i.e., it takes about 70 days from the first
meiotic divisions of sperm generation in the germinal
epithelium until the time when the sperm are fully
matured, in place, and ready for ejaculation. During
the last 2 weeks of spermatogenesis, sperm are
located in the tubules of the testes and in the
epididymis and require very little additional matura-
tion. There is a constant stream of maturing sperm,
because various seminiferous tubules are in different
stages of this long cycle. The most mature stages of
the spermatogenic cycle are most sensitive to heat
(Van Demark and Free 1970). The permanent (10-
month) sterility seen in the experiment above is due
not only to loss of the most mature and most heat-
sensitive stages, but also to the loss of sperm at all
stages, including the stages involving the germinal
epithelium. The 2-week temporary infertility seen in
the less affected males was caused by the loss of only
the most mature and most heat-sensitive sperm.
A study to demonstrate an alteration in functional
fertility was conducted by Berman et al. (1980). The
authors' report concentrated on chronic exposures of
rats to 2450-MHz radiation in an anechoic chamber.
There were three separate experiments:
(1) exposure at a power density of 5 mW/cm2 for 4
h/day, daily, from the 6th day of gestation through
90 days of age postpartum;
(2) exposure at a power density of 10 mW/cm2 for 5
h/day for 5 days, beginning on the 90th day of age
postpartum; and
(3) exposure at 28 mW/cm2 for 4 h/day, 5 days a
week, for 4 continuous weeks, beginning on the
90th day of age postpartum.
The main purpose of the experiments was to evaluate
potential mutagenic effects of RF radiation on the
•germ cells of the male rat. Male rats were bred to
untreated female rats shortly after the end of the
treatment period. No mutagenic effect was demon-
strated. The breeding data of the assays used in these
experiments were used to evaluate the effects on the
spermatogenic function in rats.
In the first experiment, the animals were exposed
daily from the 6th day of gestation to 90 days of age, at
a power density of 5 mW/cm2. In this experimental
group, the SAR varied inversely with the growth of
the animals, i.e., from approximately 4.5 WAg in
neonates to approximately 0.9 WAg at 90 days of
age. Twin-well calorimetry was not used in the other
two experiments, and SARs are estimated at 2 W/kg
at a power density of 10 mW/cm2, and 5.6 W/kg at 28
mW/cm2.
In this study, temperatures of the testes of rats
exposed up to 90 min to 2450-MHz fields at 28
mW/cm2 showed an increase from a pre-exposure
level of 34°C to almost 38°C after exposure.
Simultaneously recorded rectal temperatures were ~
3°C higher than temperatures of the testes during the
entire period. Sham-irradiated animals had testicular
temperatures ranging from almost 32°C to approxi-
mately 35°C. The exposure at 28 mW/cm2during the
90-min period produced a temperature in the testis
equivalent to the normal rectal temperature.
Chronic exposure at 5 mW/cm2 from the 6th day of
gestation through 90 days of age appeared to have no
effect on the reproductive efficiency of the male rats
when bred with normal females. Also, exposure at a
power density of 10 mW/cm2 (SAR ~ 2 W/kg) at 90
days of age for a period of 5 days had no effect on the
reproductive efficiency of the males. It was only the
most severe regimen, the exposure of adult male
rats at 28 mW/cm2 for ~ 4 weeks (estimated SAR ~
5.6 W/kg), that caused any alteration in reproductive
function. This exposure produced a severe decrease
in the reproductive ability of the males; only 50
percent of the females that were available to the
males for breeding became pregnant during the week
immediately following the exposure period. The
breeding returned to normal beginning at the third
week after irradiation (the next period of test breeding).
5-39
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The animals bred normally thereafter. No examination
was made of the testes of animals exposed at 28
mW/cm2. The temperatures reached in the testes at
the highest power density (28 mW/cm2) were similar
to those reported by Fahim et al. (1975), where
histological changes were seen.
Varma and Traboulay (1975) exposed anesthetized
male mice to 1.7-GHz or 3.0-GHz radiation at power
densities up to 200 mW/cm2for up to 100 min. The
results of the reported experiments are (frequency in
GHz; power density in mW/cm2; SAR in W/kg, and
estimated from Durney (1978); exposure duration in
minutes; and effects observed): 1.7 GHz, 10
mW/cm2, 15 W/kg, < 100 min, no effect; 1.7 GHz,
10 mW/cm2, 15 W/kg, 100 min, necrotic germinal
and tubular tissue, and intact interstitial and Sertoli
cells; 1.7 GHz, 50 mW/cm2, 75 W/kg, 30 to 40 min,
all tissues necrotic; 1.7 GHz, 200 mW/cm2, 300
W/kg, 20 min, skin burns; 3.0 GHz, 50 mW/cm2, 50
W/kg, 20 min, minimal (sic) injuries. In this
experiment, as in the earlier work described in the
document, acute effects are very dependent on the
combination of exposure duration and field strength.
Cairnie et al. (1980a) used oil-bath immersion to
modify core and testis temperature. When conscious
mice were immersed in oil baths at temperatures
from 34 to 42°C, both core and testicular tempera-
tures appeared to be physiologically regulated,
paralleled the bath temperature, and reached
equilibrium. Anesthetized mice, on the other hand,
did not appear to demonstrate any core or testicular
temperature modification, but appeared, instead, to
increase temperatures equally with the temperature
of the oil. This study assumes importance because it
clearly demonstrates that the temperature in the
testes is not normally regulated in anesthetized
animals. The investigators also studied the effects in
mouse testes after a range of whole-body exposures
of up to 30 days for 16 h/day at 2450 MHz and power
densities of up to 36 mW/cm2 (average whole-body
SAR = 7 W/kg; average testicular SAR = 14 W/kg).
These exposures caused no measurable increase in
testicular temperature. No changes were seen in the
number of dead testicular cells, the number of
epididymal sperm, or in the percentage of abnormal
sperm after exposure, even up to 8 weeks after
exposure. Four strains of mice were used, and no
strain susceptibility was observed.
Cairnie et al. (1980b), in preparation for their future
work in the RF-radiation effects in the testes,
determined the dosimetry of 2.45 GHz in mouse
testes. They found that the absorption in the
abdomen in the area of the liver was 11 times greater
than in the testes when the body is oriented parallel to
the electric-field vector. They also found that though
abdominal temperature may have been increased by
exposure to 50 mW/cm2 for 16 h, testicular
temperature was not.
Cairnie and Leach (1980) examined the viability of
testicular and sperm cells and the morphology of
sperm cells after exposure to hot-water baths of the
posterior torso in mice. Unanesthetized mice were
partly immersed in water at temperatures of 32 to
43°C for up to 4 h. The results of this experiment are
appropriate to this discussion in that they may reflect
the type of response that testicular tissue and sperm
would give to exposure to RF radiation; however,
caution should be used in attempting to equate
durations of water immersion and RF radiation
exposure, as the site and time-profile of heat
deposition may not be equivalent. Cairnie and Leach
observed that heat-damaged testicular cells are
evident within 2 h after exposure (41 °C, 30 min), that
the incidences of the damaged cells are at a
maximum from 4 to 12 h after exposure, and that the
incidences of damaged testicular cells are related to
combinations of exposure duration and bath
temperature. They also observed that a 30-min
immersion in 43°C water, but not lower tempera-
tures, significantly decreased total epididymal sperm
counts during a 10-week-long postexposure period,
and that the incidences of abnormal-appearing sperm
followed a similar pattern.
In the"studies reported by Ely et al. (1964), 2880-MHz
(PW) radiation was used to irradiate only the
testicular area in groups of dogs. The animals were
anesthetized during exposures while temperatures
were measured in the testis by a thermistor in a metal
needle. Irradiation of the testicular area continued
until a peak temperature was reached; the RF
radiation was then turned off manually so that the
testes could cool, at which point the RF radiation was
turned on once again. This cycling of exposure was
completed many times so that the animal's testes
could be kept at a "steady" temperature for a
considerable length of time. The normal temperature
of the testes of the dogs was ~ 33°C, 5°C lower than
that of the rectum.
According to this report, exposure of the testes
caused an elevated testicular temperature of 36°C at
20 mW/cm2, 38°C at 33 mW/cm , and up to 40°C at
45 mW/cm2. As 38°C is the approximate body
temperature in the dog, bringing the testes to body
temperature can expect to produce sterility if the
elevation is sufficiently chronic. It appears, then,
that 45 mW/cm2 is required to produce this type of
effect.
There is a large body of literature on the fertility
effects caused by temperature increases, such as
when the testicles are clothed to prevent the normal
thermal radiation. Even high environmental tempera-
tures, when sustained, can produce infertility in male
rats. One example of this is a report (Pucak et al.
1977) describing deaths in a large rat-production
colony in which room temperatures accidently
reached as high as 31.6°C for 2 days and as high as
5-40
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37.7°C in individual cages. Under these conditions,
approximately 3,000 of 14,000 Sprague-Dawley rats
died from heat prostration. When examined 18 days
after the incident, 25 percent of the surviving males
showed bilateral atrophy of the testicles, which were
approximately half the normal size. Histological
examination showed atrophy of the spermatic
tubules and failure of spermatogenesis. The
proportion of affected testicles ranged from 50 to 75
percent. Five weeks after the incident the animals with
small testes were still sterile. In comparison with the
temperatures seen in this study, raising the
temperatures of testes to 42°C by RF-radiation
exposure appears to be an extreme experimental
regimen. Observed testes effects are summarized in
Table 5-11.
5.3.4 Unresolved Issues
5.3.4.1 Teratology
A threshold of teratogenic effects due to RF radiation
has not been determined. The measurement of
threshold will have to include the entire range of
teratogenic effects: lethality, anomaly production,
decreased body weight in fetuses, and alteration of
postnatal function. Even at this stage of development
of the data relating to RF-radiation-induced terato-
genesis, a picture is appearing in which the degree of
response depends on the level of whole-body SAR,
the duration of exposure, the timeliness of the
exposure, and the species, all of which complicate the
threshold determination. It is not yet clear whether
threshold can be based on a finite whole-body SAR
for all species or whether some adjustment or
proportion will be necessary for species size,
metabolic rate, thermoregulatory capacity, etc. So far,
the only physiologic variable that can be supportably
associated with teratogenic effects is the colonic
temperature of the dam during or at the end of
exposure. The mouse and rat, two extensively studied
species, show a minimum temperature of approxi-
mately 40°C in the dam is associated with teratologic
symptoms. However, whole-body SARs required to
cause temperature excursions like this are much
Table 5-11. Summary of Studies Concerning Effects of RF
higher in the mouse than in the rat. Therefore, an
adequate relationship of teratogenesis to SAR alone
is not apparent. The maternal colonic temperature,
then, is the only available indicator of a threshold for
teratogenesis in mammals.
Published reports that meet the criteria for considera-
tion in this document have limited their examination of
the fetal results of gestational exposure to a gross
morphological change or one that might be seen
under low magnification (15X). There has been no
organized attempt to examine in histologic detail
fetuses that have been irradiated in utero. Authors of
one study (McRee et al. 1980b), however, made a
detailed examination of embryonic hearts but could
not demonstrate changes in morphologic, ultrastruc-
tural, or enzymatic activity. The subjects were
Japanese quail which had been exposed daily for 8
days to 2450-MHz radiation at SARs of 4 and 16
W/kg.
There are classifications of fetal changes that
represent no gross structural deficit, but nevertheless
represent some variation of structure. An example of
a variation that may not be considered by all
terajologists as a "deficit" is a small but normal fetus.
However, if the incidence of this variation is
consistently increased by the application of a toxic
agent, it could be considered an expression of
embryotoxicity. The decreased body weight so often
seen in offspring exposed to RF radiation (Berman et
al. 1978; Chernovetz et al. 1977,1979; Rugh 1976a)
might otherwise be considered as a lesser category of
"structural variation without deficit" if decreased
weight were not so consistent in these experiments.
Whether this decreased fetal weight is temporary
(i.e., only a delayed growth that will disappear in the
neonatal stage) or permanent (i.e., a stunting of the
fetus that will persist) has not yet been resolved.
There is one aspect of the literature on the
teratogenic potential of RF radiation that deserves
further discussion. More than half the papers in this
document on teratogenesis report experiments with
Radiation Exposure in Testes of Mice and Rats
Exposure Conditions
Effects
No change
Abnormal germinal cells.
normal interstitial cells
All tissue necrotic
Scrotal skin burns
"Minimal" injury
No change in tissue.
sperm
Abnormal spermatogenic
tissue
No change
No change
Temporary sterility
Species
Mouse
Mouse
Mouse
Rat
Rat
Frequency
(GHz)
1.7
3.0
2.45
2.45
2.45
Intensity
(mW/cm2)
10
10
50
200
50
<37
80
5
10
28
Duration
(days x min)
1 x<100
1 x 100
1 x 30-40
1 x20
1 x20
many x 1 6 h
1 x 10-73
5x 10-73
many x 240
5x360
20 x 240
SAR
(W/kg)
15
15
75
300
50
<8
16
16
0.9-4.5
2
5.6
Reference
Varma and Traboulay (1975)
Cairnie et al. (1980a)
Muraca et al. (1976)
Berman et al. (1980)
5-41
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the rat. Chernovetz et al. (1977) raise an interesting
point about using the rat in determining the
teratogenic potential of RF radiation. The authors
argue that because levels of microwave exposure
which are associated with high mortality rates of
dams do not also produce fetal structural abnormal-
ities in the rat, "...that the teratogenic threshold of
microwave radiation is higher than the dam's
threshold of mortality," and hence"... that maternal
mortality is more probable than malformation of the
fetus, irrespective of the dose."
The problem of using animal models in determining
teratogenic potential in humans is that there is no
assurance that any of these models is a real estimate
of effects in humans. The concepts supporting the
use of animals as models of human beings require
that the response be demonstrated in a number of
species, so that the resultant generality can be more
confidently extended to humans. Therefore, we seek
among species some generality of effects of
microwaves on the fetus. Mice and rats are the two
laboratory animals upon which rest almost all of the
data of RF-radiation-induced teratogenesis. Any
difference between the two species in their
teratogenic response to RF radiation, therefore,
becomes important.
the energy could not reach the prostate. This appears
to deserve additional attention and exploration.
The literature we have cited does not lend itself to
extrapolation of effects of RF radiation that cause only
small increases in the temperature of the testes. The
lack of data on RF-radiation effects at lower power
densities (which cause lower testicular elevations of
temperature than have been cited in the articles
above) is especially important in light of suggestions
in the popular media that thermal energy, in the form
of absorbed RF radiation, can be used as a
contraceptive in men.
One report by Rugh (1976a) contains data on survival
in RF-radiation fields that are different in males and
females. In this study, mice of both sexes and ofthree
ages (weanlings, young mature, and aged) were
irradiated with 2450-MHz RF radiation until dead. Of
the three variables (age, sex, body weight) examined
for their contribution to RFrradiation lethality, Rugh
found that "The overall conclusion would be that no
matter at what age...absorbed dose to death...is
different for the two sexes. Females are slightly more
radiosensitive..." These results are not explained
easily. Although they are not apparently related to
sexual function, they were included here on the basis
of sexual differences.
5.3.4.2 Reproductive Efficiency and Testes
The testes contain, besides sperm-producing tissues,
interstitial cells that secrete testosterone, the male
hormone. Gunn et al. (1961) described the effect of
24-GHz radiation on the morphology and function of
the interstitial cells in rats. They exposed rats once at
this frequency for a period of 5 min at a power density
of 250 mW/cm2, which caused the temperature to
rise to 41 °C in the testes. As a result, there were
scrota! burns, severe edema, and spermatic tubular
degeneration, but not interstitial-cell pathology.
The testosterone secreted by the interstitial cells of
the testes regulates zinc uptake by the dorsolateral
prostate. When Gunn examined zinc uptake in RF-
irradiated rats that had no interstitial cell pathology,
he found a decreased uptake. Gunn related the
decreased function of this secondary sex organ to
decreased testosterone secretion.
The effects seen by Gunn were produced at a
frequency at 24 GHz. At such a short wavelength
there should be no significant penetration to affect
the dorsolateral prostate directly. The tests using the
dorsolateral prostate as an indicator of sexual
function in the rat have been commonly used by Gunn
and others in other types of experimental situations.
It is not known why and how the dorsolateral prostate
lost its capacity to function normally when there was
no observable change in the interstitial tissues, the
other testicular damage appeared to be minimal, and
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5.4 Nervous System
Michael I. Gage
Ernest N. Albert
Communication with the external environment and
modification of the operation of other organ systems
are functions of the nervous system. Signals from
stimuli in the external environment, such as
chemicals, pressure, temperature, or radiant energy,
are received by specialized receptor cells and
transduced into nerve impulses that are measured as
a complex pattern of electrical and chemical events.
These impulses are combined with other signals from
the internal environment, such as chemical secretions
or feedback from intermediate neurons or neurons in
efferent paths of the nervous system, at junctions
called synapses. Information is thus transmitted
through the nervous system until some effector
change occurs (usually a chemical event at a site
called a neuromuscular junction) that activates or
modifies some gland or muscle tissue, and brings
about an integrated response to changes in the
internal and external environment of an organism.
Detailed descriptions of the organization and
functioning of the nervous system are available
(Crosby et al. 1962, Kandel and Schwartz 1981;
Carlson 1980; Cooper et al. 1982; Scientific
American 1979).
Two types of cells are found in the nervous system,
neurons and glia. Neurons consist of cell bodies and two
types of peripheral processes known asdendritesand
axons. They are considered responsible for carrying
the information throughout the nervous system. The
glia (of which there are several types) are considered
to support the neurons, to nourish them, and react to
damage of nearby neurons.
The nervous system can be divided into several
anatomical subsystems, that are not mutually
exclusive but have been formulated to unify a
particular function or anatomical similarity. One such
division is the central nervous system (CNS, i.e., the
brain and spinal cord), as opposed to the remainder of
the nervous system called the peripheral nervous
system (PNS). The brain may be subdivided into areas
which may be further subdivided into nuclei or
cortices (the gray matter containing the cell bodies
and frequently the dendrites of neurons) and tracts (the
white matter containing the axons which are covered
with a white fatty tissue called myelin and in the PNS
are wrapped by Schwann cells). Neurons in nuclei
and cortices and axons in tracts are positioned so that
each area contains a topographic projection of the
part of the peripheral location connected by the
neurons.
There is much redundancy within the nervous
system. Multiple pathways carry similar information
between the periphery and the brain, as well as
within the brain itself. Some of these paths, such as
primary sensory tracts, have few neuronal connec-
tions; others, such as the reticular formation, have
many intermediate (or internuncial) neurons. Input
neurons synapse with intermediate and output
neurons at numerous levels in the nervous system.
At synapses specific chemicals known as neurotrans-
mitiers function in complex series of reactions to
carry signals between neurons. Packets of neuro-
transmitter substance are released at the synapse by
one neuron and taken up at the postsynaptic
membrane of an adjoining neuron. Much evidence
indicates that norepinephrine, dopamine, acetylcho-
line, serotonin, and x-aminobutyric acid (GABA) are
neurotransmitters. The reactions at synaptic
connections are different from another type of
chemical activity that takes place at the membrane
along the axon at breaks in the myelin cover called
nodes, enabling conduction of electrical impulses
along the axon. At these nodes influx and efflux of
ions of potassium, sodium, and calcium establish
changes in electrical potentials.
The fine topographic organization throughout the
nervous system, coupled with multiple connections
and pathways between input and output and the
transmission of specific chemicals at particular
synaptic junctions, enables the specificity of
response to ambient changes for which the nervous
system is renown. This exquisite organization and
complexity within small areas in the brain is also
responsible for a variety of changes that might be
seen if RF radiation were to affect the nervous system.
A review of the literature of the effects of RF radiation
on the nervous system permits the following general
statements to be made:
• Acute or chronic CW or PW radiation of animals at
SARs > 2 W/kg can produce morphological
alterations in the central nervous system. These
changes are qualitatively similar after acute or
chronic exposure and at different SARs, but
quantitatively more alterations occur in the
affected neuronal structure after exposure at
higher SARs and after chronic exposure. The
changes are found less frequently if the animals
are allowed to survive several days to weeks after
exposure. Acute exposures above 2.5 W/kg alter
electrophysiological responses in thethalamusof
the cat brain.
Currently, no information conclusively shows RF
radiation affects the blood-brain barrier (BBB) at
SARs below 2 W/kg. Initially it appeared that RF
radiation at low power densities altered the
permeability of the BBB in experimental animals.
5-43
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Later experiments indicated such alterations were
due to thermal effects. Effects formerly attributed
to changes in BBB permeability are now thought
to be due to increased blood flow in the brain.
• RF radiation appears to have a potentiating effect
on drugs that affect nervous system function. Most
of the relevant studies have used pulse-modulated
waves only. Whether RF radiation also has an
inhibiting effect on neuropharmacologic drugs is
not certain.
• There are no data on the effects of RF radiation on
neurotransmitters at SARs < 2 W/kg. However,
after exposure at SARs > 8 W/kg the release of
neurotransmitters appears to be affected.
Whether there is an increased or a decreased
release depends on the specific neurotransmitter.
5.4.1 Morphological and Physiological
Observations
The nature of morphologic changes in the nervous
system of exposed animals depends on the frequency,
power density, duration, and modulation characteristics
(e.g., PW or CW) of the radiation. Gordon (1970) and
Tolgskaya and Gordon (1973) reported severe
damage in the brain of rats after short exposure to RF
radiation of various frequencies at high power
densities (> 40 mW/cm2, SAR estimated > 8 W/kg,
assuming the worst case condition which would
occur if the rats had their long body axis parallel to the
E-f ield vector) which produced rectal temperatures of
42 to 45°C. These changes consisted of hemorrhages,
edema, and vacuolation of neurons after a 40-min
exposure to 3,000 or 10,000 MHz PW or CW radiation
at 40 to 100 mW/cm2. At 20 mW/cm2 similar but less
severe effects were observed. Further, 3000-MHz
radiation (SAR estimated about 4 W/kg) produced
more marked changes than 10,000 MHz (SAR
estimated about 3.2 W/kg) at equal power densities.
However, Austin and Horvath (1954) did not observe
similar changes in brains of rats that became
convulsive and hyperthermic (rectal temperature
increase of 2.3°C, or brain temperature increase to
about 43.7°C) during a single, short irradiation. The
exposure to 2450 MHz lasted for a maximum of 7 min
or until the onset of convulsion (which was usually
less than 2 min). Exposure was of high intensity and
was presented only to the head (60 or 90 W applied
2.5 cm above or on the head). These authors observed
only mild pyknosis and hyperemia in some areas of the
brain, mostly in the pyramidal cell layer of the
hippocampus.
Albert and DeSantis (1975) did not observe
hemorrhage, gliosis, or focal necrosis in adult
Chinese hamsters exposed to 2450 MHz (CW) at 50
mW/cm2 (SAR estimated at 15 W/kg) in the far field
in an anechoic chamber for 30 min or single periods
lasting up to 24 h, but they did observe swollen
neurons with frothy cytoplasm in the hypothalamic
and subthalamic regions located near the center of the
brain. Such observations were not seen in the
cerebellum, pons, or spinal cord, which are located
more posterior than the other areas. These changes
were less severe in hamsters allowed to survive for 6
to 10 days after treatment. In a second study (Albert
and DeSantis 1976) similar histologic changes were
seen in the hypothalamus and subthalamus of
Chinese hamsters following single 1700-MHz (CW)
exposures lasting from 30 to 120 min at either 10
mW/cm2 (SAR estimated at 3 W/kg) or 25 mW/cm2
(SAR estimated at 7.5 W/kg) in the far field in an
anechoic chamber. No lessening of the severity of
these changes was seen in animals allowed to
survive for 13 to 15 days following exposure.
Histologic changes in the rat brain have also been
reported after multiple (35 or more) 30-min
exposures to 3000 MHz at lower power densities(< 10
mW/cm2, SAR estimated at 2 W/kg). The histological
alterations included cytoplasmic vacuolation of
neurons, axonal swelling and beading, and swelling
in and decreased numbers of dendritic spinesf Gordon
1970; Tolgskaya and Gordon 1973). These changes
were seen to a lesser degree or not at all in animals
allowed to survive for 3 to 4 weeks after exposure
before sacrifice. Vacuolation of neurons but not glia
was also seen in the hypothalamic region of Chinese
hamsters exposed to 2450 MHz (CW) at 25 mW/cm2
(SAR estimated at 7.5 W/kg) for 14 h on each of 22
days (Albert and DeSantis 1975).
Baranski (1972b) reported that exposure of groups of
30 guinea pigs to 3000 MHz (CW and PW at 400 Hz) in
an anechoic chamber at 3.5 mW/cm2 (SAR estimated
at 0.53 W/kg) and exposure of 20 rabbits to 3000
MHz (CW or PW not indicated) at 5 mW/cm2 (SAR
estimated at 0.75 W/kg) for 3 h daily for 30 days
resulted in myelin degeneration and increased
proliferation of glial cells in both the cerebrum and
cerebellum. More alterations were noted in the
guinea pigs exposed to PWthan those exposed to CW.
Temperatures recorded at unspecified points in the
body were reported never to increase more than
0.5°C. Single 3-h PW or CW exposures of guinea pigs
at 3.5 mW/cm2 had no effects, but single exposures
at 25 mW/cm2 (SAR estimated at 3.75 W/kg)
produced edema, hyperemia, and small necrotic
lesions indicative of damage due to heat.
Switzer and Mitchell (1977) found 3 times as many
myelin figures in the dendrites of brain neurons of 15
female rats repeatedly exposed to 2450-MHz (CW)
fields in a multimodal cavity than in the 14 sham-
irradiated control rats. Exposures lasted 5 h, 5 days
weekly for 22 weeks (a total of 550 h at an average
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SAP calculated to be 2.3 W/kg, with Ta = 24 ± 1.5°C,
RH = 50 ± 10 percent) and were followed by a 6-week
recovery period before the euthanasia. These authors
did not observe other changes such as gliosis,
perivascular edema, or synaptic pathology. However,
the irradiated rats in this study exhibited marked
disruptions of behavior during the exposure period
(Mitchell et al. 1977; see also Sec. 5.5).
Qualitatively, the morphological effects on the CNS
are similar in the range of 10 to 50 mW/cm2 (SARs
above 2 W/kg), but effects are quantitatively greater
at the higher power densities. Many scientists would
consider that irradiation at these power densities can
raise body temperature. Soviet scientists have
reported similar morphological changes at power
densities less than 10 mW/cm2 after chronic
irradiation; they do not consider these alterations to
be of thermogenic origin. Tolgskaya and Gordon
(1973) and Baranski (1972b) further state that
morphological effects are more marked after PW than
after CW and after chronic exposure than after acute
exposure. Most Eastern European studies claim full
recovery of irradiated animals in 1 to 3 weeks after
exposure at less than 10 mW/cm2 (SAR of 2 W/kg).
Albert and DeSantis (1975, 1976) found continued
existence of neuronal cytopathology in animals 2
weeks after exposure. Perhaps a longer recovery
period in the latter study would have shown complete
reversibility. We can conclude that RF radiation
causes morphological changes in the CNS of
experimental animals following acute or chronic
exposures at SARs of 2 W/kg. In most of the lower-
intensity exposure studies, effects were rarely
observed or were less severe in animals allowed to
recover for 3 or more weeks after exposure.
Electrophysiological recordings from the brain and
spinal cord of animals have been made during and
following RF radiation when precautions have been
taken to minimize artifact due to electrodes in the
microwave field. Johnson and Guy (1972) have
shown that a metal electrode of the type commonly
used in neurophysiology can greatly increase the
amount of energy absorbed in neighboring tissue by
several orders of magnitude. However, saline-filled
glass electrodes did not alter thermograms showing
RF power absorption in brain tissue. Averaged evoked
potentials were measured with glass electrodes in the
thalamus to somesthetic stimulation of the contra-
lateral forepaw (Johnson and Guy 1972). Cats
(anesthetized with alpha-chloralose and immobilized
with gallamine triethiodide) were exposed to 918
MHz (CW) for 15-min intervals at power densities
ranging from 1 to 40 mW/cm2 with a microwave
applicator located 8 cm from the head and directed so
maximum intensity was aimed at the thalamic region
of the brain. The SAR in the thalamus of a live cat was
1.88 mW/cm3 (~ 1.88 W/kg) for an incident power
density of 2.6 mW/cm2. The exposures decreased
latencies between the stimulus presentation and the
peaks of the later components of the evoked
potentials as a function of the power density
(threshold of 2.5 to 5 W/kg). Latencies between the
stimulus and initial thalamic response were not
decreased by the RF radiation. This result indicates a
change in the multisynaptic paths to the thalamus
and within the brain with little change in the primary
sensory pathway. Although microwave exposure
produced increases in thalamic and body temperatures,
similar increases in body temperature produced by a
hot pad decreased latency of both initial and later
components of the thalamic evoked potential.
Monosynaptic ventral root reflex responses of the
spinal cord to electrical stimulation of the ipsilateral
gastrocnemius nerve of cats anesthetized with pento-
barbital and immobilized by gallamine triethiodide
were measured with a polyethylene suction electrode
during and after brief exposure to microwaves (Taylor
and Ashleman 1975). Exposures of 3 min at 2450 MHz
(CW) were delivered by a parallel-plate applicator
surrounding the spinal cord. Decreases in latency and
attenuation in amplitude to zero of the monosynaptic
reflex occurred during exposures with an incident
power of 7.5 W, resulting in an absorbed power of 1.6
W/cm3 (~ 1600 W/kg) at the spinal cord. The
temperature in a bath surrounding the cord was
37.5°C. Similar but less marked changes were
observed during 3.75-W exposures. These changes
were reversible with the termination of exposure.
Increased amplitude of the monosynaptic reflex
produced by cooling the spinal cord was reversed by
microwave radiation. Raising spinal cord temperature
by heating the bath surrounding the cord produced
effects similar to those seen during microwave
radiation.
Takashima et al. (1979) exposed male rabbits
between parallel plates to RF fields having carrier
frequencies ranging from 1 to 30 MHz that were
amplitude modulated at either 15 Hz or 60 Hz during a
single 2-to 3-h exposure or during 4 to 6 weeks of
chronic exposure. The electric field strengths ranged
from 60 to 500 Vrms/m. Acute and chronic EEG
readings were obtained from animals under sodium
pentobarbital anesthesia. There was no temperature
rise in the exposed animals. The EEG recordings after
acute exposure at field strengths of 60 to 500 Vrms/m
or after chronic exposure at strengths up to 70 Vrms/m
showed no difference between control and experi-
mental animals. However, chronic irradiation at
higher field strengths was associated with abnormal
patterns, consisting of bursts of high amplitude
spindles at 90 Vrms/m, as well as suppression of
activity at 500 Vrms/m. All brain activities returned to
normal a few hours after irradiation. The results in
this study appear to be free of electrode artifacts
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because chronic exposures were made without
electrodes, and all recordings were made when the
fields were switched off. The effects of anesthesia are
not clear, and the natural fluctuations of brain activity
also complicate interpretation of the results.
Although the occurrence of high-amplitude spindles
in irradiated animals in this study is similar to that
described by Bawin et al. (1973), comparison of the
two results is difficult because in the latter study,
chronically implanted electrodes may have interfered
with the imposed fields. Takashima et al. (1979)
confirmed the existence of artifacts during irradiation
when implanted electrodes were used.
Bawin et al. (1973) exposed adult female cats
previously implanted with steel electrodes and held in
a fixed position by a wooden stereotaxic frame in a
parallel-plate exposure system to 147-MHz fields
amplitude modulated at frequencies ranging from 1
to 25 Hz at intensities of 1 mW/cm2 or less (SAR
estimated about 0.015 W/kg). Five cats were trained
(by operant behavioral reinforcement techniques) to
increase the percentage of time during which specific
brain waves were within a narrow frequency band
specified by the experimenter. Then reinforcement
was discontinued for a series of sessions until the
percentage of brain waves of the reinforced
frequency returned to preconditioning operant levels.
During these extinction sessions, three of the cats
were exposed to the RF radiation modulated at 4.5 Hz
for one cat, 3 Hz for the second, and 14 Hz for the
third. The modulation frequency was within the range
reinforced for each cat. Irradiated cats required more
sessions for the brain activity to return to precondi-
tioning levels than nonirradiated cats. Spectral
analysis of the brain waves of irradiated cats showed
a shift such that the predominant frequency centered
around the modulation frequency of the RF radiation.
No such spectra were seen in irradiated cats that had
no behavioral training. In the same study two other
cats were reinforced by amplitude-modulated
radiation. The production of specified frequencies of
brain rhythms was followed by irradiation. Increases
in the number of bursts of the reinforced frequencies
occurred, but the duration of these bursts did not
increase. The number of bursts returned to precondi-
tioning levels when the irradiation was discontinued.
5.4.2 Blood-Brain Barrier Studies
A separation between the blood and the central
nervous system (including the ventricles containing
the cerebrospinal fluid) limits the ready passage of
certain substances from the blood into the nervous
system. Such a separation acts to protect the brain
from foreign and therefore toxic substances but
allows entry of certain molecules necessary for
metabolism. This separation is an anatomical entity
consisting of special cells that have tight junctions
between them, as well as a functional property of
some glial cells. A thorough discussion of the blood-
brain barrier has been presented by Rapoport (1976).
In the past few years, contradictory reports have been
published concerning the effects of RF radiation on
the permeability of the BBB. (For reviews, see Albert
1979a and Justesen 1980).
Frey et al. (1975) were the first authors in the United
States to report a permeability increase in the BBB of
the rat after RF-radiation exposure. They observed
that a 30-min 1200-MHz exposure (CW) at 2.4
mW/cm2 (SAR estimated at 1.0 W/kg) resulted in a
statistically significant increase in fluorescein in
brain slices of experimental animals over controls.
Most of the fluorescein appeared to be concentrated
in the vicinity of the lateral and third ventricles. Some
dye also was detected in the metencephalon. The
authors also reported similar but heightened
alterations in the permeability of the BBB when rats
were irradiated with PW radiation at 2.1 mW/cm2
peak and 0.2 mW/cm2 average power density (SAR
estimated at 0.8 W/kg). Their results also indicated
that PW radiation was more effective in altering brain
permeability than CW.
Merritt et al. (1978) were unable to replicate the
fluorescein studies of Frey et al. (1975). However,
increased brain permeation of fluorescein-albumin
(mol. wt. 60,000) was produced in rats heated to40°C
by hot air or by RF radiation. They concluded that
hyperthermia per se, and not field-specific effects of
RF radiation, is the essential determinant of
increased permeability. With sodium fluorescein and
Evan's blue, Lin and Lin (1980) also found no change
in BBB permeation after a single 20-min focal
exposure within the rat head at 0.5 to 10OOmW/cm2
(local SARs ranged from 0.04 to 80 W/kg) at 2450
MHz (PW). In 1982, these authors reported increased
BBB permeability in the rat exposed similarly btit at an
SAR of 240 W/kg (in the brain); the brain temperature
was 43°C (Lin and Lin 1982).
Electron microscopic tracer methodology has been
used to follow the movement of horseradish
peroxidase into Chinese hamster brains after 2450-
MHz (CW) radiation in the far field at 10 mW/cm2
(SAR estimated at 2.5 W/kg) for 2 h (Albert 1977;
Albert and Kerns 1981), and into rat and Chinese
hamster brains after 2800-MHz (CW) radiation at 10
mW/cm2 (SAR estimated at 0.9 W/kg for rats and 1.9
W/kg for Chinese hamsters) for 2 h (Albert 1979b).
Horseradish peroxidase is an enzyme (mol. wt.
40,000) that normally does not enter the brain. Focal
areas of dark-staining material indicating increased
permeability of peroxidase were seen in about 35
percent of the irradiated animals in contrast with
about 10 percent of the controls. Oark-stainad
particles were seen in a variety of brain areas, but
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appeared with greater frequency in the thalamus,
hypothalamus, medulla, and cerebellum than in the
cortex or hippocampus (Albert and Kerns 1981). In
two of the above studies (Albert 1979b; Albert and
Kerns 1981), fewer of the animals that were allowed
to survive for 1 h following irradiation and almost no
animals that were allowed to survive for 2 h following
irradiation showed evidence of peroxidase in areas
other than those that are leaky in all animals due to
the normal absence of the BBB. This finding
demonstrated complete reversibility of the RF-
radiation effect. The increased permeability of the
BBB appeared to be due to increased pinocytotic
transpdrt of the tracer rather than to opening of the
endothelial tight junctions (Albert and Kerns 1981).
Sutton and Carroll (1979) produced a change in
permeability of the BBB to intravenously administered
horseradish peroxidase by 2450-MHz (CW) micro-
waves of sufficient power (10 to 20 W) to raise and
maintain brain temperatures of male rats to40,42, or
45°C for periods lasting from 10 to 120 min.
Exposures were limited to the head region by the use
of type A or type B applicators and by shielding of the
remainder of the body with an absorbent collar.
Increased residual peroxidase activity in brain was
found after 10-min exposure at45°C, after 15 min at
42°C, or 60 min at 40°C. If body core temperature
was maintained at 30°C during exposure by
precooling the rat before head-only irradiation,
peroxidase activity increased in the brain after 15 min
at a brain temperature of 45°C, 30 min at 42°C, and
180 min at 40°C. Precooling the rats increased the
exposure time needed to eliminate BBB integrity, and
also increased the survival time of the rats irradiated
at the lowest level from 2 to 3 h. This study indicates
that severe hyperthermia induced by the radiation
produces the disruption in the BBB and that this
disruption can be prevented or retarded by perfusion
of the brain by blood cooled in passage through the
remainder of the body.
Oscar and Hawkins (1977) exposed rats injected with
radioisotope tracers to 1300 MHz (CW or PW)
radiation for 20 min. Using the technique of
Oldendorf (1970), they found after CW irradiation at 1
mW/cm2 (SAP estimated at 0.4 W/kg) a greater
uptake of radiolabelled mannitol (mol. wt. 182) and
inulin (mol. wt. 5000), but not dextran (mol. wt.
60,000), in brains of exposed animals. Similar, but
greater, uptake of these compounds was observed
after PW irradiation (average power density 0.3
mW/cm2; SAP estimated at 0.1 W/kg) than after CW
irradiation. Uptake of mannitol by the brain was
dependent on power density, pulse width, and
number of pulses per second. Merritt et al. (1978),
who also used the Oldendorf technique, reported no
significant change in uptake of mannitol or inulin in
rats exposed to RF radiation under conditions similar
to those used by Oscar and Hawkins (1977).
Preston et al. (1979) used the Oldendorf technique in
a study of rats exposed to 2450-MHz (CW) fields for
30 min at zero or one of five power densities ranging
from 0.1 to 30 mW/cm2 (SAP estimated at 0.02 to 6
W/kg) in the far field in an anechoic chamber
(Ta=22±1°C). No change in uptake of mannitol intothe
medulla, cerebellum, diencephalon, or cerebral
cortex of the brian was found. Intracarotid infusion of
propylene glycol, however, did increase brain uptake
of mannitol. They speculated that the changes
reported by Oscar and Hawkins (1977) may have been
due to changes in blood flow. Later, Oscar et al.
(1981) measured the blood flow in several brain
regions during exposure to 2800-MHz (PW) fields at
15 mW/cm2 (average) for 5 to 60 min and found
increased local blood flow. They then suggested that
previously reported BBB permeability changes(0scar
and Hawkins 1977) may be smaller than originally
indicated.
A later report by Preston and Prefontaine (1980)
described studies on BBB permeability in rats
exposed to 2450-MHz (CW) radiation in both the near
and the far field. The exposure in the far field in an
anechoic chamber was at 1 or 10 mW/cm2 (SAR
estimated at 0.2 or 2.0 W/kg)for 30min (Ta=22±1°C).
In the near-field exposure, a microwave applicator
was placed on the rat head for a single 25-min
irradiation at 7,28, or 140 mW forward power (SAR of
the head, estimated as 12.64 W/kg for each watt of
forward power, was 0.08 to 1.8 W/kg). In the near-
field study the exposure took place after radiolabelled
sucrose was injected into the animal so that BBB
function during irradiation could be examined. No
change in permeation was found in either study.
In summary, some initial reports indicated that direct
effects of RF radiation in experimental animals might
result in increased permeability of the BBB(Freyef al.
1975; Oscar and Hawkins 1977; Albert and DeSantis
1976; Albert 1979b). Other reports indicated that
increased permeability might be mediated by
hyperthermia induced by intense RF fields (Sutton
and Carroll 1979; Merritt et al. 1978; Lin and Lin
1980). Preston et al. (1979) and Preston and
Prefontaine (1980) reported negative findings at
lower power densities. Some of these discrepancies
may be attributed to differences in techniques
employed to assess changes of permeability. These
methodologies consisted of gross examination of
brain slices, fluorescence observations, and mea-
surement of single-passage isotopic tracers and
electron microscopic tracers. All these techniques
have some inherent shortcomings, either in
quantitation or sensitivity. Some of the deficiencies of
these methods have been recently reviewed
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(Blasberg 1979; Segal and Magin 1983). Thus, unless
the changes of permeability are diffuse and
significant, positive results may not be readily
apparent. Further complications with the interpreta-
tion of the data lie in reports that average power
density, peak power, and pulse width may be
important variables affecting the BBB permeability
(Frey et at. 1975; Oscar and Hawkins 1977).
Therefore, one must consider the limitations of the
techniques and the exposure parameters before
reaching conclusions regarding effects of RF radia-
tion on the BBB.
5.4.3 Pharmacological Effects
RF radiation has been reported to alter effects of
drugs that influence CNS functions. Baranski and
Edelwejn (1968) noted altered EEG tracings and
increased effects of Cardiasol, a CNS stimulant, in
persons working in microwave fields. To understand
these observations better they conducted experiments
in rabbits. Administration of 4 mg/kg Phenactil
(chlorpromazine), a depressant of cortical activity,
followed by 3000-MHz (PW) irradiation at 20
mW/cm2 (SAR estimated at 3.0 W/kg) for 20 min,
resulted in desynchronization of the EEG, and
reversal of the synchrony of the EEG seen after
Penactil alone. According to Baranski and Edelwejn
(1968) this result indicated that microwaves
stimulated the brain-stem reticular formation (a path
of multiple short neurons lying in the middle of the
brain), which was inhibited by the chlorpromazine.
Administration of 3 mg/kg Cardiasol (pentylenetetra-
zole, a CNS stimulant and convulsant) following
irradiation or sham exposure of these rabbits resulted
in an EEG change only in the exposed animals. The
authors concluded that microwaves potentiated the
effects of the pentylenetetrazole through pathways
through the center of the brain. Chronic exposure of
rabbits (Baranski and Edelwejn 1968,1974) to 3000-
MHz (PW) radiation at 7 mW/cm2 (SAR estimated at
1.0 W/kg), 3 h/day for 23 to 26 days (a total of 70 to
80 h) resulted in convulsions that were more violent
than after single exposures or in control rabbits. This
result indicated that microwaves acted on the same
thalamic reticular formation areas as did the
pentylenetetrazole. Chronic RF exposure also
resulted in desynchronization and high-amplitude
recording potentials in the EEG. In these studies,
thermal effects of microwaves were considered
unlikely. However, it should be noted that the EEG
records were obtained with screw electrodes
implanted into the skull of the rabbits and that the
pulse modulation characteristics were not specified
in these experiments.
Servantie et al. (1974) investigated the convulsive
effects of a 50-mg/kg intraperitoneal injection of
pentetrazol (pentylenetetrazole) following chronic
exposures of mice to 3000-MHz radiation (PW, peak
power of 600 kW, average power of 350 W, pulse
duration of 1 yus, repetition rate of 525 Hz). The mice
were exposed in groups in the far field in an anechoic
chamber in front of a horn antenna for either 8,15,
20, 27, or 36 days (for an unspecified duration each
day). The mean power density measured in the
absence of the animals was 5 mW/cm2 (SAR
estimated at 5 W/kg). RF radiation affected the .time
to onset of convulsions and the mortality rate.
Nonirradiated mice had a biphasic distribution of
convulsion latency. Mice were equally distributed
between groups with a short and long onset time.
After 15 days of irradiation, a greater proportion of
mice had longer latencies to start pentylenetetrazole
convulsions. However, after 20, 27, or 36 days of
exposure, a greater number of mice had shorter
latencies to convulsion. Mice irradiated for only 8
days were not different from control populations.
Increased incidence of mortality following convulsions
was observed in the groups of mice irradiated for
more than 8 days.
Servantie et al. (1974) also investigated the effect of
curare-like drugs on rats and neuromuscular
preparations of rats irradiated for 10 to 15 days,
presumably under conditions described above (SAR
would be 1 W/kg). They found that irradiated rats
were less susceptible to the paralyzing drugs. Similar
findings were noted in sciatic and phrenic nerve
preparatons from exposed rats. Phrenic nerves
isolated from irradiated rats were paralyzed to a
lesser extent and recovered sooner than those from
control rats.
Goldstein and Sisko (1974) investigated the gross
behavior and EEG of rabbits given pentobarbital and
then exposed for 5 min to 9300 MHz (CW) in an
anechoic chamber at power densities ranging from
0.7 to 2.8 mW/cm2 (SAR estimated at 0.1 to 0.3
W/kg, assuming the rabbits were oriented with the
long axis of their body parallel to the E-field vector).
Five minutes prior to irradiation or sham exposure the
rabbits were injected intravenously with 4 mg/kg of
sodium pentobarbital. No difference was seen in EEG
patterns between control and irradiated rabbits
during the 5-min exposure period. However, after a
latent period lasting from 3 to 12 min following
exposure, periods of EEG and behavioral arousal
lasting as long as 16 min and followed by periods of
sedation occurred in the animals exposed to RF
radiation after the barbiturate, but not in the controls.
Such effects were seen after the lowest power
densities investigated but were more pronounced
after exposure at 2 mW/cm2. Similar effects of
arousal after irradiation were also seen in rabbits
injected with hallucinogens or morphine in place of
the pentobarbital before exposure. In this study the
EEG was recorded with the aid of stainless steel
electrodes implanted before the irradiation.
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A related finding, that of decreased sleeping time in
rabbits following injections of 22 mg/kg sodium
pentobarbital during 2450-MHz or 1700-MHz (CW)
RF irradiations, has been reported (Cleary and
Wangemann 1976). Exposures were in the far field in
an anechoic chamber (Ta=22±0.6°C, RH=40 to 60
percent). The exposure level for this effect was 5
mW/cm2 (SAR estimated at 0.8 W/kg) at 2450 MHz
and 10 mW/cm2 (SAR estimated at 1.3 W/kg) at
1700 MHz. Effective exposures were accompanied by
increased rectal temperatures. However, pentobarb-
ital-injected rabbits kept at an elevated room
temperature (39°C), which resulted in similarly
increased rectal temperatures (+1°C), showed an
insignificant reduction in sleeping time.
Recently, Thomas et al. (1979) reported that acute,
low-level (av 1 mW/cm2)2450-MHz(PW) radiation in
the near field (SAR estimated at 0.2 W/kg)
potentiated the behavioral response to chlordiaze-
poxide (a tranquilizer) in rats. This and other
behavioral studies are discussed in Sec. 5.5.5,
Behavior, Interactions with Other Stimuli.
It can be concluded from pharmacologic studies that
low-level microwaves may elicit a drug-specific
interaction on the nervous system. Such interactions
may prove to be potentially both useful and harmful
as more information becomes available.
5.4.4 Effects on Neurotransmitters
Specific neural systems that contain various
neurotransmitters are known to affect the inhibitory
or excitatory states of the brain. The relative firing
rates of these neuronal systems are reflected in the
turnover of their neurotransmitters. Since RF radiation
has been reported to stimulate and depress the CNS,
several scientists have investigated the effects of RF
radiation on CNS neurotransmitters.
Snyder (1971) made neurochemical measurements
in rats exposed to 3000-MHz (CW) radiation. He
observed that a 1 -h exposure at 40 mW/cm2 (SAR
estimated at 8 W/kg) resulted in a. significant
increase of 5-hydroxyindolacetic acid (5-HIAA) and 5-
HT (serotonin), indicating increased turnover rates of
serotonin in the brain. The opposite effect (that is,
reduced levels of 5-HIAA and 5-HT, indicating
reduced turnover rates of serotonin) was found in
rats exposed at 10 mW/cm2 (SAR estimated at 2
W/kg) 8 h/day for 7 days. The body temperature in
the rats exposed at 10 mW/cm2 rose by 1 to 2°C
during irradiation, and the animals showed signs of
moderate heat stress. Control rats were similarly
handled and restrained but not irradiated. The effects
of the 10-mW/cm2 exposure were compared to those
of conventional radiant heat loads by elevation of body
temperature of rats by 1 to 2°C (by placement in an
incubator maintained at 34°C by thermostatically
controlled incandescent lights) for 8 h/day for 7 days.
No difference was found in the turnover rate of
norepinephrine or 5-HT, or steady-state levels of 5-
HIAA, between conventionally heated and control
animals. Snyder concluded that exposure to RF radia-
tion produced distinctly different effects on 5-HT and
5-HIAA in rat brains from effects produced by
conventional heating.
Zeman et al. (1973) investigated the effects of acute
and chronic exposure of rats to 2860-MHz (PW, peak
power of 60 kW, average power of 300 W, pulse
duration of 1 fjs. repetition rate of 500 Hz) radiation on
brain GABA. Chronic exposures at 10 mW/cm2 (SAR
estimated at 2 W/kg) lasted for 8 h daily for 3 or 5 days
or lasted 4 h for 5 days per week for either 4 or 8
weeks. No significant increase in body temperature
was measured in randomly selected rats immediately
after exposure during the chronic series. Acute
exposures at 40 mW/cm2 (SAR estimated at 8 W/kg)
lasted 20 min, and acute exposures at 80 mW/cm2
(SAR of 16 W/kg) lasted 5 min. Rectal temperature
increased by no more than 3°C, and signs of general
hyperthermia were observed after exposures to
either of these acute conditions. There were no
significant differences in whole-brain GABA levels or
in L-glutamate decarboxylase (the enzyme synthesiz-
ing GABA) activity between control and irradiated
animals after either chronic or acute exposures.
Merritt et al. (1976) reported decreased norepineph-
rine, dopamine, and serotonin in discrete areas of rat
brains after a whole-body exposure for 10 min to
1600-MHz microwaves at 80 mW/cm2 (SAR
estimated at 24 W/kg) that raised rectal temperatures
4.1°C. Hyperthermal control rats were kept at 78°C
for 10 min, which was sufficient to raise rectal
temperatures 3.7°C. Hypothalamic norepinephrine
and dopamine were significantly decreased in
irradiated rats and were decreased (although less
severely) in hyperthermic control rats, as compared
with normotheric controls. Levels of serotonin in the
hypothalamus and striatum of the brain were
unchanged, but serotonin levels in the hippocampus
were decreased only in irradiated rats, and serotonin
levels in the cerebellum and cortex (areas usually low
in serotonin) were decreased only in hyperthermic
control rats. Merritt et al. (1976) concluded that
hyperthermia was responsible for these effects on
neurotransmitters.
In a separate study, Merritt et al. (1977) observed a
significant decrease in norepinephrine and an
insignificant decrease in dopamine in the hypothala-
mus of rats exposed for 10 min to 1600-MHz (CW)
radiation at 20 mW/cm2 (SAR estimated at 6.0
W/kg). but not at 10 mW/cm2 (SAR of 3 W/kg). The
effective exposure produced increased brain and
rectal temperatures, whereas exposure at the lower
5-49
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power density did not. Serotonin inthehypothalamus
was unaffected by exposures up to 80 mW/cm2 (SAR
of 24 W/kg).
Nervous-system effects are summarized in Table 5-
12. There appear to be ample data that suggest
effects of high power densities of RF radiation on the
nervous system of animals. It may be that most of
these effects are the result of thermal effects on the
tissues. The effect of RF radiation on calcium ion
efflux from brain and other tissues is discussed in
Sec. 5.7.5.
5.4.5 Unresolved Issues
There are several difficulties in evaluating alterations
in function of the nervous system that result from
exposure to RF radiation. Minute changes in the
energy distribution due to focusing or scattering
effects could produce changes that may be reflected
in various parts of the body. Electromagnetic energy
may affect the nervous system in many ways. The
electrical and magnetic fields surrounding the
neurons might be directly alterable by externally
imposed fields. Radiation may produce changes in
chemical reactions that could result in a variety of
effects. In addition, small differences in size and
shape among individuals could result in quite
different manifestations of exposure to a given power
density of RF radiation. Observations of anatomical
changes must be made at a time quite removed from
the exposure. Moreover, it is labor intensive to
localize where small anatomical damage might occur.
Neurophysiologists typically record patterns of
electrical activity in either individual neurons or
groups of neurons by inserting metal electrodes fn the
nervous system or on the body and amplifying the
small signals recorded by sophisticated electronic
apparatus. The use of metal in electronic equipment
precludes easy measurement of neuronal functioning
in the presence of electromagnetic fields. Chemical
measurements made by neurochemists are only just
beginning to be understood as indicators of neuronal
functioning. Techniques are only now becoming
available by which minute chemical changes known
to occur in the nervous system as it responds to
specific inputs can be measured.
Investigations of effects of RF radiation on CNS
development have usually examined behavior rather
than the nervous system at the cellular and
subcellular levels. Thus the effects of low-level
exposure to RF radiation on the morphology and
physiology of the adult and developing CNS have not
been adequately studied to permit definitive
conclusions to be drawn. Two morphological studies
have been done by Albert et al. (1981 a,b). In the first
study, he reported permanent loss of cerebellar
Purkinje cells in rat pups after exposure of pregnant
dams to 2450-MHz (CW, SAR of 2 W/kg) and both the
dams and their offspring to 100-MHz (CW, SAR of
2.77 W/kg) radiation. These authors also reported an
apparent reversibility of a decrease in cerebellar
Purkinje cells following irradiation of rat pups 6 to 10
Table 5-12. Summary of Studies Concerning RF-Radiation Effects on the Nervous System*
Exposure Conditions
Effects
Desynchronized EEC
Greater effect of CNS
stimulating drugs
Biphasic effect of latency
to a convulsive drug effect
Decrease effect of paralyzing
drugs
Changes in EEC patterns of
anesthetized animals
Potentiation of drug response
Decreased hypothalamic NE. DA,
and hippocampal serotonin in
hyperthermic animals
Decreased hypothalamic NE,
DA
No effect on neurotransmitter
levels
No effect on GABA content
Swollen neurons in
hypothalamus and subthalamus
Swollen neurons in hypo-
Species
Rabbit
Rabbit
Mice
Rats
Rabbits
Male rats
Rats
Rats
Rats
Rats
Chinese
hamsters
Chinese
Frequency
(MHz)
3000 (PW)
3000 (PW)
3000 (PW)
3000 (PW)
9300 (CW)
2450 (PW)
1600(CW)
1 600 (CW)
1600(CW)
2860 (PW)
2450 (CW)
1 700 (CW)
Intensity
(mW/cm2)
20 (av)
7(av)
5
5
0.7-2.8
1 .0 (av)
80
20,80
10
80
40
10
10
50
25
10
Duration
(days x min)
1 x20
24-26 x 180
8-36 x
Unknown
10-15 x Unknown
1 x5
1 x30
1 x 10
1 x 10
1 x 10
1 xS
1 x20
5x480
40x240
1 x30
22x840
1 x 30-120
SAR
(W/kg)
3.0 (est)
1 .0 (est)
5
1
0.1 -0.3 (est)
0.2 (est)
24 (est)
.6-24 (est)
3.0 (est)
16.0 (est)
8.0 (est)
2.0 (est)
15 (est)
7.5
3 (est)
Reference
Baranski and Edelwejn (1 968)
Baranski and Edelwejn (1968)
Servant le era/. (1974)
Servantie et al. (1974)
Goldstein and Sisko (1974)
Thomas era/. (1979)
Merrittera/. (1976)
Merrittef a/. (1977)
Merritt et al. (1977)
Zeman era/. (1973)
Albert and OeSantis (1975)
Albert and OeSantis (1976)
thalamus and subthalamus
hamsters
5-50
-------
Table 6-12. (Continued)
Exposure Conditions
Effects
Myelm figures in dendrites
6 weeks post -exposure
Increased permeability of
BBS to fluorescein
Myelm degeneration and
metabolic alterations;
glial cell proliferation
Focal areas of increased
BBB permeability to
peroxidase
Increased peroxidase in brain.
absent after recovery period
Increased peroxidase in brain
Brain temperature elevation
(40-45°C|; increased perme-
ability of BBB
Increased permeability of BBB
(mannitol and inulin)
Decreased latency of late
components of thalamic somato-
sensory evoked potentials
Attenuation of monosynaptic
spinal reflex
EEC effects seen after chronic
but not acute exposures
Change of predominant EEG
frequencies
Reversible neuronal morphology
alterations
Mild pyknosis of hippocampal
neurons, increased brain and
rectal temperature
Increased brain serotonin
turnover rate
Decreased brain serotonin
turnover rate
No decrease in cerebellar
purkinje cells in offspring
Decreased cerebellar purkinje
cells after perinatal exposure
Species
Female rats
Rats
Guinea
pigs
Rabbits
Chinese
hamsters
Rats
Chinese
hamsters
Chinese
hamsters
Rats
Rats
Cat
Cat
Rabbit
Cat
Rat
Rat
Rat
Rat
Rat
Squirrel
monkey
Rat
Frequency
(MHz)
2450 (CW;
multimodal
cavity)
1200ICW)
1200(PW)
3000 (CW.PW)
3000 (CW.PW)
3000 (CW;PW)
2800 (CW)
2800 (CW)
2450 (CW)
2450 (CW)
2450 (CW)
1300(CW)
1300(PW)
918 (CW)
2450 (CW)
1-10 (AM)
1-10 (AM)
147(AM)
3000
3000
2450
3000
3000
2450
2450
100
Intensity
(mW/cm2)
10
24
0.2 (av)
3.5
25
5
10
10
10
10
SOW
1.0
0.3 (av)
2.6
3.75 W
60-500
V^/m
90-500
V™/m
1.0
10
10
60-90 W
40
10
10
10
46
Duration
(days x min)
110x300
1 x30
1 x30
90 x 180
1 x 180
90x180
1 x 120
1 x 120
1 x 120
1 x 120
1 x 10-30
1 x20
1 x20
1 x 15
1 x3
1 x 120-180
20-30 x
120-180
Varying
35x30
35x30
1 x 2.5-7
1 x 60
7x480
368 x 180
5x 1260
110x240
SAR
(W/kg)
2.3
1 .0 lest)
0.08 (est)
0.5 (est)
3.5
0.4 (est)
1.9
0.9
2.5
2.5
—
0.4
0.1
2.5
800
10'5 -10~"
10-" -10'3
0.01 5 (est)
2 (est)
2 (est)
head only
8.0 (est)
2.0 (est)
3.4
2.0
2.7
Reference
Switzer and Mitchell (1977)
Freyefa/. (1975)
Baranski (1972b)
Albert (1979b)
Albert and Kerns (1981)
Albert (1977)
Sutton and Carroll (1979)
Oscar and Hawkins (1977)
Johnson and Guy (1972)
Taylor and Ashleman (1975)
Takashima et al. (1979)
Bawinef a/. (1973)
Gordon (1970)
Tolgskaya and Gordon (1973)
Austin and Horvath (1954)
Snvder(1971)
Snyder(1971)
Albert et al. (1981 a)
Albert el al. (1981b)
"AM = amplitude modulation, NE - norepmephrme. DA - dopamme
days postnatally at 2450 MHz. Rats killed immediately
after exposure had a 24-percent decrease in these
cells, whereas those killed 40 days after the
exposures had only an insignificant 7-percent
decrease. No histological examination was made of
other portions of the brains of these rats. In the
second study (Albert et al. 1981 b), no difference was
observed in the number of Purkinje cells in the uvula
of the cerebellum from seven squirrel monkeys
exposed for 3 h, 5 days/week, both prenatally and for
9 months postnatally to a 2450-MHz (CW) field in a
multimodal cavity (SAR calculated to be 3.4 W/kg),
when compared to cell counts in seven control
monkeys. Therefore, the extent of abnormal
development and the conditions of exposure that lead
to such development are still uncertain.
Synergistic and antagonistic effects of RF radiation
with chemical agents that affect the nervous system
have not been investigated in a systematic fashion. In
addition, existing data are quite old, and experiments
utilizing the latest neurochemical measurements and
techniques are lacking. Information on the effects of
chronic and low-level RF-radiation exposure on
neurotransmitters is lacking. Data on microwave-
produced alterations in BBB permeability are
controversial; the effects may be simply due to
increased brain temperature or increased blood flow.
In summary, the state of the art does not permit one to
assume that exposure to low-level RF radiation
produces a significant effect on nervous system
5-51
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morphology, the blood-brain barrier, CNS-active
drugs, or neurotransmitters. Reports of long-term,
low-level exposure on the developing and adult
nervous system are conspicuously absent from the
Western European and the U.S. literature. Higher-
level, acute exposure may alter nervous system
structure and function, but the effects may not be
specific to the nervous system and could be the
consequence of body heating.
5-52
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5.5 Behavior
Michael I. Gage
Behavior has been defined as "anything an organism
does" (Catania 1968), or as "the actions or reactions
of persons or things under specified circumstances"
(Morris 1976). Behavior may also be defined as the
actions of an organism in relation to its environmental
stimuli.
Behavioral effects of RF radiation have been
extensively studied for several reasons. The first is
the reports of experiments (not fully documented with
methods and detailed data analysis) from the Soviet
Union and other East European countries that
behavioral effects of microwaves are seen at
relatively low levels, i.e., 500 //W/cm2 and below at
2375t MHz in rats (Dumansky and Shandala 1974;
Shandala et at. 1977). The second is that behavior
can serve as an index of how the whole organism is
functioning, displaying the status of the nervous
system and many other organ systems of the body as
they act together. Behavior has often been defined as
the final common pathway of the nervous system.
Moreover, behavior can be analyzed in a nonterminal
fashion, without resort to surgically or biochemically
invasive preparatory techniques.
Behavior may be separated into two major categories:
naturalistic and acquired. Spontaneous or naturally
occurring behavior may be innate and is often
species-specific in frequency of occurrence. Examples
of naturally occurring behavior include locomotor
activity, eating, drinking, and mating. Elements of
these behaviors are often acquired.
There are two general categories of acquired or
learned behavior—respondent and operant, which
are distinguished by the procedures used in the
acquisition or conditioning of the behavior. Respon-
dent conditioning occurs as a consequence of the
temporal contiguity between stimuli. Stimuli paired
in time with another stimulus, which reflexively
elicits a response, gradually elicit the response.
Examples of acquired respondent behavior are
salivation and hunger pangs when one is passing a
restaurant or eye blinks to acoustic stimuli.
Responses conditioned by respondent procedures are
usually measured by their occurrence and their
magnitude.
Much complex behavior of human beings and other
higher animals in the course of daily activities can be
viewed as emitted or operant behavior. Operant
conditioning occurs as a consequence of reinforce-
ment that follows the emission of a response.
Reinforcers may be positive (such as food or water), or
negative (such as termination of electric shock or
intense radiant energy). All reinforcers maintain or
increase the frequency of response. By definition, a
positive reinforcer is a stimulus that increases or
maintains the probability of emission of an operant by
its presentation. A negative reinforcer is a stimulus
that increases or maintains this probability by its
removal after emission of the operant. Reinforcement
need not follow the occurrence of each response. It
may be intermittent according to a schedule (i.e., a
schedule of reinforcement). Responses are said to be
conditioned when they have a highly predictable
probability of occurrence. This probability is often
expressed by the average occurrence within a period
of time, or the response rate. Examples of operant
behavior include eating with a knife and fork, driving a
car, or writing a review on behavioral effects of
microwaves.
Operant conditioning may be used to answer specific
questions about behavior that are known to be similar
across species. For example, by reinforcing the
responses in the presence of light of one wavelength
but not reinforcing responses in the presence of light
of any other wavelength, animals can learn to
respond selectively in the presence of light of the first
wavelength. By presenting light at wavelengths close
to the one that is reinforced, one can obtain the
threshold for discriminability of colors.
Specific types of behaviors investigated in behavioral
research are so numerous that no attempt can be
made to describe them all here. Descriptions will be
given of behaviors that have been studied as a
function of microwave exposures. For a more
complete description of behavior as studied by
ethologists and psychologists, the reader is referred
to several standard books (Brown 1975; Hinde 1970;
Honig and Staddon 1977; Kling and Riggs 1971;
Konorski 1967; Pavlov 1960; and Skinner 1953).
Some general statements can be made regarding the
effects of RF-radiation exposure on behavior:
• Some microwave effects have been reported for a
variety of animal behaviors. Most of the studies
have used rats as subjects; only a few have used
mice, squirrel monkeys, and rhesus monkeys.
• Changes in locomotor behavior have occurred
after CW exposures at an SAR as low as 1.2 W/kg
in rats (D'Andrea et a/. 1979). Changes in food and
water intake or body mass have not been
consistently reported at such levels.
• Decreases in rates of ongoing operant behavior
have been seen during exposures at SAR = 2.5
W/kg in rats (de Lorge and Ezell 1980), and
cessation of operant behavior has been seen at an
SAR of 10 W/kg in rats (D'Andrea et al. 1976).
• Alterations in operant performance measured
after exposure was terminated also occurred
with SARs of 2.5 W/kg or more in rats (Gage
1979a).
• The threshold for detection of microwaves may be
as low as 0.6 W/kg in rats (King et al. 1971).
5-53
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However, it is not certain that animals avoid or
attempt to escape from CW microwaves, even at
very high power levels.
• Drug effects on behavior in rats have been
augmented after PW-radiation exposures lasting
0.5 h at average SAR = 0.2 W/kg (Thomas et al.
1979). Behavioral thermoregulation has been
altered after only several minutes of exposure at
SAR = 1.0 W/kg in the rat (Stern era/. 1979)andat
SAR = 1.0 W/kg in the squirrel monkey (Adair and
Adams 1980b).
• Although the same behavioral effects during or
after microwave exposure of the same magnitude
may not be consistently predictable, enough
behavioral changes have been reported after
similar exposures to warrant the conclusion that
behavior is disrupted by microwaves with an
energy input that approximates one quarter to one
half of the resting metabolic rate of many animals.
• When the persistence of behavioral changes
after the termination of exposure has been
investigated, the behavioral alterations reported
were reversible with time after the exposure
ended.
5.5.7 Naturalistic Behavior
Spontaneous locomotor behavior has been studied
with both acute- and chronic-exposure regimens in
the rat. Hunt et al. (1975) found decreased initial
exploratory activity by male Wistar rats after a 30-min
exposure to 2450-MHz fields in a multimodal cavity
(Ta = 24°C, RH from 20 to 40 percent), with power
adjusted to produce an SAR of 6.3 W/kg. The activity
of exposed animals returned to control values within
a 2-h period. The decrease in initial exploratory
activity was the same whether the rat was placed in
the apparatus immediately after or 1 h after exposure
was terminated. Core body temperature was in-
creased to 40.3°C at termination of exposure but
dropped to 37.8°C, within the normal range, 1 h after
exposure. Decreased swimming speed in water at
24°C was also seen in rats that were practiced
swimmers after 30-min exposures to 2450-MHz
fields at SARs of either 6.3 or 11 W/kg. The effects
were seen only after 1.2 km of swimming following a
6.3-W/kg exposure. After an 11-W/kg exposure,
effects were seen immediately for the first few
meters and again after 0.6 km of swimming despite
the fact that water at 24°C would reduce persistence
of a microwave-related hyperthermia.
Robert! et al. (1975), on the other hand, did not see
changes in spontaneous motor activity, as measured
in a glass cage, in male Wistar rats after four different
exposure conditions in the far field of an anechoic
chamber (Ta = 22 ± 1°C, RH = 50 ± 5 percent). The
locomoter activity measured by Robert! et al. may
not have required as much physical effort as
continuous swimming. The four exposure conditions
were (1) 10,700-MHz (CW) fields at 0.6 to 0.9
mW/cm2 (SAR, based on single animal exposures,
can be estimated at 0.15 W/kg) for 185 continuous
hours (24 h daily for 7 2/3 days); (2) 3000-MHz (CW)
fields at 0.5 to 1.0 mW/cm2 (SAR can be estimated at
0.3 W/kg) for 185 continuous hours; (3) 3000-MHz
(PW) fields, 769 pulses/s, at 1.5 to 2.0 mW/cm2 (SAR
estimated at 0.6 W/kg) for 185 continuous hours; or
(4) 3000-MHz (PW) fields, 769 pulses/s at 24 to 26
mW/cm2 (SAR estimated at 8.3 W/kg) for 408
continuous hours (24 h daily for 17 days). After this
last exposure condition, no change was also observed
in running speed during forced runway running by
the rats.
Locomotor activity on a small platform was increased
(as compared with five controls) in five female
Sprague-Dawley rats during the course of repeated
exposures to 2450-MHz (CW) fields in a multimodal
cavity (Mitchell et al. 1977). Exposures of 5-h
duration occurred 5 days weekly for 22 weeks (TB = 24
± 1.5°C). The average SAR was determined to be 2.3
W/kg, which is similar to the SAR at power density of
10 mW/cm2 in a plane-wave environment. The
activity increased within the first week of exposure
and remained high throughout the course of the
exposure period.
Decreases in activity, measured by visual observation,
were reported during repeated exposures of eight
Wistar male rats to 918-MHz (CW) fields in a circular
waveguide (Moe eta/. 1976). Each exposure lasted 10
h (from 2200 to 0800) and occurred nightly during the
dark and usually more active period of the circadian
cycle of a rat for 3 weeks for a total of 210 h (T,= 21.8
± 0.13°C). The range of whole-body average SARs
was measured as 3.6 to 4.2 W/kg (10 mW/cm2
average power density). Most of the decreased
activity occurred shortly after the microwave field
was activated. The exposed rats were stretched out in
a prone position more frequently than control rats in
the early morning hours. In addition, exposed rats
were reported to consume less food than did the
controls over the course of the exposure, even though
their body mass was not different from that of
controls. A repeat of this experiment, where eight
male Wistar rats were exposed 10 h/night for 13
weeks at an average power density of 2.5 mW/cm2
(average SAR = 0.9 to 1.0 W/kg; T. = 21.1 ±0.15°C),
resulted in no differences in food consumption or in
activity measured during the eleventh week (Lovely et
al. 1977). The two studies indicate that a dose-rate-
related threshold for these effects might be somewhere
between 1.0 and 3.6 W/kg. Unfortunately, in the
circular waveguide, the power density is twice the
average on axis and falls off rapidly toward the wall,
which may lead to fluctuating and uncertain
quantitative description of SAR at specific times
during exposure (Guy and Chou 1976).
5-54
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Effects on spontaneous behavior of rats were
reported in two other chronic-exposure experiments.
Both experiments used 15 exposed and 15 control
male Long-Evans rats irradiated during the illuminated
portion of the circadian cycle from 0900 to 1700(8 h),
5 days/week for 16 weeks in an anechoic chamber
with a central monopole antenna and ground plane
(Ta = 22 ± 2°C, RH from 20 to 40 percent). The rats
were adapted to the exposure and testing apparatus
for 4 or 8 weeks before irradiation. In one experiment
(D'Andrea et al. 1979), exposures were to 2450-MHz
(CW) fields at a power density of 5 mW/cm2 (average
SAR = 1.2 W/kg); and in the other (D'Andrea et al.
1980), exposures were to 915-MHz (CW) fields at a
power density of 5 mW/cm2 (average SAR = 2.5
W/kg).
In the study at 2450 MHz, rats showed decreases in
activity as measured on a stabilimetric platform
throughout the course of exposure but increased
running-wheel activity overnight through the course
of exposure. (This latter effect was not significant.) No
significant differences were seen in food and water
intake and in body mass. In the study at 915 MHz,
exposed rats showed increased activity as measured
both in the running wheels and on the stabilimeter.
Again, no significant changes in food and water
intake or body mass were observed.
Rudnev et al. (1978) reported effects of exposure of
25 male albino rats to 2375-MHz (CW) fields at 0.5
mW/cm2 (SAR estimated at 0.1 W/kg for individual
animal exposure) for 7 h daily for 1 month. Open field
activity was measured in irradiated rats and in 25
controls as the number of squares crossed in 3 min on
2 successive days. The count on the first day was
defined as exploratory activity, and on the following
day, as motor activity. Shock-induced aggression was
measured by observation of battles between an
exposed and control rat. Maintenance of balance on a
rotating treadmill (dynamic-load endurance) and on
an inclined rod (static-load endurance) was measured,
as was the amount of food consumed in 20 min after
23 h of deprivation. Electrodermal skin sensitivity
was measured as the voltage of 100-Hz square-wave
electrical stimulus that was needed to elicit paw
withdrawal from the metal bars on the cage floor. The
above measurements were made at the start of the
series of exposures and again prior to irradiation
periods on the 10th, 20th, and 30th days of exposure,
and every 15 days for 3 months after exposure.
A significant reduction in food intake, time on the
treadmill, and in time on the inclined rod was seen by
the 10th day of exposure. Exploratory activity was
significantly decreased, and shock sensitivity was
increased after 20 days of exposure. At the end of
exposure, exploratory and motor activity, time on the
inclined bar, and shock sensitivity were significantly
decreased. The latency to start eating when food was
presented was increased for 30 days after exposure
ended. Time on the treadmill was reduced for 15 days
after the termination exposure. Exploratory activity
was increased throughout the 3-month postexposure
period. Sensitivity to electric shock was reduced
significantly on the 30th and 60th day after exposure
ended and was still below control levels on the 90th
day.
5.5.2 Learned Behavior
5.5.2.1 Respondent Conditioning
Currently, there appear to be no reports by U.S.
investigators of microwave exposure altering
respondent behavior, although the description of an
experiment that used RF radiation as an unconditional
stimulus has been published. Some studies using
respondent conditioning techniques that report
changes in behavior as a consequence of microwave
exposure appear in the Soviet literature (e.g.,
Dumansky and Shandala 1974; Lobanova 1974).
Unfortunately, details regarding exposure conditions
or behavioral methodology and results are too
sketchy to permit inclusion in this review. An attempt
was made to use microwave exposure as an
unconditional stimulus in one experiment (Bermant
et al. 1979). A 30-s presentation of a 525-Hz tone
that preceded 2450-MHz sinusoidally modulated
microwaves that were either presented for 10 s (SAR
= 420 W/kg) or 30 s (SAR = 220 W/kg), or that
preceded an electric shock to the tail, produced rises
in rectal temperature of 0.7, 0.5, or 0.37°C,
respectively, during a base-line period over the
course of 10 conditioning sessions at an unspecified
Ta. Control female Sprague-Dawley rats presented
with the tone alone showed a decrease of 0.47°C in
rectal temperature during this period. The microwave
exposure itself was designed to produce an increase
in rectal temperature of 1.5°C. Aside from this study
there are no reports of microwaves altering
respondently conditioned behavior in which exposure
parameters allow clear determination of the SAR.
5.5.2.2 Operant Conditioning
There is a large body of literature that examines
alterations of operant behavior produced by micro-
waves for which SAR values have been, or can be,
determined.
Reduction in response rates on an operantly
conditioned task has been observed during the course
of microwave irradiation. Rats were trained to lever-
press for food pellets on a random-interval, 30-s
schedule. After behavior on this task stabilized, the
rats showed a response rate that was in general
linearly uniform and typical of random- or variable-
interval schedule-controlled performance. The rats
were then exposed to microwaves under each of
several conditions in sessions lasting 25 min, or until
the rat's response rate fell below one third of its base-
line control rate. In an initial experiment (D'Andrea er
5-55
-------
a/. 1976), six male Long-Evans rats were exposed to
360-, 480-, or 500-MHz (CW) fields (Ta from 21.1 to
22.2°C, RH from 12 to 40 percent) in a parallel-plate
apparatus at an incident power density of 25
mW/cm2 with the long axis of the rat parallel either to
the electric-field vector or to the vector of wave
propagation. Responding was reduced only during
exposures to 500-MHz fields when the .long axis of
the body was parallel to the electric-field vector.
Behavior stopped abruptly after ~11 min of exposure,
and upon removal from the apparatus the animals
appeared flaccid, wet, and, according to the authors,
heat stressed. At this exposure, the SAR was
comptued from the measured 0.16°C/min rise in
rectal temperature to be ~ 10 W/kg. Exposures that
produced no change in behavior had SARs ranging
from 5 to 6 W/kg.
In a second experiment (D'Andrea etal. 1977), these
results were confirmed and extended. Exposures
were conducted in a monopole-above-ground
radiation chamber and lasted for up to 55 min, or until
responding on the random-interval schedule fell
below one third of the base-line rate. Exposures of
five male Long-Evans rats for periods up to 55 min to
400-, 500-, 600-, and 700-MHz (CW) fields at 20
mW/cm2 power density (Ta = 22± 1 °C; RH = 50 ±1.5
perent) yielded a U-shaped function of time to the
criterion reduction in rate, with the minimum of ~ 23
min at 600 MHz when rectal temperature increased
0.09°C/min (SAR estimated at 16.4 W/kg). At the
time they stopped responding, all rats appeared heat
stressed and were engaged in spreading saliva on
their fur. Six additional rats, exposed to 600-MHz
(CW) fields at power densities of 5, 7.5, 10, and 20
mW/cm2, showed decreased times to stop their
responding at power densities above 7.5 mW/cm2
when rectal temperature increased- 0.04°C/min or
more. At 10 mW/cm2 (SAR estimated at 7.5 W/kg)
the rats stopped responding after—45 min, and rectal
temperature increased 0.04°C/min. Three rats
exposed to PW microwaves with 170 mW/cm2 peak
and 5.1 mW/cm2 average power density showed no
change in performance. As in the earlier experiment
of D'Andrea et at. (1976), response reduction was
abrupt and was correlated with the rectal temperature
increase.
A series of experiments by 'te Lorge (1976,1979) also
examined alterations in operant performance during
exposure to microwaves. In most 'of these experi-
ments, the schedule of reinforcement was used to
measure observing and detection responses in an
operant task. Two levers were present in a testing
chamber or in front of a primate restraint chair made
of Styrofoam and sheet plastic for optimal trans-
parency to microwaves. Responses on the right lever,
called observing responses, produced either a low- or
a high-frequency acoustic signal. The high-frequency
signal was scheduled to occur on a variable interval of
either 30 or 60 s. If the animal made a response on the
left lever when the high-frequency signal occurred—
a detection response, it received a food pellet as a
reinforcer. Observing responses occurred at fairly
linear response rates, a pattern similar to that seen on
variable interval schedules of reinforcement.
In the first experiment (de Lorge 1976) five male
rhesus monkeys (Macaca mulatta) showed no change
in behavior on this schedule during 1 or 2 h of
exposure to 2450 MHz in the far field of an anechoic
chamber (Ta from 21 to 24°C, RH = 70 ± 15 percent)
when power densities ranged to 16 mW/cm2 (SAR
estimated at 1.2 W/kg). The field was 100-percent
amplitude modulated at 120 Hz. Three of these
monkeys showed reduced rates of observing
response during 1-h exposure to this field at 72
mW/cm2 (SAR estimated at 5.0 W/kg) but not at 32,
42, 52, or (in two monkeys) 62 mW/cm2. At 72
mW/cm2, rectal temperatures rose ~ 2°C and were
still increasing at the end of the hour-long session.
The animals moved more in their chairs after 20 min
and were observed to take short naps after — 30 min
at this power density. When observing responses
decreased, reaction time to respond on the left lever
increased.
In the second experiment (de Lorge 1979) four male
squirrel monkeys (Saimeri sciureus) were tested and
exposed to 2450-MHz 120-Hz modulated microwaves
under conditions similar to those described above at
10, 20, 30, 40, 50, 60, and 70 mW/cm2 (T. = 22.5 to
23.2°C, RH = 57 percent during 0.5-h exposures and
74 percent during 1 -h exposures). No reduction in the
mean rate of right lever observing responses > 1
standard deviation belqwthe mean of the control rate
was seen at any power density during the 30-min
exposures. But brief pauses in responding were seen
at microwave onset and offset at 50 mW/cm2 and
above (SAR estimated at 2.75 W/kg). At this power
density rectal temperature rose > 1°C. Three of the
monkeys were also given 1-h exposures. Graphic
representation of data from one monkey showed
observing response rate decreased more, and this
decrease began earlier, in sessions at the higher
power densities (de Lorge 1979, Figure 6). One of the
three monkeys exhibited an increase of response rate
as power density increased. After microwave
exposure, all monkeys also showed decreased
responding that was directly related to the power
density during the exposure. These decreases were
apparent for a 30-min period following exposure but
gradually returned to base-line values. All monkeys
showed increases in frequency of incorrect respond-
ing on the left lever for food, which was a direct
function of power density. Changes in behavior
consistently occurred only at power densities of 40 to
50 mW/cm2 at a time when rectal temperatures had
risen by > 1 °C.
5-56
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In a third experiment (de Lorge and Ezell 1980), eight
male Long-Evans rats were exposed in an anechoic
chamber (Ta varied from 23 to 26.5°C, RH from about
50 to 52 percent) to 5620-MHz (PW) fields at 662
pulses/s, and then to 1280-MHz (PW) fields at 370
pulses/s. They were tested on the behavioral task of
vigilance during exposures (SARs were reported at
0.19 W/kg per mW/cm2 at 5620 MHz, and 0.25
W/kg per mW/cm2 at 1280 MHz). Rates of observing
responses during exposures to 1280-MHz fields
decreased somewhat at 10 mW/cm2 (average power
density) and decreased markedly after 15 to 20 min
during 15 mW/cm2. At 5620 MHz, rates of observing
responses decreased only during exposures at 26
mW/cm2 and above. Behavior decrements occurred
at SAR = 2.5 W/kg at 1280 MHz but required SAR =
4.9 W/kg at 5620 MHz.
In a related experiment (Sanza and de Lorge 1977),
four male Sprague-Dawley rats were trained to
respond on a fixed-interval 50-s schedule for food
pellets as reinforcers. With this schedule, the first
response emitted 50 or more seconds after arrival of
the last food pellet produced another food pellet.
Exposures for 60 min to 2450-MHz, 120-Hz
modulated fields at 37.5 mW/cm2 in the far field of an
anechoic chamber (Ta = 24 ± 0.6°C, RH = 70 ± 5
percent) produced decreases in response rates that
had a fairly abrupt onset. The response decrements
were seen only in two rats that had high base-line
rates and not in two rats with low response rates.
Exposures at 8.8 and 18.4 mW/cm2 produced no
decrements in performance. All rats spent more time
at the wall opposite the food cup during 18.4- and
37.5-mW/cm2 exposures than during sham or 8.8-
mW/cm2 exposures. The SAR was not given but is
estimated at 3.7 W/kg at 18.4 mW/cm2 and 7.5
W/kg at 37.5 mW/cm2.
Responding of three male rhesus monkeys trained to
a high level of proficiency on a visual tracking task
was not disrupted by exposures at 10 or 20 mW/cm2
to 1200-MHz (CW) fields (reported SAR estimated at
0.8 and 1.6 W/kg; Ta = 27 ± 3°C, RH = 50 ± 3 percent)
during behavior sessions lasting ~ 2 h (Scholl and
Allen 1979).
Some other studies have looked at changes in
previously learned operant behavior at the termination
of single or multiple exposure periods. Thomas et a/.
(1975) trained four male Sprague-Dawley rats to
respond on a multiple schedule. One component was
fixed ratio 20 (FR20): Every 20th response on the right
lever was reinforced by a food pellet. The other
component was a differential-reinforcement-of-low-
rate of 18 s with a limited hold of 6 s (DRL 18 LH 6):
Responses on the left lever separated by at least 18 s,
but by no more than 24 s, were reinforced.
Components alternated on an irregular basis. Only
one of the schedules was in effect during a given time
period. Exposures to microwaves lasted for 30 min.
and behavioral testing began 5 to 10 min after
exposure. Exposure parameters were as follows: 5,7,
15, and 20 mW/cm2 to 2450-MHz (CW) fields; 5, 10,
15, and 20 mW/cm2 to 2860-MHz (PW) fields at 500
pulses/s and 1 -fjs pulse width; and 1, 5, 10, and 15
mW/cm2 to 9600-MHz (PW) fields at 500 pulses/s
and 1-yt/s pulse width. All rats were exposed to all
parameters while restrained in the far field of an
anechoic chamber. In general, response rates
increased on the DRL schedule and decreased on the
FR schedule. Increased rates on the DRL schedule
were seen following exposures to 9600-MHz fields at
5 mW/cm2 and above (SAR estimated at 1.5 W/kg),
to 2450-MHz (CW) fields at 7.5 mW/cm2 and above
(SAR estimated at 2.0 W/kg), and to 2860-MHzf ields
at 10 mW/cm2 and above (SAR estimated at 2.7
W/kg). Decreased response rates on the FR schedule
were observed following exposures to all frequencies
at 5 mW/cm2 and above (SAR estimated at 1.5 W/kg
for 9600 MHz, and 1.4 WAg for 2450 and 2860
MHz). Increased response rates during time-out
periods between components were seen following
exposures to all three frequencies at 5 mW/cm2.
Time-out responses peaked and then dropped after
exposures at higher power densities.
In a second study, Thomas et al. (1976) trained four
male Sprague-Dawley food-deprived rats on a fixed-
consecutive-number-eight (FCN 8) schedule. With
this schedule, at least eight presses had to be made
on the right lever before depression of the left lever
would yield a food pellet reinforcer. If the rat made
fewer than eight consecutive responses on the right
lever before switching, the count was restarted at
zero. Well-trained rats were tested after 30-min
exposures in the near field at 5,10, and 15 mW/cm2
to 2450-MHz (PW) fields at 500 pulses/s, and 1 -//s
pulse width. Because exposures were in the near
field, SAR cannot be precisely estimated but may be
assumed at 0.4 W/kg for each 1 mW/cm2 (Durney et
al. 1980). The percentage of eight or more consecutive
responses on the right lever (reinforced runs)
decreased, and the length of these runs decreased
after all exposures. Those decreases were direct
functions of power density. However, the overall rate
of responding and the running rate (i.e., the rate after
the first response following reinforcement) hardly
decreased during these postexposure sessions.
Gage (1979a) reported decreases in response rates
of eight adult male Sprague-Dawley rats trained to
alternate between levers either 11 or 33 times for a
food-pellet reinforcer. The decrements occurred in
sessions following overnight, 15-h exposures (Ta =
22°C, RH = 50 percent) to 2450-MHz(CW)f ields at 10,
15, and 20 mW/cm2, but not after exposures at 0.5
and 1.0 mW/cm2. Only very small decrements were
seen after 55-min exposures at power densities up to
30 mW/cm2. (The SAR measured in rats under
similar exposure conditions was0.3 W/kg for each 1
mW/cm2.)
5-57
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Discrimination was tested immediately after 30 min
of irradiation in 10 well-trained, young adult male
Wistar rats (Hunt et al. 1975). Exposures produced
SARs of 0.0, 6.5, and 11.0 W/kg at 2450 MHz
(modulated in a quasi-sinusoidal fashion at 120 Hz in
a multimodal cavity at Ta = 24°C, RH from 20 to 40
percent). All rats were exposed at both SAR values,
but the sequence of exposures was varied. The task
required the rats to obtain saccharin-flavored water
reinforcers by pressing a bar when a light flashed, and
by not pressing a bar when a sonic stimulus was
presented. One of the two stimuli was presented
every 5 s, and the light was presented 12.5 percent of
the time. Rats exposed at both SARs had an increased
number of omission errors (i.e., failures to respond to
the light after exposure), but there were no increases
in errors of comission (i.e., responding wrongly when
the noise was presented). The failure to respond
correctly was more frequent at the start of the
session, as well as after exposure at the higher SAR.
Schrot et al. (1980) experimented with three male
albino rats trained to learn a new sequence of
pressing three levers for food reinforcers daily in a
repeated-acquisition procedure. The rats increased
their number of errors and decreased their rate of
sequence completions when tested immediately after
30-min exposures to 2800-MHz (PW) fields (500
pulses/s, 2-fis pulse width) at 5 and 10 mW/cm2
average power density (Ta = 21 ± 1.5°C). No effects
were seen at lower average power densities of 0.25,
0.5, and 1 mW/cm2. Peak powers were 0.25,0.5,1,5,
and 10 W/cm2 in these exposures. The rats were
exposed in a sleeve holder with the electric-field
vector perpendicular to the long axis of the animal's
body. The reported SARs based on temperature
measurements were 0.7 and 1.7 WAg at 5 and 10
mW/cm2, respectively.
Operant behavior has also been examined during or
following the course of chronic microwave exposures
in some reports also described in Sec. 5.5.3,
Naturalistic Behavior. Mitchell era/. (1977)measured
performance on two schedules in separate groups of
rats pretrained before the start of 22 weeks of 5-h
exposures, 5 days/week, to 2450-MHz fields (aver-
age SAR at 2.3 W/kg) in a multimodal cavity (T. = 24 ±
1.5°C, RH = 50 ± 10 percent). Five exposed and five
control female Sprague-Dawley rats were tested for
30-min sessions on a schedule of multiple FR5
extinction for 15 s (MULT FR5 EXT 15 s). When a
white lamp was on, every fifth response was
reinforced by a food pellet, but during periods when
the lamp was off, no responses were reinforced.
Although the control rats had higher response rates
during the FR component, this difference was not
significant. Exposed rats had higher response rates
than controls during the extinction component, and
this difference was statistically significant. The ratio
of response rate during the FR5 component to
response rate during the EXT15 component was
significantly different in exposed as compared with
control rats: Exposed rats exhibited a higher ratio,
indicating poorer discrimination over the course of
exposure, although they had a value like that of the
control rats before irradiation began. Another
schedule, Sidman avoidance, was used to test escape
and avoidance response. Five exposed and four
control rats were trained to postpone an unsignaled
2.0-mA foot shock for 15 s (response-shock interval)
by pressing a lever. During 30-min sessions, the
animals received a shock every 0.5 s (shock-shock
interval) until they pressed the lever. No significant
effects of microwave exposures were seen with this
schedule, although improvement in avoidance was
seen in all rats both within and over the course of
testing sessions.
Conditioned taste aversion was studied in experiments
where rats were exposed chronically to 918-MHz fields in
circular waveguides at 10 mW/cm2 (Moe et al. 1976)
and 2.5 mW/cm2 (Lovely era/. 1977). Rats were given
a saccharin solution to drink in place of water during
the microwave exposure period. Presumably, if the
saccharin were drunk in conjunction with an agent,
such as microwave radiation, which made the rat sick
or produced a yet unspecifiable effect, a connection
would be learned between the drinking of the agent
and the consequences, and the solution would be
avoided in the future. The investigators measured
preference after exposure by allowing a water-
deprived rat to choose between drinking the
saccharin solution and water for 20 min. In the
experiment at 2.5 mW/cm2 (Lovely et al. 1977),
saccharin preference was tested only from the 9th to
the 13th week of exposure. No difference between
exposed and control rats was seen in amount of
saccharin solution consumed either at 2.5 mW/cm2
(average measured SAR at 1.0 W/kg) or at 10
mW/cm2 (average measured SAR at 3.9 W/kg).
Several studies have investigated the ability of
animals to detect or to take behavioral action to
minimize, avoid, or escape from microwaves. In an
early paper, King et al. (1971) showed that three
irradiated and three control male albino rats could
respond to 2450-MHz microwaves doubly modulated
at 60 and 12 Hz as the conditioned"stimulus in a
measure of conditional suppression. The microwave
radiation was presented in a multimodal exposure
cavity (T, = 24 ± 2°C, RH from 20 to 40 percent). In this
experiment, rats were reinforced with sugar water on
a random interval schedule for licking at a water tube.
At various times during each 2-h session either a
525-Hz tone or the microwaves were presented for 1
min, and an unavoidable 0.5-s electrical foot-shock
followed. Conditioned suppression to the tone was
reliably indicated by no licks being emitted during the
tone. Microwave dose rates of 0.6,1.2, 2.4,4.8, and
6.4 W/kg were substituted for the tone in some
sessions. During irradiation at SAR = 0.6 W/kg one of
three rats suppressed responding, at SAR = 1.2 W/kg
5-58
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two rats suppressed, and at SAR = 2.4 W/kg all three
suppressed reliably.
Johnson et al. (1976) trained two male Wistar-
derived rats to nose poke in a restraint for food pellets
on an FR5 schedule in the presence of an acoustic-
pulse stimulus of 7.5 kHz, 10 pulses/s, 3-//s pulse
duration for 3-min periods, which alternated with 3-
min periods of no stimulation during which nose
pokes were not reinforced (extinction). When
microwaves at 918 MHz (10 pulses/s, 10-//S pulse
durations) were presented for 30-s intervals during
an extinction period, or when microwaves were
substituted for the auditory stimulus during
reinforced periods, response rates were observed
that were similar to those seen in periods when the
acoustic stimulus was present. The energy density
per pulse of microwaves was 150 fjj/cm2, and the
average power density was 15 mW/cm2. (The SAR
would be near 7.5 W/kg if the rats were in the far
field.)
Detection of microwaves does not imply that there are
affective properties of this stimulus, i.e., that they
hurt or feel good. In fact, such detection may be
further evidence of the RF hearing phenomenon(Frey
and Messenger 1973). Indeed, in several experiments
in which PW microwaves are presented during
exposure, the alteration in behavior of the exposed
animal might be due to effects of acoustic stimulation
by the microwave pulses. Such experiments should
have as a control the presentation of pulsed auditory
stimuli.
Frey et al. (1975) experimented with female Sprague-
Dawley rats exposed to 1200-MHz (PW) fields at 1000
pulses/s (0.5-s pulse duration) at an average power
density of 0.2 mW/cm2 (SAR estimated at 0.2 W/kg)
and a peak power density of 2.1 mW/cm2. Six rats
spent only 30 percent of a 30-min period of exposure
in an unshielded half of a Styrofoam shuttle box
during the last 2 of 4 successive daily exposures. Six
other rats exposed to 1200-MHz (CW) fields at 2.4
mW/cm2 (SAR estimated at 2.2 W/kg) spent 52
percent of the time in the unshielded half of the box
on these days. Six other control rats spent 64 percent
of the 30-min period in the unshielded half. Only the
rats exposed to PW microwaves could be said to
escape from the stimulus or exhibit a modest
preference that would decrease their exposure. A
similar finding was also reported by Frey and Feld
(1975) to occur in male rats during exposures to a
1200-MHz (PW) field at 100 pulses/s at 0.4 or 0.9
mW/cm2 average power densities (SAR estimated at
0.4 and 0.81 W/kg, respectively) and at 133 or 300
mW/cm2 peak power densities (Ta=22°C). These rats
spent an average of only 29 percent of their time in the
unshielded half during seven 90-min sessions, and
this side preference was maintained throughout all 7
days. Sham-irradiated rats spent an average of 57
percent of their time in the unshielded half of the box.
Two groups of eight male Wistar rats spent more than
half of each of nine weekly hour periods in the side of
a shuttlebox when occupancy of that side kept a PW
microwave field turned off (Hjeresen et al. 1979). The
2880-MHz field was pulsed at 100 pulses/s (3.0-//S
pulse width) with a 9.5-mW/cm2 average and 33-
mW/cm2 peak power density (SAR calculated at 2.1
W/kg). The exposure was in the far field of an
anechoic chamber (Ta from 22 to 24°C, RH from 20 to
50 percent). A group of eight rats that could not
extinguish the field and another group that received
no microwaves showed no side preferences.
Preference for occupancy of the side that extinguished
the field increased across each weekly session as
judged from the data in Table 1 of Hjeresen et al.
(1979). Statistically significant preferences for
the unexposed side occurred during the hour periods
of weeks 2, 4, 6, and 8, during which times the
original positions of the exposed and unexposed sides
of the shuttlebox were reversed. Substitution of a
37.5-MHz (PW) acoustic stimulus for the microwaves
in one session resulted in the rats spending most of
the session in the side that kept the acoustic
stimulus off. A continuously occurring broadband
"pink" noise in the anechoic chamber prevented
appearance of side preference in two other groups. In
addition to confirming that rats &void or escape from
pulsed microwaves, this experiment suggests that
pulsed microwaves may be detected as an auditory
stimulus.
Monahan and Ho (1976) showed that male CF1 mice
irradiated for 10 or 15 min at 2450-MHz(CW)fields in
a waveguide (TB = 24 ± 0.5°C, RH = 50 ± 1.5 percent)
when forward-power levels were stabilized at 0.4,
0.8,1.6, 2.4, 3.2, 4.0, or 4.8 W exhibited a decline in
energy absorption rate at 2.4 W and above. This
decline usually occurred within the first 5 min of
exposure and stabilized toward the latter part of the
period. Monahan and Ho interpreted the results to
show that the rats changed their behavior to minimize
exposure to the microwaves. However, they did not
directly measure any animal behavior. During the
first 5 min of exposure the SARs measured in this
apparatus ranged from 7.7 to 65.7 W/kg. The lowest
SAR at which the mice clearly altered their rates of
energy absorption was 28 W/kg. In a second study
Monahan and Ho (1977) showed that the SAR
associated with reduction of absorption during 20min
of irradiation (RH = 50 ± 1.5 percent) decreased
reliably from 43.6 W/kg when ambient temperature
was 20°C, to 0.6 W/kg when ambient temperature
was 35°C. The reduction in absorption was greater
with higher forward-power levels at any given
temperature. Forward powers used were 1.62 to 3.84
at20°C, 1.12 to 3.11 at 24°C, 0.42 to 2.45 at 30°C.
and 0.004 to 0.40 at 35°C. The mice did not altertheir
energy absorption at SARs of 28 W/kg or below until
temperature was 30°C or higher.
5-59
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Videotape observations of rats and mice exposed to
2450-MHz (CW) fields at 15 mW/cm2 for 1 h in the far
field below a radiating horn in an anechoic chamber
did not reveal any preferential behavior that
minimized whole-body absorption rates through
parallel orientation to the magnetic- as opposed to the
electric-field vector (Gage et al. 1979). These
observations occurred at ambient temperatures of 22
or 28°C (RH = 50 percent) while the animal was held
in a cuboid or cylindrical enclosure. Usually, the
animals assumed a curled, sleep-like posture in the
hour before the microwaves were turned on and
maintained that posture throughout most of the expo-
sure period. However.mice exposed at 28°C more
often assumed positions that were oriented parallel to
either of the two field vectors than positions oriented
in other directions. The SAR of the rats without any
enclosure was 3.3 W/kg at 15 mW/cm2, independent
of their orientation. The SAR of the mice when
parallel to the electric-field vector was 12.3 W/kg,
and the SAR when the mice were parallel to the
magnetic-field vector was 6.2 W/kg, without any
enclosure. The animals changed positions more
frequently when some difference in SAR existed
relative to the position assumed.
Rats cannot easily learn to escape from or avoid high-
intensity electromagnetic radiation. Carroll et al.
(1980) reported that 20 female Long-Evans rats did
not go to a marked-off floor area in a multimodal
cavity to reduce the intensity of 918-MHz microwaves
(modulated at 60 Hz with 3-Hz mode stirrer
modulation) from 60 W/kg to either 40, 30, 20, or 2
W/kg (Ta = 21.1 ± 2°C; RH = 53 ± 10 percent). The
mean number of entries into the marked-off "safe"
area and the percentage of time spent there during
22-min sessions were not different when the
microwaves were on (for five 2-min periods) or off.
SARs > 60 W/kg were associated with lethality
within 8 min of continuous exposure in tests of a
separate group of rats. However, in the same
apparatus 10 rats quJckly learned to escape from an
800-//A electric foot shock by going to this marked-off
area within a 22-min session. Shocked rats would
remain in this area over 90 percent of the session
time. A later study (Levinson et al. 1982), extending
these findings, showed that rats spent significantly
more time in the marked "safe" area (which when
entered extinguished radiation and light) on the fifth
day of repeated light and microwave pairings when
microwave radiation was accompanied with the
photic stimulus than when the radiation was
presented without the light. Groups of four female
Long-Evans rats were exposed to a 350-lux stimulus
light alone, microwave radiation alone (918 MHz
modulated at 60 Hz with a 3-Hz mode stirrer
modulation at 60 W/kg in the same multimodal cavity
used by Carrol et al. [1980]), the microwave radiation
in combination with the light, or faradic shock (800
//Arms) to the feet and tail during alternate 2-min
periods of five successive 22-min daily sessions. The
average time spent in the marked area on the last day
(of 1320 s maximum) was about 100 s for rats
receiving light, 300 s for rats receiving microwave
radiation alone, about 700 s for rats receiving
radiation plus light, and about 1200 s for rats
receiving shock alone. Additionally, acquisition
curves indicated rats were learning to escape from
both the microwave radiation presented alone and in
combination with light over the course of the
sessions, but escape learning occurred sooner in the
rats given the multiple stimulus.
Sanza and de Lorge (1977) noted that their rats first
tried to jump out of a testing chamber and then
assumed a stationary position after failing to escape
during exposures to 2450 MHz at 37.5 mW/cm2 (SAR
= 7.5 W/kg).
5.5.3 Interactions with Other Stimuli
Interactions of microwaves with two other types of
stimuli have been reported to affect behavior. One
type of stimulus is chemical, specifically, several
commonly used psychoactive drugs; the other is
physical, e.g., ambient temperature during exposure.
Response rates of rats performing on a fixed-interval
1 -min schedule of reinforcement beginning 0.5 h
after 2.5- to 20-mg/kg dosages of chlordiazepoxide
(Librium) (Thomas et al. 1979) were increased over
control values. These increases were further
augmented if an exposure at an average power
density of 1 mW/cm2 to a 2450-MHz (PW)field (500
pulses/s, 2-/us pulse width, 100-mW/cm2 peak
power density; Ta = 23 ± 2°C) occurred in the half hour
between the injection and behavioral testing. In a
second study (Thomas and Maitland 1979), the dose-
response function of rats given d-amphetamine
sulfate was shifted to a lower range after exposure to
microwaves with the same parameters and conditions
of exposure as those mentioned above. The shift to a
lower range of the dose-response function indicated
an increased potency of the drug. After microwave
exposure, as opposed to sham exposure, given
changes in response rate were produced by lower
drug doses. Rats in this second study were reinforced
for responses separated by more than 18s(DRL18 s).
Although the rat was in the near field in these studies,
and the exposure field may not have been as uniform
as if it were in the far field, the average SAR
measured in a Styrofoam-insulated water model was
0.2 W/kg. Thomas and Maitland (1979) also showed
that 0.5-h exposure to microwaves, at the parameters
indicated above, 4 days/week when amphetamine
was not administered, shifted the dose-response
function of this drug to a lower range when it was
administered on the fifth day of the week when a
microwave exposure did not occur. In both of these
studies, exposure to microwaves alone or after saline
injection had no effect on behavior. The shift to a
lower range of a dose-response function indicated
5-60
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that an exposure to microwaves, which by itself did
not affect behavior, acted synergistically with
chlordiazepoxide or amphetamine to increase the
sensitivity of the organsm to the drug. Similar results
have not been seen with chlorpromazine or with
diazepam (Valium), an analog of chlordiazepoxide, in
experiments in the same laboratory (Thomas et al.
1980).
In a related experiment, Monahan and Henton (1979)
showed that chlordiazepoxide and, with less
consistency, chlorpromazine and d-amphetamine
altered response rates of mice trained in an operant-
conditioning procedure to escape from or to avoid
2450-MHz (CW) fields at an average dose rate of 46
W/kg (Ta = 24 ± 0.5°C; RH = 50 ± 1.5 percent).
Although this experiment showed that drug effects
can interact to alter microwave exposure effects, the
design of the experiment does not allow any conclu-
sion to be drawn about interactions between drugs
and microwaves on performance.
Interactions with ambient temperature and humidity
were predicted by Mumford( 1969). Monahan and Ho
(1977) showed that reduction in the rate of energy
absorption by mice exposed in a waveguide to 2450-
MHz (CW) fields occurred at a low dose rate of 0.6
W/kg when ambient temperature was 35°C but
required higher doses at lower ambient temperatures.
Although the mice were not directly observed, the
authors presumed the mice reoriented in the
microwave field to reduce the amount of absorbed
energy.
Gage (1979b) showed that overnight exposures at 5,
10, or 15 mW/cm2 to 2450-MHz (CW) fields (SAR =
0.2 mW/g per mW/cm2) at an ambient temperature
of 28°C (RH = 50 percent) reduced operant response
rates of male Long-Evans rats measured the morning
after exposure was terminated. Similar exposures
when ambient temperature was22°C did not result in
reduced response rates except after exposure at the
highest power density. The rats were reinforced with
food on a random interval 1.33-min schedule.
Response rates in control sessions that did not follow
exposures ranged from about 0.25 to over 2
responses/s for the 1 2 rats but were consistent over
sessions for each rat.
Two reports have indicated that mammals alter
thermoregulatory behavior in the presence of as little
as 5 mW/cm2 of 2450-MHz (CW) microwaves. In one
(Stern et al. 1979), six male rats were trained to press
a lever to switch on an infrared (IR) heat lamp for 2 sin
a cold chamber (Ta from 3.9 to 5.3°C). Microwaves at
power densities as low as 5 mW/cm2 reduced the
rate of responding for the heat lamp. The reduced
response rate occurring shortly after microwave
onset was a direct function of power density in the
range of 5 to 20 mW/cm2 and returned to base-line
values when microwaves were switched off. The rats
were exposed in a far field (SAR = 0.2 W/kg per
mW/cm2) in which the distribution of power densities
varied within 11 percent of the mean value.
Adair and Adams (1980b) showed that thermoregula-
tory behavior of the squirrel monkey (a New World
primate found in equatorial jungle areas) was
significantly altered at power densities as low as 6
mW/cm2 in the far zone of a 2450-MHz (CW) field
within 10 min of onset of exposure. In this study, the
monkeys were trained to select a preferred ambient
air temperature by making an operant response to
obtain 15 s of 55°C air when the air was otherwise
15°C or to obtain 15 s of 15°C air when the air was
otherwise 55°C. Preferred air temperatures ranged
between 35 and 36°C without microwaves and
decreased as a direct function of the microwave
power density during exposure. (The SAR in this
experiment was determined calorimetrically on
saline models to be 0.2 W/kg per 1 mW/cm2.) As in
the experiment by Stern et al. (1979) with rats,
preferred temperatures returned to base-line levels
when the microwave field was extinguished.
In conclusion, there is ample evidence to suggest that
microwaves alter a variety of unlearned and learned
behaviors occurring during and after exposures. In
most cases the behavior change can be described as a
reduction in the level of ongoing activity. However,
there are some situations in which increased activity
has been seen. When measured, the magnitude of
behavioral change seems to be related to the power
density or SAR of the exposure. Behavioral changes
usually revert to base-line levels after removal of the
microwave field. The above studies of behavioral
effects caused by microwave exposure are summa-
rized in Table 5-13.
5.5.4 Unresolved Issues
Most unresolved issues regarding behavioral effects
of microwaves arise because observed findings have
not been verified within the same laboratory or in
other laboratories. Repeating a study involves high
cost and the risk of failure to confirm a finding due to
small unnoticed differences, e.g., between standard
procedures in two laboratories. Possibly for these
reasons verification has not been often attempted.
However, verification and systematic replication
would allow determination of the limits of conditions
within which a behavioral effect may be expected, as
well as definition of the range of conditions adequate
to observe a threshold of effect.
There is no unifying hypothesis to explain all the
observed behavioral changes. The research on
interaction between microwaves and chemicals has
not been verified in independent laboratories, and it
has not been extended to determine whether the
interaction is limited to particular classes of
compounds. Delineation of differences between
effects of single and multiple exposures would help
5-61
-------
Table 5-13. Summary of Studies Concerning RF-Radiation Effects on Behavior
Exposure Conditions
Effects
Decreased exploratory activity
an swimming speed. AT increase
2.5°C
No effect on spontaneous activity
or activity and forced running
Increased locomotor activity
Decreased spontaneous activity and
food intake
No effect on spontaneous activity
or food intake
Decreased activity on stabilimetric
platform, no significant increase
in wheel running
Increased activity on stabilimetric
platform and in wheel running
Decreased time on treadmill and
inclined rod, decreased exploratory
activity, increased then decreased
shock sensitivity. Decreased
activity and shock sensitivity
persisted 90 days after exposure
Rectal temperature rise = 0.37°C
before start of test, AT = 1 .5°C
with microwaves
Response decreased during exposure
on random interval schedule (lowest
intensity for effect. AT = 1 .8°C)
Response decreased during exposure
(maximum effect) on random
interval schedule, AT = 1 .8°C
Decreased observing responses
on vigilance task, AT = 2°C
No effect on observing responses
Decreased observing responses
on vigilance task
No effect on observing responses
Decreased observing responses
on vigilance task
Response rate decreased on fixed
interval schedule in rats with
high base-line rates, spending time
away from lever
No effect on response rate
No effect on visual tracking task
Response rate decreased on FR and
increased on DRL schedules
Decreased length of runs and fewer
remforcers on FCN schedule
Decreased response rate on FR
operant schedule
Increased rate of missed observing
responses on vigilance task
Decreased rate of responding on
repeated acquisition task
Increased response rates in
extinction, decreased stimulus
control, no effect on Sidman
avoidance
Species
(Weight, g)
Young male
rat
Male rat
(160-180)
Female
rat (307)
Male rat
(360-410)
Male rat
(316-388)
Male rat
(350-375)
Male rat
(350-375)
Male rat
Female
rat
Male rat
(350-380)
Male rat
(357-382)
Male rhesus
monkey
(4kg)
Male squirrel
monkeys
(850-950)
Male rat
(362-400)
Male rat
(290-340)
Male rhesus
monkey
(6.2-7.9 kg)
Male rat
(120 days.
150?)
Male rat
(250-300)
Male rat
(284-439)
Young male
rat
Male rat
(275)
Female
rat
Frequency
(MHz)
2450 (PW.
multimodal cavity
120 Hz. AM)
10700(CW)
3000 (CW)
3000 (PW)
3000 (PW)
2450 (CW, multi-
modal cavity)
918ICW)
918(CW)
2450 (CW)
915(CW)
2375 (CW)
2450 (PW, multi-
modal cavity.
60 and 1 2 Hz AM)
500 (CW)
600 (CW)
2450
(120 Hz, AM)
2450
(120H,. AM)
1280(PW)
5620 (PW)
2450
(120 Hz. AM)
1200ICW)
2450 (CW)
2860 (PW)
9600 (PW)
2450 (PW)
2450 (CW)
2450 (PW,
AM, multimodal
cavity)
2800 (PW)
2450 (CW,
multimodal
cavity)
Intensity
(mW/cm'l
?
0.6-0.9
0.5-1.0
1 .5-2.0
24-26 (av)
10
10
2.5
5
5
0.5
25
10
72
16
50
10
26
37.5
8.8-18.4
20
5
5
5
5
10
5
10
Duration
(days x min)
1 x30
7.7 x 1440
7.7 x 1440
7.7 x 1440
17x 1440
110x300
21 x 600
91 x 600
80x480
80x480
30 x 420
10x0.17
10x0.5
1 x 11
1 x55
1 x60
1 x20
1 x30
1 x60
1 x60
1 x40
1 x40
1 x60
1 x60
1 x 120
1 x30
1 x30
1 x30
1 x30
1 x900
1 x30
1 x30
110x300
SAR*
(W/kg)
6.3
0.2
0.3
0.6
8.3
2.3
3.6
1.0
1.2
2.5
0.1
420
220
10
7.5
5.0
1.1
2.8
0.6-1.7
2.5
4.9
7.5
1.8-3.7
1.6
1.4
1.4
1.5
?
2.7
6.5
0.7
2.3
Reference
Hunt eta/ (1975)
Robert, era/ (1975)
Mitchell et at. (1977)
Moeetal (1976)
Lovely era/. (1977)
D'Andrea et al. (1979)
D'Andrea « a/. (1980)
Rudnevef a/. (1978)
Bermant et al. (1979)
D'Andrea et al. (1976)
D'Andrea et al. (1977)
deLorge(1976)
deLorge(1976)
deLorge(1979)
deLorge(1979)
de Lorge and Ezell
(1980)
Sanza and de Lorge
(1977)
Sanza and de Lorge
(1977)
Scholl and Allen
(1979)
Thomas et al. (1975)
Thomas et al. (1976)
Gage (1979a)
Hunt era/. (1975)
Schrot era/. (1980)
Mitchell er al. (1977)
5-62
-------
Table 5-1 3. (Continued)
Effects
No effect on flavor aversion test
No effect on flavor aversion test
Microwaves detected as stimulus
Microwaves detected as stimulus
Spending more time in shielded vs.
unshielded compartment
Spending equal time in shielded vs.
unshielded compartment
Spending more time in shielded vs.
unshielded compartment (occurrred
in first of 7 sessions)
Spending more time in unirradiated
compartment
Decrease in SAR at 24°C
Decrease in SAR when ambient
temperature increased from 20°C
to 35°C
No preferential orientation of rats
or mice in far field of plane wave
Cannot take specific action to
reduce intensity of irradiation
Augmentation of increased
response rates produced by
chlordiazepoxide
Shift to lower doses of
d-amphetamine on dose-response
curve for DRL schedule
No effect on dose response curve
for chlorpromazine or diazepam
Chlordiazepoxide reduced responses,
decreased avoidance responses, and
increased escape responses to
microwaves
Response rate decreases were
augmented after exposures at
higher ambient temperatures
Reduced responding for heat lamp
in a cold room
Selection of a lower ambient
air temperature
Species
(Weight, g)
Male rat
(360-410)
Male rat
(316-388)
Male rat
(409-427)
Male rat
(300-350)
Female
rat
Female
rat
Male rat
(250)
Male rat
Male mouse
(30-34)
Male mouse
(30-34)
Male rat
(200-360)
Male mouse
(25-33)
Female
rat
(290)
Male rat
(325-375)
Male rat
(250-300)
Male rat
(360-380)
Male mouse
(35-44)
Male rat
(315-365)
Male rat
(325-450)
Squirrel
monkey
(750-1100)
Frequency
(MHz)
918ICW)
918(CW)
2450 (PW,
120 Hz, AM,
multimodal
cavity)
918IPW)
1200(PW)
1200ICW)
1200IPW)
2880 (PW)
2450 (CW)
2450 (CW)
2450 (CW)
2450 (CW)
918(PW,
60 Hz, AM,
multimodal
cavity)
2450 (PW)
2450 (PW)
3800 (PW)
2450 (CW)
2450 (CW)
2450 (CW)
2450 (CW)
Exposure Conditions
Intensity Duration
(mW/cm2) (days x mm)
10 21x600
2.5 91 x 600
1 x 1
15 1 xO.5
0.2 4 x 30
2.4 4 x 30
0.4 1 x 90
9.5 9 x 60
1 x 15
1 x20
15 1 x60
15 1x60
5x2
1 1 x30
1 1 x30
1 4x30
1 1 x30
1 x30
10 1 x 930
5 1 x 15
6 1x10
SAR'
(W/kg)
3.9
1.0
0.6-2.4
7.5
0.2
2.2
0.4
2.1
28
43.6-0.6
3.3
6.2-12.3
(depending on
orientation)
60
0.2
0.2
0.2
0.2
46
2.0
1.0
1.0
Reference
Moeera/. (1976)
Lovely era/. (1977)
King era/. (1971)
Johnson era/. (1976)
Frey et al. (1975)
Frey era/. (1975)
Frey and Fold ( 1975)
Hjeresen er al. (1979)
Monahan and Ho (1976)
Monahan and Ho (1977)
Gage era/. (1979)
Carroll et al (1980)
Thomas era/. (1979)
Thomas and Maitland
(1979)
Thomas era/. (1980)
Monahan and Henton
(1979)
Gage (1979b)
Sterner al. (1979)
Adair and Adams (1980b)
•If measured SAR was not reponed, SAR was estimated when possible.
determine whether effects of chronic exposure are
qualitatively different from repeated measurement of
effects of each single exposure.
Behavioral experiments have used only a limited
sample of microwave exposure conditions. Exploration
of frequency spectrum, modulations, waveforms, and
interactions between waves of different parameters
has hardly begun. Most behavioral work has used rats
as subjects. Animals more like humans in physical
size and shape have been studied only infrequently to
help extrapolate findings to humans. Specific
conditions of exposure in addition to the microwave
stimulus, such as ambient temperature and humidity,
have not been consistently controlled and reported
so that their influence on behavior may be
determined. There is no information on exposure
effects of specific or limited areas of the body in
comparison to total-body exposure to evaluate the
effects of localized energy absorption.
5-63
-------
5.6 Special Senses
Joe A. Elder
5.6.1 Cataractogenic Effects
A cataract is an opacity in the crystalline lens of the
eye. These lens defects may be clinically insignificant
or may cause partial or total blindness. The following
conclusions may be drawn from animal experiments
on the cataractogenic potential of RF radiation (Tables
5-14 and 5-15):
1. RF radiation is cataractogenic if exposure is of
sufficient intensity and duration.
2. For single acute exposures, the threshold
intensity for cataract production exceeds 100
mW/cm2. Multiple exposures at intensities near
threshold values for single acute exposures
results in lens opacities.
3. The cataractogenic potential of RF radiation varies
with frequency; the most effective frequencies
appear to be microwave frequencies in the 1 - to
10-GHz range.
4. Similar ocular effects are produed by CW and PW
radiation of the same average intensity.
5. In contrast with the above conclusions, which are
based on acute, near-field exposures to the eye or
head, no cataracts have been reported in
unrestrained animals after far-field exposure at
power densities near lethal values or in rabbits
exposed at 10 mW/cm2 (2450 MHz) for 180 days.
Although the RF power density for cataract
induction for long-term exposure of animals
(including humans) has not been defined, the
threshold is, most probably, significantly higher
than that required to induce many other
physiological changes.
The review of the literature on human cataracts is in
Sec. 5.10, Human Studies.
5.6.1.1 Microwave Radiation in Experimental
Cataractogenesis
The rabbit eye has been the experimental model most
often used in animal studies because of its similarity
in size and anatomy to the human eye (Figure 5-3). Its
diameter is ~ 75 percent that of the human eye; the
cornea is as large, and although the lens is thicker, its
diameter is the same as that of the human eye. In a
typical study (Carpenter et al. 1960b), one eye of an
^anesthetized rabbit was exposed to microwave
'radiation in the near field, and the nonirradiated eye
served as the control. The eyes were then examined
at various intervals by an ophthalmoscope, slit-lamp
biomicroscope, or both instruments. The earliest
positive reaction in t!~iis type of study, occurring
within 24 to 48 h after a cataractogenic exposure, is
the appearance of one or two narrow translucent or
milky bands in the posterior cortex of the lens, just
under the capsule, which extends no further than the
lens equator. These bands can be seen only by slit-
lamp examination with an angled beam. If the ocular
injury is minimal, no further change occurs, and the
cortical banding disappears within a few days.
Otherwise, in 2 to 4 days after exposure small
granules appear in the region of the suture of the
posterior lens. If a more intense reaction occurs,
larger numbers of granules appear over a larger area
within the next few days, and small vesicles may
develop. These early changes may develop further
and become either well-defined circumscribed or
diffuse cataracts. These changes in the lens remain
as permanent ocular defects. In general, it has been
found that microwave cataracts in rabbits involve
only the posterior cortex of the lens, unless the
exposure is so intense that the opacity extends
throughout the lens.
At exposure levels that cause cataracts, other ocular
reactions also occur, but they are transient and differ
in severity with the intensity and duration of the
exposure. Examples include swelling and chemosis
of bulbar and palpebral conjunctivae, pupillary
constriction, hyperemia of iris and limbal vessels, and
vitreous floaters and filaments (Carpenter 1979).
5.6.T.2 Exposure Threshold Values for Cataracts
Following the publication of reports demonstrating
that microwaves can cause cataracts in experimental
animals (Richardson et al. 1948; Daily era/. 1950a,b),
three laboratories (Williams et al. 1955; Carpenter et
al. 1960b; Carpenter and Van Ummersen 1968; and
Guy et al. 1975a) published time vs. power-density
threshold curves for cataract induction in rabbits by a
single exposure to near-field 2.45-GHz radiation. The
time vs. power-density threshold curves originally
published by the three laboratories are similar in
shape but are quantitatively different. The more
recent studies found lower threshold values than
those reported by Williams et al. (1955). This finding
probably reflects differences in the irradiation
method and in techniques used to measure power
density. In fact. Carpenter (1979) has determined that
his power densities were 50 percent higher than
originally published. His corrected data are plotted in
Figure 5-4 along with the results of Williams et al.
(1955) for comparison. Guy et al. (1975a) replicated
Carpenter's work for single acute exposures with
essentially the same results, and also quantified the
threshold of cataractogenesis in terms of SAR (Figure
5-4). For example, these workers found the
cataractogenic threshold for a 100-min exposure, the
longest period of irradiation, to be 150 mW/cm2 (138
W/kg peak absorption) (Figure 5-5).
The cumulative effect of microwave radiation on
cataractogenesis in the rabbit has been examined by
repeated irradiation of the eye at power densities
below the threshold for single acute exposures
(Carpenter 1979). For example, daily 1 -h exposures at
5-64
-------
Table 6-14. Summary of Studies Concerning Ocular Effects of Near-Field Exposures
Exposure Conditions
Effects
Cataract
Cataract
Cataract and other
ocular effects
No cataract
Cataract
Cataract
Cataract and other
Species
Rabbit
Rabbit
Rabbit
Rabbit
rabbit
Rabbit
Rabbit
Frequency
(MHz)
5,500 (CW and PW)
800 (CW)
4,200 (PW)
4.600 (PW)
5,200 (PW)
5,400 (CW and PW)
5,500 (CW and PW)
6,300 (PW)
2,450 (CW)
2,450 (CW)
2,450 (CW)
2,450 (CW)
10,000 (CW)
2,450 (CW)
Intensity Duration
(mW/cm2) (days x min)
470-785* 1 x 2-100
785*
785*
785*
500-785*
500-785*
500-785*
785*
x25
x17
x15
x5-12
x3-4
x2-3
x5
180* 1 x240
120-180 20x60
75 20 x 60
150 1 x100
295 1 x 30
375 1 x30
180 1 x140
SAR
(W/kg)
300-500t
500t
500t
500t
350-500t
300-500t
300-500t
500t
138tt
100tt
Reference
Birenbaum et al. (1969a)
Birenbaum era/. (1969b)
Carpenter (1979)
Carpenter (1979)
Guy era/. (1975a)
Hagan and Carpenter ( 1 976)
Kramarera/. (1978)
ocular effects
Second- to third-degree Rhesus 2,450 (CW)
nasal burns; no ocular Monkey
effects
No cataract; keratitis Rabbit 35,000
(inflammation of cornea) 107,000
300
40
40
x22
x60
x60
115tt
>175#
>238#
Kramarera/. (1978)
Rosenthal era/. (1976)
'Estimate of average power density calculated by dividing the microwave power by the irradiated area (d = 1.27 cm) of the eye.
tEstimate based on the assumption that ail the incident power was absorbed by the eye (2 g).
ttMaximum SAR in the eye. «
//Estimated SAR values for the cornea. (See text for discussion of Rosenthal et al. studies of frequency specificity.)
Table 5-15. Summary of Studies Concerning Ocular Effects of Far-Field Exposures
Exposure Conditions
Effects
Species
Frequency
(MHz)
Intensity
(mW/cm2)
Duration
(days x min)
SAR
(W/kg)
Reference
No ocular effects, including no
lenticular changes
Acute ocular changes, e.g.,
hyperemia of lids and conjunctiva,
meiosis, anterior chamber flare,
engorgement of iris vessels, and
periorbital cutaneous burns; no
lenticular changes
Rabbit
3000 (CW) 100, 200 1 x 15, 30
300, 400,
500
x15
14, 28* Appleton et al. (1975)
42, 56*
70*
Death
No catarats
No cataracts
No ocular effects
No ocular effects
Rabbit
Rabbit
Rabbit
Monkey
(M. mulattaj
385 (CW)
385 (CW)
468 (CW)
2450 (CW)
2450 (CW)
9310(PW)
300
500
60
30
60t
10
10
1 50 (av)
1 x30
1 x15
10x 15
10x90
10x20
5 x 480
(x 8- 17 weeks)
180 x 1380
30-40 x 294-665ft
42*
70*
48*
24*
8.1
1.5*
17#
Cogan et al. (1958)
Ferri and Hagan (1976)
Guy era/. (1980b)
McAfee era/. (1979)
'Estimated average whole-body SAR values (Durney et al. 1978, Figure 31).
tWaveguide average whole-body exposure.
ttTotal exposure time in minutes for the entire 30- to 40-day experimental period.
//Maximal SAR in head.
5-65
-------
Figure 5-3. Cross-sectional sketch of the human (left) and the rabbit (right) eye (from Birenbaum ft al. 1969a, Figure 1).
f Ciliary Body
Retinas
Choroid
Sclera
Fovea
Optic
Nerve
Central
Artery and
Vein of Retina
Suspensory
Ligament
of Lens
Iris
Lens
Cornea
Anterior
Chamber
Posterior
Chamber
Conjunctiva
Ciliary Body
Cornea
Lens
Anterior
Chamber
Optic
Nerve
Vitreous Body Conjunctiva
Vitreous
Body
Posterior
Chamber
180 mW/cm2 for 13 to 20 days were found to be
cataractogenic in 8 of 10 animals, whereas single
exposures at this power density were not effective. At
150 mW/cm2, 4 of 10 rabbits gave a positive
response after 18 to 32 daily exposures. No cataracts
were observed after 20 daily 1 -h exposures at 75
mW/cm2.
The power densities used in the cumulative-effect
experiments were only slightly lower than those that
cause cataracts after a single exposure (Figure 5-4).
For example, the lowest effective power density (120
mW/cm2) given for 1 h daily for 20 to 24 days
produced only one positive response in nine animals
(See Table I in Carpenter 1979). But that would be a
"thermalizing" level if extended to the whole body. If
the entire body of an unanesthesized rabbit is
exposed at power densities similar to those that
cause cataracts under near-field conditions, the
animal exhibits signs of acute stress; Appleton et al.
(1975) reported that rabbits became heat stressed
and struggled out of the field during a 15-min
exposure at 100 mW/cm2. This report is described in
more detail in Sec. 5.6.1.4, along with other
experiments in which no evidence of cataracts was
observed in animals exposed in the far field. In one of
these studies, Guy et al. (1980b) found no change in
the eyes of rabbits exposed at 10 mW/cm2 (2450
MHz) for 23 h/day for 180 days. Although a
cumulative effect on the lens of rabbits has been
described by Carpenter and his colleagues at high
exposure levels, the report by Guy et al. (1980b)
provides evidence against such an effect at power
densities <10 mW/cm2.
5.6.1.3 Frequency Specificity
As indicated above, most studies of experimental
cataractogenesis were conducted at 2.45 GHz, but
5-66
opacities in rabbit eyes have been reported after near-
field exposures at 0.8,4.2,4.6,5.2,5.4,5.5,6.3, and
10 GHz (Birenbaum et al. 1969a,b; Hagan and
Carpenter 1976). In several studies, the cataracto-
genic potential of different frequencies was
addressed. For example, after Hagan and Carpenter
(1976) determined the relative effects of 2.45- and
10-GHz (CW) radiation on the rabbit eye, they
concluded that the cataractogenic potential for single
acute exposures is greater at the lower frequency. At
both frequencies, the opacities were characteristically
located in the posterior subcapsular cortex of the
lens, although the initial appearance and subsequent
development differed. These differences probably
reflect differences in the pattern of absorbed
microwave energy in the eye due to the different
depths of penetration of the radiation at these two
frequencies.
Guy et al. (1974,1975a) measured the distribution of
absorbed energy in rabbit eyes exposed to 918- and
2450-MHz radiation and found the patterns to be
significantly different. At 2450 MHz, energy
absorption was maximal in the vitreous body at a
point midway between the posterior surface of the
lens and the retinal surface (Figure 5-5). The locus of
peak absorption thus correlates well with the
observation of irreversible changes in the posterior
cortical lens. Exposure to 918-MHz fields in a
specially devised cavity resulted in relatively uniform
absorption in the eye, but maximal absorption was
only ~ 25 percent of the peak absorption at 2450 MHz
(Figure 5-6). Therefore, one would expect the
threshold for cataractogenesis in rabbits exposed to
918 MHz to be considerably higher than the threshold
at 2450 MHz. But more important, at 918 MHz, peak
absorption in the rabbit brain was 36 percent higher
than in the eye. It is possible that lens effects or ocular
-------
Figure 6-4. Time and power-density threshold for cataracto-
genesis in rabbits exposed to near-field 2450-MHz
radiation; values of maximal SAR are also given
(from Guy et al. 1975a, Figure 7).
700'
600-
-500H
o
x
Jsoo-l
l_
0>
£200-1
100-
Carpenter et al. (1960b, 1979)
Williams et al. (1955)
Guy et al. (1975a)
20 40 60 80
Exposure Time (min)
600
-500
^400
C
300 «
a
E
200
-100
100
Figure 6-5.
1.25-1
Distribution of energy absorption rate (W/kg) per
mW/cm2 incident power density in the rabbit's eye
and head exposed to 2450-MHz radiation (from
Guy et al. 1974, Figure 3).
E
o
$ 1 00-|
E
I
5*0.75-
5
0.50-
0.25-
0.00
Posterior Pole
Retina
— Cornea
-i 1 1 =»>-
1234
Depth from Cornea! Surface (cm)
changes may not occur before more severe damage
occurs in other sensitive tissues, such as the brain,
during exposure to 918-MHz fields.
Both Hagan and Carpenter (1976) and Guy et al.
(1975a) used exposure systems that applied
microwave energy across an air space to the eye, and
both reported lenticular cataracts in the posterior
Figure 5-6.
0.30-,
Distribution of energy absorption rate (W/kg) per
mW/cm* incident power density in rabbit's head
and eye exposed to 918-MHz radiation (from Guy
atal. 1974. Figure 27).
E
i
0.25-
§ S
^_ m
5 0.20 H
EC
C
o
0.15-
-L
0
234
Depth from Cornea! Surface (cm)
subcapsular cortex. Birenbaum et al. (1969b)
produced cataracts in the anterior cortex of rabbit
lens with an exposure system that applied PW
microwaves to the cornea! surface. Furthermore, as
the frequency decreased from 6.3 to 5.2 to 4.6 to4.2
GHz, longer exposure times at a constant field
strength were required to produce lens defects.
Under similar experimental conditions, even longer
exposure times were required to induce cataracts at a
lower frequency, i.e., 0.8-GHz (CW) radiation.
Furthermore, Birenbaum et al. (1969a) found no
substantial difference in the cataractogenic threshold
values for CW and PW 5.5-GHz radiation and
concluded that the average, not the peak, rate of
energy absorption determines whether lens injury
will occur. The peak power density of the pulses was
1000 times greater than the estimated average
power densities shown in Table 5-14.
Rosenthal et al. (1976) examined the effects of 35-
and 107-GHz radiation on the rabbit eye. At both
frequencies keratitis (inflammation of the cornea)
occurred at lower intensities than required to produce
any other demonstrable ocular effect, such as lens
injury (cataract) or iritis. Irradiation at 107 GHz was
more effective in producing immediate cornea!
damage, but this change was generally gone by the
next day. Effects at 35 GHz were persistent, were
almost always present the next day, and were
associated with marked injury to the cornea!
epithelium. Effects on the cornea correlate well with
the pattern of microwave-energy absorption because
most of the energy at these high frequencies is
absorbed in the outer regions of the eye. The earliest
stage of keratitis or minimal cornea! stromal injury
occurred after a 30-min exposure at an incident
5-67
-------
power of 50 mW or after a 60-min exposure at 25
mW. Estimates of the rate of energy absorption in the
eye at the lower incident power (25 mW) are 35 mW
at 35 GHz and 47.5 mWat 107GHz(Rosenthalera/.
1976); therefore, the average SARs of a rabbit eye
weighing 2 g are 17.5 and 23.8 W/kg, respectively.
Since maximal absorption occurs in the outer
structures of the eye, the SAR in the cornea is
estimated to exceed the average SAR of the eye by
more than one order of magnitude.
Although the above data cannot be compared directly
because of widely varying experimental procedures,
these results indicate that the potential for cataract
induction in rabbits is higher in the frequency range
between 1 and 10 GHz than at either lower or higher
microwave frequencies. Power densities that would
cause cataracts at frequencies below 1 GHz and
above 10 GHz give rise to insult in other ocular sites
and extra-ocular tissues. Rosenthal et al. (1976)
found that 35- and 107-GHz radiation primarily
affected the outer structure of the eye, the cornea
for example; and at 918 MHz, Guy et al. (1974)
showed that maximal energy absorption occurred in the
brain, not in the eye.
The effects of near-field microwave exposures on the
rabbit eye have been summarized by Cleary (1980) as
follows:
The induction of cataracts in experimental animals,
principally New Zealand white rabbits, has been
described by a number of investigators using a
variety of microwave exposure modalities. Gene-
rally microwave field intensities necessary for
cataract induction in the rabbit are such that acute
whole body exposures would be lethal due to
hyperthermia. Most cataract studies have, there-
fore, employed focused or near-zone fields which
limit exposures to the head or eyes. Localized
thermal trauma is still of such a magnitude to
necessitate the use of general or local anesthesia.
Cornea! irrigation with physiological saline
solutions have also been used to prevent corneal
damage due to tissue dehydration during microwave
exposure. Anesthesia and corneal irrigation, as
well as air temperature and humidity, may
significantly affect the temperature of ocular
structures.
The experimental results strongly suggest that
radiation-induced temperature elevation may be
essential for the cataractogenic effect of microwaves.
Additional evidence for this position has been
provided by Kramar et a I. (1975), who reported that
rabbits kept under general hypothermia during
irradiation at known cataractogenic levels of 2.45-
GHz (near-field) radiation did not develop cataracts.
This study is described more fully in Sec. 5.6.2.
Kramar et al. (1978) did a comparative study of the
cataractogenic threshold and SAR patterns in the
eyes of rabbits and rhesus monkeys exposed in the
near field at 2450 MHz. In this experiment, the
radiator was designed to simulate a leaky microwave
oven door. In rabbits, a time and power-density
threshold curve for cataractogenesis was found that
was similar to earlier results (see Figure 5-4), and the
peak SAR occurred within the lens. These authors
reported that the microwave exposure caused
immediate effects similar to those described by
Carpenter era/. (1960b), i.e., constricted pupil, dilated
conjunctiva! and iris vessels, a turbid anterior
chamber, and a milky band in the posterior cortex of
the lens.
The monkey eye was irradiated at 400 mW/cm2 for
30 or 60 min or at 500 mW/cm2 for 60 min with the
applicator centered, over one eye. Following these
exposures at time and power density values that
exceeded those required to produce cataracts in
rabbits, no lens opacities were observed in three
monkeys for a period of 13 months. At the highest
exposure, lid edema, contracted pupil, and changes in
the anterior chamber were noted. It is interesting that
the SAR pattern in the monkey eye revealed that the
peak SAR occurred in the anterior chamber and not in
the lens. Additional evidence for a marked difference
in the pattern of energy absorption in the monkey was
the observation that the exposures caused varying
degrees of nasal burns in the three animals. A fourth
monkey was exposed to an applicator centered
between the eyes. An exposure of 300 mW/cm2 for
22 min caused second- to third-degree burns on the
nasal bridge, but the eyes were not affected.
These results show that exposure conditions that
cause cataracts in rabbits do not induce cataracts in
monkeys. Monkey eyes are better shielded by facial
bones and tissues than rabbit eyes. Because of the
different anatomical features, the peak SAR, i.e., peak
temperature increase, was not observed at the
posterior surface of the lens. For example, the peak
retrolental temperature following an exposure of 300
mW/cm2 was only40.2°C in the monkey but 45.1°C
in the rabbit. Kramar et al. (1978) stated that an
additional factor that helps explain the differential
effects on the eyes of rabbits and monkeys might be
the relative as well as the absolute size of the lens.
The anterio-posterior diameter of the adult rabbit lens
is ~ 7 mm, which represents almost one-third of the
eye's diameter. In the rhesus monkey and man, the
eye is larger but the lens is about 4 mm thick (Figure
5-3).- The smaller lens is probably more effectively
cooled by the larger pool of surrounding fluid. Since
the facial features and eye structure of human beings
are more like those of the monkey than those of the
rabbit, extrapolation of the results with monkeys is
more useful. Based on studies at 2450 MHz, one may
conclude that under conditions of acute exposure, the
threshold for cataracts in monkeys, and presumably in
human beings, is greater than the threshold for
rabbits. The reader should note that the report by
5-65
-------
Kramar et al. (1978) vividly describes a number of
other clearly undesirable effects, e.g., facial burns,
that occur at subthreshold conditions for cataracts in
monkeys.
5.6.1.4 Far-field Exposure Studies
In contrast with the acute, near-field exposures that
can cause cataracts and other ocular effects,
cataracts have not been produced in rabbits whose
entire bodies were exposed to radiation in the far field
(Table 5-15). Appleton et al. (1975) exposd anesthe-
tized rabbits to far-field radiation at 3000 MHzfor 15 or
30 min at 100 or 200 mW/cm2. No ocular changes
were observed during or immediately after exposure.
Fourteen daily examinations and four weekly
examinations, followed by monthly examinations for
1 year, revealed no lenticular changes. During
exposure at higher levels (300,400, or 500 mW/cm2
for 15 min) animals exhibited acute ocular changes
consisting of hyperemia of lids and conjunctiva,
meiosis, anterior chamber flare, engorgement of iris
vessels, and periorbital cutaneous burns. Subsequent
examinations revealed no morphologic lenticular
abnormalities. The authors concluded that "It is
noteworthy that one year after a single microwave
exposure, sufficient in intensity to cause both thermal
cutaneous and acute gross ocular effects, no lens
changes or cataracts were observed." It is also
noteworthly that these power levels and durations
were well above the cutaneous sensation level,
because unanesthetized animals became heat
stressed and struggled out of the field during a 15-
min exposure at 100 mW/cm2. Exposures at 300
mW/cm2 for 30 min or 500 mW/cm2 for 15 min were
lethal to some of the rabbits.
Ferri and Hagan (1976) exposed unanesthetized
rabbits to 2450-MHz (CW) radiation in the far field at
10 mW/cm2,8 h/day, 5 days/week for 8 to 17 weeks.
Weekly examinations of the eye showed no abnormal
changes during the study, and no post-irradiation
changes were observed during the following 3
months. Guy et al. (1980b) exposed four rabbits
individually (2450 MHz, 10 mW/cm2)for 23 h/day for
180 days; the peak SAP in the head was 17 W/kg. An
equal number of animals were sham-exposed. The
authors stated that "Aside from normal aging
changes found in the lenses of the 8 animals, no
differences were noted in the eyes of the two
groups."
Cogan et al. (1958) found no cataracts in rabbits 4
weeks after exposure at 385 MHz; the rabbits were
irradiated twice weekly for 5 weeks at 60 mW/cm2 for
15 min or 30 mW/cm2 for 90 min. Six weeks after
exposure in a waveguide, no cataracts were observed
in rabbits irradiated at 468 MHz, 60 mW/cm2 (SAR =
8.1 W/kg), for 10 days (20 min daily). Although the
authors reported that the exposure levels at both
frequencies were near lethal values, the 8.1-W/kg
SAR is considerably lower than the value other
investigators have found to be sublethal to rabbits
(Table 5-15). The environmental conditions (tempera-
ture, airflow, etc.) within the waveguide were not
given; therefore, one must assume that the ambient
conditions were significantly different from normal
values or that the measured SAR is in error.
McAfee et al. (1979) trained unfettered monkeys
(Macaca mulatta) to expose their faces and eyes to
9.31-GHz (PW) radiation at 150 mW/cm2 average
power density (peak power density = 300 W/cm2).
Over a period of about three months, the animals
were irradiated for a total of 294 to 665 min during 30
to 40 daily sessions. No cataracts or cornea! lesions
were observed in these monkeys during a 1-year
period following irradiation.
5.6.2 Unresolved Issues
Exposure of the rabbit eye to microwave radiation at
sufficient power densities and durations causes an
immediate increase in intra-ocular temperature, and
after a latent period of a few days, opacities develop in
the posterior subcapsular cortex of the lens (Kramar
et al. 1975). This sequence of events has led to the
assumption that microwave-induced lens opacities
are thermally caused. Several experiments have been
designed to test directly the cause-and-effect
relationship between temperature increase and
cataract formation. Kramar et al. (1975) exposed
rabbit eyes to cataractogenic levels of microwave
radiation while the animal's body was submerged in
cold water. By this means, microwave-induced intra-
ocular temperature was limited to < 41 °C, and no
lens opacities developed. In a later experiment,
Kramar et al. (1976) used heated water to produce
ocular and rectal temperatures characteristic of those
in rabbits exposed to a cataractogenic level of
microwaves. Although the vicinity of the lens was
heated to temperatures above those known to be
associated with microwave cataracts, no lens
opacities were observed; however, the rate of ocular
temperature rise was about one-tenth the rate of
increase with microwaves. Kramar et al. (1976)
concluded that a combination of a sharp temperature
gradient and rapid rise in temperature following
irradiation may be more traumatic to the lens than a
critical temperature per se.
Carpenter et al. (1977) reported no cataracts of the
posterior cortex of the lens in rabbits after 6 weeks of
treatment in which "the eye was heated at the same
rate, to the same extent, and for an equal period of
time as it would experience during a cataractogenic
microwave exposure, the difference being that the
equal heating was provided by other means, namely,
direct application of heat to the surface of the eye." In
addition, elevating retrolental and rectal temperatures
to values characteristic of a cataractogenic microwave
exposure, through a combination of restricted body
heat loss and irradiation of one eye to power densities
5-69
-------
slightly below the cataractogenic threshold, produced
cataracts in only 3 of 10 rabbits. According to their
hypothesis, if cataracts were solely of thermal origin,
all animals given the two treatments should have
developed cataracts. Carpenter et al. (1977), therefore,
concluded that the increase in intra-ocular tempera-
ture occurring during microwave irradiation is not the
sole causative factor in microwave cataractogenesis.
The reason for the apparent disagreement between
the conclusions of Carpenter et al. (1977) and Kramar
et al. (1976) probably rests with the difficulty of
duplicating by nonmicrowave heating techniques the
temporal and spatial temperature profiles induced by
microwave irradiation of the eye. Note that the
temperature at a single site in the eye was the basis
for evidence of duplicating microwave heating of the
eye at the same rate and to the same extent.
Furthermore, even though retrolental and rectal
temperatures characteristic of cataractogenic
microwave exposures were produced, the overall
effects on the rabbits were more traumatic than a
near-field microwave exposure to one eye. Within 24
h after heated water was applied directly to the eye,
almost all the eyes exhibited hemorrhage into the
anterior cavity, so that observation of the lens became
impossible. Only 21 of 32 rabbits survived the heat
treatment. Of these, five developed lenticular
cataracts of the anterior cortex, and only three
developed cataracts of the posterior cortex of the lens
that are characteristic of microwave-induced
opacities (Carpenter et al. 1977).
As mentioned above, the difficulty of duplicating by
nonmicrowave techniques the time-temperature
profile of microwave energy absorption in the eye is
probably responsible for the unsuccessful attemptsto
prove that an elevation of temperature is responsible
for microwave cataracts (cf. Kramar et al. 1976;
Carpenter et al. 1977). On the other hand, strong
evidence for thermalization being the causative factor
in microwave cataracts is provided by the experiment
of Kramar et al. (1975), which showed that cataracts
were not produced in hypothermia rabbits receiving a
cataractogenic microwave exposure. At present, it is
generally understood that intense localized exposure
of the eye for substantial durations (i.e., 150 mW/cm2
for 100 min) is necessary to induce cataracts in
laboratory animals, and that such acute exposures
cause death by hyperthermia if the entire animal is
irradiated.
5.6.3 Auditory Effects
When the human head is exposed to PW RF radiation,
an audible sound described as a click, buzz, chirp, or a
knocking sensation is perceived by some individuals;
the sound appears to originate from within or behind
the head. This auditory phenomenon is called "RF
sound" or "RF hearing." Our present knowledge of
RF hearing is summarized below.
1. The RF sound occurs only upon exposure to PW
sources; it appears to originate from within or
near the back of the head regardless of orientation
of the head in the RF field, and the sound varies
with pulse width and pulse repetition rate.
2. RF hearing has been reported at frequencies of
216 to 7500 MHz. The effect has been found to
occur at average power densities as low as 0.001
mW/cm2 with peak power densities in the range
of 100 to 300 mW/cm2. Effective pulse widths
vary from 1 to 1000//s; however, it is the energy in
the first 30 fjs or so of the pulse that determines
the threshold and loudness levels regardless of
pulse widths greater than about 30 /us (Table 5-
16).
3. The ability to perceive RF pulses has been shown
to be related to bone-conduction hearing and to
the ability to hear high-frequency acoustic waves
above 5 to 8 kHz.
4. The available data support the conclusion that the
RF auditory effect is evoked by a mechanism
similar to that for conventional acoustic stimuli
and that the primary site of interaction is
peripheral to the cochlea.
5. The most generally accepted mechanism respon-
sible for the RF auditory sensation isthermoelastic
expansion. That is, the absorption of the energy in
a brief RF pulse causes a small temperature rise
(~ 10~*°C) in a short time(~ 10/us), which results in
thermoelastic expansion of matter within the
head, which then launches a pressure wave that
is detected by the hair cells in the cochlea via bone
conduction. After stimulation of the auditory
nerve in the high-frequency region of the cochlea,
transmission of the PW-induced response to the
auditory center of the brain follows the same
auditory pathways as do all acoustically induced
responses.
5.6.3.1 Human Perception of Pulsed RF
Radiation
In their recent review article on the RF hearing
phenomenon, Chou et al. (1982) wrote:
The earliest report we have found on the auditory
perception of pulsed microwaves appeared in 1956
as an advertisement of the Airborne Instruments
Laboratory in Vol. 44 of the Proceedings of the IRE.
.The advertisement described observations made in
1947 on the hearing of sounds that occurred at the
repetition rate of a radar while the listener stood
close to a horn antenna. When the observers first
told their coworkers in the Laboratory of their
hearing experiences, they encountered skepticism
and rather pointed questions about their mental
health.
Frey (1961) was the first to study systematically the
human auditory response to pulse-modulated
5-70
-------
radiation. The subjects, who were more than 30 m
from an enclosed antenna, reported hearing a
transient buzzing sound upon exposure to the
intermittent rotating beam. The apparent location of
the sound, which was described as a short distance
behind the head, was the same no matter how the
people were oriented in the RF field. When an RF
shield (aluminum flyscreen) was placed between the
subject and the RF source, the subject did not perceive
RF sounds (Frey 1973). When earplugs were used, a
reduction in the ambient noise level and an increase
in the RF sound level were reported. The sensitive
area for detecting RF sounds was later described as a
region over the temporal lobe of the brain, because
the placement of a small piece of metal screen (5x5
cm) over this area completely stopped the RF sound
(Frey 1962).
Guy et al. (1975b) described the effect of PW radiation
on two of the coinvestigators. Three pulses, 100 ms
apart, were presented each second to keep the
average power density below 1 mW/cm2. Each
individual pulse was heard as a distinct and separate
click, and short pulse trains were heard as chirps with
the tone pitch corresponding to the pulse repetition
rate (PRR). The RF.sound appeared to originate from
within or near the back of the head. This report also
included the note that transmitted digital codes could
be accurately interpreted by the subject when the
pulse generator was keyed manually. Guy et al.
(1975b) also reported that the threshold for RF
hearing was lower when earplugs were used.
In a study by Constant (1967), the RF sound was
described as being in the area of the ear on the side
opposite to the one that was irradiated. All three of his
subjects readily detected 2-//S pulses, whereas0.5-//s
pulses were not perceived. All three experienced a
buzzing sensation at PRRs greater than 100/s,
whereas individual pulses were heard when subjects
were exposed to PRRs below 100/s.
Five of eight human subjects reported hearing
distinct clicks either inside the head or behind the
head when exposed to 15-yus pulses (Cain and
Rissmann 1978). The remaining three people heard
faint clicks when the pulse width was increased to 20
/us.
5.6.3.2 Effective Radiation Parameters
In the initial report by Frey (1961), human subjects
perceived PW radiation at frequencies of 1310 and
2982 MHz. Although the peak of power-density
thresholds for RF hearing was 266 mW/cm2 for
1310-MHz and 5000 mW/cm2 for 2982-MHz fields,
the average power density thresholds were 0.4
mW/cm2 and 2 mW/cm2, respectively. When
earplugs were used to attenuate the ambient noise
level of 70 to 80 dB, the subjects reported an increase
in the RF sound levels.
In the following year, Frey (1962) reported that
humans could perceive PW radiation at 425 MHz with
an average power density threshold of 1 mW/cm2;
the peak of power density was 263 mW/cm2. A
frequency of 8900 MHz was not effective even at an
average power density of 25 mW/cm2; the peak of
power density was 25,000 mW/cm2. At 216 MHz, the
lowest effective frequency reported in the literature,
the average power density threshold was 4 mW/cm2;
the peak of power density was 670 mW/cm2 (Frey
1963).
Table 5-16. Summary of Studies Concerning Auditory Effects of RF-Radiation in Humans
Exposure Conditions
Effect
RF hearing
"distinct'
clicks"
RF hearing:
buzz heard
at PRR > 100:
individual
pulses heard
at PRR < 100
No auditory
response
RF hearing
"buzzing sound"
RF hearing
"buzz.
clicking, hiss.
or knocking"
No auditory
response
RF hearing
"buzzing sound"
RF hearing
"clicks, chirps"
RF hearing
Comment
Threshold
values
Threshold
values
Threshold
values
Threshold
values
Polytonal
sound
Number
of
Subjects
8
3
4
Not
given
8
7
1
18
Frequency
(MHz)
3,000
3.000
6.5OO
9.500
1.245
1.245
216
425
425
425
425
8900
1.310
2982
2.450
BOO
Pulse
Repetition
Rates Is")
05
<1OO-1.0OO
0 00-1.000
50
50
_
27
27
27
27
400
244
400
3
1.000-1.200
Pulse
Width
(us]
5
10
15
1-2
1-2
05
10
70
_
125
250
500
1.000
25
6
1
1-32
10-30
Peak
Intensity
(mW/cm'l
2500
225-2.000
300-1.000
2,500-50.000
2.500-50.000
370
90
670
263
271
229
254
25.000
267
5.000
1.250-40.000
>SOO
Average
Intensity
(mW/cm'l
0.006
0 001 -0.01
OOO2 -0.007
5
5
019
032
40
1.0
1.9
3.2
7.1
25
04
2
0.1
_
Energy/
Pulse Noise Level
(jjj/cm1) (dB)
125 45 (* plastic
2.3-20.0 foam earmuffs)
4.5-15.0
40
70-90 1+ ear
stopples)
70-90 (+ ear
stopples)
70-80
(+ earplugs)
40- 45
— 40 (» ear
stopples)
References
Cam and Rissmann ( 1 978)
Constant (1967)
Frey and Messenger
(1973)
Frey (1962. 1963)
Frey (1962)
Frey (1961)
Guy era/. (1975b)
Tyazhelov « «/. (1979b|
•Calculated peak-absorbed-energy density per pulse is 16 mJ/kg
5-71
-------
In the study by Constant (1967), three human
observers were exposed to PW radiation at 3,6.5, and
9.5 GHz at an average power density of 5 mW/cm2
(pulse width was 0.5 to 2.0 //s; PRR was up to
1000/s). Only two of the three observers perceived 3-
and 6.5-GHz radiation; none experienced a response
to the highest frequency. Cain and Rissmann (1978)
reported that all eight of their subjects heard RF
pulses at 3 GHz. In this study, plastic foam earmuffs
were worn to attenuate the ambient noise, which
was 45 dB. The average threshold energy density per
pulse was 10.6 yuJ/cm2 (range of values was 3.4 to
17.5 /yJ/cm2). Expression of the peak power
threshold (225 mW/cm2) for the most sensitive
individual in units of average incident power density
yields 0.001 mW/cm2, the lowest threshold value for
human beings found in the literature. For a given peak
power, average power density depends on the pulse
repetition rate; the low threshold average power
density was a result of a pulse repetition rate of only
0.5/s(Table5-16).
The range of microwave pulse widths varied from 1 to
32 fjs in the study by Guy era/. (1975b) on one human
subject. The results indicate that regardless of the
peak power of the pulse or the pulse width, the
threshold for RF hearing of 2450-MHz radiation was
related to an energy density of 40 //J/cm2 per pulse,
or energy absorption per pulse of 16 fiJ/g. as
calculated with the aid of a spherical model. The
background noise of the exposure chamber was 45
dB. When earplugs were used, the threshold level
decreased to 28 /yJ/cm2. The threshold for a second
subject, who had a hearing deficit, was approximately
135 /uJ/cm2. Guy et al. (1975b) stated that two pulses
which occurred within several hundred microseconds
of each other were perceived as a single pulse with
energy equal to the sum of the two pulses.
The human studies cited above indicate that the
highest effective frequency of RF hearing is between
6.5 and 8.9 GHz and that the lowest effective
frequency is 216 MHz. Also, the results describe
other radiation parameters (peak power density,
energy density per pulse, and pulse width) that are
important in determining the threshold for RF hearing
in humans. Again, the RF hearing phenomenon
depends on the energy in a single pulse and not on
average power density.
5.6.3.3 Dependence of RF Hearing on Acoustic
Hearing
Standard audiograms measure hearing thresholds
for air conduction at acoustic frequencies of 250 to
8000 Hz and for bone conduction to 4000 Hz. Cain
and Rissmann (1978) measured the hearing ability of
eight subjects over the frequency range of 1 to 20 kHz
in addition to determining their standard audiograms.
They found that, although there was no apparent
correlation between the ability to perceive pulsed
microwaves at 3000 MHz and hearing ability as
measured by standard audiograms, there was a
strong correlation between microwave-hearing
threshold and hearing thresholds to air-conducted
acoustic signals above 8 kHz. For example, three of
the subjects who had normal hearing below 4 kHz
could not hear microwave pulses of less than 20-fJS
duration under conditions in which the other subjects
could perceive RF sounds. All three had a hearing
deficit at frequencies above 8 kHz.
Frey (1961) compared human acoustical hearing and
RF hearing and reported that a necessary condition
for perceiving the RF sound was the ability to hear
audiofrequencies above approximately 5 kHz,
although not necessarily by air conduction. This
conclusion was based on one subject who had normal
air-conduction hearing below 5 kHz but failed to hear
the microwave pulses. The person was subsequently
found to have a substantial loss in bone-conduction
hearing. On the other hand, a subject with good bone-
conduction hearing but with poor air-conduction
hearing perceived the RF sound at approximately the
same power density that induced threshold perception
in subjects with normal hearing. The studies by Cain
and Rissmann (1978) and by Frey (1961) show RF
hearing to depend on high-frequency hearing above 8
kHz and bone-conduction hearing at lower acoustic
frequencies. It is interesting that the 1956 report from
Airborne Instruments Laboratory stated that two
persons with hearing loss above 5 kHz did not
perceive RF sounds as well as did observers with
normal hearing up to 15 kHz.
5.6.3.4 Similarity of Auditory Response to
Microwave and Conventional Acoustic Stimuli
Taylor and Ashleman (1974) measured the electrical
response in three successive levels of the cat auditory
nervous system (eighth cranial nerve, medial
geniculate nucleus, and primary auditory cortex) to
both acoustic and pulsed-microwave (2450-MHz)
stimuli. They concluded that the microwave-induced
auditory effect on the animal is exerted similarly to
that of conventional acoustic stimuli. Furthermore,
these authors reported that inactivation (perforation
of the round window and aspiration of perilymph) of
the cochlea, the known first stage of transduction for
acoustic stimuli, affected the central nervous system
(CNS) response to acoustic and microwave energy in
the same way; i.e., the evoked electrical activities of
all three sites were abolished by cochlear destrution.
These results indicated that the locus of the initial
interaction of pulse-modulated microwave energy
with the auditory system might reside peripheral to
the cochlea.
In an experiment in which the thresholds of evoked
electrical responses from the medial-geniculate body
in cats were determined as a function of background
noise, Guy et at. (1975b) found that as the noise level
(50- to 15,000-Hz bandwidth) increased from 60 to 80
dB, there was only a negligible increase in the
5-72
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threshold for the 2450-MHz microwave stimuli, a
moderate increase in the threshold for a piezoelectric
bone-conduction source, and a large increase in the
threshold for loudspeaker-produced stimuli. The
finding that the evoked response to microwave
stimuli did not increase in relation to background
noise, which included acoustic frequencies to 15,000
Hz, indicates that microwaves may interact with the
high-frequency portion of the auditory system.
Guy et al. (1975b) also demonstrated that potentials
evoked by microwave stimuli could be recorded at
CNS sites other than those that correspond to the
auditory nervous system. This finding indicates that
elicited potentials recorded from any CNS location
could be misinterpreted as indicating a direct
microwave interaction with the particular system in
which the recording is made.
Prior to 1970, Frey (1962) had suggested that RF
hearing might be a result of direct cortical or neural
stimulation. He based this suggestion on (1) his
observations that the perception of RF pulses was
instantaneous and occurred at low average-incident-
power densities and on (2) the failure to record
cochlear microphonics at power densities much
higher than those required to elicit auditory nerve
responses. Cochlear microphonics are electrical
potentials that mimic the sonic waveforms of acoustic
stimuli; they are the signature of mechanical distor-
tion of cochlear hair cells, the first stage of sound
transduction. The failure to observe microwave-
induced cochlear microphonics had led to the
suggestion that pulsed microwaves, unlike conven-
tional acoustic stimuli, may not act on any sensor
prior to acting directly on the inner-ear apparatus
(Frey 1967).
In 1975, Chou et al. reported their success in
overcoming the technical problems that had
prevented investigators from recording cochlear
microphonics from microwave-irradiated animals.
The cochlear microphonics of guinea pigs exposed to
918-MHz (PW) radiation were found to be similar to
those evoked by acoustic stimuli.
The results of the above studies of evoked electrical
potentials in the auditory system, including the
demonstration of pulsed-microwave-evoked cochlear
microphonics, strongly indicate that the microwave-
induced auditory sensation is detected similarly to
conventional sound detection and that the site of
conversion from microwave to acoustic energy
resides peripheral to the cochlea. However, it is not
known what structure(s) in the head transduce(s) the
microwave energy to acoustic energy.
5.6.3.5 Mechanism of RF Hearing
As mentioned above, Frey (1967) had suggested that
RF hearing might be a result of direct cortical or
neural stimulation because of the failure to record
cochlear microphonics and because the perception of
RF pulses was instantaneous and occurred at low
average-incident-power densities. The latter points
were evidence against a radiation-pressure/bone-
conduction hypothesis. (See also Guy et al. 1975b.)
Sommer and von Gierke (1964) had suggested that
radiation pressure exerted by the RF pulse impinging
on the surface of the head could launch an acoustic
signal of sufficient amplitude to be detected by the
inner ear via bone conduction. Other types of
pressure much greater than radiation pressure can
be produced in tissue exposed to RF pulses. They
include thermal-expansion forces, which are
proportional to the square of the electric field in the
material. For example, Gournay (1966) has shown
that pressures greatly exceeding radiation pressure
result when visible light from a laser is converted to
acoustic energy by thermal expansion due to
absorbed energy in various liquids.
Foster and Finch (1974) extended Gournay'sanalysis
to a physiological solution exposed to microwave
pulses similar to those that produce RF hearing in
humans. They showed both theoretically and
experimentally that radiation-induced pressure
changes would result from the absorption of RF
pulses and could produce significant acoustic energy
in the solution. In fact, audible sounds were produced
by rapid thermal expansion, resulting from only a 5 x
10~6°C temperature rise in the physiological solution,
because of the absorption of the energy in the RF
pulse.
The following experimental results led Foster and
Finch (1974) to propose thermoelastic expansion as
the mechanism for RF hearing.
(1) Acoustic transients were recorded with a
hydrophone immersed in a 0.15 N KCI solution
exposed to 2450-MHz pulses that would elicit RF
sounds in a human subject. In addition, they
reported the measurement of acoustic transients
in blood, muscle, and brain exposed in vitro to
microwave pulses.
(2) The radiation-induced pressure wave generated
in distilled water inverted in phase when the
water was cooled below 4°C, and the response
vanished at 4°C, in agreement with the tempera-
ture dependence of the thermoelastic properties
of water.
(3) The thermoelastic theory predicts that the
maximal pressure in the medium is proportional
to the total energy of the pulse for short pulses
and is proportional to the peak power for long
pulses. Foster and Finch found the relationship
between pulse width and the microwave-
generated acoustic transient in the KCI solution to
be consistent with the theory.
Based on these findings, they concluded that the RF
sounds involve perception, via bone conduction, of
5-73
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the thermally generated sound transients caused by
the absorption of microwave pulses. The pulses must
be moderately intense (typically 500 to 5000
mW/cm2 at the surface of the head). However, they
can be sufficiently brief (< 50 //s) such that the
maximum increase in tissue temperature after each
pulse is very small «10"S°C).
A year earlier. Prey and Messenger (1973) published
the results of a study of RF hearing in four human
subjects. The data in this report are in agreement with
the mechanism proposed by Foster and Finch (1974).
That is, the loudness of the RF hearing sensation in
the human subjects depended upon the incident-
peak-power density for pulse widths < 30 //s; for
shorter pulses, their data show that loudness is a
function of the total energy per pulse.
More recently, Chou and Guy (1979) reported that the
threshold for RF hearing in guinea pigs, as measured
by auditory brainstem-evoked electrical responses, is
related to the incident energy per pulse for pulse
widths > 30 fjs and is related to the peak power for
longer pulses. The threshold dependence on pulse
width is in agreement with the predictions of the
thermoelastic mechanism as stated above.
The results on threshold and loudness may be
summarized as follows. The energy in the first 30 (js
or so of the pulse determines the threshold and
loudness levels regardless of pulse widths greater
than about 30 /us. For wider pulses (> 90 fjs),
loudness is related to peak power rather than energy
because the energy associated with the first 30ps of
the pulse increases directly with peak power. Thus, if
sufficient energy is deposited within a 30-fjs period, an
RF sound will result without regard to pulse width.
And, for pulses > 30 fjs, loudness increases with an
increase in peak power. Thus, the auditory response
undergoes a gradual transition from an energy-
related effect at pulse widths < 30 /js to an effect
dependent on peak power at pulse widths > 90 //s
(Frey and Messenger 1973; Chou and Guy 1979).
The hypothesis of Foster and Finch (1974) predicts
also that the RF hearing effect is related to
thermoelastically induced mechanical vibrations in
the head. Vibrations of this type can be produced by
other means, such as by a laser pulse or by a pulsed
piezoelectric crystal in contact with the skull (Chou et
al. 1976). Frey and Coren (1979) used a holographic
technique to test whether the skull and the tissues of
the head of an animal have the predicted vibrations
when exposed to a pulsed RF field. No displacements
were recorded, but subsequent to this report, Chou et
al. (1980a) demonstrated that the sensitivity of the
holographic technique used by Frey and Coren (1979)
was 3 to 4 orders of magnitude too low to detect
displacements related to vibrations from microwave-
induced thermoelastic expansion in biological
tissues.
Tyazhelov et al. (1979b) conducted a series of
psychophysical experiments with 18 subjects to
evaluate the adequacy of the thermoelastic hypothesis
and to study the perceptual qualities of RF-induced
sounds. Audiofrequency signals were presented
alternately to or concurrently with microwave pulses
(see Table 5-16) under conditions in which the
subject could adjust the amplitude, frequency, and
phase of the audio signal. The authors concluded that
the thermoelastic hypothesis adequately explained
some of their findings for microwave pulses of high
peak power and short width (< 50 fjs), but other
results were interpreted as inconsistent with a
thermoelastic mechanism for RF hearing. For
example, pulse widths greater than 50 /us, which
increased the mean power level, produced increases
in loudness that rose more rapidly than predicted by
the thermoacoustic model. In addition, suppression of
RF sounds by the audio signal was reported to be
inconsistent with the model.
Lebovitz and Seaman (1977) compared the response
to pulsed microwaves (915 MHz) with the response to
acoustic clicks by monitoring single auditory neurons
in the cat. A response of these neurons to pulsed
microwaves was predicted by earlier studies that
demonstrated subjective auditory perception (Frey
1962), auditory evoked potentials (Taylor and
Ashleman 1974), and cochlear microphonics (Chou
et al. 1975). Furthermore, the thermoelastic model
predicts that a mechanical wave of pressure
stimulates the inner ear via bone conduction. Thus, the
response of the neurons in the auditory pathway to
pulsed microwaves should be similar to their
response to transient mechanical stimuli such as
acoustic clicks. The results indicated that mechanical
factors within the cochlea are similarly involved in
determining both the acoustic and the pulsed
microwave response (Lebovitz and Seaman 1977).
Other data in this report (Lebovitz and Seaman 1977)
appeared to be inconsistent with the thermoelastic
model that predicts a high-frequency component
such as the microwave-induced cochlear microphonic
recorded by Chou et al. (1975). That is, Lebovitz and
Seaman (1977) observed a decrease in sensitivity of
high-frequency auditory units to microwave pulses.
However, they used long pulses of 250 to 300 //s in
duration to obtain maximal energy per pulse. More
recently, Tyazhelov et al. (1979b) reported that long
pulses (~ 100 //s) result in a lower pitch of the RF
sound in humans. Two of their observers who had a
high-frequency auditory limit of 10 kHz could not hear
short RF pulses but could hear long pulses. Thus, the
results of single unit recordings in cats are consistent
with human perception of RF pulses when the pulse
widths are long.
Lin (1977) developed a theoretical model that
estimates the characteristics of acoustic signals
induced in laboratory animals and humans by
5-74
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microwave pulses; his model is based on thermal
expansion in spherical heads irradiated by pulsed
microwave energy. The frequency of the induced
sound was found to be a function of head size and of
acoustic properties for brain tissues; hence, the
acoustic pitch perceived by a given subject is the
same regardless of the RF frequency. The calculations
of Lin show that thefundamental frequency predicted
by the model varies inversely with the radius of the
head; i.e., the larger the radius, the lower the
frequency of the perceived RF sound. He estimated
the fundamental frequency of vibration in guinea
pigs, cats, and adult humans to be 45,38, and 13 kHz,
respectively. The frequency for an infant head was
estimated to be about 18 kHz. These calculations
provide further evidence that a necessary condition
for auditory perception by adult humans is the ability
to hear sound above 5 to 8 kHz (Frey 1961; Rissmann
and Cain 1975).
The results of Lin (1977) appear to be in good
agreement with the measurements of Chou et al.
(1975), who found cochlear microphonics in guinea
pigs to be 50 kHz. In a later report, Chou et al. (1977)
found the frequency of the cochlear microphonic in
guinea pigs and cats to correlate well with the longest
dimension of the brain cavity. Extrapolation of these
results indicates that the frequency of the microwave-
induced cochlear microphonic in human beings
should be between 7 and 10 kHz. Chou et al. (1977)
concluded also that the frequency of the cochlear
microphonic was independent of microwave fre-
quency (915 or 2450 MHz) and exposure method
(horn applicator or cylindrical waveguide).
In summary, evidence from many studies—the
measurement of acoustic transients in water, KCI
solution, and tissues (Foster and Finch 1974) and in
muscle-simulating materials (Olsen and Hammer
1980); the relationship of pulse duration and
threshold (Foster and Finch 1974; Frey and
Messenger 1973; Chou and Guy 1979); the
characteristics of the field-induced cochear micro-
phonics in laboratory animals (Chou et al. 1975,
1977) and the theoretical calculations (Lin 1978)—
indicates that thermoelastic expansion is the
mechanism that explains most of the characteristics
of the RF hearing phenomenon.
5.6.4 Unresolved Issues
Several investigators have tried to determine the
thresholds for the RF-induced auditory sensation in
human beings and in laboratory animals (Table 5-17).
Human studies and animal experiments, in general,
are few and have used small sample sizes, different
frequencies, and different experimental procedures.
However, the radiation parameters that are most
important in determining the threshold for the
auditory response in humans (discussed in Sec.
5.6.3.2, Effective Radiation Parameters) and in
laboratory animals (discussed below) are being
characterized.
The threshold for an auditory response in cats
exposed to 918- and 2450-MHz (PW) radiation was
studied by recording of electric potentials from the
medial geniculate body (Guy et al. 1975b). As the
pulse width increased from 0.5 to 32/ys, the threshold
value for the peak of power density decreased
proportionately for pulse widths below 10 /us. The
thresholds of average power density and energy
density per pulse also increased with pulse width, but
these parameters did not show the strong proportiona I
relationship with pulse width as did the peak of power
density. Guy et al. (1975b) concluded that the
threshold for the evoked auditory response was
related to the incident energy density per pulse, at
least for pulse widths less than 10/us. In the cat, the
threshold energy density per pulse was found to be
about one-half of that which had produced a
sensation in one human subject.
In a similar experiment conducted at frequencies
between 8670 and 9160 MHz, Guy et al. (1975b)
found that the threshold values of power density and
of energy density per pulse, which include the
auditory response of cats, were an order of magnitude
higher than those required at 918 and 2450 MHz
(Table 5-17). Furthermore, no auditory response was
obtained at 8670 to 9160 MHz until the brain was
exposed by enlarging the hole in the skull that served
as the electrode access port.
Cain and Rissmann (19.78) determined the threshold
for auditory responses in animals exposed to 3000-
MHz (PW) radiation. Although their results are in
general agreement with Guy et al. (1975b) in that the
threshold energy density per pulse was relatively
constant for pulse widths of 5, 10, and 15 /us, their
results are confounded by the use of scalp electrodes
and only few animals of three species (two cats, two
chinchillas, and a dog).
In the following year, Chou and Guy (1979)
determined the threshold for RF hearing in guinea
pigs by measuring auditory brainstem-evoked
electrical responses with carbon-loaded Teflon
electrodes attached to the skin of the head. In this
experiment, the head of the guinea pig was inserted
into a 918-MHz circular waveguide exposure system.
The threshold dependence on pulse width was
found to be in agreement with the predictions of the
thermoelastic expansion mechanism; that is, the
threshold was related to the incident energy per pulse
for short pu Ise widths « 30 fjs) and was related to the
peak power for longer pulses. At the shortest pulse
width (10/us), the threshold absorbed energy density
of RF hearing in the guinea pig was about 6 /uJ/g.
Wilson et al. (1980) described an autoradiographic
technique in which [14C]2-deoxy-D-glucose was used
5-75
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Table 5-17. Summary of Studies Concerning Threshold Values for Auditory-Evoked Potentials in Laboratory Animals
Exposure Conditions
Effect
Response obtained
with scalp
electrodes
Response obtained
from round window
with carbon lead
Response obtained
with carbon-loaded
Teflon electrodes
Response obtained
from medial
geniculate with
glass electrode
Response obtained
from individual
auditory neurons
with glass electrode
Species
(n)
Cat (2)
Guinea
Pig (5)
Guinea
pig (not
given)
Cat (2)
Cat
(not
given)
Frequency
(MHz)
3000
918
918
918
2450
8.670-9.160
915
Pulse
Repetition
Rate
(s-)
0.5
100
30
1
1
1
<10
Pulse Width
Uis)
5
10
15
•1-10
10-500
3-32
0.5-32
32
25-250
Pulse
Intensity
(mW/cmJ)
2.200, 2.800
1.300
580
•
62-156
800-5.800
600-35.600
14.800-38.800
—
Average
Intensity
(mW/cm'l
*
0.05-1.4
0.017-0.028
0.015-0.047
0.472-1.24
S1.0
Incident
Energy Density
Per Pulse
11. 14
13
87
1.56-468
17.4-28.3
15.2-47.0
472-1.240
Peak Absorbed
Energy Density
Per Pulse
20
6-180
12.3-20.0
8.7-26,7
4-40
References
Cam and Rissmann ( 1 978)
Chou era/ (1975)
Chou and Guy (1979)
Guv era/ (1975b)
Lebovitz and Seaman
(1977)
•Direct comparison of power density in the waveguide exposure system to free-field power density is improper because the efficiency of energy coupling is 10 times higher than for free-
field exposure. (See Chou el »l. 1975. p. 362.)
to map auditory activity in the brain of rats exposed to
acoustic stimuli and to PW and CW microwave
radiation. With this technique, in vivo determination
of metabolic activity (i.e., glucose utilization and
associated functional activity in the brain) can be
visualized. Prior to exposure to the acoustic stimuli
or to microwaves, one middle ear was ablated. First,
the authors showed the expected bilateral asymmetry
of radioactive tracer uptake in the auditory system of
rats exposed to acoustic clicks or weak background
noise. Second, in contrast, a symmetrical uptake of
tracer was found in animals exposed to PW
radiation. Thus, the autoradiographic results
confirmed the finding that RF hearing does not
involve the middle ear (Frey 1961; Chou and
Galambos 1979). Unexpectedly, Wilson et al. (1980)
found similar patterns of radioactive tracer uptake in
the auditory system of rats exposed to CW radiation
(918 MHz; 2.5 and 10 mW/cm2) and to PW radiation
(2450 MHz).
This result, indicating an auditory response to CW
microwaves, was unexpected, because no report of
a direct hearing sensation due to exposure to CW
microwaves had appeared in the literature. Since the
thermoelastic hypothesis of RF hearing is based on
the properties of PW radiation, this observation
suggests that another mechanism may be involved
in the interaction of RF radiation with the auditory
system of the brain.
It is well documented that some human beings can
hear pulsed RF radiation as a buzz, click, or knock.
Furthermore, the thermoelastic expansion mecha-
nism explains how the pulse of RF energy can be
transformed to an acoustic impulse in the head.
Since a single pulse of RF radiation can be heard,
calculation of the threshold energy in terms of the
average-incident-power density results in a very
small number. Because a very low average-power
density can cause an acoustic response in the head
and there is the potential for exposure of the public
to pulsed fields that induce the effect, an unresolved
issup is the need to assess the psychological effects
of RF hearing, particularly in populations that may
have no knowledge as to the origin of the RF sounds
in the head.
5.6.5 Human Cutaneous Percept/on
Exposure of the human body to microwave radiation
can cause heating that is detectable by the
temperature-sensitive receptors in the skin. As
shown in Table 5-18, several investigators have
experimentally determined the microwave intensities
that cause sensations of warmth and thermal pain in
human subjects.
5.6.5.1 Frequency Specificity
Hendler and colleagues (1963, 1968) exposed a
circular area (37 cm2) of the forehead to 3- and 10-
GHz (PW) radiation and to infrared (IR) radiation. The
forehead was selected for a study of warmth
sensations because the temperature receptors in the
skin of the forehead are relatively numerous and are
evenly distributed, so that the area constitutes a low-
threshold region of uniform temperature sensitivity.
The lower-frequency microwaves (3 GHz) had a
higher-intensity threshold for warmth sensation. The
higher-frequency IR radiation was more effective
than either microwave frequency, because the IR
energy was absorbed more effectively in the outer
skin layers containing the thermal sensors.
The study by Justesen et al. (1982) confirmed the
earlier work on perception of microwave radiation.
Four human adults individually exposed the ventral
surface of the forearm for 10 s to 2450-MHz or
infrared radiation; two additional subjects experienced
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Table 5-18. Summary of Studies Concerning Human Cutaneous Perception of RF-Radiation
Effect
Sensation of
warmth on
forehead
Sensation of
warmth on
forehead
Sensation of
warmth on
inner forearm
Sensation of
warmth on
inner forearm
Sensation of
pain on inner
forearm
Frequency
(MHz)
3,000
(PW)
10,000
(PW)
2,880
2450 (CW)
3,000
(PW)
3,000
Intensity
(mW/cm*)
—
74
56
26.7
300-2,500
2,500
1,000
Durtion
(s)
1-5
1-5
15-73
50-180
10
<6
30
130
SAP*
(W/kg)
20-40
25-35
—
^~
"
2,000
Reference
Handler (1968)
Hendler et al.
(1963)
Schwan et al. (1966)
Justesen et al. (1982)
Vendrick and Vos
(1958)
Cook (1952)
*SAR value is estimated.
microwave radiation only. Thresholds of detection of
just-noticeable warming were determined to be 26.7
mW/cm2 for microwave radiation and 1.7 mW/cm2
for infrared waves. The 15-fold difference between
thresholds was attributed to (1) differential scatter
(nearly two-thirds of the incident microwave energy
is scattered and not absorbed), and (2) the differing
depths of penetration of the two forms of energy (a
relatively small proportion of the total absorbed
microwave energy is absorbed at the skin's surface).
The total energy absorbed at threshold values was
estimated to be 10.2 joules (9.5 mJ/cm2) and 1.8
joules (1.7 mJ/cm2) for microwave and infrared
radiation, respectively. Although absorption of
microwave energy was more than five times greater
at threshold, none of the four observers who
experienced both types of radiation could distinguish
a difference in sensory quality. The authors
concluded that the same set of superficial thermore-
ceptors was being stimulated, only less efficiently so,
by the more deeply penetrating, more diffusely
absorbed microwave energy.
5.6.5.2 Temperature Thresholds
For both microwave and IR radiation at intensities
producing warmth sensations, a threshold of warmth
was experienced when the temperature of a more
superficial layer of subcutaneous tissue ~ 0.2 mm
below the skin's surface was increased ~ 0.01 to
0.02°C over the temperature of a deeper layer in the
skin lying ~ 1 mm below the surface. In this study it
was also noted that there was a persistent
sensation of warmth for ~ 7 s after cessation of the
exposure, which indicated the continued existence of
an effective temperature difference between the
subcutaneous tissue layers (Hendler 1968).
Schwan et al. (1966) exposed a small area of the
forehead (7-cm diameter) equivalent to the area
exposed in Hendler's studies to 2.88-GHz radiation
and measured the length of time that elapsed before
the person was aware of a sensation of warmth. The
times for four subjects varied from 15 to 73 s at 74
mW/cm2 and from 50 to 180 s at 56 mW/cm2. The
authors found that the reaction times were not
linearly proportional to the reciprocal of the incident
power density and concluded that subjective
awareness of warmth was not a reliable indication of
microwave hazard.
Vendrik and Vos (1958) exposed a 13-cm2 area of the
inner forearm to 3-GHz (PW) radiation (300 to 2500
mW/cm2) and found the threshold for temperature
changes to be 0.4 to 1.0°C. Skin temperature
increases that were kept below 1 °C were linear with
microwave intensity for six exposure durations. In
contrast to the regularity of skin temperature changes
induced by microwaves, the reports of temperature
sensations were variable. Sensations of warmth
occurred < 0.5 to 3.5 s after rapid rises in skin
temperature. The sensations did not cease when the
skin temperature began to drop. In this study,
microwave radiation (3 GHz) was found to be a factor of
10 less effective in producing a temperature elevation
than was IR radiation at a similar intensity.
Cook (1952) determined the pain threshold in six
subjects who were exposed to 3-GHz radiation at five
different sites on the body's surface. The initial skin
temperature ranged from 31.5 to 33.5°C. Pain
resulted when a critical skin temperature (~ 46°C)
was reached rather than from a critical temperature
rise (AT). For an inner forearm area of 9.5 cm2, the
power density pain thresholds varied from 2500
mW/cm2 for a 30-s exposure to 1000 mW/cm2 for an
exposure of 130 s. The pain threshold was lower for a
larger exposed area of 53 cm2. The skin temperature
corresponding to burning pain was found to be
5-77
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independent of the area of exposure, radiation
intensity, exposure time, and anatomical site. At high
intensities, the exposure time needed to produce pain
was an inverse function of radiation intensity. The
author reported that the sensations of warmth and
pain with microwave heating differed little from those
resulting from IR. radiation.
5.5.5 Unresolved Issues
The few studies on thermal pain and warmth
sensations in human beings exposed to frequencies
in the range of 3 to 10 GHz provide useful data on
exposure levels that are clearly undesirable for the
general population. Cutaneous perception, however,
may be a reliable indicator of an unsafe exposure
level only at RF frequencies with wavelengths small
in comparison to the length of the exposed body, i.e.,
wavelengths comparable to or smaller than the
thickness of skin. Under these conditions, most of the
energy is absorbed in the outer tissue layers
containing thermal sensors. At lower frequencies,
which have wavelengths approximately equal to or
longer than the human body, modeling studies have
shown that much of the energy is absorbed within the
body belowthe superficial skin layers. In all mammals
tested, the threshold temperature (~42°C) of cellular
injury for sustained elevations (seconds to tens of
seconds) is below the threshold (~ 45°C) of pain
(Hardy et al. 1967). These results strongly indicate
that cutaneous perception of RF energy is not a
reliable sensory response that protects against
potentially harmful levels of RF radiation over the
broad frequency range of 0.5 MHz to 100 GHz.
5-78
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5.7 Endocrine, Physiological and
Biochemical Effects
Charles G. Liddle
Carl F. Blackman
5.7.1 Endocrine Effects
The endocrine system in coordination with the
nervous system is a major regulatory system in the
body. Alterations in the function of the neuroendocrine
system often reflect the efforts on the part of the
animal to maintain homeostasis when subjected to
stressful internal and external stimuli. Detection of
changes in the endocrine system is a sensitive means
of analyzing the animal's responses either to direct
stimulation of the endocrine organs themselves or to
stimulation of the CNS.
Animals exposed to a wide variety of stimuli generally
respond with a rather specific pattern of physiologic
changes, usually referred to as the general
adaptation syndrome, and the stimuli that can
provoke the syndrome are usually called stressors.
An increase in the concentration of corticosteriods in
the blood above that which would normally occur at
that time of day in the absence of a stimulus is
considered by many to be an indicator of an animal's
response to stress. Such an increase results when an
internal or external stimulus, either chemical,
physical, or emotional, excites neurons of the
hypothalamus to release corticotropin-releasing
hormone, which drives the pituitary to release
adrenocorticotropic hormone (ACTH). This hormone
then stimulates the adrenal cortex to secrete
corticosteroids. Among the strongest stressful
stimuli are surgery, anesthesia, cold, narcosis,
burning, high environmental temperature, and
rough handling or restraint.
The thyroid gland plays a principal role in regulating
basal metabolism, as well as in generating metabolic
heat in the tissues. Changes in thyroid activity can
result from changes in thyroid-stimulating hormone
from the hypothalamic-hypophyseal system and/or
increased metabolic activity of the thyroid gland due
to heating. Direct interaction with the CNS could also
produce changes in thyroid activity. Moderate or
gradual heating results in a reduction of thyroid
hormone; rapid or marked elevation of body
temperature results in an increase in thyroid activity.
The effects of RF radiation on the endocrine system
are discussed below and summarized in Table 5-19.
Thyroid function of rats following exposure to 2450-
MHz (CW) microwaves at 10, 20, and 25 mW/cm2
(SARs estimated at 0.25 W/kg per mW/cm2)for 4 or
16 h was studied by Parker (1973). No effects on
thyroid gland function were found at these exposures.
However, at 15 mW/cm2 (SAR estimated at 3.75
W/kg), exposure for a longer period (60 h) was
reported to produce a significant decrease in serum-
protein-bound iodine, thyroxine, and thyroid/serum
iodine ratio. A significant rectal temperature increase
(1.7°C) was reported at 25 mW/cm2, but not at lower
power densities.
Magin et al. (1977a,b) irradiated the surgically
exposed thyroid gland of anesthetized dogs with
2450-MHz (CW) microwaves using a waveguide
applicator at power densities of 72, 162, and 236
mW/cm2 (SARs from 58 to 190 W/kg) for 2 h. One
thyroid was irradiated while the other was used as a
control. Tissue temperatures of 39, 41, and 45°C
were maintained in the thyroid at the three power
densities. They reported an increased release of
thyroxine (TH) and triiodothyronine (T3) at all power
densities, which showed that the thyroid gland in the
dog can be stimulated directly by microwave heating.
Milroy and Michaelson (1972) exposed rats to 2450-
MHz microwaves at 1, 10, and 100 mW/cm2 (SAR =
0.25 W/kg per mW/cm2) for single exposures of 10,
20,30, and 45 min and at 1 and 10 mW/cm2,8 h/day,
for 8 weeks, and reported no effect on T3 levels,
thyroxine levels, or on the uptake of radioactive
iodine. No rectal temperature increase was observed
at 10 mW/cm2 or less. At 100 mW/cm2 there was a
constant rise in rectal temperature throughout
exposure, up to 42°C at the end of the exposure
period. Histopathological examination of the thyroid
glands also showed no effect from the exposure.
An increased production of thyroid hormone in
rabbits as measured by increased incorporation of1311
and increased radioactivity per gram of thyroid
(verified by autoradiography) was reported by
Barahski et al. (1972). The animals were exposed for
3 h/day for 4 months to 10-cm (3-GHz, PW)
microwaves at an average incident power density of 5
mW/cm2 (SAR estimated at 0.25 to 0.75 W/kg).
They reported no increase in body temperature or
thyroid temperature. (The pulse parameters were not
given, so peak power density cannot be calculated.)
Lu et al. (1977) reported serum thyroxine levels in
rats exposed to 2450-MHz microwaves at 1, 5, 10,
and 20 mW/cm2 (0.25, 1.25, 2.5, and 5 W/kg) for 1,
2, 4, or 8 h. Decreased thyroxine levels were observed
at 20 mW/cm2 following 4- and 8-h exposures. The
thyroxine values at shorter exposures and lower
power densities were not significantly different from
the sham values, except for an increase after 4 h at 1
mW/cm2, which appears to be a chance variation,
since at both higher and lower power densities and at
longer and shorter periods of exposure no effect was
detected. There were small but statistically significant
rectal temperature increases at 1 mW/cm2 after 4 h,
at 5 mW/cm2 after 1 and2h,andat 10 mW/cm2 after
2 and 4 h of exposure. The increases were in the
range of 0.2 to 0.56°C. The lack of correlation
between power density, exposure time, and rectal
temperature increase, along with the small rectal
5-75
-------
temperature change, suggests that the effects may
not have been due entirely to the microwave
exposure but possibly from the stress of confinement.
At 20 mW/cm2, however, the rectal temperature was
significantly elevated at all four exposure times and
tended to increase with longer exposures. At 1 and 2
h the changes were small (0.64 and 0.54°C), but
larger (1.01 and 1.35°C) increases occurred after 4
and 8 h. Serum corticosteroid levels were decreased
at 20 mW/cm2 after 8 h only, which the authors
report as a shift in the circadian periodicity. Serum
growth hormone measurements showed no change
at any of the power densities or times reported. They
also measured no change in the mass of the thyroid,
pituitary, and adrenal glands following irradiation.
In another study on the effects of microwaves on
acute endocrine responses in rats, Lu et al. (1981)
exposed animals to 2450-MHz microwaves (AM at
120 Hz) for 1 and 4 h, and measured colonic
temperature, thyrotropin and corticosterone levels
immediately after exposure. The 1 -h exposures were
conducted at power densities of 1, 5, 10, 20, 40, 50,
60, or 70 mW/cm2, and the 4-h exposures at 0.1,1,5.
10, 20, 25, and 40 mW/cm2 (measured SAP = 0.21
W/kg per mW/cm2). The results for the 1 -h exposure
showed an increase in colonic temperature with
increasing power density with a significant increase
at 20 mW/cm2 and above, but not at 10 mW/cm2 or
below. Corticosterone also showed an increase with
increased power density.with evidence of a threshold
between 20 and 40 mW/cm2. Thyrotropin values
showed a decrease with increasing power densities,
with significant results at 40 mW/cm2 and above,
and equivocal results in the 10- to 20-mW/cm2
range. (The 10-mW/cm2 values were significantly
lower; those at 20 mW/cm2 were not.) Similartrends
were observed following 4-h exposures, with a
significant increase in colonic temperatures at 10
mW/cm2 and above, and no increases at 5 mW/cm2
Table 5-19. Summary of Studies Concerning RF-Radiation Effect* on Endocrinology
Exposure Conditions
Effects
Species
Frequency
(MHz)
Intensity
(mW/cm*)
Duration
(days x min)
SAR (W/kg)
AT" (°C)
Reference
Increased thyroxine and Dog 2450 (CW)
triiodothyronine
No effect on thyroid gland or Rat 2450 (CW)
thyroid hormone
No effect on thyroid function Rat 2450 (CW)
Decrease in serum-protein-bound Rat 2450 (CW)
iodrne. thyroxine and thyroxine/
serum ratio
Increase in thyroid hormone Rabbit 3000 (PW)
Decrease in serum thyroxine Rat 2450 (CW)
levels
Increase in corticosterone Rat 2450 (120 Hz
levels AM)
Decrease in thyrotropin levels
Increase in corticosterone levels
Decrease in thyrotropin levels
No effect on thyroid, pituitary. Rat 2450 (CW)
or adrenal glands weight or
growth hormone levels
72-236
1. 10. 100
1. 10
10. 20. 25
1 x 120
1 x 10-45
56 x 480
1 x 240-960
25 x 1440
58-190
0.25-25
0.25-2.5
2.5, 5.
6.5 lest)
3.8 lest)
2-8
(thyroid temp)
£ 10 mW/cm3 = 0
lOOmW/cm'fiS
§ 20 mW/cm' = 0
25 mW/cm! = 17
5
20
Negt 1-10
40-70
Neg 1-20
10. 4O-70
Neg 1-5. 20
10-40
Neg 1-5
25. 40
Neg 1-20
1-20
48 x 180
1 x 240-480
1 x 60-480
1 x60
1 x240
5.2, 84
002-42
1 x 60-480
0.25-0.75
lest)
5
025-25
84-14
Neg 021 -4.2
2.1-14.7
Neg 0.21 -4.2
2.1-8.4
Neg 0.2- 1.0
06-2.1
0-1
0.25-25
Not reported
0-0.6
0.6-1 4
1.3-3.0
0-0.6
0-3.0
0-0.6
03-2.1
0
0-1-4
Maginer*/. (1977a.b)
Milroy and Michaelson
(1972)
Parker (1973)
Parker (1973)
Baranski et al
(1972)
Luetal. (1977)
Luet al (1981)
Luetal (1977)
No effect on thyroid, anterior
pituitary gland, adrenal, prostate
or testes weights; no change in
follicle-stimulating hormone or
gonadotropic hormone levels
Increase in leutmizing hormone
Increased adrenal weights and
significant adrenal response
Increased plasma corticosterone
levels
Increase in corticosterone
No effect on serum corticosterone
levels
Rat
Rat
Infant
Rat
Rat
Rat
Rat
2860-2880 ICW)
2860-2880 (CW)
2450 (CW)
2450 (CW)
2450 (AM.
120 Hz)
918 (CW)
10
10
40
50. 60
Neg 13-40
20-40
Neg 13
50. 60
25
36
36
6x
1 x
1 x
1 x
91
x360
x360
5
30-60
120
60
X600
1 -2 lest)
1 -2 (est)
20-60 lest)
11 5-13.8 lest)
Neg 3.0-9.2
4.6-9.2 es
Neg 13 lest)
8.3. 9.6
1.0
Not reported
Not reported
1 5-2.5
13 mW/cmJ
20 mW/cm!
30 mW/cm'
40 mW/cmJ
50 mW/cm'
60 mW/cm'
Not reported
0
= 0.5
= 0.7
= 09-1.4
= 1.3-1.4
= 1 6-2.4
= 2.5-2.9
Mikolajczyk<1976)
Mikolajczyk (1976)
Guillen and
Michaelson (1977)
Lotz and Michaelson
(1978)
Lou and Michaelson
(1979)
Lovely •(»/. (1977)
•AT = Rectal temperature mcreii
tNeg = Effect not found at value indicated
5-50
-------
or below with the exception of one small group at 1
mW/cm2. The trends for the increase in corticosterone
levels and the decrease in thyrotropin levels were not
significant; however, the corticosterone level at 40
mW/cm2 was significantly increased, but not at 25
mW/cm2 or lower values. Also, the thyrotropin
values at 25 mW/cm2 and 40 mW/cm2 were
significantly decreased, whereas those at 20
mW/cm2 and below were not. Comparing the effects
of 1 - and 4-h exposures on the three parameters, the
change in colonic temperature was similar for both
exposures; however, the stimulatory effect on serum
corticosterone levels was less for the 4-h exposures
than for the 1-h exposures, but the depression of
serum thyrotropin was more pronounced after 4 h
than after 1 h. The authors concluded that the
hormonal changes probably represented a general
nonspecific stress reaction that was related to the
intensity and duration of the stressing agent, rather
than to the nature of the agent itself.
No change in thyroid weight was seen in a study by
Mikolajczyk (1976), where rats were exposed to
2860- to 2880-MHz microwaves at 10 mW/cm2, 6
h/day, 6 days/week for 6 weeks. The SAR is
estimated to be 1 to 2 W/kg for a single animal
exposure, but the animals were exposed close
together in a box with dividers every 10 cm, which
should give a somewhat higher SAR value. The
author did find a significant increase in leuteinizing
hormone from the anterior pituitary gland but no
chance in follicle-stimulating or gonadotropic
hormone levels. The weights of the anterior pituitary,
adrenal, prostate, or testes were not affected by the
exposure.
Lovely et al. (1977) exposed rats to 918-MHz
microwaves at 2.5 mW/cm2 (SAR ~ 1.04 W/kg), 10
h/day for 13 weeks, and no changes in serum
corticosterone levels were observed. In a study by
Guillet and Michaelson (1977), rat pups were
exposed to 2450-MHz microwaves at 40 mW/cm2
(SAR estimated at 20 to 60 W/kg), 5 min/day for 6
days beginning at 1 day postpartum; no change in
basal corticosterone levels was found. There was a
significant adrenal response to the microwaves, but
this response was the same as seen following ACTH
administration, which would suggest a stress
reaction. Rectal temperatures of the exposed animals
averaged 1.5 to 2.5°C higher than those of the sham-
exposed animals. Adrenal mass of the irradiated
animals was significantly greater than those of the
control animals.
In another study, Lotz and Michaelson (1978)
irradiated rats with 2450-MHz microwaves at power
densities of 13, 20, 30, and 40 mW/cm2 for 30,60, or
120 min and at 50 and 60 mW/cm2 for 30 or 60 min
(SAR estimated at 0.21 W/kg per mW/cm2). Plasma
corticosterone levels were increased at power
densities at or above 50 mW/cm2, but not at 40
mW/cm2 or less, for the 30- and 60-min exposures.
At the longest exposure time (120 min), increased
levels were seen at or above 20 mW/cm2 but not at
13 mW/cm2. Graphs were presented of the rectal
temperature taken at the completion of exposures;
estimates of the rectal temperature increases taken
from the graphs for 50 mW/cm2 were 1.6 and 2.4°C
and for 60 mW/cm2 were 2.5 and 2.9°C for 30 and 60
min, respectively. The temperature increases for 40
mW/cm2 were 1.3 and 1.4°C for 30 and 60 min. For
the 120-min exposures, rectal temperature increased
0.5°C at 13 mW/cm2 and 0.7°C at 20 mW/cm2.
A study by Lotz and Michaelson (1979) suggests that
the change in corticosterone levels is due to
stimulation of the pituitary gland, probably due to
hyperthermia. They exposed hypophysectomized rats
to 2.45-GHz microwaves (AM at 120 Hz) at 60
mW/cm2 (9.6 W/kg) and found significantly lower
levels of corticosterone compared to normal and
sham-hypophysectomized rats. In another study,
dexamethasone effectively suppressed the cortico-
sterone response in rats exposed to 50 mW/cm2 (8.3
W/kg), but only partial suppression was observed at
70 mW/cm2 (11.2 W/kg). These results provide
further evidence for a stimulatory effect of microwave
radjation on the pituitary gland rather than the
adrenal gland.
In summary, microwave effects on thyroid function
have been reported at SARs as low as 2.1 W/kg, and
negative results have been reported at values as high
as 25 W/kg. The duration of exposure, as well as the
exposure rate, appears to be important, as demon-
strated by the study by Parker (1973) where
exposures at 6.25 W/kg for 16 h produced no
changes, whereas 3.75 W/kg exposures for 60 h
resulted in a decrease in serum thyroxine levels.
Changes in corticosterone levels have been reported
from microwave exposure at SARs as low as 10 W/kg
but not at 6.25 W/kg, and adrenal responses have
been reported at levels as low as 4.6 W/kg but not at 3
W/kg.
5.7.2 Clinical Chemistry and Metabolism
An individual's response to many stresses manifests
itself through changes in some of the clinical
chemistry indices. Serum calcium and phosphate
levels normally increase initially and then decrease
below normal in response to stress; whereas serum
glucose, blood urea nitrogen, and uric acid levels
increase following stress. These blood chemical
responses are consistent with induction of release of
adrenocortical hormones in response to stress.
Physiological responses, including thermal responses,
to RF-radiation exposure may occur at exposure
levels too low to produce large changes in thermo-
tregulatory behavior or colonic temperature. In such
instances there may be changes in various metabolic
parameters. There are few clinical chemistry and
5-81
-------
metabolism reports where exposures were sufficiently
defined to relate results to the power density or SAR.
These studies are described below, and are outlined
in Table 5-20.
A study of the effects of microwaves on serum
chemistry values was reported by Lovely et al. (1977),
who exposed rats in circularly polarized waveguides
to 918-MHz (CW) radiation. The animals were
irradiated 10 h/day for 13 weeks at a power density of
2.5 mW/cm2 (SAR ~ 1.04 W/kg). They reported no
change in Na+, K*, ion gap, Cf, blood urea nitrogen, or
glucose values compared to the sham-irradiated
animals. They did report a significant difference in the
serum calcium values at the end of the 12-week
exposure period. However, this is most probably a
spurious result, because the calcium levels in the
sham-irradiated animals were decreased from
previous values, whereas the levels in the irradiated
animals remained unchanged from earlier values.
These results, therefore, are interpreted to mean that
918-MHz microwaves at 2.5 mW/cm2 do not alter the
measured clinical chemistry values. Colonic temper-
ature measurements were made on the animals, and
no detectable changes were observed.
Somewhat differing from these results, Wangemann
and Cleary (1976) reported an increase in serum
glucose levels in rabbits exposed for 2 h to 2450-MHz
microwaves (CW and PW) at power densities of 5,10,
and 25 mW/cm2 (SARs estimated at 0.8,1.6, and4.0
W/kg, respectively), and an increased blood urea
nitrogen value in animals exposed to 25-mW/cm2
microwaves only. Increased uric acid levels were
found at 10 and 25 mW/cm2, but not at 5 mW/cm2
(both CW and PW). Levels of calcium, phosphorus,
cholesterol, total protein, alkaline phosphatase, lactic
dehydrogenase, and serum glutamic oxalic trans-
aminase were unaffected at the three power densities.
The authors stated that the PW and CW results could
not be compared directly because the exposure
conditions were different. The results were those that
would be expected from heat stress. Animals exposed
at 25 mW/cm2 for 2 h showed a significant rectal
temperature increase of 1.7 and 2.9°C for PW and
CW exposures, respectively. Those exposed at 10
mW/cm2 showed evidence of mild heat stress, such
as peripheral vasodilation, but no significant increase
in rectal temperature. One possible explanation for
the difference between these results and those of
Lovely et al. is the difference in absorbed energy
patterns in rats and rabbits at 2450 MHz.
Brains from rats exposed at 1600 MHz for 10 min at a
power density of 80 mW/cm2 (SAR estimated at 48
W/kg) were analyzed for selected heavy metals by
Chamness et al. (1976). Iron levels were increased in
all the areas of the brain (hypothalamus, corpus
striatum, midbrain, hippocampus, cerebellum,
medulla, cortex). Manganese was increased in the
cortex and medulla, and copper was increased in the
cortex; while calcium, zinc, sodium, and potassium
levels were unchanged. The observed changes were
probably a result of hyperthermia, since most
alterations seen were also observed in rats subjected
to a hyperthermal environment, and the irradiated
animals showed a rectal temperature increase of
4.5°C.
Platelet-rich human plasma was irradiated in vitro
with 2450-MHz microwaves at power densities from
10 to 280 mW/cm2 (SARs 1.3 to 38 W/kg) for 0.5 to
24 h by Boggs et al. (1972), and effects on blood
coagulation were analyzed. They reported no
significant changes in platelet count, coagulation
time, or clot strength at these power densities. The
plasma temperature was maintained below 37°C
during the exposures. They also conducted studies on
the effect of heating on coagulation time and clot
strength. Samples were heated either by microwaves
or by radiant heating, and the results were compared
to unheated control samples. The relative coagulation
time for the microwave-heated samples remained
unchanged throughout the temperature range studied
(34, 37, 39, and 42°C), and the samples heated by
radiant energy showed increases in the relative
coagulation time (1.58 and 2.03 times the nonheated
samples) at 39 and 42°C, respectively. A similar but
reverse effect was seen in the relative clot strength.
The samples heated to 42°C by microwaves showed
a decrease to 0.74 times the control samples, and the
radiant-heated samples showed a decrease to 0.31
times the control values. A possible explanation for
these differences is that it is difficult to produce the
same heating rate and pattern within a sample with
different sources of heat.
Ho and Edwards (1977b) measured the rate of oxygen
consumption of mice exposed to 2450-MHz micro-
waves in a waveguide for 30 min at dose rates from
1.6 to 44.3 W/kg at an environmental temperature of
24°C. They found a significant decrease in the
specific metabolic rate (SMR) at 10.4 W/kg or higher,
but not at 1.5 or 5.5 W/kg. In measurements taken
immediately after exposure, there was no detectable
rectal temperature increase at or below 10.4 W/kg,
but there was a 0.5°C increase at 23.6 W/kg and a
1.0°C increase at 44.3 W/kg. These results indicate
that the mouse compensates for large dose rates of
microwave energy by adjusting its metabolic rate
downward to compensate for the thermal load.
In'a more recent report, Ho and Edwards (1979)
reported on a continuation of the previous study.
Exposure conditions were identical to those of the
previous study except environmental temperatures of
20, 30, and 35°C were also used. At 20°C, they found
a significant decrease during exposure in the SMR at
12.1 W/kg and above, but not at 6.0 W/kg or below. A
significant decrease was found in the SMR during the
30-min postexposure period at 45.1 W/kg, but not at
27.0 W/kg or less. For the exposures at 30°C there
5-52
-------
Table 6-20. Summary of Studies Concerning RF-Radiation Effects on Clinical Chemistry and Metabolism
Exposure Conditions
Effects
Frequency
Species (MHz)
Intensity Duration
(mW/cm2) (days x min) SAR (W/kg) AT* (°C)
Reference
No effect on serum chemistry Rat 918(CW)
values
Increase in serum glucose Rabbit 2450 (CW
and PW)
Increase in blood urea Rabbit 2450 (CW)
nitrogen
No increase in blood urea Rabbit 2450 (CW)
nitrogen Rabbit 2450 (PW)
Increase in uric acid values Rabbit 2450 (CW
and PW)
1.0
2.5 91 x 600
5, 10,25 1 x120
25 1 x 120 4.0 (est)
Lovely era/. (1977)
0.8-4.0 (est) 0, 0, 1.7 (PW) Wangemann and Cleary
0, 0.2.9 (CW) (1976)
2.9
No effect on other serum Rabbit
chemistry values
Increased iron and manganese Rat
levels in brain
2450 (CW
and PW)
1600(CW)
5 and 10 1 x 120
5,10,25 1x120
10.25 1x120
Negt5
5, 10, 1 x 120
and 25
80 1x10
Mouse 2450 (CW) —
Decrease in specific
metabolic rate
(Ambient T = 24°C)
Increase in specific
metabolic rate
(Ambient T = 35°C)
Increased NADH fluorescence Rat 591 (CW)
Decreased ATP (exposed
Mouse 2450 (CW) —
13.8
x30
x30
1 xO.5
0.8, 1.6 (est) 0
0.8-4.0 (est) 0,0, 1.7
1.6, 4.0 (est) 0, 1.7(PW)
0, 2.9 (CW)
Neg 0.8 0
0.8-4.0 (est) 0,0, 1.7(PW)
0, 0, 2.9 (CW)
48 (est) 4.5
10.4
(Neg 5.5)
8.6 0
(Neg 3.6)
0.36-2.2 0
Chamness et al. (1976)
Ho and Edwards (1977b)
Ho and Edwards (1979)
Sanders et al. (1980)
Decreased CP
Decreased ATP
Decreased CP
Increase in oxygen
consumption
Decreased in metabolic
heat production
No effect on blood
coagulation
brain)
Rat
(exposed
brain)
Rat
Monkey
Human
plasma
591 (CW) 5
2450 —
(120HzPW)
2450 (CW) 6
2450 (CW) 10-280
1 xO.5
1 x30
1 x 10
1 x30
0.13-0.8
6.5, 11.1
(Neg 4.5)
0.9
1 .3-38 (est)
0
0.9, 1.8
0.4
0
Not reported
Sanders et al. (1980)
Phillips et al.
(1975b)
Adair and Adams
(1982a)
Boggsera/. (1972)
*AT = Rectal temperature increase.
fNeg = Effect not found at value indicated.
was no change in the SMR at any of the dose rates
used (1.4 to 23.7 W/kg) either during exposure or in
the postexposure period. At 35°C there was a
significant increase in the SMR at 8.6 W/kg and
higher, but not at 3.6 W/kg or lower during exposure,
and no changes were observed during the postexpo-
sure period. The authors reevaluated their first report
(Ho and Edwards 1977b) by comparing the results
during exposure with the pre-exposure values, not
with those of sham-exposed animals. With this
method of evaluation, the SMR values during
exposure at 24°C were not significantly different
from the pre-exposure values. They reported that this
method of comparison accounted for the lack of
uniformity among animals at the beginning of each
experiment and therefore was a better method of
comparison.
The general trends indicated by their studies are that
microwave exposure at the lowest ambient tempera-
ture resulted in a reduction in the SMR, exposure at
the highest ambient temperature resulted in an
increase in the SMR, with no significant changes at
the intermediate temperatures. A possible interpreta-
tion of these trends is that at the lower ambient
temperatures the animals are producing heat to
maintain thermal neutrality; addition of the microwave
heating reduces the animals' demand for additional
endogenous heat. At the higher ambient temperatures
the animals may be actively trying to dissipate the
additional heat from the microwaves as evidenced by
spreading saliva, thereby increasing their SMR.
Adult rats were exposed to 2450-MHz microwaves
pulsed at 120 Hz in a multimodal cavity for 30 min at
SARs of 4.5, 6.5, and 11.1 W/kg; and their metabolic
rate was measured beginning within 10 min after the
completion of exposure by determining oxygen
consumption and carbon dioxide production (Phillips
et al. 1975b). Room temperature was maintained at
24.2°C. They found no change in metabolic rate at 4.5
W/kg, a decrease at 6.5 W/kg, and a greater
5-83
-------
decrease at 11.1 W/kg. Colonic temperature measure-
ments were made at the end of exposure, and the
temperatures were elevated 0.4, 0.9, and 1.8°C for
the 4.5-, 6.5-, and 11.1 -W/kg exposures, respectively.
These results tend to confirm those initially reported
at 24°C by Ho and Edwards (1977b), where they
compared the exposed animals to sham-exposed
animals, but not the reanalyzed results (Ho and
Edwards 1979), where they compared the exposure
values with pre-exposure values on the same
animals.
Squirrel monkeys were exposed to 2450-MHz CW
microwaves for 10-min periods at 2.5,4,6,8, and 10
mW/cm2 (SARs from 0.4 to 1.5 W/kg) at ambient
temperatures of 15, 20, and 25°C by Adair and
Adams (1982a), and the metabolic heat production
was calculated from oxygen consumption measure-
ments. They found thatfor monkeys restrained at cool
temperatures and exposed at power densities of 4 to 6
mW/cm2 and above, the metabolic heat production
was reduced in direct relationship to the microwave
energy absorbed. They also exposed monkeys at 8
mW/cm2 (1.2 W/kg) for 90-min (ambient temperature
= 20°C) and found that the metabolic heat production
initially decreased and then leveled off at ~ 1.2 W/kg
below pre-exposure values; i.e., the reduction in
metabolic rate was equal to the rate of microwave
energy deposition.
A study on the effects of microwaves on energy
metabolism of the rat brain was reported by Sanders
et al. (1980). First, a small area of the brain of
anesthetized animals was surgically exposed. Then a
horn antenna was positioned so that exposures were
in the far field and only the exposed surface of the
brain was irradiated with the electric field parallel to
the body axis. Animals were exposed at 591-MHz
(CW) radiation for 0.5, 1, 2, 3, or 5 min at 13.8
mW/cm2 or for 0.5 or 1 min at 5 mW/cm2.
(Calculated SAP for 5 mW/cm2 = 0.13 W/kg using a
2-cm sphere model or 0.8 W/kg using a semi-infinite
plane model.) During exposures at 13.8 mW/cm2
they found an increase in nicotinamide adenine
dinucleotide (NADH) fluorescence to a maximum of
4.0 to 12.5 percent above pre-exposure control levels.
In addition, adenosine triphosphate (ATP) levels were
significantly decreased at all exposure times, as were
creatine phosphate (CP) levels. At 5 mW/cm2, ATP
and CP levels were also significantly decreased
following 0.5- and 1 -min exposures. The ATP and CP
changes at 5 mW/cm2 were not significantly
different from those seen at 13.8 mW/cm2. There
were no changes in rectal temperature at any of the
exposures and no significant difference in brain
temperature between exposed and sham-exposed
animals. The authors concluded that the results
(increased NADH fluorescence, decreased ATP and
CP levels) support the hypothesis that RF radiation
inhibits mitochondria! electron transport chain
function and that the changes cannot be attributed to
general tissue hyperthermia.
In summary, changes in clinical chemistry values
have been reported at dose rates as low as 0.8 W/kg
in rabbits, and negative results have been reported at
exposures as high as 1 W/kg in rats. The clinical
chemistry changes that have been reported are those
that would be expected from heat stress. In other
studies, effects on the rate of oxygen consumption of
mice have been reported at 10.4 W/kg, in rats at 6.5
W/kg, and in squirrel monkeys at 0.9 W/kg; and
changes in brain energy metabolism have been found
at an SAR estimated to range from 0.13 to 0.8 W/kg
(Table 5-20).
5.7.3 Growth and Development
Few investigators have reported the effects of a
combination of pre- and postnatal exposure or
postnatal exposure only to RF radiation on the growth
of laboratory animals (Table 5-21). Smialowicz et al.
(1979a) exposed rats for 4 h per day, beginning on day
6 of gestation through 40 to 41 days postpartum to
2450-MHz (CW) microwaves at 5 mW/cm2 (SARs =
0.7 to 4.7 W/kg), and reported no difference between
the weight gains of the exposed and sham-exposed
animals.
In another study, Smialowicz et al. (1981 a) reported
the growth and development of rats exposed to 100-
MHz (CW) microwaves at an incident power density of
46 mW/cm2 (average SAR = 2.8 W/kg) for 4 h/day
from day 6 of gestation through 97 days of age. The
ambient temperature was maintained at 22°C except
for days 1 to 14, when it was maintained at 27°C (RH =
50 percent). There was no consistent difference
between the body weights of the exposed and sham-
exposed animals, though the exposed animals tended
to be larger than the sham-exposed animals. Some of
the animals were tested for neurological development,
and no differences were observed in the development
of a startle response or righting reflex. There was a
significant difference in the age of eye opening, with
the mean age of eye opening in the sham-irradiated
animals occurring almost one day later than the
irradiated animals. The authors stated that the
change probably did not represent an acceleration of
eye opening, as the age of eye opening in the
irradiated animals was similar to that normally seen
in control animals in other experiments, but that eye
opening was delayed in the sham-irradiated animals.
Tests for development of motor activity at 35 and 84
days of age showed no difference between exposed
and sham-exposed animals. No difference was
observed between the exposed and sham-exposed
animals for complete blood counts, mitogen-
stimulated response of lymphocytes, frequency of T-
and B-lymphocytes, or antibody response to Strepto-
coccus pneumoniae capsular polysaccharide. No
mutagenic effect was observed on the sperm cells
after 20 days using the dominant lethal assay. Seven
5-84
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regions of the brain were weighed at 22, 40, and 97
days of age, and there was a significant increase in
the weight of the medulla in the irradiated animals at
40 days of age but not at 22 or 97 days of age. There
were no differences in the weights of any other brain
region. There were also no differences in the brain
protein concentrations for the seven regions. Brain
acetylcholinesterase (AChE) activity, however, was
reduced in the striatum and medulla at 22 days of age
and in the midbrain at 40 days of age. No effects on
AChE activity were noted in the other regions at 22
and 40 days of age, and no differences were noted at
97 days of age. The differences were small, and there
appeared to be no pattern to the changes; the sample
size was small (3 to 5 animals), and out of 21
comparisons made at the 5-percent confidence level,
one significantly different result would be expected.
Consequently, without replication with a larger
sample size, it is difficult to ascribe these changes to
the microwave exposure.
The effect of postnatal exposure to microwaves on
growth and development was studied by McAfee et
at, (1973). Weanling mice were exposed to 2450-MHz
microwaves at 10 mW/cm2, 2 min each hour for 24
days; no effect on animal growth was found. There
was no elevation of body temperature in the exposed
animals. The authors also stated that a previous
study, in which a stimulatory effect on growth from
microwaves was claimed, was probably in error
because of inaccuracies in weighing the animals
(Nieset era/. 1958).
Guillet and Michaelson (1977) exposed neonatal rats
to 2450-MHz microwaves at 40 mW/cm2 (SARs at 20
to 60 W/kg), 5 min/day for 6 days beginning on day 1
postpartum. No effect on body mass was found,
though the authors did report adrenal changes, as
discussed in Sec. 5.7.1, Endocrine Effects.
Stavinoha et al. (1975) irradiated 4-day-old mice at a
field intensity of 5800 V/m (8.92 W/cm2) for 20 min
with 10.5-, 19.27-, or 26.6-MHz radiation, and
observed no change in growth rate to 22 days of age
compared to the control animals (SARs estimated at
0.9, 1.8, and 3.6 W/kg). Mice were also exposed to
19-MHz microwaves for 40 min/day for 5 days from a
near-field synthesizer that delivered an E field of 800
V/m (17 W/cm2) and an H field of 55 A/m (114
W/cm2); no change in body mass through 120 days of
age was found (SAR estimated at 6.3 W/kg).
In a chronic study, Lin et al. (1979a) exposed 4- to 7-
day-old mice to 148-MHz microwaves at 0.5
mW/cm2 (SAR = 0.013 W/kg), 1 h/day, 5 days/week
for 10 weeks and reported no significant effect on
weight gain.
Albert et al. (1981 a) reported a significant decrease in
the number of Purkinje cells in the cerebellum of rats
exposed in utero (days 16 to 21 of gestation) and
postnatally for 97 days (4 h/day) to 100-MHz (CW)
microwaves at 46 mW/cm2 (SAR = 2.8 W/kg). The
animals were from the study by Smialowicz et al.
(1981 a), as reported above. A similar decrease was
found in rats exposed 21 h/day in utero (days 17 to
21) to 2.45-GHz (CW) microwaves at 10 mW/cm2
(SAR = 2 W/kg). In rats exposed 7 h/day for 5 days
beginning at 6 days of age, a decrease in the number
of Purkinje cells was seen in animals immediately
after exposure, but after 40 days there was apparent
recovery.
In a report by Kaplan et al. (1982) squirrel monkeys
were exposed to 2.45-GHz microwaves for 3 h/day in
utero and through 9.5 months of age at 0.034, 0.34,
and 3.4 W/kg. The results indicated a possible
increase in mortality at 3.4 W/kg. Because of the
small number of animals involved, a follow-up study
was done with larger number of animals (Kaplan
1981), and this study showed no difference in the
mortality between the irradiated (3.4 W/kg) and
sham-irradiated animals. Other aspects of these
papers are discussed in Sec. 5.3.1.2, Reproductive
Effects in Mammalian Models.
Albert et al. (1981b) examined the squirrel monkeys
described in the preceding paragraph (Kaplan et al.
1982) and found no change in the number of Purkinje
cells as compared to the sham-irradiated animals.
These studies indicate that RF exposures at SARs <
2.8 W/kg have no effect on growth and development
of animals exposed pre- and postnatally or postnatally
on ly. Exposures at 20 to 60 W/kg postnata lly for short
exposure times also did not alter the growth rate of
animals even though adrenal changes were seen.
5.7.4 Cardiovascular System
5.7.4.1 Whole-Body Exposures
Some of the initial studies of biological effects of
microwave radiation were made on the cardiovascular
system. Presman and Levitina (1962) reported that
whole-body or ventral exposure to CW microwaves at
2400 MHz, 7 to 12 mW/cm2, promoted a decreased
heart rate (bradycardia) in the rabbit. However,
exposing only the head to microwaves at the same
power densities resulted in an inceased heart rate
(tachycardia). The SAR could not be estimated as the
animals were exposed in the near field; therefore, the
study is not listed with other cardiac physiology
studies in Table 5-22. The report is mentioned here
because it provided the impetus for other studies
discussed below.
Kaplan et al. (1971) attempted to replicate the
tachycardia reported by Presman and Levitina by
exposing the head of rabbits to 2400-MHz (CW)
microwaves at an incident power density of 10
mW/cm2 (SAR estimated at 2 W/kg) for 20 min. The
exposure conditions differed in that Kaplan et al.
exposed the animals in the far field, whereas
Presman and Levitina had used near-field exposures.
5-85
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Table 5-21 . Summary of Studies Concerning RF-Radiation Effects on Growth and Development
Exposure Conditions
Effects
No effect on weight gain
No effect on growth, neuro-
logical or immunological
development or mutagenicity
Possible decrease in brain
acetylcholinesterase activity
Decrease in Purkinje cells
Decrease in Purkinje cells
Decrease, then recovery,
in Purkinje cells
No change in Purkinje cells
No change in infant mortality
No effect on growth
No effect on body weights
No effect on growth
No effect on weight gain
Species
Rat
Rat
Rat
Rat
Rat
Monkey
Monkey
Mouse
Infant
rat
Mouse
Mouse
Mouse
Frequency
(MHz)
2450 (CW)
100 MHz (CW)
100 MHz (CW)
2450 MHz (CW)
2450 MHz (CW)
2450 MHz (CW)
2450 MHz (CW)
2450 (CW)
2450 (CW)
10.5, 19.27,
26.6 (CW)
19
148 (CW)
Intensity
(mW/cm2)
5
46
46
10
10
10
40
8900
17,000-
114,000
0.5
Duration
(days x min)
55x240
112x240
37.55
x240
112x240
5x 1260
5x240
285 x 180
285x180
24x48
6x5
1 x20
5x40
50x60
SAR (W/kg)
0.7-4.7
2.8
2.8
2
2
3.4
3.4
6-8 (est)
20-60 (est)
0.9, 1.8
3.6 (est)
6.3 (est)
0.013
AT' (°C)
Not reported
Not reported
Not reported
Not reported
Not reported
Not reported
Not reported
Not reported
1.5-2.5
Not reported
Not reported
Reference
Smialowicz et al. (1979a|
Smialowicz et al. (19818)
Albert era/. (198 la)
Albert « •/. (1981 a)
Albert era/. (1981a)
Albert era/. (1981 b)
Kaplan (1981)
McAfee era/. (1973)
Guillet and Michaelson
(1977)
Stavinoha el al.
(1975)
Lin era/. (1979a)
"AT = Rectal temperature increase.
Kaplan et al. reported no change in heart rate. They
then exposed rabbits at increasing power densities
(20, 40, 60, 80, and 100 mW/cm2) and measured
respiration rate, body temperature, and heart rate.
Respiration increased at 40 mW/cm2 and greater,
and body temperature was elevated at 80 and 100
mW/cm2 (0.5°C at both power densities). Heart rate
was increased at 100 mW/cm2 only.
Birenbaum et al. (1975) exposed the heads of
unanesthetized rabbits to 2.4-GHz (CW) microwaves
for 60 min at 20, 40, 60, and 80 mW/cm2 (SAR
estimated at 3 to 12 W/kg), and found increases in
heart rate, respiration rate, and subcutaneous
temperature (lower back) at all four power densities,
with greater increases at higher exposure levels.
They also compared 2.8-GHz (CW and PW, 1000
pulses/s, 1.3 /us) microwaves at 20 mW/cm2 for the
same three parameters and found no differences in
the responses to CW or PW irradiation.
Phillips er al. (1975b) exposed adult rats to 2450-MHz
microwaves pulsed at 120 Hz for 30 min (SARs = 4.5,
6.5, and 11.1 W/kg) and measured colonic and skin
temperatures and heart rate after exposure. They
reported increases in colonic and skin temperatures
with increased exposure levels immediately after
irradiation. At the highest exposure, the colonic
temperature dropped below normal at 1 h after
exposure and remained subnormal for 4 h. There was
no postexposure effect on heart rate at 4.5 W/kg;
however, there was a mild bradycardia at 6.5 W/kg
and the more pronounced decrease in heart rate at
11.1 W/kg. They attributed the effect to the heat
stress induced by the microwaves. They also
discussed the possibility that heating the regulatory
center in the hypothalamus may have stimulated the
fall in body temperature.
Hamrick and McRee (1980) assessed the effects of
body temperature on the heart rate of embryonic
quail. They exposed the embryos to 2450-MHz
(CW) microwaves for 5 to 10 min (SARs = 3, 6, 15,
and 30 W/kg) at incubation temperatures from 35 to
38°C, and to 2450-MHz (PW) microwaves (10-^s
pulses, varied from 10 to 50 pulses/s; SARs at 0.3,
1.5, and 3 W/kg) at incubation temperatures of 35 to
39°C. There were no significant differences between
the heart rates of the exposed and control embryos in
any of the groups at any of the temperatures used. The
authors did observe that the embryonic heart rate
increased ~ 23 beats/min for each 1°C rise in
incubation temperature in the 36 to 39°C range.
Chou et al. (1980b) exposed rabbits both dorsally and
ventrally to 2.45-GHz microwaves 20 min/day for 10
days to both continuous and pulsed waves (100
pulses/s, 1 -fjs pulse width, and 10-/us pulses
triggered by the R wave at various delay times). The
incident power density for the CW and the PW
condition was 5 mW/cm2, with a calculated local
SAR to the heart of 0.093 W/kg for dorsal irradiation
and 0.3 W/kg for ventral irradiation. No effect on
heart rate was found. Rabbits exposed at 80 mW/cm2
showed an increase in heart rate, presumably from
heat stress.
5-86
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5.7.4.2 Isolated Heart Preparations
Although the data supporting a microwave-induced
bradycardia in the intact animal are equivocal, some
researchers have exposed isolated heart preparations
and reported an effect of microwaves on heart rate.
Tinney et at. (1976) attempted to determine the locus
of microwave-induced bradycardia in the isolated
turtle heart using 960-MHz (CW) microwaves.
Although the heart was isolated from the CMS, it was
still capable of responding to neurohumoral agents.
They found that exposing the isolated heart to
microwaves at 8 mW/cm2 caused bradycardia. When
the heart was treated with atropine to block the
sympathetic system, tachycardia resulted. However,
when the heart was treated with propranolol to block
the parasympathetic system, the heart rate decrease
was more significant than that following microwave
exposure alone, which would show that microwaves
may have affected the parasympathetic reflexes.
With both blocking agents added to the heart,
microwave exposure had only slight effects on the
heart rate. Tinney et at. postulated that microwave
exposure of the isolated heart equally enhances the
release of acetylcholine and norepinephrine; however,
since the activity of the former usually predominates
over the latter (Johansen 1963), the net effect of
microwave exposure is a decrease in heart rate.
A similar drug-microwave interaction has been
observed in the isolated rat heart by Olsen et al.
(1977). They exposed the heart to 960-MHz (CW)
microwaves for 4 min at 1.3 and 2.1 W/kg and
observed a decrease in heart rate. The decrease was
greater at 1.3 W/kg than at 2.1 W/kg. They also
conducted studies at 2.1 W/kg with drugs to block the
sympathetic and parasympathetic nervous system
and obtained the same results as Tinney et al. (1976).
Table 5-22. Summary of Studie* Concerning RF-Radiation Effect* on Variou* Aspect* of Cardiac Physiology
Exposure Conditions
Effects
Species
Frequency
(MHz)
Intensity
(mW/cm2)
Duration
(total min)
SAR
(W/kg)
Reference
Bradycardia develops after
whole-body exposure, along
with hyperthermia
Exposure to head promotes
tachycardia; exposure to
back raises respiratory rate
but not heart rate
Increased respiration
Increased heart rate from
dorsal exposure of the head
Alterations in ECG
(shortening of QT interval,
increased height of T-wave,
appearance of U-wave)
No effect on heart rate that
cannot be attributed to
microwave heating
Pulses synchronized with each
R-wave do not affect heart
rate
Synchronized pulses with QRS
complex causes increase in heart
rate with some arrhythmias
Increased heart rate
No effect on heart rate
Low power levels cause
bradycardia in the isolated
turtle heart
Causes slight decrease in the
isolated heart
Synchronized exposures with ECG
have no effect on heart rate
Rat 2450 (PW) 28,48
Rabbit
Rabbit
Rabbit
72-h
Chick
haart
Quail
embryo
Frog
Frog
Rabbit
Turtle
Rat
Frog
2400 (CW and 20
PW)
2400
2400
40-100
100
24,000 (PW) 74
2450 (CW and NAt
PW)
2450 (CW) 80
5
960 (CW) NA
960 (CW)
NA
1420-3000 0.0006
(PW)
30
60
20
20
6.5, 11.1
5 to 10
1420-10,000 32/yW/cm2 100-^s
(PW) pulses
1425 (PW) 0.6/uW/cm2 10-jus
pulses
20x10d
20 x 10 d
60
5 to 10
2-, 10-,
150-/US
pulses
8-20 (est)
20 (est)
NG"
0.3-30
NG
Phillips et al. (1975b)
Birenbaum et al. (1975)
Kaplan et al. (1971)
Kaplan et al. (1971)
Paff era/. (1963)
Hamrickand McRee(1980)
Liu et al. (1976)
Frey and Seifert (1968)
12 Chou et al. (1980b)
0.3 and 0.093
2-10 Tinney ef al. (1976)
1.3 and 2.1 Olsen et al. (1977)
NG Clapman and Cain (1975)
*NG = Not given.
tNA = Not applicable.
5-87
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Paff et al. (1963), working with the isolated embryonic
chicken heart, were unable to detect changes in heart
rate during exposure to 24,000-MHz (PW) radar fields.
They did, however, detect effects on the electrocar-
diogram (ECG), including abnormal P andT waves from
3-min exposures at 74 mW/cm2.
Frey and Seifert (1968) showed that 10-//S pulses at a
carrier frequency of 1.425 GHz given at a synchronous
period with the ECG (220 ms after the P wave)
resulted in tachycardia or heart arrhythmia in the
isolated frog heart. The peak power density was 60
mW/cm2 (average power density — 0.6/uW/cm2). Liu
et al. (1976) reported no effect on heart rate with
isolated frog hearts or in hearts irradiated in situ in a
similar study. The in situ hearts were exposed to 100-
fjK pulses of either 1.42 or 10 GHz, and the isolated
frog hearts were exposed to 100-//S pulses of 1.42
GHz. The pulse was delivered on the rising phase of
the R-wave from the ECG, which as somewhat
similar to, but not exactly the same as, the 200-ms
delay following the P-wave used by Frey and Seifert.
(The R-wave follows the P-wave by about 200 ms.)
The peak and average power densites of 320mWand
32 (AN were also considerably higher than those used
by Frey and Seifert. These factors, plus differences in
the manner of preparing the isolated hearts (Liu et al.
curarized the frogs, whereas Frey and Seifert
decapitated the frogs), make it difficult to compare the
results of the two studies.
Clapman and Cain (1975), however, tried to replicate
the study of Frey and Seifert using similar pulse
widths (10 //s), peak and average power densities (60
mW/cm2 and 0.6 //W/cm2), carrier frequency (1.42
GHz), and method of isolating the frog heart; they
reported no change in heart rate. Also, no heart rate
changes were found when they conducted studies
with a different peak power (5.5 W/cm2), frequency (3
GHz), and pulse widths (2 and 150 /us). Clapman and
Cain were able to produce an increased heart rate
with 20-mA current pulses synchronized 200 ms after
the P-wave peak.
The results of microwave exposure on the cardiovas-
cular system (Table 5-22) indicate that whole-body
exposure of sufficient intensity to produce heating
also produces an increase in heart rate similar to that
which would be expected from heating alone. In the
isolated heart there appears to be a stimulation of the
autonomic nervous system from microwave exposure
at levels where very little heating would be expected
(1 to 2 W/kg). Low levels of synchronized PW
microwaves (0.6 to 32 mW/kg) apparently are
ineffective in producing detectable alterations in
heart rate.
5.7.5 Biological Effects of Low Frequency
Modulation of RF Radiation
Interest in the biological effects of low frequency
modulation of RF radiation stems from reports of
changes caused by exposure to electric and magnetic
fields in the sub-ELF range (0 to 30 Hz). It has been
reported that exposure to low-frequency electric
fields changes the reaction time in humans (Konig
and Ankermuller 1960; Hamer 1968; Konig 1971) and
in monkeys (Gavalas; etal. 1970; Gavalas-Medici and
Day-Magdaleno 1976), and alters circadian activity
in human beings (Wever 1973). Friedman etal. (1967)
observed that magnetic fields modulated at low
frequencies also change reaction time in human
beings.
Two other studies that provide important background
information are reported by Kaczmarek and Adey
(1973, 1974). In the first report, they described
release of calcium ions and x-aminobutyric acid
(GABA) from the cerebral cortex of cats in response to
small changes in the extracellular concentration of
calcium. In 1974, they demonstrated release of
calcium ions and GABA from the cat cortex in
response to low intensity electric currents, pulsed at
200 Hz, applied directly to the cerebral cortex. Thus,
extracellular calcium and electric current have
similar effects on the release of GABA and calcium
ions from brain tissue.
The studies of (1) behavioral changes in animals and
human beings induced by low frequency signals and
(2) biochemical changes in the cat brain caused by
electric currents led to a study of the influence of
electric fields on EEG patterns associated with a
conditioned behavioral response in cats (Bawin et al.
1973). To increase the penetration of the signals into
the tissue, they chose an RF carrier wave of 147 MHz,
which was amplitude modulated at sub-ELF frequen-
cies (e.g., 3 to 14 Hz). Alterations were observed in
the rate of performance, accuracy of reinforced
patterns, and resistance to extinction in learned
behavior of the exposed animals compared to
controls, indicating that the fields were acting as
reinforcers. In order to determine whether these
effects were mediated via peripheral receptors or
occurred as a result of changes induced directly on
the CNS, experiments were designed to examine the
effects of modulated RF carrier waves on brain tissue
in vitro.
5.7.5.1 Calcium Ion Efflux In Vitro: A
Fundamental Finding
The association of calcium ions with brain tissue was
selected as the biochemical marker to examine the
influence of modulated RF fields because calcium ion
efflux has been shown to be sensitive to electric
currents applied directly to brain tissue in vitro, and
because calcium ions have a prominent role in many
biochemical and biophysical processes (e.g., cellular
membrane integrity and function, enzyme cofactor,
putative second messenger for the conduction of
extracellular signa'ls to the nucleus of the cell, neural
tissue excitation and secretion of transmitter
5-88
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substances at synapses). The first report of
the influence of modulated RF fields on excised brain
tissue was Bawin et al. (1975), who showed that a 20-
min exposure of chick brain tissue in vitro to a 147-
MHz field at 1 to 2 mW/cm2 (SAR estimated at 0.002
W/kg) caused enhanced efflux of calcium ions, but
only if the field was sinusoidally amplitude modulated at
frequencies of 6, 9, 11, 16, or 20 Hz. Maximal efflux
was measured at 16 Hz. Modulation frequencies of 0,
0.5,3, 25, and 35 Hz were ineffective. This frequency-
specific response, which occurred while the 147-
MHz carrier field was maintained at the same power
density, indicates that the field-induced efflux of
calcium ions was not due to heating of the samples.
In another report, Bawin et al. (1978) exposed chick
brain tissue for 20 min to 450-MHz fields, amplitude
modulated at 16 Hz, at 0.75 mW/cm2 (SAR estimated
at 0.0035 W/kg) under a variety of chemical
conditions. The results demonstrated that (a) the
enhanced efflux of calcium ions is not highly sensitive
to the external calcium concentration, (b) bicarbonate
appears to be important for enhanced efflux, (c)
lowering the pH from 7.6 to 6.8 in the presence of
bicarbonate may enhance the magnitude of efflux,
and (d) lanthanum causes a reversal to field-induced
retardation of calcium ion efflux.
Corroboration of the frequency-specific response
described by Bawin and co-workers was provided by
Blackman et al. (1979), who showed that 16-Hz
amplitude modulation of 147-MHz carrier waves
caused enhanced efflux in chick brain tissue in vitro,
whereas modulation frequencies of 3, 9, and 30 Hz
did not. Although the data had large variances, an
unusual intensity response was described, i.e., only
0.83 mW/cm2 (SAR estimated at 0.0014 W/kg)
produced a statistically significant efflux enhance-
ment (intensity values are corrected based on
discussion in Blackman era/. 1980a); power densities
(0.11,0.55,1.11 and 1.38 mW/cm2) below and above
the effective value did not cause efflux. In a later
report, Blackman et al. (1980a) used a revised
statistical model and experimental procedure to
reduce the influence of the large sample variance. An
intensity response identical to their earlier result was
found. However, when the distance between samples
was halved, the range of intensities that produced
enhanced efflux increased to include 0.55,0.83,1.11
and 1.38 mW/cm2, whereas lower and higher values
of 0.11 and 1.66 mW/cm2 were ineffective. In
addition, an intensity region from 0.55 to 1.11
mW/cm2 caused enhanced efflux when 9 Hz was
used as the modulation frequency. These data,
obtained with a more rigorous experimental protocol,
provided additional support for the results of Bawin et
al. (1975) and Blackman et al. (1979); however, the
explanation for the dependence on sample spacing
awaited further developments.
Joines et al. (1981) examined the dependence on
sample spacing by calculation of the electrical
coupling between the samples; for similicity the
samples were modeled as spheres. They found that
increased electrical interaction between the more
closely packed spheres produced a broader range of
internal field strengths within each sphere. Thus, if a
given internal field strength were necessary to cause
enhanced efflux, the chance would be greater for that
internal field strength to occur in closely coupled
samples exposed to a specific range of incident
intensities. Joines et al. (1981) found this result to be
consistent with the experimental findings in
Blackman et al. (1980a). Thus a potential artifact was
shown to be a logical result of the experimental
procedures.
The intensity response observed by Blackman et al.
(1979) with modulated 147-MHz carrier waves was
confirmed by Sheppard ef al. (1979) with 450-MHz
carrier waves, modulated at 16 Hz; calcium-ion efflux
was enhanced at 0.1 and 1.0 mW/cm2 but not at
0.05, 2.0, or 5.0 mW/cm2. (The estimated SAR at 1.0
mW/cm2 is 0.0047 W/kg.) The results of these two
reports show that the intensities producing calcium-
ion efflux from chick brain tissue in vitro are within
the range of 0.1 to 1.38 mW/cm2for modulated 147-
MHz and 450-MHz carrier waves.
The apparent carrier-frequency independence of
effective intensities was tested with a 50-MHz carrier
wave, amplitude modulated at 16 Hz. Enhanced efflux
of calcium ions occurred within two intensity regions
(between 1.44 and 1.67, and at 3.64 mW/cm2; SARs
were 0.0013 and 0.0035 W/kg, respectively)
separated by intensities of no effect, including 0.72
mW/cm2 (Blackman et al. 1980b). These effective
intensity values were different from the corresponding
values of 147-MHz radiation; thereby indicating a
dependence on carrier frequency. In addition this
result revealed the existence of more than one range
of effective intensities.
The apparent discrepancy in effective power
densities at the three different carrier frequencies
(50, 147, and 450 MHz) has been resolved by the
finding that efflux is dependent on the electric field
strength within the tissue and not on incident
intensity (Joines and Blackman 1980). The calcula-
tion to transform the incident intensity to internal
field strength was based on an empirical model
described by Joines et al. (1981). With the data
available at 50 and 147 MHz, the model was used to
predict intensities that would produce both altera-
tions and no alterations in calcium-ion efflux; some
predictions were tested and found to be valid
(Blackman et al. 1981). These reports described two
intensity ranges that appear effective for enhanced
efflux at both 50 and 147 MHz, identified the internal
electric field strength ratherthan incident intensity as
the important exposure parameter, and showed the
5-89
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importance of frequency-dependent complex permit-
tivity values of brain tissue in the conversion of
incident intensity to internal field strength. The
exposures at 50 and 147 MHz caused no generalized
heating of the sample. The maximum temperature
rise was calculated to be <0.0004°C, and SAR
calculated at each carrier frequency was <0.0014
W/kg (Blackman et a/. 1980b).
Subsequent to the critique by Athey (1981) that the
simple spherical model used by Joines and Blackman
(1980) was too idealized, these authors showed that a
layered sphere model produced relationships between
incident intensities at 50, 147, and 450 MHz and
internal field strengths that were also consistent with
the experimental results (Joines and Blackman
1981). The success of the initial, simple models to
predict intensity regions of both field-induced efflux
enhancement and no enhancement demonstrates
the utility of the approach. More refinements in the
models are necessary before the experimental
situation is realistically described.
Shelton and Merritt (1981), who used different
procedures from those described by Bawin et af.
(1975), Blackman et a/. (1979, 1980a,b), and
Sheppard et a/. (1979) reported no change in calcium-
ion efflux from rat brain. Brain tissue, labeled in vitro
with radioactive calcium, was irradiated at 1 GHz,
pulse-modulated with square waves at 16 or 32 Hz
(0.5, 1.0, 2.0, and 15 mW/cm2). In a second report,
Merritt et a/. (1982) exposed rat brain tissue labeled in
vivo with radioactive calcium to microwave radiation,
pulse modulated at 16 Hz (20-ms pulse width). The
intensities for the 1-GHz carrier frequency were 1
mW/cm2 (SAR = 0.29 W/kg) and 10 mW/cm2 (SAR =
2.9 W/kg); and for the 2.45-GHz carrier frequency, 1
mW/cm2 (SAR = 0.3 W/kg). In addition, animals
labeled with radioactive calcium were exposed for 20
min to 2.06-GHz radiation at one of 17 different
combinations of intensity and pulse repetition rate: 0,
0.5, 1.0, 5.0,10.0 mW/cm2 (SAR was 0.24 W/kg per
mW/cm2); and 0, 8, 16, 32 Hz (pulse width was 10
ms). After exposure, brain tissue was analyzed for
radioactivity. No statistically significant field-induced
enhancement of calcium-ion efflux or change of
calcium content in the brain tissue was found. The
reason for these negative findings is not known;
however, the use of square wave rather than sine
wave modulation, the different biological preparation,
and different medium composition are factors that
may have influenced the outcome.
5.7.5.2 Additional CNS Studies
The reports of field-induced calcium-ion efflux from
chick brain tissue in vitro have led to other CNS
studies. Synaptosomes, prepared from rat cerebra
and labelled with radioactive calcium, were exposed
for 10 min at 0.5 mW/cm2 to 450-MHz fields,
amplitude modulated at 0, 16, or 60 Hz (Lin-Liu and
Adey 1982). Only 16 Hz affected the efflux kinetics of
calcium ions. Although the SAR can be estimated as
low, an exact value cannot be unequivocally
established because the exposure chamber may have
been operated in a multimodal condition. (See Weil et
a/. 1981.) Nevertheless, this result is modulation
dependent, and it is unlikely that heating is involved
as a causative agent.
Similar field-induced efflux enhancement has been
reported in a live animal. Adey et al. (1982) exposed
awake, immobilized cats to 450-MHz fields, amplitude
modulated at 16 Hz, at 3.0 mW/cm2 (SAR = 0.29
W/kg). The release of calcium ions from the cortex
was observed as a function of time. Irradiation for 60
min caused episodes of enhanced efflux lasting 20 to
30 min and extending into the postexposure period.
Although focusing on a different component of the
efflux kinetics than that studied by Lin-Liu and Adey
(1982), these results demonstrate that RF fields
modulated at 16 Hz can cause changes in both a
subcellular membrane system and in the live
mammal. Thus, the field-induced phenomenon is not
restricted to an avian species nor to in vitro
preparations.
Recently, Dutta et al. (1984) observed field-induced
enhancement of calcium ions from cells of human
origin. Monolayer cultures of human neuroblastoma
cells were exposed for 30 min at ten SARs from 0.01
to 5.0 W/kg to 915-MHz fields, with or without
sinusoidal amplitude modulation (80 percent) at
frequencies between 3 and 30 Hz. Significant
increases in the efflux of calcium ions occurred at two
SARs (0.05 and 1.0 W/kg). The increased efflux at
0.05 W/kg was dependent on the presence of 16-Hz
modulation but not at the higher value. Exposure at
modulation frequencies between 3 and 30 Hz (SAR -
0.05 W/kg) revealed a peak in the response at 16 Hz.
Although the effective SAR (0.05 W/kg) for 16-Hz
modulation is more than 38 times greater than the
SARs for enhanced efflux of calcium ions from chick
brain tissue in vitro, the low-frequency response
pattern was similar to that reported by Bawin et al.
(1975) and Blackman et al. (1979). The relation of
enhanced efflux with unmodulated fields at 1.0 W/kg
with the effects of modulated fields is not known at
this time; however, it is not due to a temperature
increase in the sample because enhancement was
not found at SARs of 2.0 and 5.0 W/kg.
The effect of modulated RF fields on the EEG was
investigated by Takashima et al. (1979). Rabbits were
exposed 2 h daily for 6 weeks to 1.2 MHz, amplitude
modulated at 15 Hz, or 5 MHz amplitude modulated at
14 Hz. Following exposure, the EEG was recorded
with scalp electrodes and, when compared to the
pretreatment EEG pattern, was found to be altered
with enhanced low-frequency components and
decreased high-frequency components. The EEG
pattern returned to the pretreatment pattern after
5-50
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several weeks postexposure. Although the electric
field intensity was given as 500 V/m, with an error
factor as large as 2, the important aspect of the
results was that unmodulated fields of similar
intensity had no effect on the EEG pattern. The
absence of metallic electrodes in the animal during
exposure avoids the major criticism of earlier studies
that reported field-induced changes in EEG patterns
(Gavalas et al. 1970; Bawin et al. 1973).
Sagan and Medici (1979) studied the influence of
450-MHz fields, sinusoidally amplitude modulated at
either 3 or 16 Hz, on locomotor activity in young
chickens. The experiments were performed in a
plastic, modified Skinner box with light beams to
monitor activity; the complete apparatus was placed
in an anechoic chamber and exposed in the far field.
The authors found no statistically significant change
in performance during or immediately after a 23-min
exposure at 1 or 5 mW/cm2 (SAR estimated at 0.2
and 1.0 W/kg). They concluded that the lack of a field-
induced response could be due to the use of
modulation frequencies not present in the chicken's
EEG during performance on the particular (fixed-time
schedule) task. An alternative possibility, based on
the multiple-intensity ranges observed for field-
induced calcium-ion efflux, is that the two intensities
used in this study may have been outside the effective
ranges.
In summary, four groups (Adey et al.: Blackman et al.;
Dutta et al.; Takashima et al.) have shown that RF
fields, sinusoidally modulated at sub-ELFfrequencies,
especially 16 Hz, cause CNS changes in different in
vitro preparations and in the live animal. Many of
these studies have been analyzed in reviews (Adey
1981; Blackman et al. 1981; Greengard et al. 1982;
Myers and Ross 1981). It is generally agreed that both
the mechanism of interaction and the physiological
consequences of these changes are yet to be
established.
5.7.5.3 Non-CNS Studies
The effects of exposure of pancreatic tissue and T-
lymphocytes to RF fields, sinusoidally amplitude
modulated at low frequencies, have been examined.
An increase of calcium-ion efflux from rat pancreatic
tissue exposed in vivo at 2 mW/cm2 for 1 to 2.5 h at
147 MHz, modulated at 16 Hz (estimated SAR <
0.075 W/kg), has been reported by Albert et al.
(1980). However, the efflux was not accompanied by
a change in protein secretion, which is normally
associated with calcium mobilization in the pancreas.
The authors attributed the lack of protein secretion to
a limitation imposed by the exposure conditions, i.e.,
a relatively small volume of medium was available to
the tissue for normal metabolic activity.
In another in vitro assay, the cytotoxic activity of
mouse T-lymphocytes was suppressed by a 2-h
exposure (1.5 mW/cm2)to450-MHzfields, modulated
at frequencies between 16 and 100 Hz (Lyle et al.
1983). Peak suppression occurred at 60-Hz modula-
tion, with smaller effects at 16, 40, 80, and 100 Hz.
The exposed cells recovered full cytotoxic activity
12.5 h after the termination of exposure. This result
demonstrated an inhibitory but reversible effect on a
cell-mediated immune response by modulation
frequencies.
5.7.5.4 Sinusoidal ELF and Sub-ELF Signals
Most of the studies reviewed above demonstrate an
absolute requirement for low-frequency sinusoidal
modulation of the RF carrier wave in order for the
signal to be effective biologically. For completeness,
several reports are mentioned that describe biological
effects of exposure to low frequencies in the absence
of an RF carrier wave. Bawin and Adey (1976,1977)
exposed chick and cat cerebral tissue for 20 min to 1,
6,16, 32 or 75 Hz at electric field gradients of 5,10,
56, and 100 Vp-p/m in air. Only two frequencies, 6
and 16 Hz, caused a reduction in calcium-ion efflux at
10 and 56 V/m for the chick tissue, and at 56 V/m for
the cat tissue. Because all other combinations
produced no field-induced responses, the authors
described "amplitude and frequency windows" for
calcium-ion efflux. Electric field gradients within the
tissue were estimated to be 10r5 V/m. The field-
induced reduction in efflux is in contrast to the
enhancement caused by modulated RF carrier waves.
Nevertheless, the frequency dependence observed in
the two studies was similar, which suggests an
interaction with a common substrate as the site of
interaction.
Blackman et al. (1982) used chick brain to study the
influence of 16-Hz signals at 15 intensities between 1
and 70 Vp-p/m on the efflux of calcium ions. Two
intensity regions that included 5,6, and 7.5 V/m and
35, 40, 45, and 50 V/m caused enhanced efflux. No
field-induced effects were seen below (1, 2, and 3.5
V/m), between (10, 20, and 30 V/m), or above (60
and 70 V/m) the two effective intensity regions.
Moreover, 1 - and 30-Hz signals at 40 V/m caused no
change in efflux. This finding is consistent with the
reports of multiple-intensity regions of enhanced
efflux caused by modulated RF radiation (Blackman
et al. 1980b, 1981). In addition to the intensity
response, the frequency dependence corroborated
reports by Bawin and Adey (1976) for low-frequency
signals, and by Bawin et al. (1975) and Blackman et
al. (1979) for modulated RF fields.
In these two low-frequency studies, the cause of the
slight difference in effective intensities is unknown.
The major disagreement in the results of Bawin and
Adey (1976) and Blackman et al. (1982) is the
direction of the change in efflux; the latter authors
state that the "cause may be found in the slightly
different preparations and procedures used in the two
laboratories."
5-91
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Several research groups have reported biological
changes induced by low-frequency, sinusoidally
oscillating magnetic fields. The myxomycetePhysarum
polycephalum has a longer mitotic cycle and reduced
respiration rate after chronic exposure to 2.0-gauss
magnetic fields at 75 Hz (Goodman et al. 1979).
Human fibroblasts in culture exposed to sinusoidally
varying magnetic fields for a wide range of
frequencies (15 Hz to 4 kHz) and amplitudes (0.25 to
5.6 gauss) exhibit enhanced DNA synthesis (Liboff et
al. 1984). Fruit flies (Drosophila melanogaster)
preferred not to deposit eggs in a 10-gauss,
sinusoidally varying 50-Hz magnetic field; similar
exposure during development of the egg produced
less viable eggs and pupae in the exposed samples
than in controls (Ramirez et al. 1983). These results
suggest that low-frequency, sinosoidally varying
fields may alter fundamental biological processes.
Low-frequency, pulsed magnetic fields have also
been reported to produce alterations in diverse
biological systems. These 'systems include the
developing chick embryo (Delgado et al. 1982; Ubeda
et al. 1983), Drosophila egg laying and mortality
(Ramirez et al. 1983), the de-differentiating amphibian
red blood cell (Chiabrera et al. 1979), transcription in
the Dipteran chromosome (Goodman et al. 1983),
nerve cells in culture (Dixey and Rein 1982), and
mouse bone cells in culture (Luben era/. 1982). Many
of these studies used an intricate pulsed waveform,
which has been used in therapeutic devices for bone
nonunions. All the studies used pulse repetition rates
below 500 Hz, with most below 100 Hz. Recently,
Liboff et al. (1984) questioned the need for the
particular wave shapes because it appears that the
essential element is the low-frequency field.
5.7.5.5 Summary
Many reports of effects of RF fields that are amplitude
modulated at very low frequencies have not been
independently corroborated. The major exception is
calcium-ion efflux from chick brain tissue in vitro at
intensity levels far below those that cause heating.
This exception, combined with the results of studies
of brain biochemistry and EEGs in animals and with
synaptosomes and human neuroblastoma cells in
culture, provides evidence that CNS tissue from
several species, including human beings, is affected
by low-intensity RF fields sinosuoidally amplitude
modulated at specific low frequencies (Table 5-23).
The physiological significance of these field-induced
effects is not established.
5.7.5 Unresolved Issues
In addition to the CNS-related changes, amplitude-
modulated RF fields have been reported to alter an
immune response and a pancreatic tissue function.
These reports with diverse biological systems are
without apparent connection to each other except for
the physical agent causing the change. The biological
effects of frequency-modulated RF radiation, e.g., FM
radio signals, are not known. The reports cited above
of Merritt and co-workers indicate that pulsed
square-wave modulation may not cause calcium-ion
efflux, whereas data from the Bawin et al. and
Blackman et al. studies show that sine wave
modulation is effective.
No report has yet described a mechanism of action in
sufficient detail to identify the conditions necessary
and sufficient to explain unequivocally calcium-ion
efflux in the brain or the other biological changes
caused by modulated RF fields. The response to
specific frequencies and intensities is unusual and at
present unexplained. This response to amplitude-
modulated RF radiation or to sub-ELF signals alone
may be a true field effect at a very low SAR and at
biologically relevant frequencies, i.e., in the range of
frequencies normally present in the EEG. The
frequency-specific nature of the responses provides
evidence against heat as the underlying cause. The
unusual, multiple-intensity-range response challenges
standard dose-response analyses, and by its very
nature, may prohibit the invocation of threshold
levels.
Other areas of unresolved issues include comparisons
of CW vs. PW microwaves under identical exposure
conditions. Such studies would help determine if the
differences seen by Wangemann and Cleary (1976)
were due to different exposure conditions or to the
irradiation parameters (CW or PW). There is also a
paucity of information on the effects of RF radiation at
different frequencies, particularly at frequencies of
environmental importance. Studies at different
frequencies would help to determine the reasons for
differences in effects at similar SARs. Such studies
might help explain why Wangemann and Cleary
(1976) reported serum chemistry changes in rabbits
at 0.8 W/kg (2450 MHz), and why Lovely et al. (1977)
reported no change in serum chemistry values in rats
at 1 W/kg (918 MHz).
There are also data such as those reported by Boggs
et al. (1972) where the results from microwave
heating to a predetermined temperature are different
from those resulting from the same temperature
produced by other means of heating. Perhaps there
are differences in the uniformity of heating or in the
rate of heating which would account for these
differences. In addition, a study by Oeficis etal. (1979)
reported elevated serum triglyceride and/Hipoprotein
levels in mice exposed to 2450 MHz at 1.5, 3.3, or 4
mW/cm2, but not at 1 mW/cm2. Because the
exposures were conducted in a multimodal cavity,
SAR values were not reported and cannot be
predicted. If this study is repeated, particular attention
should be given to dosimetry. An alternative is to
5-92
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make or report dosimetric measurements in the
exposure system used.
The reported effects on thyroid function at 3.75 W/kg
for 60 h contrasted with no effect at 6.25 W/kg for 16
h (Parker 1973) suggests that the total amount of
energy absorbed may also be an important considera-
tion. Additional studies could define further the
relative importance of dose rate compared with total
dose.
Table 5-23. Summary of Studies Concerning Biological Effects of Low Frequency Modulation of RF-Radiation
Effects
RF Modulation Intensity Time SAR
Species (MHz) (Hz) (mW/cm2) (min) (W/kg)
Reference
Altered calcium-ion efflux in
brain tissue in vitro
frequency specificity Chicken 147 6-20
influence of pH and lanthanum Chicken 450 16
frequency and intensity Chicken 147 16
specificity
intensity specificity and
sample spacing
theoretical analysis of
sample spacing
intensity specificity
two intensity ranges
theoretical analysis of
RF dependence
test of predictions of
theoretical analyses
no effect for pulse
modulation
no effect for pulse
modulation
change in calcium efflux
kinetics in synaptosomes
frequency and intensity
specificity in cultured
neuroblastoma cells
Altered calcium-ion efflux in
brain tissue in vivo
no effect for pulse
modulation
change in efflux kinetics
from awake animal
Changed EEC patterns
No change in behavior
Suppressed T-lymphocyte
activity
Altered calcium ion efflux
in pancreatic slices
in vitro
Chicken 147 9, 16
Chicken 147 16
Chicken 450 16
Chicken 50 16
Chicken 50 16
147
450
Chicken 147 16
Rat 1000 16*, 32*
Rat 1000 16*
2450 8*, 16*.
32*
Rat
450 16
Human 915 16
being
Rat 2060 8*, 16*.
32*
Cat 450 16
Rabbit 1.2 15
5.0 14
Chicken 450 3, 16
Mouse 450 16-100
Rat
147 16
1-2
0.75
0.83
0.83
0.83
0.1-1
1.5
3.6
0.37
0.49
0.5-15
1, 10
1
0.5
0.5-10
3
20
20
20
20
20
20
20
20
20
20
20
10
30
20
60
0.002*
0.0035*
0.0014*
0.0014*
0.0014
0.0005-
0.005*
0.0013
0.0035
-0.001
0.0006
0.0008
0.15-4.35
0.29-2.9
0.3
0.05
Bawin etal. (1975)
Bawin etal. (1978)
Blackman et at. (1979)
Blackman et al. (1980a)
Joines ef al. (1981)
Sheppard et al. (1979)
Blackman etal. (1980b)
Joines and Blackman (1980);
Athey (1981); Joines and
Blackman (1981)
Blackman et al. (1981)
Shelton and Merritt (1981)
Merritt ef a/. (1982)
Lin-Liu and Adey (1982)
Duttaef a/. (1984)
500 V/m 120 x 6wk —
500 V/m 120 x 6wk —
1,5 23
1.5 120
0.12-2.4 Merritt etal. (1982)
0.29 Adey etal. (1982)
Takashima etal. (1979)
0.2. 1.0* Sagan and Medici (1979)
- Lyle etal. (1983)
60-150 <0.075 Albert et al. (1980)
*Est. SAR.
'Square wave.
5-55
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cs and Mutagenesis
r/na/i
ie branch of biology that deals with the
variation of organisms. The biochemical
dity lies in the sequence of bases found
: acids, deoxyribonucleic acid (DNA), and
v.., a ,c« v,c,*os) ribonucleic acid (RNA). All living cells
have the biochemical machinery to detect the
sequence of bases in the DNA and to transcribe
sections of DNA information into similar sequences
of bases in RNA. The RNA molecules then move to
other locations inside the cell, where their information
is translated into various series of amino acids joined
together in sequences that were precisely defined in
the original DNA molecule. These specifically
arranged amino acids form proteins, some of which
are enzymes. Enzymes, in turn, catalyze biochemical
reactions that ultimately result in the growth and
propagation of intact organisms. Hereditary (genetic)
material can be either nucleic acids alone, as found in
bacteria and viruses, or a nucleic acid in association
with proteins, which form the chromosomes found in
more complex organisms, including man.
Heat is a physical agent that can disrupt genetic
material by causing the temperature to rise above
normal physiological range. The effect of heat, or
temperature rise, has been studied in many biological
systems. As examples, heat has been shown to cause
physicochemical damage in isolated DNA preparations
(Lindahl andNyberg 1974; Ginoza era/. 1964; Ginoza
and Miller 1965) and in bacteria (Pellon et al. 1980);
chromosome changes in Drosophila melanogaster
(Grell 1971) and in the Locusts migrator/a (Buss and
Henderson 1971), including a change from diploid to
haploid in pollen from maize (Mathur et al. 1980);
enhanced sensitivity to other agents in mammalian
cell cultures (Ben-Hur et al. 1974) and in D.
melanogaster (Mittler 1979); reduced fertility in rats
(Bowler 1972; Fahim et al. 1975); and mutations in
bacteriophages (Bingham et al. 1976), in bacteria
(Zamenhof and Greer 1958) and in D. melanogaster
(Muller and Altenburg 1919). Because absorbed RF
energy is usually dissipated as heat, all reports of
genetic and mutagenic changes caused by exposure
to RF radiation must be examined closely to
determine whether temperature rise, or some other
mechanism, is the causative agent.
Mutations are relatively permanent changes in the
hereditary material involving either a physical
change in chromosomal relations or a biochemical
change in the sequence of nucleic acid bases that
make up the genes. These changes can be passed on
to future generations of cells. Two different types can
be affected: germ cells, which are egg or sperm or
their antecedent cells; and somatic cells, which form
all other tissues in the body. Mutations in germ cells
can be passed on to future generations of the
organism, whereas mutations in somatic cells of an
organism may lead to impairment of organ function
and, in the extreme case, to cancer. Most mutations
are considered harmful because they disturb the
biochemical processes necessary for the survival of
the organism and for the propagation of the species.
Evaluation of the mutagenic potential of RF radiation
has generally followed the procedures established for
testing the mutagenic activity of chemicalsfHollaender
1971). This evaluative scheme utilizes
• molecular systems, to detect changes in the
hereditary material;
• single-cell organisms, to detect changes in
structure and function that are transmissible to
the next generation;
• multicellular systems, including plants and
animals, to detect changes in reproductive
potential;
• infra-human primates, to detect changes in
reproductive potential.
The evaluation scheme starts with simple, well-
defined genetic systems that enable rapid analysis
and identification of suspected agents meriting
further evaluation. The more complex biological
systems used in further testing require substantially
larger investments of time and resources.
In summary, the following conclusions may be drawn
from the review of the literature on the genetic and
mutagenic effects of RF radiation. Experiments
designed to examine the genetic consequences of
exposure to RF radiation have been conducted with a
variety of test systems, including isolated DNA,
prokaryotic and eukaryotic cells, and whole animal
systems. Radiation-induced effects on biochemical
properties of DNA, on chromosomal structure, on
mutation induction, and on reproductive capabilities
have been investigated. The reports demonstrate that
(1) RF irradiation of low-to-moderate intensity
does not cause mutations in biological systems
in which temperature is adequately controlled,
and
(2) the only exposures that are potentially
mutagenic are those at high power densities of
CW or PW radiation, i.e., exposures that result
in substantial thermal loading at sensitive
sites or result in extremely high electric-field
forces.
These conclusions must be qualified because (a) only
specific frequencies or small regions of the RF
spectrum have been experimentally examined, (b)
few detailed dose-response analyses have been
performed, (c) the influence of modulated radiation has
not been sufficiently examined, an (d) potential
synergistic reactions with other environmental
stresses have not been adequately studied.
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5.8.1 Effects on Genetic Material of Cellular and
Subcellular Systems
5.8.1.1 Physical and Chemical DNA and
Chromosome Studies
Mechanisms for the absorption of RF radiation by
DNA molecules are treated elsewhere in this
document (Sec. 3.2, RF-Field Interactions with
Biological Systems, and Sec. 5.1, Cellular and
Subcellular Effects). This section addresses the
experimental studies that have examined changes in
genetic material induced by RF radiation. Purified
DNA or DNA extracted from the testes of exposed
mice has been examined to determine whether the
physical properties of the molecule can be altered by
the exposure to RF radiation. Hamrick (1973)
examined the thermal-denaturation profiles of
aqueous solutions of isolated DNA exposed in vitro at
37°C to 2450-MHz (CW) radiation (SAR = 67 W/kg).
No changes were found. Even elevated temperatures
(to 50°C) produced by microwaves (1 h at an SAR
estimated to be 160 W/kg) did not cause a difference
in the thermal denaturation profile. (See Sec. 5.1 for
details.)
Varma and Traboulay (1976) reported radiation-
induced changes in thermal denaturation profiles
(i.e., shift to lower temperature in the midpoint of the
transition curve [Tm] and reduction in the maximum
hyperchromicity) as well as changes in the base
composition of testicular DNA extracted from
anesthetized mice whose testes were irradiated in the
near field. Ten animals were exposed individually
either to 1.7-GHz radiation at 50 mW/cm2 for 30 min
(SAR estimated at 2.4 W/kg for testes alone) or at 10
mW/cm2 for 80 min (SAR estimated at 0.48 W/kg for
testes alone), or to 0.985-GHz radiation at 10
mW/cm2 for 80 min (SAR estimated at 0.26 W/kg for
testes alone). The animals exposed to 1.7-GHz fields
at 50 mW/cm2 or to 0.985-GHz fields at 10 mW/cm2
were given a 1 -day recovery period before they were
subjected to euthanasia, and the DNA was extracted.
The animals exposed to 1.7-GHzf ields at 10 mW/cm2
were used in another test for 8 weeks before
euthanasia, and the DNA was extracted. Identical
results are reported for the 1.7-GHz exposure at 50
mW/cm2 in another publication (Varma and
Traboulay 1977). They conclude "that biological
damage may be due to the combined effect of thermal
and nonionizing radiation."
To evaluate the relative contributions of the thermal
effects versus nonionizing radiation per se. the
results reported by Varma and Traboulay must be
examined with careful attention to the control
experiments and to the potential size of the thermal
insult. A critical examination of the base composition
and hyperchromicity data reveals that the authors'
explanations are not supported by the data. Although
the higher percent adenine/thymine in the DNA
extracted from exposed animals could be responsible
for the drop in Tm, the variability normally inherent
in the extraction procedures and in the base
composition measurements is not given. Without an
explicit indication of this variability, one cannot
conclude that the differences between control and
exposed samples are significant; nor can it be
concluded that the differences result from the
radiation exposure directly, rather than from the
extraction procedures. Similarly, the potential size of
the thermal insult must be examined. The SAR values
for testicular exposures were crude estimates based
on incomplete information and appear too low to
produce the types of damage described in the report.
For example, in an anesthetized animal exposed in
the near field to 1.7-GHz radiation at 50 mW/cm2
(SAR estimated at 2.4 W/kg) and shielded with
Eccosorb except for the testes, a 1 to 2°C recta I-
temperature rise was recorded following exposure
(Varma and Traboulay 1977). Since no description of
the exact shielding technique was provided, it is
possible that more than just the testes of the animal
was exposed, thus accounting for the rectal
temperature increase. In another report (Varma and
Traboulay 1975), animals were exposed under the
same conditions as described above, except that the
exposure time varied between 30 and 40 min, and the
testes were examined histologically. The authors
report that "the lumens were empty with complete
disintegration of spermatids, Sertoli cells and the
delicate connective tissue which surrounds the
seminiferous tubules." This type of damage can be
caused by abnormal temperature elevation of the
tissue (Muraca et al. 1976). Since anesthesia has
been shown to impair thermoregulation (Cairnie etal.
1980b), it is possible that sufficient energy was
deposited in the anesthetized animals to cause the
temperature elevation responsible for many of the
changes that are attributed to microwave-specific
effects. (See Sec. 5.3.3, Reproductive Effects—
Testes, for further discussion of the influence of
abnormal temperature rise on radiation-induced
damage in the testes.) Thus, an alternative explanation
for the results described by these authors is that the
causative agent is elevated temperatures, produced
at sensitive sites in the tissue by the radiation
exposures. This explanation is consistent with the
available data, and there is no need to advocate an
unknown mechanism for radiation-induced damage.
Thus, an evaluation of the existing evidence from
physical studies on DNA indicates that RF irradiation at
low-to-moderate intensities not accompanied by
temperature rise causes no changes in DNA bases,
the fundamental unit of the genetic code. However, if
substantial elevations of temperature occur during
exposure, disruptions in the pairing of the two
complementary strands, as well as other damage,
may result.
Other researchers have used cytogenetic techniques
to examine some physical and chemical properties of
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chromosomes in intact cells to determine if the
relationship of various parts of the genetic material is
altered by RF-radiation exposure. Huang etal. (1977)
stated that no RF-induced chromosomal aberrations
were found in white blood cells from Chinese
hamsters exposed to 2450-MHz radiation at power
densities up to 45 mW/cm2 (SAR = 20.7 W/kg) for 15
min/day on 5 consecutive days; however, the data
are presented in a manner which does not permit
independent statistical analysis. McRee et al. (1978)
in a preliminary report found no sister chromatid
exchanges in bone-marrow cells of mice exposed to
2450-MHz fields at 20 mW/cm2 (SAR = 15.4 W/kg),
for 8 h daily, 28 days total. Alam etal. (1978)showed,
in great detail, that chromosomal aberrations
occurred in a Chinese-hamster-cell line (CHO-K1)
exposed 30 min to 2450-MHz radiation from a
diathermy applicator, but only if the temperature of
the culture was allowed to rise to 49°C during
exposure. These authors demonstrated that irradiation
of cell lines at high (> 200 mW/cm2) power densities
(SAR estimated at 360 W/kg) would cause no
detectable cytogenetic effects, provided proper
temperature control was maintained. Thus, heating
seems to account for the observed cytological
changes.
Authors of one detailed study used a frequency well
below the 1.7- to 2.45-GHz range. McLees et al.
(1972) exposed rats treated to undergo liver
regeneration either to 13.12-MHz CW(4.45 kVp-p/m)
fields or to PW (44.1 kVp-p/m, 200-/us pulse width,
50-Hz pulse repetition rate [PRR]) radiation for 28 to
44 h. They examined the effects of radiation on liver
cell mitotic activity (i.e., the percentage of cells in
mitosis and the number of chromosomal aberrations).
Rat liver cells may be very sensitive to exogenous
stresses during this regenerative process because
they are normally nondividing cells in an intact
animal unless challenged to divide in situ. However,
the authors found no RF-induced alterations in
chromosomal morphology (SAR estimated at 1.2 to
1.3 W/kg). Their results indicate that no cytogenetic
changes would be expected in the range of
frequencies studied for low-intensity exposures.
Thus, although there are reports indicating that
exposure to RF radiation can cause cytogenetic
changes, these changes appear to result from
radiation-induced elevations of temperature.
McRee et al. (1981) have recently published the paper
that was reviewed when in preliminary format
(McRee et al. 1978). Twelve 10-we.ek-old female mice
(CD-1 strain) were exposed to 2450-MHz CWfields at
20 mW/cm2 (SAR = 21 W/kg) for 8 h daily (4 h in
morning, 1 h delay, 4 h in afternoon) each day for 28
days. Exposure was dorsal. Immediately after the last
exposure, procedures were initiated that produced,
19 h later, labeled bone marrow cells that-were
processed to give a measure of sister chromatid
exchanges. Upon analysis, no statistical differences
were detected in the mean number of sister
chromatid exchanges per cell between the exposed
and either of the unexposed control groups (sham and
cage control). Based on the percentage of mitotic cells
in each group, the microwave treatment did not have
an effect on the rate of cell proliferation in bone
marrow of mice. These results are consistent with
those given in the preliminary report.
5.8.1.2 Biological Studies of DNA and
Chromosomes
Bacteria have been used to study the mutagenic
potential of RF radiation, because the single-cell
system is simple, easy to culture, quick to test, and
relatively sensitive to the action of mutagenic agents.
By using the bacterial system and the biological
amplification it provides for any DNA change,
molecular biologists have been able to decipher the
genetic code and to identify a change in as few as one
DNA subunit out of 10'° to 1012 subunits. In contrast,
biologists using standard physical techniques such as
DNA melting curves usually can detect changes in no
better than 0.1 percent of the DNA. Blackman et al.
(1976) exposed growing cultures of the bacterium
Escherichia coli either to 1.7- or to 2.45-GHz (CW)
radiation for 3 to 4 h. Exposure at 1.7 GHz was in the
near field at 88 V^s/m or ~ 250 Vp-p/m (SAR = 3
W/kg). The 2.45-GHz exposures were in the far field
at either 10 or 50 mW/cm2 (SAR = 15 or 70 W/kg,
respectively). Although exposure of growing cells
provided enhanced sensitivity to mutagenic agents,
no mutagenic activity was detected. A positive
control, ultraviolet (UV) light, caused mutations and
was used to demonstrate the sensitivity of the assay
method. Dutta et al. (1979a) exposed growing
cultures of various bacterial strains of Salmonella
typhimurium, commonly used in the Ames testing
procedures to detect chemical mutagens (Ames et al.
1975), to 2.45-GHz (CW) radiation for 90 min at 20
mW/cm2 (SAR =40 W/kg) and to 8.6-, 8.8-, 9.0-, 9.2-,
9.4-, and 9.6-GHz (PW) radiation (1 -yus pulse width, 1 -
kHz PRR) at 10 and 45 mW/cm2 average power
densities, and 10,000 and 45,000 mW/cm2 peak
power densities. (The SAR at 45 mW/cm2 was
estimated at 80 W/kg.) No mutagenic activity was
observed under any of these exposure conditions.
Another approach with bacterial systems is to test for
radiation-induced alterations in genetic processes,
including cell death. Since most mutations are
detrimental, they might be detected indirectly by this
method. Corelli et al. (1977) exposed cultures of E.
coli to microwaves at frequencies swept between 2.6
and 4.0 GHz for 8 h (SAR = 19 W/kg). Although at
26°C these cultures were probably growing slowly,
no change was noted in the number of colony-
forming units (CFUs) in the cultures following
irradiation, indicating no detectable lethal events
because of the exposure. These workers also
examined the infrared (IR) spectrum of these cells
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when exposed to 3.2-GHz radiation for 11 to 12 h
(SAR is either 21 or 16 W/kg). There was no
observable effect on the molecular or conformational
structure of these cells, in contrast to results obtained
with a positive control, ionizing radiation. Two strains
of E. coli, one deficient in an enzyme needed to repair
damaged DNA, were tested for survival following
microwave exposure (Outta et al. 1979b). The
exposure conditions were 8.6-GHz (PW) radiation (1 -
/us pulse width, 1 -kHz PRR, SAR = 12 W/kg) for 1, 2,
4, or 7 h. There was no significant change in the
relative growth patterns of these strains that could be
attributed to microwave-induced ONA damage that
was repaired in one strain, but not in the other.
Blackman eta/. (1975) exposed a different strain of f.
coli in log phase (actively dividing) and in lag phase
(undergoing metabolic activities preparatory to
division) at 32°C for 4 h to 2.45-GHz radiation at
0.005, 0.5, 5.0, or 50 mW/cm2. (At 50 mW/cm2
power density the SAR = 75 W/kg.) Additional
experiments were conducted at 5 mW/cm2 and 25°C
to test for the influence of cold stress, and in two-
culture media at 30 and 35°C to compare the relative
influence of a rich medium with a minimal medium;
the latter required greater utilization of the genetic
apparatus of the cell for growth to occur. Except for
enhanced growth at 50 mW/cm2, which was
attributed to slight temperature rises in the exposed
cultures, no change was found in the colony-forming
ability of the cultures due to the exposure.
Few researchers have used single-cell systems more
complex than bacteria specifically to look for RF-
radiation-induced mutagenesis. Dutta et al. (1979a)
exposed a diploid strain of the yeast Saccharomyces
cerevisiae, a primitive eukaryote, to 2.45-GHz (CW)
radiation for 2 h at 20 mW/cm2 (SAR = 40 W/kg).
They found essentially no change in the number of
mutations at either of two loci affecting the
nutritional requirements for adenine or tryptophan.
These investigators conducted additional tests at 8.5-,
8.6-, 8.8-, 9.0-, 9.2-, 9.4-, and 9.6-GHz(PW)radiation
(1-/JS pulse width, 1-kHz PRR) for 2 h at average
power densities of 1, 5, 8.9, 10, 15, 30, 35, 40, or 45
mW/cm2. Although no measurements of SAR are
cited, so that comparisons with CW exposures are
difficult, the highest power density was reported to
raise the temperature of the culture by 12°C, which
would mean substantial absorption of the radiation.
(At 45-mW/cm2 power density the estimated SAR =
80 W/kg.) In no case did the exposures cause a
change in the frequency of genetic events, altering
the requirements for either adenine or tryptophan, in
the treated population as compared with the control
population. Saccharomyces cerevisiae was also used
in two studies by Dardalhon and co-workers. In the first
report, Dardalhon et al. (1979) exposed two haploid
and one diploid strain of the yeast at 20°C in the near
field to either 70.5- or 73-GHz CW fields at power
densities up to 60 mW/cm2 (SAR estimated at 17
W/kg) for durations up to 3 h. In the second report,
Dardalhon et al. (1980) exposed a diploid strain of S.
cerevisiae at 20°C in the near field of 9.4-GHz (CW)
radiation (SAR estimated at < 2 W/kg) for 1 to 5 h, or
in the near field of 17-GHz (CW) radiation at either of
two power densities (SARs estimated at 28 or < 6
W/kg, respectively) for various times to 24 h. No
significant changes attributable to the irradiation
were observed in the percent survival, in the
induction of cytoplasmic "petite" mutations, in the
induction of mitotic recombinations, or in sporulation.
Thus, no changes were detected in complex single-
cell systems used to examine directly the mutagenic
potential of microwaves at frequencies of 9.4, 17,
70.5, or 73 GHz (CW) and SARs of < 2 to 28 W/kg.
Some work has been done with bacteria and yeast
cultures that compares the lethal and mutagenic
effects of microwaves with those induced by
conventional heating. Dutta et al. (1980) examined
the responses of various strains of the bacteria S.
typhimurium and E. coli and those of a diploid strain
of the yeast S. cerevisiae, exposed to 8.6-, 8.8-, or
9.0-GHz (PW) radiation (1 -kHz PRR, 1 -A»S pulse width)
at average power densities to 45 mW/cm2 (SAR
estimated maximum at 80 W/kg). The bacteria were
exposed 90 min at an ambient temperature of 37°C,
whereas the yeast were exposed 2 h at 30°C. The
comparison of these irradiation treatments with
those obtained from treatments at elevated tempera-
tures produced by conventional heating indicated that
conventional heating could produce cellular damage
leading to reduced survival in a manner similar to the
changes caused by microwave-induced elevations of
temperature (to 10°C above normal growth tempera-
tures). Nd mutational events occurred in bacteria to
42°C, or in the yeast to 40°C, however, at 45°C, a
slight increase in mutational events occurred in the
yeast, and at 47°C, in S. typhimurium. To obtain some
indication of the temperature rise associated with
exposure to RF radiation, Dardalhon et al. (1979)
developed a response curve for zygote formation, the
production of a diploid cell from the union of two
haploid cells, as a function of temperature. Exposure
to 70.5-GHz CW fields at 60 mW/cm2 (SAR estimated
at 17 W/kg) produced a response in zygote formation
that could result from a 3°C temperature rise. This
result demonstrated that biological systems could be
used as sensitive indicators of temperature change
under exposure conditions in which temperature can
not be readily measured. In another study, Dardalhon
et al. (1980) exposed a diploid strain of S. cerevisiae
for 3 h at 52°C. (Normal growth temperature is 30°C.)
Large changes were observed In the percent survival,
in the induction of cytoplasmic mutations, and in the
induction of mitotic recombinations after 3 h,
compared to no changes in these end points during
microwave exposure at 20°C to 9.4-GHz or 17-GHz
fields (SAR estimated at < 28 W/kg), described
above. Both groups of authors conclude that care
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must be exercised in evaluating genetic changes in
microbial assay systems when elevated temperatures
accompany microwave exposure.
Since 1980, three groups have published reports in
this subject area. Dutta extended his previous work
(Dutta et at. 1979b, 1980) with two strains of E. coli,
one deficient in an enzyme needed to repair damaged
DNA, to compare bacterial growth under high-
intensity microwaves and conventional heating
(Hossain and Dutta 1982). Both bacterial strains were
grown for 2. 5,10, or 15 h either at 35.2 °C or42.2°C,
or exposed to 8.8-GHz (PW) radiation (1-/as pulse
width, 1-kHz PRR, SAR = 12 W/kg) at 35.2°C (final
temperature of the sample was 42.2°C) and assayed
for growth, as colony-forming units. The results
demonstrated that although the microwave exposure
caused a change in the bacterial growth when
compared with the 35.2°C control, it had no effect on
the growth of E. coli beyond that associated with the
radiation-induced temperature increase.
Dardalhon and co-workers (1981) exposed the yeast
S. cerevisiae, and both normal and repair-deficient
strains of the bacterium E. coli, to microwave fields
and tested for survival and induction of mutations. In
diploid yeast, they tested for sporulation capacity and
gene segregation during meiosis. They found no
evidence for altered survival in any of the bacterial
strains following near-field exposure for 30 min to
9.4-GHz CW fields (SAR = 23 W/kg), 17-GHz CW
fields (up to SAR = 28 W/kg), or 70- to 75-GHz CW
fields (SAR = 9 W/kg), nor any evidence of mutation
induction following exposure for 30 min to 70- to 75-
GHz CW fields (SAR = 28 W/kg) or 17-GHz CW fields
(SAR = 6 W/kg). Exposure of haploid yeast strains to
70- to 75-GHz CW fields (SAR = 28 W/kg), 17-GHz
CW fields (up to SAR = 28 W/kg), or 9.4-GHz CW
fields (SAR = 23 W/kg) produced no detectable
changes in survival, induction of cytoplasmic
mutations, induction of reversions, or genetically
altered colonies. Similarly, exposure of diploid yeast
to 9.5-GHz CW (SAR = 23 W/kg) or 17-GHz CW (SAR
= 28 W/kg) fields for 48 h produced no significant
alterations in the sporulation capacity nor in meiotic
gene segregation. Thus with both prokaryotic and
eukaryotic cells these investigators did not detect any
significant genetic effects from exposure to microwave
radiation at selected frequencies between 9.4 and 75
GHz.
In a series of three detailed papers, Swedish
researchers studied the possible genetic effects in
bacteria of exposure to high-frequency RF fields
(Anderstam et al. 1983; Ehrenberg et al. 1983;
Hamnerius 1983). Tests for forward mutations were
performed in two E. coli strains and three S.
typhimurium strains, for backward mutations in three
E. coli strains and two S. typhimurium strains, and for
prophage induction in three E. coli strains. The
bacterial samples were exposed in the far field at
37°C to either 3.07-GHz pulsed fields (500 Hz PRR, 2-
fjs pulse width) at average power densities up to 210
mW/cm2 (SAR = 100 W/kg), or 2.45-GHz CW fields
(which were essentially 100-percent amplitude
modulated at 100 Hz) at power densities up to 170
mW/cm2 (SAR = 80 W/kg). Bacterial samples were
exposed similarly to 27.12-MHz CW field components:
electric fields at 72 V/m in the sample generated
between two parallel plates (SAR = 3 W/kg), and
magnetic fields at 20 A/m in the sample generated by
a Helmholtz coil (SAR = 20 W/kg). Exposures were
conducted for 1 to 7 h, followed by measurements of
cellular growth for viability, mutation or prophage
induction, or RNA synthesis. The battery of bacterial
test systems used in this detailed study was designed
to provide a measure of resolving power and thus to
place an upper confidence limit on the number of
mutagenic events that would be probable for a given
result. The authors state that the pooled mutation
frequency did not differ from that of the controls,
although a weak prophage-induction capability and an
ability to modify the response to UV-radiation (DNA
repair) were noted. The most prevalent finding was a
stimulation of growth, especially for certain strains
and as the cultures were entering stationary phase.
This result was also exhibited in the RNA synthesis
studies. Although the authors discounted at length
the influence of temperature difference as the
underlying cause of the growth stimulation, because
of the high SARs that were used, a 1 °C temperature
gradient was known to exist between the bacterial
samples and the cooling bath. Other workers, notably
Livingston er a/. (1979), have emphasized the
extreme caution that must be exercised in interpreting
data obtained under conditons where local hot spots
could occur. To support their contention that
temperature change contributed in only a minor way
to the observed growth stimulation, the authors could
have conducted exposures at temperatures below
and above the optimum growth temperature. If
temperature increases were a major factor in the
field-induced growth-rate changes, one would expect
a reversal in the response between the lower and
higher temperatures. The complex biochemical
changes that occur as the cells transfer from
exponential to stationary growth phase adds further
uncertainty to any evaluation of altered growth
patterns. Nevertheless, with a comprehensive battery
of test systems, the authors were unable to
demonstrate any mutagenic activity due to exposures
to 27.12-MHz CW, 2.45-GHz CW, or 3.07-GHz pulsed
fields.
In another study to determine temperature change
during RF exposure, Dardalhon et al. (1979) exposed
one diploid and two haploid strains of the yeast S.
cerevisiae, at 20°C in the near field to either 70.5 or
73-GHz CW fields at power densities up to 60
mW/cm2 (est. SAR = 17 W/kg) for up to 3 h. No
changes were observed in cell survival, or in induction
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of mitotic recombination or of cytoplasmic mutations.
To obtain some indication of the temperature rise
associated with these exposures, the authors
developed a biological indicator, namely a response
curve for zygote formation as a function of
temperature. Exposure to 70.5-GHz CW fields at 60
mW/cm2 (est. SAR = 17 W/kg) produced a response
that could result from a 3°C temperature rise. This
result demonstrates the usefulness of biological
systems as sensitive indicators of temperature
change under exposure conditions where temperature
can not be readily measured.
All these reports are consistent with the conclusion
reached above that no well-defined genetic effects
have been reported occurring from exposure to
microwave radiation that could not be attributed to
temperature rise. However, the work of Grundler and
Keilmann (1983) identifies possible frequency-
specific alterations in the growth of yeast (Sec. 5.8.3).
The mechanism for this response has not been
identified.
5.8.2 Effects on Genetic Material of Higher-Order
Biological Systems
5.8.2.1 Plants
Plant systems are sensitive to mutagenic agents and
thus can serve to identify conditions that should be
examined more carefully in mammalian systems.
Although several studies are reported in the
literature, none has sufficiently described experi-
mental conditions to allow independent evaluation of
the work. Thus, useful mutagenic testing of RF
radiation with respect to plant systems has yet to be
accomplished and documented.
5.8.2.2 Invertebrates
Several investigators have studied D. melanogaster.
a standard model for testing mutations induced by RF
radiation. No mutagenic effects were reported by
Hamnerius et al. (1979) in embryos exposed 6 h in
water at 24.5°C to 2450-MHz (CW) fields at 100
W/kg. Similar negative effects were reported by Pay
et al. (1972), who exposed adult males to 2450-MHz
fields for 45 min at 4600, 5900, or 6500 mW/cm2
(SARs estimated at 140, 190, and 210 W/kg,
respectively) and mated each of the surviving males
individually with two virgin females during 15
consecutive days. No changes were observed in the
generation time or sex-ratio pattern of the offspring.
These offspring were then mated and observed for
possible sex-linked lethal mutations in their
offspring. No such mutations were found at
frequencies > 1 percent, a detection limit based on
the small number of chromosomes (< 800) actually
evaluated. An additional caveat by the authors was
that the most sensitive stages to detect recessive sex-
linked lethal mutations (late spermatocytes and early
meiosis) were not tested in their study, because few
sperm were still in meiosis at the time of exposure.
Mittler (1976), who exposed adult males from various
strains of D. melanogaster to 29-MHz (CW) fields at
600 Vrms/m (SAR roughly estimated at 0.024 W/kg
and to 146-MHz (CW) fields at 62.5 Vms/m (SAR
roughly estimated at 0.015 W/kg) for 12 h, mated
them with virgin females for 12 h every 2 days in
production of 4 or 5 broods. In these experiments,
brood 4 was produced from sperm irradiated "in or
about meiosis." No mutations were induced by these
treatments as evidenced by the lack of chromosome
loss, nondisjunction, or sex-linked recessive lethals.
In addition, Mittler (1977) observed no mutagenic
effects (recessive lethals) when exposing adult
females to 98.5-MHz frequency-modulated fields
(composed of standard commercial broadcast audio
frequencies) at 0.3 Vm,,/m (SAR estimated at 0.0004
W/kg), 134 h per week for 32 weeks. Although the
results with D. melanogaster are difficult to
extrapolate to the human condition, this test system
as a qualitative index could not detect any mutagenic
alterations by RF radiation over a wide range of
frequencies.
5.8.2.3 Vertebrates
Experiments with vertebrates address the impact of
the genetic effects of RF radiation most directly be-
cause of the general biological similarities between man
and other vertebrates. However, there are very few
such experiments directed at this subject. Three
studies have been reported that are directly focused
on the mutagenic potential of microwaves in mice
and rats. Varma et al. (1976) used the dominant-
lethal test to investigate the effects of 2.45-GHz (CW)
radiation. The testes of anesthetized mice were
treated either by a single 10-min exposure at 100
mW/cm2 (SAR estimated at 11.4 W/kg), or by three
exposures of 10 min each at 2-h intervals on the same
day at 50 mW/cm2 (SAR estimated at 5.7 WAg), or by
four exposures of 10 min each at 3-day intervals over 2
weeks at 50 mW/cm2 (SAR estimated at 5.7 W/kg).
Varma and Traboulay (1976) in a similar study exposed
the testes of anesthetized mice to a single dose of 1.7-
GHz radiation, at 10 mW/cm2 for 80 min (SAR
estimated at 0.48 W/kg) or at 50 mW/cm2 for 30 min
(SAR estimated at 2.4 W/kg). Following a 24-h recovery
period, the males were bred with virgin females—one
group of females per week for 6 to 8 weeks. In the 2.45-
GHz study, the authors used the week-6-group results
for comparison; they found a higher mutagenicity index
in the results of the 100-mW/cm2 group bred at week 1,
and in results of the 50-mW/cm2 group exposed three
times in one day and bred at week 4. The authors
concluded that a single intense exposure or multiple
exposures during one day induced a number of
significant mutations in the mice. The results of the 1.7-
GHz studies at 50 mW/cm2 for 30 min indicated a
radiation-induced increase in infertility, in pre-
implantation losses, and in the mutagenicity index of the
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groups bred at 3, 4, 5, and 6 weeks. In addition, for the
group exposed to 1.7-GHz fields at 10 mW/cm2 for 80
min, an increase was seen in the mutagenicity index of
the groups bred at 1, 2, 3, and 6 weeks. The authors
concluded that the "biological damage may be due to the
combined effect of thermal and nonionizing radiation."
Both these reports should be evaluated on the basis
described in Sec. 5.8.1.1, Physical and Chemical DNA
and Chromosome Studies, for the physical and chemical
studies reported by these authors. Basically, the reports
do not describe the exposure conditions in sufficient
detail to allow an unequivocal evaluation of the results.
Also, it is not possible to determine the extent of the
biological damage caused by elevated temperature in
either of these reports, especially because anesthetized
mice lack an effective temperature-regulatuion
capability (Cairnie et a/. 1980). However, if the
histological damage found in the testes of animals
exposed under similar conditions (Varma andTraboulay
1975} is reflected in damage to sperm, it could account
for many if not all changes in the mutagenic index,
fertility, and pre-implantation loss reported by those
authors in later studies.
The conclusion that radiation in the frequency range
of 1.7 to 2.45 GHz could cause mutagenic changes in
mice was challenged in a detailed study by Berman et-
al. (1980). Unanesthetized male rats were exposed to
2.45-GHz (CW) radiation under three treatment
regimens: 4 h/day from day 6 of gestation to 90 days
of age at 5 mW/cm2 (SAR varied from 4.7 W/kg to
somewhat less than 0.9 W/kg at day 90, because
growth of the animals changed their energy
absorption efficiencies); 5 h/day for 5 days beginning
on day 90 at 10 mW/cm2 (SAR estimated at 2 W/kg);
and 4 h/day, 5 days/week, for 4 weeks beginning on
day 90 at 28 mW/cm2 (SAR estimated at 5.6 W/kg).
During selected weekly periods after -treatment, the
exposed males were bred to untreated females that
were examined in late pregnancy by the dominant-
lethal assay. No significant germ-cell mutagenesis
was detected under any treatment condition, even
though significant increases in rectal and testicular
temperature were observed during the 28-mW/cm2
exposure and were associated with a concomitant
decrease in incidence of pregnancy during some of
the breeding periods, which indicates temporary
sterility. In addition, these authors reexamined the
data of Varma and concluded they had been
interpreted incorrectly because the effects of litter
size on fetal mortality had been ignored and the
differences between treated and control groups had
been overemphasized when the control values were
not representative of normal values. Berman et al.
(1980) concluded that "it still remains to be
demonstrated that microwaves, even at near-lethal
doses, can cause a dominant lethal mutagenic effect
in the mouse or the rat." Thus, well-designed
experiments with biological systems having complex
genomes similar to man's have demonstrated no
mutagenic effects from low- to moderate-intensity RF
radiation when the temperature of the biological
system is maintained in the physiological range. Most
of the reported changes are consistent with the
effects expected from elevations in temperature,
caused by CW exposure to high-intensity RF
radiation. The other purported changes cited in this
section may have resulted from incomplete experi-
mental design.
Recently, dominant lethality was tested by Saunders
et al. (1983), who exposed the lower half of adult male
C3H mice one time for 30 min in a waveguide at
2450-MHz CW fields (average SAR = 43 W/kg). The
exposed males were then mated with pairs of virgin
females each week for 10 weeks. The uterine contents
of the females were examined either on day 14 or day
18. The post-implantation survival, defined as the
number of living implants divided by the total number
of implants, was used as a measure of the dominant
lethality. There were no significant changes in the
dominant lethal test for any of the 10 mating periods,
which indicated that no stage of spermatogenesis
was preferentially sensitive to the RF treatment. This
result is in agreement with the other results cited in
this section. Other measures made by Saunders eta/.
are distussed in Sec. 5.3.3.
5.8.3 Unresolved Issues
Heating, which raises the temperature of biological
samples above normal physiological ranges and may
result in genetic and mutagenic changes, is a well-
known result of exposure to high-intensity RF
radiation. The choice of exposure conditions to study
the genetic and mutagenic effects of moderate to low
intensity radiation is arbitrary because no well-
defined mechanism of RF interaction other than
heating has been developed to address this biological
problem. The experimenter must select the frequency,
intensity, and duration of exposure, as well as the
type and characteristics of modulation. To compound
the problem further, the number of biological systems
that could be selected for study is limitless. Several
guides can be developed from recent experimental
findings to help delineate a future experimental plan.
Although the conclusion has been stated above that
no strong evidence exists in the cited reports to
demonstrate activity for low-intensity RF radiation
per se, it should be qualified by the following
observations:
1. These experiments are limited to small portions of
the RF region of interest, i.e., 0.5 MHz to 100 GHz.
This 106-Hz frequency range is so large that if
detrimental effects occurred over very narrow
frequency ranges, they might have gone unde-
tected.
2. Many of the experiments were conducted with
CW radiation. If effects exist, they may occur with
5-100
-------
amplitude-, frequency-, or PW-modulated radiation
at frequencies associated with ongoing biological
or biochemical processes. An exposure to a short-
duration, high-intensity PW radiation (radar-like)
may not produce the same biological response as a
CW exposure of the same average power density.
Thus, the concept of averaging the intensity of PW
radiation over time to determine an effective
intensity may not be generally valid.
3. The general approach in most experimental
studies has been to assume that the higher the
radiation intensity, the more pronounced the
biological effect. It is possible that several
mechanisms are operative during radiation
exposure and that mechanisms with thresholds at
relatively high intensities (e.g., heating) mask the
effects, which may be caused by the more subtle
mechanisms.
4. RF radiation may enhance the effects of known
mutagenic agents as a co-stressor. In environ-
mentally relevant situations, biological systems
are exposed simultaneously to many agents, both
chemical and physical.
5. Standard test procedures that have been
optimized to identify ionizing and chemical
mutagens are not necessarily applicable to
examining the interaction of RF radiation with
complex biological structures and genetic
material. No test system should be overlooked as
potentially sensitive for detection of mutagenic
activity. For example, plant systems have been
shown to be extremely sensitive indicators of
environmental pollution.
Recent experimental developments support some of
the suggestions made above. Possible frequency-
specific responses were reported by Smolyanskaya
and Vilenskaya (1973), who described the induction of
colicin in E. coli by extremely high-frequency
radiation, near 37 GHz, at power densities of 0.001,
0.01,0.1, or 1.0mW/cm2for0.5,1, and 2 h. Colicin is
a protein usually not made by the cell. Its induction,
though not well understood, requires the transcription
of a new portion of the DNA molecule. This induction
demonstrates that specific microwave frequencies
can induce changes in the genetic processes of cells.
More recently, Grundler et al. (1977) described
frequency-dependent growth responses in the yeast
S. cerevisiae exposed for periods to 11 h to
microwave frequencies between 41 and 42 GHz at 1
to 3 mW/cm2 (average SAR estimated at 4 to 11
W/kg). (See Sec. 5.1, Cellular and Subcellular
Effects, for details.) Although this work is controver-
sial, it does support the frequency-specific-response
concept.
The importance of examining the effects of RF
radiation as a co-stressor with other agents is
emphasized in the report by Dardalhon et al. (1980)
that was discussed earlier with respect to exposure
either to heat or to microwave radiation. These
authors exposed haploid and diploid strains of S.
cerevisiae tor 1 h to 17-GHz(CW) radiation, near field,
at 50 mW/cm2 (SAR estimated at < 6 W/kg) and
20°C, followed by exposure to various doses of UV
light (254 nm), which is known to cause damage
directly to the DNA. Both haploid and diploid strains
were affected. The exposure combination caused a
tendency—but apparently not a statistically signifi-
cant change—toward diminished survival, increased
mitotic recombination, and increased cytoplasmic
"petite" mutations, when compared with the effects
caused by exposure to the same doses of UV light
alone. This possible microwave-radiation enhance-
ment of effects due to UV-light exposure would be
unusual, because it was observed only at high doses
of UV light, where additional repair systems are
presumably operative. The authors found similar
trends by replacing microwave-radiation exposure
with temperature elevation to 46°C before treatment
with UV light. No influence from exposure to
microwave radiation,- followed by UV light, was
observed for 17-GHz fields at 2.5 mW/cm2, or for 9.4-
GHz fields at 5 mW/cm2. Because the microwave-
radiation treatment caused only a 1°C global
temperature rise in the sample that was 10°C below
its normal growth temperature, the authors reasoned
that if temperature rise is the basic agent enhancing
the UV-light-induced response, it must be occurring
selectively at specific sites within the biological
system other than on the DNA itself, so that change
is perhaps caused in metabolic processes or in the
structural integrity of cytoplasm, or of membranes. In
this case, a differential sensitivity among the various
repair systems may be induced by the UV light.
Similar investigations might reveal biological
processes, including repair of damage or detoxification
of chemicals, that may be particularly sensitive to
microwave-radiation exposure.
In another area, radiation-induced efflux of calcium
ions from in vitro brain tissues has been shown to
depend on the modulation frequency of a carrier wave
(Bawin et al. 1975; Blackman et al. 1979). The
effective modulation frequencies were in the same
frequency range as the natural biological rhythms
associated with the EEG in the intact animal, and thus
the radiation may have coupled with an existing
oscillatory system. Further studies by Blackman et al.
(1979; 1980a,b) and Sheppard et al. (1979) indicated
that higher and lower intensities of radiation can lead
to the disappearance of the effect. This result
suggests that examining biological processes only at
a single power density may provide misleading
information.
Three additional, incomplete reports have been
included in this section. These studies are included
either because they present positive findings at
5-101
-------
frequency ranges or intensities seldom studied or
because of a strong claim by the authors. Heller
(1970) and Mickey and Koerting (1970) reported
chromosomal aberrations in cultured Chinese-
hamster lung cells exposed for 30 min to 19- or 21-
MHz fields, although no changes were observed after
exposure to 15- or 25-MHz (PW) fields (100-Hz PRR,
50-fjs pulse width) at field intensities to 300 kVp-p/m.
It is very likely either that the extremely high peak
voltages (up to 300 kVp-p/m) were producing intense,
rapid heating within the cells, or that the field per se
was causing major stresses within the system.
These reports provide insufficient descriptions to
allow an estimate of the SAR values, and thus these
results cannot be compared with those found by
others,. It is possible that fields at extremely high
intensities can account for some cytogenetic changes.
Manikowska et a/. (1979) reported a dose-indepen-
dent increase in chromosomal translocations and in
chromosomal pairs remaining as univalents at
Metaphase I in the sperm cells of mice exposed 1
h/day, 5 days/week, for 2 weeks to 9.4-GHz (PW)
radiation at 200-, 1000-, 2000-, or 20,000-mW/cm2
peak power densities (0.5-//S pulse width; 1 -kHz PRR;
0.1-, 0.5-, 1-, and 10-mW/cm2 average power
densities, respectively). (Average SAR is roughly
estimated at 5 W/kg, and peak SAR roughly at 9000
W/kg for the highest power density used.) The
authors do not describe the relation of the animals'
testes to the incident field, which thus raises the
question of the actual quantities of energy coupled to
the target cells at 9.4 GHz, where tissues exhibit large
attenuation coefficients. A description of the
environmental conditions during exposure is also
absent. These omissions prevent any critical
assessment of the results. Furthermore, because of
the small number of animals used in the study, the
authors themselves state that "the findings...
obviously need confirmation on larger numbers of
animals."
In another study, based on bacteria exposed to
extremely high temperatures, an incomplete analysis
of the distribution of temperatures within the
samples led to an unjustified conclusion. Blevins et
al. (1980), who exposed several strains of S.
typhimurium commonly used in the Ames testing
procedures (Ames et al. 1975) to 2.45-GHz radiation
in a microwave oven at a calculated power density of
5100 mW/cm2 for periods of 2 to 23 s, examined the
cultures for lethality and for mutation induction.
These exposures caused extremely large elevations
of temperature. Corollary heating experiments were
performed in high-temperature water baths to
determine the extent to which temperature change
alone contributed to lethality and mutations. Their
crnclusion that microwave radiation is a potent
mutagen, because it caused mutations in excess of
those expected from the radiation-induced tempera-
ture rise, is not supported by their data. The authors
failed to demonstrate that the uniformity of
microwave heating was duplicated by the water bath
experiments. The authors acknowledge that "differ-
ences in the kinetics of water bath and microwave
heating are possible" but do not evaluate this
possibility further. Because of the larger temperature
increases in their culture systems—apparently as
large as 46°C in 14 s—more definitive temperature
distribution work must be done to establish
accurately the contribution that temperature change
makes to induction of mutations before additional
mutagenic properties are assigned to microwaves.
Blevins et al. (1980) reported using a power density
500 times greater than the current U.S. occupational
guidelines. Because the apparent mechanism (i.e.,
heating) is based on such high, nonphysiologic
temperatures, .the authors' conclusions are not
applicable to the other cited studies, which have used
2.45-GHz radiation. However, the study may support
a reevaluation of the concept that brief, high-intensity
exposures can be averaged over a longer time period
to define the average intensity. For example, an
exposure to 5100 mW/cm2 for 2 s is 28 mW/cm2 if
averaged over 6 min, and an exposure for 14 s
becomes 200 mW/cm2 if averaged over 6 min. The
Blevins et al. study would also support the concept
that'high-intensity pulses of microwaves may affect
biological systems differently from convection or
conduction heating.
Although no solid evidence exists (i.e., there are no
independently verified reports) to indicate that low-
intensity RF radiation is mutagenic, sophisticated
concepts and designs are just beginning to appear in
experiments concerning the biological effects of RF
radiation. Thus, although it is premature to proclaim
unequivocally that RF radiation is not mutagenic, the
majority of evidence at present indicates, in the
absence of temperature elevation, that is the case.
The above studies of the biological effects of RF
radiation that relate to genetics and mutagenesis are
summarized in Table 5-24.
Since 1980, several recent reports at scientific
meetings have supported or extended the concerns
raised in this section. Kremer et al. (1983) examined
the puffing pattern of giant chromosomes from the
salivary gland of the midge Acricotopus lucidus
following a 2-h exposure to fields swept between 64
and 69 GHz CW, or at single, stabilized frequencies of
67.2 or 68.2 GHz CW. Power densities were less than
or equal to 5 mW/cm2 and resulted in temperature
rises of less than 0.03°C. There was up to a 10 times
reduction in the Balbiani ring BR2 in chromosome II;
that is, the normal mass of DNAfibers usually seen at
one chromosome locus was dramatically retarded
following microwave exposure. No change in the
normal puffing pattern was observed in either the
sham treated samples or the sham plus heat treated
samples (2.5°C temperature increase). This result
5-102
-------
Table 5-24. Summary of Studies Concerning Genetic and Mutagentc Effects of RF-Radiation Exposure
Exposure Conditions
Ol
*•*
8
Effects
No change in thermal denaturation profile.
except at elevated temperature
Change in thermal denaturation profile and
hyperchromicity of DNA extracted from
testes following exposure
No chromosome aberrations in white blood
cells
No sister chromatid exchange in bone
marrow cells
No chromosome aberrations in CHO-K1 cell
line if temperature maintained
No chromosome aberrations or change in
mitotic activity in regenerating liver
cells in rat
No mutation induction
No mutation induction observed in Ames
tester strains
Reduction in survival concomitant with rise
in sample temperature
No reduction in survival or mutational
events
No reduction in survival or mutational
events
No detectable lethal events due to no
change in CPUs
No observable change in molecular
structures because no change in IR spectrum
No repairable DNA damage
No change in growth pattern;
enhanced colony-forming activity
No change in mutation frequencies at
either of two loci controlling requirements
for adenine and tryptophan
No mutagenic effects in exposed embryos
No changes in generation time, sex ratio,
or sex-linked lethal mutations in offspring
No mutations in adult males as evidenced by
chromosome loss; nondisjunction; or sex-
Species
DNA
Mouse
Chinese hamster
Mouse
Chinese hamster
Rat
E COll
E coli
S typhimurium
£ coli
S typhimurium
S cerevisiae
S cerevisiae
S. cerevisiae
E. coli
E coli
E coli
E coli
S. cerevisiae
D. melanogaster
D. melanogaster
D. melanogaster
Frequency
(MHz)
2.450ICW)
1.700ICW)
985 (CW)
2,450 (CW)
2,450 (CW)
2,450 (CW)
13.12 (CW)
1312 (PW)
2.450 (CW)
1,700(CW)
2.450 (CW)
8.600-9,600 (PW)
8,600-9,000 (PW)
8.600- 9,000 (PW)
8.600-9,000 (PW)
70.500 (CW)
73.000 (CW)
9,400 (CW)
1 7.000 (CW)
2,600 4,000 (CW)
3.2OO(CW)
8,600 (PW)
2.450 (CW)
2.450(CW)
8,500-9,600 (PW)
2,450 (CW)
2,450 (CW)
29 (CW)
146(CW)
Intensity
(mW/cm2)
134
<50
10
5-45
20
<200
4.45 kVD-p/m
44.1 kVp.p/m
10 or 50
250 Vp-p/m
20
10, 45
1-20
<45
<49
• 60
0005-50
20
1-45
—
4.600-6,500
600 Vm./m
62.5 V^/m
Duration
(days x mm)
1 x 960
1 x 80
5x 15
28x480
1 x 30
1 x 1,680-2,640
1 x 180-240
1 x210
1 x90
1 x90
1 x90
1 x90
1 x 120
1 x180
1 x 300
1 x 1,440
1 x480
1 x 660-720
1 x 60-420
1 x240
1 x 120
1 x120
1 x 360
1 x45
1 x720
1 x720
SAR"
(W/kg)
67 (est)
<2.4 (est-testes)
<0.26 (est-testes)
21
21
<360 (est)
1.3 (est)
1 5 or 70
3
40
18. 80 (est)
>50
<80
<80
£17 (est)
<28 (est)
19
21 or 16
12
0008-75
40
<80 (est)
100
150-2 10 (est)
0.024 (est)
0015 (est)
Reference
Hamrick(1973)
Varma and Traboulay
(1976. 1977)
Huang el al (1977)
McReeera/ (1981)
Mam eta/ (1978)
McLeesef at. (1972)
Blackman el al
(1976)
Dutta el al. (1979a)
Dutta el al (1980)
Dardalhon er al
(1979)
Dardalhon et al
(1980)
Corelli el al
(1977)
Corelli et at
(1977)
Dutta et al (1979b)
Blackman et al
(1975)
Dutta el al (1979a)
Hamnerius et al
(1979)
Pavel al (1972)
Mittler (1976)
linked recessive lethals
-------
Table 6-24. (Continued)
Exposure Conditions
Oi
Effects
No mutagenic changes (recessive lethals)
in adult females
No significant germ-cell mutagenesis in
weekly breedings
No significant germ-cell mutagenesis in
weekly breedings
Same, except decrease in prec, lancies,
indicating temporary sterility caused
by elevated testicular temperatures
Induction of a repressed protein, colicin.
indicating a change in the genetic processes
Change in growth rate that was very fre-
quency specific, indicating an alteration
in the processes of the cell
Chromosome aberrations in lung cells in
vitro at two frequencies but not at two
closely related frequencies, 15 or 25 MHz
Increase in chromosome translocations in
sperm cells
Increased mutations and lethality
No change in growth when compared to
temperature controls
No change in survival or mutation
induction
No change in dominant lethality
No change in mutation induction
Higher mutagencity index perhaps
due to heating and RF
Species
D melanogaster
Rat
Rat
Rat
E coli
S cerevisiae
S cerevisiae
Chinese hamster
Mouse
S tvphimurium
E coli
E coli
S. cerevisiae
Mouse
E. coli
S. typhimurium
Mouse
Frequency
(MHz)
98 5(CW)
2.450 (CW)
2,450 (CW)
2,450 (CW)
37,000 (CW)
41. 000-42.000 (CW)
41,650-41, 825 (CW)
19(PW)
21 (PW)
9,400 (PW)
2,450 (CW)
8.800 (PW)
9,400 (CW)
1 7,000 (CW)
70.000-75.000 (CW)
9,400 (CW)
1 7.000 (CW)
70,000-75.000 (CW)
2.450 (CW)
27.12(CW)
2.450 (CW)
3,070 (PW)
27.12(CW)
2,450 (CW)
3.070 (PW)
2,450 (CW)
2,450 (CW)
1.700(CW)
Intensity
(mW/cm')
03 V,m,/m,
(FM) at
audio
5
10
28
0001-1
1-3
/10
up to
300 kVD-p/m
0 1-10
5,100
100
50
10
Duration
(days x min)
224 x 1,140
106 x 240
5 x 300
20 x 240
1 x 30-120
1 x 660
1 x 180
1 x 30
10 x 60
1 x 0.03-0.48
1 x 900
1 x 30
1 x 30
1 x30
1 x 30-2,880
1 x 30-2,880
1 x 30
1 x 30
1 x 60-400
1 x 60-400
1 x 60-400
1 x 60-400
1 x 60-400
1 x 60-400
1 x 10
3x 10
1 x80
SAR-
(W kg)
0.0004 (est)
4.7-0.9
2
56
4-11 (est, av)"
0.05-5 (est)
12
23
<28
9
23
28
28
43
-4
35-100
35-100
35-100
35-100
1 1.4 (est-testes)
5 7 (est-testes)
05 (est-testes)
Reference
Mittler (1977)
Berman et al. (1980)
Berman et al (1980)
Berman el al. (1980)
Smolyanskaya &
Vilenskaya (1973)
Grundler et al.
(1977)
Grundler and
Keilmann (1983)
Heller (1970) and
Mickey and
Koertmg (1970)
Manikowska et at.
(1979)
Blevins el al
(1980)
Hossain and Dutta
(1982)
Dardalhon et al
(1981)
Saunders et al.
(1983)
Anderstam et al
(1983)
Varma et al
(1976)
"est = estimated, est-testes - estimated for testes only; av = average.
-------
reinforced the concerns expressed above that specific
interactions may occur in unexamined frequency
domains. Edwards et al. (1983) reported microwave
absorption in isolated DNA molecules in salt solution
when exposed over the 8- to 12-GHz range. This
absorption was strongly dependent on the number of
single strand breaks in each molecule. Since these
breaks occur naturally, as during DNA replication or
repair, this result provides a basis for assuming that
certain biochemical states of DNA could be highly
susceptible to change by exposure to microwaves.
(For example, see discussion of co-stressors, above.)
Manikowska-Czerska et al. (1983a,b) reported, in
abstract form, further work with unanesthetized male
IRC mice exposed to 9.4-GHz pulsed, 2450-MHz CW,
and 915-MHz CW fields (Manikowska et al. 1979).
Exposures were 30 min/day, 6 days/week, for 2
weeks at SARs between 0.05 and 20 W/kg. Two
studies were performed. In one, increased chromo-
somal translocations were observed in meiotic cells
from the testes of exposed mice. The numbers of
translocations followed the same unusual dose-
response profile described in the earlier preliminary
report (Manikowska et al. 1979). In the other study,
exposed and sham treated males were mated with
unexposed females each week for 3 weeks. Post-
implantation loss was assayed on day 13-14 of
gestation. Significantly increased loss was reported
for the group mated to the exposed males. This result
is different from that obtained by Saunders et al.
(1983), who exposed at a higher SAR, 43 W/kg
(reviewed in Sec. 5.8.3.3), and found no change in
post-implantation survival. The incompletely de-
scribed exposure conditions and analyses in the
Manikowska-Czerska abstracts, which did not
receive peer review, preclude rigorous evaluation of
the reports; however, the occurrence of intensity-
specific effects is consistent with qualification 3,
stated above. Conversely, if the animal restraint
produced additional stress in the exposed animals
(Justesen et al. 1971), the results may address
qualification 4. Nevertheless, because the procedures
and exposure levels employed by these two research
groups differed, additional experiments are needed to
resolve the influences of particular exposure
geometries, SAR, stress produced by animal
restraint, ambient temperature and cooling capacity,
and animal species to determine the general nature of
this response.
A recent publication by Grundler and Keilmann
(1983) has corroborated their earlier report (Grundler
et al. 1977) of frequency-specific alterations in
growth rates of the yeast S. cerevisiae. In this new
study, the growth rate of yeast was monitored
spectrophotometrically during exposure by either one
of two different antenna systems. Numerous narrow
frequency ranges between 41.650 and 41.825 GHz
(CW) caused up to 10 percent change in either growth
enhancement or retardation compared to control
samples. There was substantial agreement in results
observed from the two exposure systems. The
emphasis on improved frequency resolution also
revealed that a residual modulation up to 0.5 MHz
was present. No SAR was given by the authors nor
could one be estimated from the data presented;
however, the authors stated that this effect occurred
and saturated above a threshold intensity that is
much less than 10 mW/cm2. Because the exposure
i ncreased the sa mple temperature from 0.16 to 0.4°C
for the power (10 to 25 mW) usually applied, results of
a small thermal increment on the growth rate were
established separately and displayed along with the
results of exposure at different powers. These results
reinforce the concern expressed above that low-
intensity, frequency-specific effects may exist but
have not been widely detected because of inade-
quacies either in the experimental design or in the
stability of the exposure sources. Although there are
theoretical models that are consistent with these
results, no mechanism of action has yet been
established.
5-105
-------
5.9 Life Span and Carcinogenesis
William P. Kirk
The generalizations that can be drawn from the
literature on the effects of RF radiation on life span
and carcinogenesis are:
• There is no convincing evidence that exposure to
RF radiation shortens the life span of human
beings or experimental animals or that RF
radiation is a primary carcinogen (cancer inducer);
however, (1) few studies have used longevity or
cancer incidence as end points, and (2) human
studies have lacked statistical power to exclude
life shortening or cancer.
• There is evidence from one group of investigators
that chronic exposure to RF radiation (SAR = 2 to 3
W/kg) resulted in cancer promotion or co-
carcinogenesis in three different tumor systems
in mice.
5.9.1 Life Span
5.9.1.1 Human Studies
There are few data and no definitive studies on which
to judge the long-term effects of RF-radiation exposure
on human survival. Two studies have evaluated
cause of death several years after exposure of the
study populations (Table 5-25). First, information has
been developed on the mortality experience of U.S.
Government employees assigned to the Moscow
Embassy during the period 1953 to 1976, when
microwave irradiation of the embassy by the Soviets
was taking place. Comparisons were made with a
group of employees who had been stationed at other
U.S. embassies in Soviet Bloc cities (Budapest,
Leningrad, Prague, Warsaw, Belgrade, Sophia, and
Zagreb). The comparison was chosen to be as similar
as possible to the 1800 employees in the Moscow
group for selection, i.e., posting, criteria, and
environmental influences, except that the posts were
not subject to microwave exposure (Lilienfeld et al.
1978). No evidence was found that the Moscow group
had experienced any higher mortality or any
differences in specific causes of death up to the time
of the report. Investigators noted that because the
population was relatively young it was too early to
detect long-term mortality effects except for those
serving in the earliest period of the study. The
methods and other results of this study are detailed in
Sec. 5.10, Human Studies.
Robinette et al. (1980) examined the records of a
group of 40,000 U.S. Navy personnel who enlisted
during the period 1950 to 1954. Approximately
20,000 had job classifications with maximum
potential exposure to radar; a similar number of
employees, believed to have minimum potential for
exposure, were used as a comparison group. The
authors found no apparent difference in mortality
patterns between the two exposure groups more than
20 years post-exposure. This study is also described
in more detail in Sec. 5.10, Human Studies. Exposure
data for both of these studies are given in Table 5-25.
5.9.1.2 Animal Studies
Although there have been many median-lethality
experiments to determine the lethal effects in
animals exposed to RF radiation, data on life span
effects of experimental animals exposed to low power
levels are scarce. Only one report is known of a study
in which animals were exposed to microwave
radiation as the sole stressor and observed
throughout their life span. Spalding et al. (1971)
exposed 24 adult female mice to 800-MHz fields at a
power density of 43 mW/cm2 for 2 h/day, 5
days/week for 35 weeks. A waveguide apparatus
was used to irradiate the animals, which were cooled
by forced air. No temperature or relative humidity
data are reported. The whole-body-averaged SAR is
estimated to be 12.9 W/kg. Four exposed mice died of
"thermal effects" during the experiment, and a fifth is
reported to have died during exposure because it
became too obese for the exposure chamber. The
mean life span of the remaining 19 exposed mice was
664 ± 32.2 (SEM) days, and that of the 24 sham-
irradiated mice was 645 ± 32.2 (SEM) days,
differences that are not statistically significant.
Prausnitz and Susskind (1962) studied pathological
and longevity effects on male Swiss mice exposed to
9270-MHz (PW) radiation (duty cycle = 0.001) at an
average power density of 100 mW/cm2 for 4.5 min
daily, 5 days/week for 59 weeks. The daily exposure
produced an average body temperature rise of 3.3°C.
This daily dose is stated to be half the LDso for the
mice. Originally, there were 200 irradiated mice and
100 control mice. Five percent of each group was
killed for pathological and hematological examination
7 months after the beginning of irradiation, and an
additional 10 percent of each group was killed at 16
months, within a month of the final irradiation.
Because of a partial contradiction in pathological
findings in the animals killed at 7 and 16 months, all
surviving mice (19 controls and 67 irradiates) were
killed 19 months after the beginning of irradiation (4
months after final irradiation). The data from this
experiment are summarized in Table 5-26. The
authors state that the longevity of the mice djd not
appear to be affected under the prevailing conditions
and suggested that "conceivably microwave irradia-
tion in this modality, with periodically induced slight
artificial fevers, is of some benefit to the animal in
combating disease." The data generally appear to
support this statement—and perhaps even the
stronger statement that significantly more irradiated
mice than controls survived until the termination of
the experiment. If simple 2x2 contingency tables are
5-106
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Table 5-25. Summary of Studies Concerning RF-Radiation Exposure Effects on Life Span/Carcinogenesis
Exposure Conditions
Effects
No effect on life span or cause
of death
No effect on mortality in a
military population followed
for 20 years
Slight increase in mean life span
Increased mean and maximum life
span for "irradiated mice with
tumors." Increased mean life span
but no change in maximum life span
of non-tumor-bearing mice. Delay
in development of tumors in
irradiated mice but no change in
ultimate number of tumors
Increased mean life span in
irradiated mice (concurrent
infection-pneumonia)
Species
Human adult
male & female
Human adult
male
Adult mouse
Infant mouse
Adult mouse
Frequency
(MHz)
2560-4100
600-9500
200-5000
(est) (PW)
800
2450
9270
(PW)
Intensity
(mW/cm2)
0.005 (max)
0.01 8 (max)
~ 1
(routine)
100
(occasional)
43
100
Duration
(days x min.)
8030* x 600
180 x 1200
730 x 480
(est)
175 x 120
4x20
fin uteroj
4.5 min/day
5 days/week
59 weeks
SAR
(W/kg)
2x 10~*(max)
7x lO^lmax)
<0.05 (est)
<5 (est)
12.9 (est)
35
40 (est)
References
Lilienfeld er al.
Robinette er al
Spalding et al.
Preskorn et al.
(1978)
(1980)
(1971)
(1978)
Prausnitz and Susskind
(1962)
'The duration of 8030 days equals the number of years (22) of irradiation of the embassy and length of the study period, but the average
exposure of individuals is estimated to be 2 to 4 years.
used with data from Prausnitz and Susskind (1962,
Figure 3) and from Table 5-26, ignoring all animals in
sacrifice series #1 and #2, the difference in survival is
not significant at 14 months into the experiment (x2 —
2.2) but is significant at 19 months (x2 =4.9,0.05 > p
> 0.025). The data provided are not sufficiently
detailed to permit application of the subsequently
developed, more refined methods of analyzing
survival (Peto et al. 1976, 1977). The calculation
would be perturbed slightly by the fact that sacrifice
series #1 and #2 were not predesignated prior to the
beginning of exposure but rather selected randomly
from survivors at that point in the experiment. This
Table 5-26. Summary of Prausnitz and Susskind Data (1962)
procedure would have the effect of decreasing the
proportion of survivors in both control and irradiated
groups.
There have been some reports of altered and possibly
enhanced immunological competence after micro-
wave exposure. These reports are discussed in detail
in Sec. 5.2, Hematologic and Immunologic Effects. In
a relevant study, Preskorn et al. (1978) compared
tumor development and longevity in female mice
prenatally exposed to 2450-MHz microwaves with
sham-irradiated controls. The irradiated mice were
offspring of dams exposed for 20 min/day on days 11,
Series
Sacrifice Series #1
Sacrifice Series #2
Sacrifice Series #3
(all animals
surviving at 1 9
months)
Longevity Series
Spontaneous Deaths
When
Sacrificed No
(months) Animals
7 5
16 10
(1 month post-
irradiation)
19 19
(4 months post-
irradiation)
As 40
occurred
No data 26
given
Controls (100 Total)
% of No. with % This Series
Total "Leucosis" with "Leucosis"
5 None —
apparently
given
10 1 10
19 4 21
40 4 10
26 - _
Irradiates (200 total)
No. % of No with % This Series
Animals Total "Leucosis" with "Leucosis"
10 5 None —
apparently
given
20 10 6 30
67 33.5 12 18
60 30 21 35
43 22 — —
Comment
Reported as
negative for
"leucosis"
Reported as
positive for
"leucosis";
not statis-
tically sig-
nificant
XJ<1 df) = 1.49
Reported as
negative for
"leucosis"
See text
Autolysis too
advanced for
diagnosis of
cause of
death
5-107
-------
12, 13, and 14 of gestation in a multimodal cavity
(SAR = 35 W/kg). Both groups were injected with
sarcoma cells at age 16 days. Both the mean and
maximum survival time of "irradiated mice with
tumors" exceeded those of "non-irradiated mice with
tumors" (p < 0.05). The mean survival time of
"irradiates without tumors" was also greater than
"non-irradiated mice without tumors." When 50
percent of the controls had died, 67 percent of the
irradiates were alive. The difference was not
significant (0.05 < p <0.1), however, and maximum
life span did not differ.
Rotkovska and Vacek (1972,1977) reported increased
survival and increased LD50-30 in mice for sublethal
(600 to 750 R) acute exposures to 200-kV X rays if the
X-ray exposures were preceded (1, 3, 14 days) or
followed (30 min) by a 5-min exposure to 2450-MHz
microwaves at 100 mW/cm2. In their initial
experiment, the 30-day survival after an X-ray
exposure of 600 R was increased from 14 percent
(controls) to 53, 88, or 90 percent when such
exposure followed the microwave irradiation by 1, 3,
or 14 days, respectively. In their second experiment,
the LDso-so was increased by 100 R with all
microwave-irradiated groups having significantly
higher survival at 30 days than their control
counterparts. These data, together with the interaction
with psychoactive drugs, are illustrative of the
potentially confounding variables that may have to be
considered in determining RF-radiation exposure
limits.
5.9.2 Carcinogenesis
5.9.2.1 General
Carcinogenesis is the process of inducing cancer or
malignant neoplasia. Neoplasia 'is uncontrolled
growth or cell division in a tissue; a malignant
neoplasm or cancer is a group of cells that replicate
uncontrollably and has the capacity to shed cells which
enter the blood and travel to other parts of the body to
colonize and form new tumors (metastases).
Metastasis is characteristic of malignancy but is not
required for diagnosis which is done histologically A
tumor that does not metastasize is considered
benign, although it may well grow to sufficient size to
be life threatening. Consideration of the various
theories of Carcinogenesis is beyond the scope of this
discussion, except that most authorities believe that
the initiating event(s) on the cellular level involves
physical or chemical alterations of a cell such that its
descendant cells are abnormal and may override the
body's cellular proliferation control processes. In
recent years Carcinogenesis has come to be viewed
as a multistaged process that for simplicity can be
divided into two major stages, i.e., induction (actual
induction of malignant transformation by genetic
damage) and promotion (enhanced growth and/or
survival of malignantly transformed cells). Promotion
is increasingly seen as an essential phase in the
carcinogenic process since it is assumed that many
cells capable of resulting in malignant tumors simply
die, or remain dormant unless stimulated to divide, or
are somehow protected from potentially lethal DNA
damage. Promoters are substances that result in
enhanced progression to malignant tumors when
applied in close proximity to transforming events. A
given moiety, chemical or physical, may act as an
inducer, promoter, or -both. (Ionizing radiation, for
example, is both a weak inducer and promoter.) The
role that the immune system plays in primary
Carcinogenesis has not been well documented and is
somewhat controversial. However, it is thought that
neoplasia may arise through an epigenetic mechanism
in which immunosuppression allows the development
of tumors initiated by a genetic event
Potential carcinogenicity has been periodically
discussed in connection with RF-radiation exposure
since 1953 when J.R. Mclaughlin, a medical
consultant to the Hughes Aircraft Corporation,
submitted a report to the military, listing leukemia as
one of the possible effects of radar exposure
(Mclaughlin 1953). The relevant literature, which is
sparse, has been reviewed by Baranski and Czerski
(1976), Justesen et al. (1978), and Dwyer and Leeper
(1978), with little supportable evidence that RF
exposures are likely to be carcinogenic. However, the
subject remains controversial for many reasons,
including:
(1) the failure of the public and the media to
distinguish between ionizing radiation, a proven
carcinogen, and nonionizing radiation (specifically,
RF radiation);
(2) the existence of several anecdotal and/or case
reports associating cancer in humans with RF-
radiation exposure;
(3) report of studies indicating that RF exposure may
cause leukemia (Prausnitz and Susskind 1962;
Susskind 1962) or promote the development of
several types of cancer in mice (Szmigielski et al.
1980, 1982);
(4) the lack of well-designed human or animal
studies that have adequate exposure data that
are free from artifact and are statistically
adequate to draw reliable conclusions.
5.9.2.2 Human Studies
The two relevant and acceptable studies in this area
deal with the health status of (1) U.S. Government
employees stationed at the U.S. Embassy in Moscow
(Lilienfeld et al. 1978) and (2) U.S. Navy personnel
exposed to radar duringthe Korean War(Robinette et
al. 1980). For these two studies, only those aspects
dealing with Carcinogenesis are discussed here.
In the Moscow Embassy study, the Moscow group
experienced less overall mortality from all causes of
5-108
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death than did the comparison group; however, the
death rate in Moscow group females from malignant
neoplasms was slightly, but not significantly, higher
than expected, and when exposure to microwaves
was considered, it was found that the death rate was
highest for those having the least exposure to
microwaves. The incidence of malignant neoplasms,
other than of the skin, was significantly higher in the
Moscow female group. In both cases, the numbers
were very small. In the former case, 7 different cancer
sites were involved in 8 cases, which according to the
authors, virtually eliminates a single causal factor; in
the latter case, there were 10 cases involving 7
different sites.
One of the end points examined in the U.S. Navy study
(Robinette et at. 1980) was the effect of exposure
from 1950 to 1954 on the relative incidence of cancer
during 1950 to 1976. No statistically significant
differences between the high- and low-exposure
groups were evident for malignant neoplasms as a
cause of death from 1950 to 1974, or as a cause of
hospitalization in Navy or VA hospitals. Within the
high exposure group, three subgroups were developed
to provide a gradient of potential exposure. (Sec. 5.10,
Human Studies, gives details.) There were signifi-
cantly more malignant neoplasms of the respiratory
tract in the subgroup rated as highly exposed. A
significant trend for increased death from increased
exposure was also noted when these subgroups were
used. However, information relevant to the develop-
ment of lung cancer, such as smoking histories, was
not available because the study used death
certificates to obtain data on cause of death. Also,
when many statistical comparisons are made, as was
done in this study, with a p=0.05 criterion, one or two
positive findings would be expected by chance.
5.9.2.3 Animal Studies
The only animal study reported to date that was of
sufficient duration and employed end points
appropriate to detect the induction of cancer by RF
exposure was that of Prausnitz and Susskind (1962).
They conducted an experiment to determine the
pathological and life-shortening effects of chronic
microwave exposure of mice. Two hundred male
Swiss mice were irradiated with 9270 MHz(PW) at an
average power density of 100 mW/cm2 for 4.5 min
daily. This exposure produced an average body
temperature increase of 3.3°C. Exposures were
conducted 5 days/week for 59 weeks; and survival,
body mass, blood parameters, and certain postmortem
pathological findings were compared with those of a
concurrently sham-irradiated group of 100 animals.
Tissues taken for histopathology included liver,
spleen, lymph nodes, kidneys, adrenals, gut, lungs,
and testes. No data were given regarding ambient
temperature during exposure. Between exposures,
the mice were housed 10 to the cage in a cabinet
maintained between 21 and 24°C. Animals were
sacrificed at 7,17, and 19 months afterthe beginning
of irradiation. In addition, 23 percent of the animals
were lost to the study by spontaneous death and
autolysis prior to necropsy. The remaining 100
animals (40 controls, 60 irradiates) formed a
"longevity" study group. One of the findings reported
in this group was "cancer of the white cells," defined
as monocytic or lymphocytic leucosis, or lymphatic or
myeloid leukemia. Leucosis was defined as a
noncirculating neoplasm of the white cells, whereas
leukemia was defined as a circulating leucosis. Data
were grouped and reported as "leucosis." A
contemporary medical dictionary (Taber 1953)
defines leucosis as (1) unnatural pallor, (2) presence
of an abnormal number of leukocytes in blood, (3)
increase in leukocyte-forming tissue; however, it is
not a usual pathological term. Although the liver,
spleen, and lymph nodes were removed for examina-
tion at necropsy, they were not considered in
determining lymphoid infiltration, even though these
organs are usually involved in this kind of reaction.
Data describing the differential composition of the
blood cell types are not given. A summary of the fate
of the 200 irradiates and 100 controls is shown in
Table 5-26.
The results as reported are confusing. The authors
performed a third sacrifice series at 19 months to
resolve a perceived contradiction in the "leucosis"
findings from the first and second sacrifice series,
even though a 2 x 2 contingency table analysis to test
the prevalence of leucosis in the control and
irradiated animals sacrificed in the second series
yields a x2 of only 1.49 (uncorrected for continuity)
with one degree of freedom (p > 0.20). Thus, the
prevalence of leucosis in irradiated animals was not
significantly different from that in the control animals
for any of the "sacrifice" groups.
Although leucosis in the "longevity" series is highly
significant (p < 0.005, x2 > 8.0), these data are
severely compromised by (1) the marked loss due to
autolysis of animals that would have fallen in this
group, (2) the differential loss of control animals due
to infection, and (3) the premature sacrifice of all
remaining animals to resolve an apparent paradox.
Comparing data from two groups of animals that
selected themselves (by dying prior to 19 months and
being found in time for necropsy) is not an acceptable
statistical analysis of experimental data. An
acceptable method would be to compare the
prevalence rates of leucosis in the controls and
irradiates in combined groups that include all the
animals at risk in the original longevity group
(longevity and third sacrifice series). If that is done,
the following results are obtained:
Group
With Leucosis Without Leucosis Total
Control 8 (a)
Irradiated 33 (c)
Total 41 (a+c)
51 (b)
94 (d)
145 (b+d)
59 (a+b)
127 (c+d)
186(n)
6-109
-------
To test whether the leucosis rates are different in
controls and irradiates, the following statistic may be
used:
S = n(ad - bc)2/[(a + b) (c + d) (a + c) (b + d)J
If the animals comprising the table represent a random
sample from a larger population, S approximately
follows a x2 distribution with one degree of freedom.
Upon substitution, the value of 3.62 (p ~ 0.06) is
obtained. Since x2 < 3.84 (p = 0.05), the rates would
not be declared different at the 5-percent significance
level. Furthermore, if a continuity correction were
used in computing this statistic, the resultant x2 -
2.93, with a probability of 0.09 (not significant).
There are now better statistical methods available to
analyze survival data (Peto era/. 1976,1977), but they
require detailed documentation of the fate of each
animal during the course of the experiment. Given (a)
the loss of histopathological data on animals because
of autolysis and infection, (b) the further complication
that different pathologists were used for different
sacrifice series, and (c) the absence of historical
data on the incidence of leucosis in the mouse strain
used, it is not feasible to apply these methods
retroactively. In summary, because of the previously
described problems with the biological protocol, the
lack of sound statistical methodology in experimental
design and data analyses, and the questionable
significance of what was reported, the 1962 study of
Prausnitz and Susskind is of limited value in defining
the pathological effects of chronic wholebody
microwave radiation. As noted previously, the data on
survival times (Sec. 5.9.1.2) are of considerable
interest due to similar findings by Spalding el al.
(1971) and Preskorn et al. (1978).
There have been several acceptable reports dealing
with the effects of RF exposure in the development of
experimental, spontaneous, or chemically induced
tumors in mice (Preskorn et al. 1978; Szmigielski et
al. 1980, 1982). In their paper, discussed in Sec.
5.9.1, Life Span, Preskorn et al. (1978) reported that
the development of tumors following injection of
sarcoma cells into 16-day-old CFW mice was
significantly delayed if the mice had been exposed to
2450-MHz radiation in utero on day 11,12,13, and 14
of gestation (20 min/day, SAP = 35 W/kg). However,
there was no difference in the ultimate number of
tumors.
Szmigielski et al. (1980, 1982) demonstrated that
repeated exposure of mice to 2450-MHz radiation (far
field) at 5 or 15 mW/cm2 (SAR = 2 to 3 or 6 to 8 W/kg),
2 h per day, 6 days per week for varying times up to 10
months accelerates the appearance of spontaneous
mammary cancer (female C3H/HeA mice) and of skin
cancer in male Balb/c mice treated with 3,4-
benzopyrene during or after microwave treatment.
Animals were exposed in plastic cages containing 10
mice per cage. The chamber temperature was
maintained at 22 to 23°C with humidity of 60 to 70
percent. Stress produced by chronic confinement in
compartments 5 x 6 x 10 cm, 1 animal per
compartment, 20 compartments/cage produced
approximately the same effect as the 5-mW/cm2
exposure. An additional finding is that this exposure
regimen increases the number of neoplastic nodules
developing in the lungs of Balb/c mice injected with
Li sarcoma cells (2 x 105 cells) and examined 14 days
later. Challenge with the sarcoma cells after a 3-
month exposure to 5 or 15 mW/cm2 or confinement
produced the following results.
Dose Groups
Nodules (X ± SO)
Cage Controls
Sham Irradiates
5 mW/cm2
15mW/cm2
Chronic Confinement
2.8 if 1.6
3.6 ± 2.2
6.1 ± 1.8
10.8 ±2.1
7.7 ± 2.0
It seems clear that exposure of mice to RF radiation in
these experiments resulted in the acceleraction, or
promotion, of three completely different tumors.
Whether the effect is by direct action of RF radiation
at the cellular or subcellular level, a nonspecific
stress reaction (caused by RF radiation, crowding, or
thermal stress), or a general effect on immune
response cannot be said with any confidence.
Exposure of 10 animals in a cage is certainly open to
criticism on grounds of nonuniformity of energy
absorption and resulting thermal load.
Comparison of the Preskorn etal. (1978) data with the
Szmigielski et al. (1980, 1982) data is difficult since
the biological models and exposure conditions were
substantially different (offspring of pregnant female
mice exposed at 35 W/kg, 20 min daily for 4 days,
resulting in elevation in body temperature by several
degrees, as compared with months of exposure for 2
h daily at 2 to 3 or 6 to 8 W/kg, levels that do not
produce noticeable heating). The Preskorn et al.
conditions resulted in slower development of
experimental sarcomas in mature offspring irradiated
in utero. whereas the Szmigielski et al. work resulted
in increased incidence of cancer, and/or accelerated
growth of experimental, chemically induced, or
spontaneous tumors.
5.9.2.4 Anecdotal and Other Unsupported
Reports
Much of the impetus for public and media belief in the
carcinogenicity of RF radiation can be traced to the
popularization of anecdotal and other unsupportable
reports by Brodeur (1977), Zaret (1976,1977), Dwyer
and Leeper (1978), and others. Most of these reports
deal with a perceived increase in cancer incidence in
one of several groups of defense contract personnel
working in RF-radiation research and development,
usually in situations having the potential for
substantial X-ray exposure from the RF generators
5-110
-------
being used. No reliable reports on these incidents
have appeared in the scientific or medical literature.
A good illustration of the kind of misunderstanding/
misinterpretation that has occurred is the so-called
North Karelia Connection. In the early to mid-1970's,
the Finnish government, with the World Health
Organization, conducted a program known as the
North Karelia Project, designed to decrease morbidity
and mortality from the high levels of cardiovascular
disease (CVD) in eastern Finland by identifying
causative factors, devising means for primary
prevention, and strengthening treatment and
secondary prevention (Puska et al. 1978; Keys 1970).
The proximity of North Karelia to the Soviet border
prompted Dr. Milton Zaret, who is known for his
investigations into causation of cataracts and lens
opacities from radiation, to speculate in a presentation
(at the 1973 Warsaw Symposium on the Biologic
Effects and Health Hazards of Microwave Radiation)
that microwave radiation from Soviet communications
or radar might be contributing to the incidence of
CVD. His remarks do not appear in the Symposium
record. This CVD hypothesis was restated, however,
in a published article (Zaret 1976) and letter to the
editor (Zaret 1977), both of which include allegations,
without data or reference other than a newspaper
article, of the emergence of an increased incidence of
cancer in North Karelia. The Zaret article (1976) was
later misinterpreted by Dwyer and Leeper (1978),
who presented the North Karelia project as being
designed to test the hypothesis that RF radiation
caused or contributed to heart attacks or cancer. The
Finnish government (K. Jokela, personal communication
to M. Hattunen, Scientific Counselor of Embassy of
Finland, 2133 Wisconsin Avenue N.W., Washington,
DC 20007, November 22, 1978) specifically denies
the existence of an abnormal cancer incidence in
eastern Finland and knowledge of any possible
linkage to microwave fields.
5.9.3 Unresolved Issues
Because few RF radiation studies in man or animals
have employed life span or cancer as end points and
none has had sufficient statistical power and
adequate quality control to place an upper limit of risk
at less than twice control incidences, the questions of
RF-radiation carcinogenesis or life shortening are
still open. None of the complete reports in the
literature presents a convincing case for the
existence of a significantly increased risk of cancer
induction or life shortening in exposed populations.
Neither theory nor the existing data on RF-radiation
mutagenesis support the notion of a role for RF
radiation in cancer induction except, very remotely, at
exposures causing substantial tissue heating. The
data of Szmigielski era/. (1980,1982), however, raise
the possibility that RF radiation may act as a cancer
promoter even at levels within the physiologic limits
of thermal regulation of the animal. In a different
system with higher exposures, Preskorn et al. (1978)
observed a delay in development of experimental
sarcomas. The existence of either promotion or
inhibition is yet to be confirmed in other systems and
laboratories and the mechanisms of action determined.
Two letters to the editor have appeared recently in the
New England Journal of Medicine suggesting an
association of polycythemia vera with occupational
microwave exposure (Friedman 1981) and of
leukemia with occupational exposure to a variety of
electric and magentic fields, including radio, TV, and
other electronic devices (Milham 1982). Neither of
these letters meets the literature selection criteria
established for this review but should lead to more
elaborate studies to resolve the questions raised. A
critical issue is the difficulty of developing exposure
data or information in human population studies.
The relationships of RF radiation to other physical and
chemical moieties in carcinogenesis or other
physiologic interactions having the potential to affect
survival have not been characterized sufficiently. For
example, (1) microwave-induced hyperthermia has
been demonstrated to increase the effectiveness of
X-ray treatment of various cancers and to increase
the LDso for mice exposed to X rays; (2) in
nontherapeutic situations, as noted above, both
inhibition and promotion of growth of experimental
and chemically induced tumors in mice have been
reported; (3) Riddle et al. (1982) demonstrated that
exposure (2450 MHz, CW) at 20 or 30 mW/cm2 (SAR
= 12 to 18 W/kg) after the injection of Salmonella
typhimurium lipopolysaccharide (IPS) in male mice
significantly decreased the LPS dose required to kill
50 percent of the mice. Irradiation prior to the LPS
injection did not affect the LDso; (4) Chang et al.
(1981) found that exposure to 5 mW/cm2 of 1-GHz
radiation for 20 min significantly inhibited the ability
of methotrexate (MTX) to delay the development of
CNS leukemia in mice when irradiation occurred after
MTX treatment.
It is easy to postulate feasible scenarios where
interactions of RF radiation with neurologically active
drugs (tranquilizers, medication for treatment of
various cardiovascular problems, etc.) or synergistic
effects with increased temperature, both noted in Sec.
5.5.5 (Interactions with Other Stimuli), result in life-
threatening situations. In view of the relatively few
multiple-agent-effects studies involving RF radiation
as one of the agents, the foregoing reports could well
be the harbingers of future developments in the study
of the biological effects of RF radiation.
5-111
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5.10 Human Studies
Doreen Hill
The general approach used in this document for the
evaluation of the health-effects literature is stated in
Sec. 2. Rigorous criteria were established and applied
to the reports of experimental results in order to
establish what is believed to be a credible data base.
However, it is difficult to apply these selection and
review criteria uncompromisingly to the human
studies or epidemiological literature, largely because
the research method is population based and
observational rather than experimental. The papers
included here were selected because they were
judged to present relatively more information on
exposure parameters and/or more rigorous or
analytical study designs. The amount of detail in
reporting and the degree of specification of study
methods and procedures (use of controls, statistics,
control of confounding variables, and so forth) were
considered important. Case reports are not reviewed.
From this review, the following general conclusions
can be drawn:
• The currently available epidemiological data on RF
radiation are very limited and not useful for
deriving environmental exposure limits. This
conclusion is based on various problems in the
data on human beings, as discussed in Sec.
5.10.5, Unresolved Issues.
• Two recent exploratory studies of physiotherapists
who use RF equipment in their occupation
describe potentially significant findings of heart
disease, primarily ischemic heart disease, in adult
males and poor pregnancy outcome in female
physiotherapists. However, neither study provided
quantitative information on radiation levels in the
work environment.
• Although some studies have associated ocular-
lens defects with microwave radiation exposure,
no data would at present support a conclusion that
low-level, chronic exposure to microwave
radiation induces cataracts in human beings.
Table 5-27 summarizes those studies on human
beings for which SAR values could be estimated.
5.10.1 Occupational Surveys/Clinical Studies
The majority of reports in the literature concern
people occupationally exposed in military or
industrial settings. A wide variety of conditions,
symptoms, and clinical measurements are usually
evaluated. The health conditions investigated usually
are pre- or subclinical instead of overt or diagnosed
disease. Studies of this type that focused on single
rather than multiple end points are described later.
Barron er a/. (1955) presented results of a study
conducted to evaluate changes in various physical
characteristics of radar personnel employed by an
airframe manufacturer. A total of 226 exposed workers
were initially included in the medical surveillance
program. The radar workers were characterized by
their duration of exposure, as shown in Table 5-28.
Controls totaling 88 subjects, stated to have had no
industrial radar exposure, were also examined.
Methods of selection of cases or controls were not
specified. The age distribution of all subjects ranged
from 20 to more than 50 years, with the majority
under 40 years of age. However, the controls were
older (Table 5-29).
A decrease in the number of polymorphonuclear cells
below 55 percent was observed in 25 percent of the
radar workers vs. 12 percent of the controls, but this
change did not occur in a second study (Barron and
Baraff 1958). An increase in monocytes and eosinophils
was also observed for the exposed group, but in the 1958
report these effects were attributed to a technical
error. Platelet counts and urinalyses were similar in
the two groups. Ophthalmological examinations
revealed ocular anomalies of several diverse types
among 12 exposed persons vs. 1 case in the control
group. The medical surveillance program was
extended to permit periodic reexaminations (Barron
and Baraff 1958). No significant changes in physical
health status were noted.
The radar bands of exposure included S-band (2880
MHz) and X-band (9375 MHz); the majority of
personnel worked with or around APS-45 and
AN/APS-20-B and E radars. Exposure times and
power densities for individuals could not be
developed, but zones at various distances from the
antenna were specified and used to estimate three
ranges of power densities. The minimal average
power density in Zone A was 13.1 mW/cm2. The field
strength in Zone B ranged from 3.9 to 13.1 mW/cm2,
and in Zone C the levels were <3.9 mW/cm2. The
authors stated that because of the relatively low
power densities, personnel working in Zone C were
eliminated from the study. By establishing these
zones of potential exposure, steps were taken to limit
entry of personnel to Zone A. Zone B was judged to be
safe for occasional but not constant exposure. As a
result, most subjects continuing in or added to the
examination program are believed to have had
incidental exposures to power densities less than
13.1 mW/cm2.
The strengths of this study are the attempts to
estimate potential exposures and to reexamine the
workers periodically. But there are some major
problems with study methods and analyses. For
example, there were fewer control subjects than
radar workers. Also, the comparability of the two
groups is questionable because of age differences
(Table 5-29). None of the observed results was tested
statistically.
5-112
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Table 5-27. Summary of Selected Human Studies Concerning Effects of RF-Radiation Exposure
Exposure Conditions
Effects
No significant change in health status
of exposed personnel
No differences in three major
diagnostic categories between
the two groups of microwave workers
No differences observed in clinical
evaluations; more subjective
complaints in exposed group
No effect on life span or cause
of death
No effect on mortality in a
military population followed for
more than 20 years
Decreased number of sperm/ml
of ejaculate; reduced percentages
of normal and motile sperm in
ejaculate
Species
Human
adult
male
Human
adult
male
Human
adult
male
Human
adult male
and female
Human
adult
male
Human
adult
male
Frequency
(MHz)
400 (PW)
2880 (PW)
9375 (PW)
Radar
Radar
2560-4100
600-9500
200-5000 (est, PW)
3600-10,000
Intensity
(mW/cm2)
~4 (avg)
—4 (avg)
~4 (avg)
<0.2 (avg)
X).2 (avg)
6.0 (max)
<5
0.005 (max)
0.01 8 (max)
"""*!
(routine)
100
(occasional)
Tens to
hundreds
/M//cm2
Duration
(Years)
0-13
1-10
5-10
22*
0.5
2
1-17
8 (avg)
SAR (W/kg)
(est)
-0.16
-0.12
-0.12
<8x10"3
>8x10'3
0.24 (max)
<0.2
2x10"
(max)
7x10"
(max)
<0.05
<5
0.3-4x10"2
Reference
Barren and Baraff
(1958)
(See also Barren el al
1955)
Czerski ef al. (1974);
Siekierzynski et al.
(1974a,b)
Djordjevic et al. (1979)
Lilienfeld et al. (1978)
Robinette et al. (1980)
Lancranjan et al. (1975)
•Number of years of irradiation of the embassy and length of the study period, but the average exposure of individuals is estimated to be 2 to
4 years.
Table 5-28.
Distribution of Years of Exposure for 226 Radar
Workers*
Years of Exposure
No. of Workers Percent of 226
Oto2
2 to 5
5 to 13
106
83
37
47
37
16
'Data from Barron et al. 1955.
Table 5-29.
Age Distribution of 226 Microwave Workers
and 88 Controls*
Radar
Controls
Age
20 to 29
30 to 39
40 to 49
50+
% of 226
34
49
13
4
Cumulative % % of 88 Cumulative %
34
83
96
100
14
40
27
19
14
54
81
100
*Data from Barron et al. 1955.
It is in occupational surveys and industrial health
surveillance programs that the potential for neuro-
logical and behavioral changes has been investigated.
The Soviet and Eastern European literature frequently
describes a collection of symptoms reported to occur
in personnel industrially exposed to microwaves.
These collective symptoms, which have been
variously called the "neurasthenic syndrome," the
"chronic overexposure syndrome," or "microwave
sickness," are based on subjective complaints that
include headaches, sleep disturbances, weakness,
decrease of sexual activity (lessened libido),
impotence, pains in the chest, and general poorly
defined feelings of non-well-being (Baranski and
Czerski 1976, p. 157). Also described are labile
functional cardiovascular changes including brady-
cardia (or occasional tachycardia), arterial hyperten-
sion (or hypotension), and changes in cardiac
conduction; this form of neurocirculatory asthenia is
also attributed to nervous system influence (Silverman
1980).
Czerski, Sierkierzynski, and co-workers in Poland
evaluated 841 men occupationally exposed to pulse-
modulated microwave radiation (Czerski et al. 1974;
Sierkierzynski et al. 1974a,b). The radiation
frequencies were not explicitly stated, but one can
infer from the references to pulse modulation and
radiolocation that the working environment dealt
with radar frequencies. The age distribution of the men
ranged from 20 to 45 years. The men had worked
various periods of time, with some employed over 10
years. An unexposed control population comparable
in general working conditions and socioeconomic
status could not be established; therefore, the study
group was subdivided into two groups on the basis of
level of microwave exposure. One group consisted of
507 men exposed to mean power densities greater
than 0.2 mW/cm2, with short-term exposures
estimated to reach 6 mW/cm2 The other group was
334 men exposed to mean power density levels less
than 0.2 mW/cm2.
The health end points evaluated covered three major
categories: neurotic syndrome, digestive-tract
functional disturbances, and cardiocirculatory
disturbances with abnormal electrocardiogram (ECG)
5-113
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findings. According to Polish occupational exposure
criteria, these conditions are considered contraindi-
cations for work in a microwave environment. The
neurotic syndrome was defined by a variety of
symptoms such as fatigue, headaches, sleep
disturbances, and difficulties in memorizing and
concentrating. Psychologic examinations were given.
Comparisons were made between and within
exposure groups according to age and duration of
occupational exposure. The two groups were found to
be similar with respect to the distribution of these
symptoms and conditions. There was no dependence
on the duration of exposure.
In 1979, Djordjevic et al. reported on medical
evaluations of radar workers, aged 25 to 40 years,
with a work history of 5 to 10 years. Specific
frequencies of exposure were not cited but were
stated to be within the whole range used in radar
operations. Evaluation of the working environment
was undertaken, including power-density measure-
ments. Although the environmental analyses are not
given in the paper, it was concluded that the workers
were exposed to pulsed microwaves within a wide
range of intensities but generally at levels less than 5
mW/cm2. The lower limit of this exposure may have
been 1 mW/cm2, but the discussion does not clarify
whether this estimate refers to the workers included
in this study or to radar station personnel in general.
The control group consisted of 220 persons reported
to be similar in age, character of work regime, and
socioeconomic status. The controls did not have
work experience with microwave sources. Selection
criteria or further descriptive information was not
given for either the cases or controls.
Ten major end points or diagnoses were covered in the
clinical evaluation, including ophthalmologic exam-
inations. The medical evaluations were conducted
by clinical specialists who followed the same scheme
for classification of abnormalities. The two groups did
not differ with respect to the 10 diagnostic categories.
Functioning of the nervous and cardiovascular
system was analyzed in greater detail. Electrocardio-
gram results, multiple biochemical and hematologic
indicators, frequency of sleep disturbance, inhibition
of sexual activity, and impairment of memory were
not different between the groups. Radar workers
reported more subjective complaints of headache,
fatigue, and irritability. Based on their survey of
working conditions, the authors attribute the latter
result to specific problems such as poor lighting, poor
ventilation, and high noise levels in the environment
of the radar workers as well as the need to
concentrate on the radar screen. If that is true, the
working environments for the two groups were
evidently not similar in all respects, even though the
authors stated that the controls had been matched
on the basis of comparable work regimes. Other
factors could also have been operating to produce
more subjective complaints. One possibility is
reporting bias on the part of the radar workers, e.g.,
enhanced awareness of the possible "microwave
sickness" syndrome. Another environmental factor
may have been present that may not have been
measurable in the type of environmental survey
conducted or detectable through these clinical
evaluations; however, microwave exposure cannot
be clearly excluded.
An exploratory study was published recently of male
physical therapists who use RF, infrared, and
ultrasound diathermy equipment in their occupation
(Hamburger et al. 1983). The study population
consisted of 3004 men who responded to a mail
questionnaire survey. The cohort was divided into
subgroups according to the types of exposures they
had experienced, that is, by their use of the various
types of diathermy equipment and treatment
modalities—ultrasound, microwave, shortwave, and
infrared. High and low exposures were approximated
by considering length of employment, frequency of
treatments per week, and combinations thereof. An
association between heart disease (primarily
ischemic heart disease) and exposure to shortwave
(27-MHz) radiation was the only consistently
significant finding in comparisons between high and
low exposure groups. In general, the prevalence rates
for heart disease were lower than rates in a general
population comparable with respect to sex, age, and
race. The lower prevalence rates were attributed to
higher socioeconomic status in the study group, to a
health care occupation in a medical setting, and to a
"healthy worker effect." The authors considered their
report to be an exploratory analysis because the
response rate to the questionnaire was low (58
percent), the nonresponderits could not be character-
ized, and individual exposures could not be estimated.
5.10.2 Mortality Studies
Lilienfeld and associates (1978) completed a broad
survey of the mortality and morbidity experience of
Foreign Service employees and their dependents to
assess the potential health consequences of
microwave irradiation of the U.S. Embassy in
Moscow. The health status of Foreign Service
employees and those from other agencies who had
served in the Moscow Embassy during 1943 to 1976
was compared with that of employees at eight other
embassies or consulates in Eastern Europe over the
same time period.
The microwave irradiation of the Moscow Embassy
was first detected in 1953 and subsequently varied in
intensity, direction, and frequency over time. The
frequencies ranged from 0.6 to 9.5 GHz (U.S. Senate,
Committee on Commerce, Science, andTransportation
1979; Pollack 1979). The measured average power
densities oyer time are given in Table 5-30.
5-114
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Table 6-30. MicrowaveExposureLevelsattheU.S. Embassy
in Moscow*
Exposed Power Density and
Time Period Area of Chancery Exposure Duration
1953 to May 1975 West Facade Max of 5 /M//cm2
9 h/day
June 1975 to Feb. 1976 South and East Facade 18 /yW/cm2
18 h/day
Since Feb. 7, 1976 South and East Facade Fractions of a^W/cm2
18 h/day
•Data from Lilienfeld et al. 1978.
Extensive efforts were launched to identify and trace
the populations. Information on illnesses, conditions,
or symptoms were sought from two major sources: (1)
employment medical records, which were fairly
extensive, given examination requirements for
foreign duty, and (2) a self-administered health
history questionnaire. Questionnaire responses were
validated for a stratified sample by review of hospital,
physician, and clinic records. Death certificates were
also sought, although other sources also were used
to ascertain mortality status.
Standardized mortality ratios for various subgroups
were calculated for each cause of death, were
standardized for age and calendar period, and were
specific for sex. Similar procedures were used to
develop summary indices of morbidity.
A total of 4388 employees and 8283 dependents
were studied. More than 1800 with 3000 dependents
were employed at the Moscow Embassy and 2500
with more than 5000 dependents worked at the
comparison posts. Ninety-five percent of the
employees were traced. Receipt of completed
questionnaires was less successful, with an overall
response rate of 52 percent for State Department
personnel.
Based on information in medical records, various
health problems were generally similar, with two
exceptions. Moscow employees had a threefold
greater risk of acquiring protozoal infections than
comparison-post employees. In general, both sexes in
the Moscow group had somewhat higher frequencies
of most of the common kinds of health conditions
reported. Lilienfeld et al. (1978) stated, "However,
these most common conditions represented a very
heterogeneous collection and it is difficult to
conclude that they could have been related to
exposure to microwave radiation since no consistent
pattern of increased frequency in the exposed group
could be found."
Some excesses were reported by Moscow employees
in the health history questionnaire. Both sexes
reported more eye problems due to correctable
refractive errors. More psoriasis was reported by men
and anemia by women. The Moscow employees,
especially males, reported more symptoms such as
irritability, depression, difficulties in concentration,
and loss of memory. It is possible, however, that a bias
due to awareness of potential adverse effects is
operating, since the strongest differences were
present in the subgroup with the least exposure.
The observed mortality was less in both male and
female employees than expected, based on U.S.
mortality rates; the male employees had more
favorable experience than female employees. In both
sexes, cancer was the predominant cause of death.
The Moscow and comparison groups did not differ
appreciably in overall and specific mortality.
However, the population was relatively young; it may
have been too early to detect long-term mortality
effects.
The authors concluded that no convincing evidence
was discovered to implicate microwaves in the
development of adverse health effects at the time of
the analysis. But they also carefully discussed
the limitations inherent in the study: uncertainties
associated with the reconstruction of the employee
populations and dependents, difficulties of obtaining
death certificates, the low percentage of responses
for the questionnaire, and the statistical power of the
study. The limitation most critical for consideration in
a document such as this relates to ascertainment of
exposure. Problems relative to individual mobility
within the embassy and variation of field intensities
within the building are present in this study as in any
other. No records were available on where employees
lived or worked, so one had to rely on questionnaire
responses to estimate an individual's potential for
exposure. The highest exposure level (18 /M//cm2)
was recorded for only 6 months in 1975-76; thus, the
group exposed to the most intense fields had the
shortest cumulative time of exposure and of
observation in the study.
Robinette and Silverman (1977) and Robinette et al.
(1980) examined mortality and morbidity among U.S.
naval personnel occupationally exposed to radar.
Records of service technical schools were used to
select subjects for the study; the men graduated from
technical schools during the period from 1950
through 1954. Exposure categorizations were made
on the basis of occupational specialty. The exposure
group (probably highly exposed) consisted of
technicians involved in repair and maintenance of
radar equipment. The controls (probably minimally
exposed) were involved in the operation of radar or
radio equipment. It was estimated from shipboard
monitoring that radiomen and radar operators (in the
low-exposure group) were generally exposed at less
than 1 mW/cm2, and gunfire control and electronics
technicians (in the high-exposure group) were
exposed to higher levels during their duties. Over
40,000 veterans were included in the study, with
about equal numbers in these two major exposure
classifications. The mean age in 1952 of the low-
exposure group was 20.7 years and of the high-
exposure group, 22.1 years. In conjunction with naval
5-115
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personnel, an effort was also made to develop an
index of potential exposure, termed Hazard Number,
for a limited portion of the population. This number
was based on the duty months multiplied by the sum
of the power ratings (equipment output power of
gunfire-control radars (ship) or search radars
(aircraft)) where technicians were assigned.
Medical information was obtained through Navy and
Veterans Administration records. Records were
searched for information on four major end points: (1)
mortality, (2) morbidity via in-service hospitalizations,
(3) morbidity via VA hospitalizations, and (4) disability
compensation.
Mortality was ascertained through the VA beneficiary
system. Strokes, cancers of the digestive tract and
respiratory system, and leukemias were elevated for
the high exposure group, but none of the increases
was statistically significant. The authors noted that
the differences in mortality from malignant neoplasms
of the lymphatic and hematopoietic system were not
statistically significant. As seen in Table 5-31,
comparisons were also made within the high
exposure group across Hazard Number categories. In
this case, only two comparisons were statistically
significant: (1) the difference in respiratory tract
cancer between those with a Hazard Number smaller
than 5000 vs. larger than 5000 and (2) the test for
trend for all diseases combined. These results maybe
fortuitous since one or two positive findings might be
expected when many statistical comparisons are
made. Furthermore, additional information relative to
the development of lung cancer, e.g., smoking
histories, could not be obtained; the mortality data
were obtained from death certificates, and obtaining
background information from next of kin was not
feasible. Differential health risks with respect to
hospitalized illness around the period of exposure
were not apparent. Subsequent VA hospitalizations
and disability awards provided incomplete information.
Because the study focused largely on the use of
automated VA record systems, it was not possible to
determine non-Navy or non-VA hospitalizations,
nonhospitalized conditions, reproductive histories, or
subsequent employment histories. Since actual
individual exposure could not be reconstructed
retrospectively, only an estimate of the potential
exposure of the individuals was possible.
5.10.3 Ocular Effects
The potential of RF radiation to induce cataracts and
less significant lens defects and opacities has been
cited in both U.S. and foreign literatures. Ocular
effects have, in fact, been the major end point of study
in U.S. research, primarily in military populations. For
this health end point more than others, much
attention has been devoted to careful, detailed clinical
examinations and to use of standard procedures or
protocols. However, population selection criteria are
not well elaborated; therefore, the possibility of
selection bias cannot be excluded for most of these
surveys. Ocular studies have largely taken the form of
cross-sectional clinical surveys in actively working
Table 5-31. Number of Deaths from Disease and Mortality Ratios* by Hazard Number: U.S. Enlisted Naval Personnel Exposed to
Microwave Radiation During the Korean War Periodf
Number of Deaths
Cause of Death
All diseases
Malignant neoplasms
Digestive organs
Respiratory tract
Lymphatic and
hematopoietic
system
Other malignant
neoplasms
Diseases of
circulatory system
Other diseases
International
Classification
of Diseases
(8th Rev.)
000-796
140-209
150-159
160-163
200-209
Residue
390-458
Residue
High Exposure
Low
Exposure
325
(1.04)
87
(0.96)
14
(0.85)
16
(0.85)
29
(6.83)
37
(1.19)
167
(1.07)
71
(1.08)
Total
309
(0.96)
96
(1.04)
20
(1.14)
24
(1.14)
26
(1.18)
26
(0.82)
150
(0.93)
63
(0.92)
0
63
(0.82)
22
(0.99)
6
(1.49)
4
(0.82)
6
(1.09)
6
(0.78)
36
(0.94)
5
(0.30)
Hazard Number
1-5000
160
(0.91)
45
(0.90)
11
(1.14)
10
(0.86)
12
(1.04)
12
(0.70)
73
(0.83)
42
(1.13)
5000+
86
(1.23)
29
(1.44)
3
(0.78)
10
(2.20)
8
(1.64)
8
(1.17)
41
(1.17)
16
(1.08)
"Mortality ratio (in parentheses) standardized for year of birth; the combined experience of the low and high exposure groups is taken as the
standard.
tTable from Robinette et al. 1980.
5-116
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populations and, as such, have focused on minor lens
changes. Longitudinal studies of populations with
known exposure, with follow-up of either a
prospective or retrospective nature, are nonexistent
despite the identification of potential cohorts from the
cross-sectional surveys. The research to date has not
determined whether lens changes lead to overt
clinical eye disease or conditions, e.g., the functional
and clinical significance of minor lens changes in
general and over time. Thus, although it appears
reasonable that RF radiation at high levels could
influence cataractogenesis, it cannot be confirmed
without more rigorous follow-up studies in already
identified exposed populations. This would be a
reasonable line of future research if such epidemio-
logical studies prove feasible.
More than 50 cases of cataract development have
been attributed to microwave exposure (Zaret 1974).
These instances have generally been related to acute
exposure to high-intensity fields in the workplace. For
most cases, work history information sufficient to
estimate dose rates or exposure conditions is lacking
(Zaret 1970).
Utilizing Veterans Administration hospital records
and military personnel records, Cleary et al. (1965)
conducted a case-control study to examine cataract
formation among U.S. Army and Air Force veterans.
This is the only case-control study of clinically
diagnosed cataracts. Cases were defined as white
males born after 1910 who were treated for cataracts
between 1950 and 1962, based on diagnoses given in
VA hospital records. The restriction on year of birth
resulted in a study population under 55 years of age.
According to the authors, this was done to minimize
dilution of the sample with senile cataracts. Also,
cases with certain specific cataract diagnoses were
not included in the study because the diagnoses are
unrelated to microwave exposure. These cases were
congenital cataracts, cataracts in Down's Syndrome,
traumatic cataracts, and diabetic cataracts. Controls,
also born after 1910, were drawn from the same
sources by selection of men with adjacent hospital
register numbers; therefore, the control group had a
sample of diagnoses made in the same hospitals at
the same time the cataract cases were diagnosed.
Military occupational specialties, as abstracted from
service records, were used to denote radar or
nonradar workers. Job classification was then used
as an indicator of potential exposure. The distribution
of cases and controls according to radar exposure is
seen in Table 5-32. The frequency of microwave
exposure as denoted by radar work history was
similar between cases and controls; the odds ratio
was less than one (0.67) and was not statistically
significant. The distribution in different age groups is
shown in Table 5-33. Excess risk was noted for U.S.
Air Force veterans, but the numbers were small. Only
40 radar workers were found in over 5000 cases and
controls.
Table 5-32. Classification by Military Occupation of World
War II and Korean War Veterans With and
Without Cataracts, Based on Discharges from
VA Hospitals*
Veterans' Cataract Status
Military Occupationt
Yes
No
Total
Radar Workers
Nonradar Workers
TOTAL
19
2625
2644
21
1935
1956
40
4560
4600
Odds Ratio = OR = (19>(1935) = 0.67
(21) (2625)
*Data are from Cleary et al. 1965.
tBased on Military Occupational Specialties.
Table 5-33. Estimated Relative Risk of Cataracts Among
Army and Air Force Veterans by Age Group and
Occupation*
Age
Group
Total
20-39
40-49
50-59
Cataracts
Yes
No
Yes
No
Yes
No
Yes
No
Radar
Workers
19
21
3
4
7
13
9
4
Nonradar
Workers
2625
1935
418
522
1517
1101
699
316
Odds
Ratio
0.67
0.94
0.39
1.02
X1
1.26NS
0.08 NS
3.39 NS
0.09 NS
'Data are from Cleary et al. 1965.
Cleary and Pasternack (1966) examined and scored
subclinical or minor lens changes in 736 microwave
workers and 559 controls. The population was drawn
from 16 microwave installations of various types at
different locations. Sampling constraints did not
permit matching on age. The mean age of each group
was very similar (32.8 years for microwave workers
and 33.2 for controls), but the age distributions were
different. The age frequency distribution for controls
was broader than for the exposed group, with more
younger and older individuals, whereas more of the
exposed group were 26 to 30 years of age. Slit lamp
examinations were performed, and a grading
procedure revised by Zaret and Eisenbud (1961) was
used to provide a relative measure (eye score) of
minor types of lens changes. Detailed occupational
histories were taken. The work environment in terms
of microwave exposure parameters was not reported;
that is perhaps the greatest drawback of the study.
However, a relative microwave exposure index or
score was developed by use of various parameters
such as power output and distance from the
microwave-generating source. The exposure score
was used to compare lens findings with occupational
microwave exposure.
By linear regression techniques, the number of
defects was found to increase significantly in both
groups with increasing age, and microwave workers
were found to have more lens changes than controls
(Figure 5-7). The authors suggested that the
5-117
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Figure 5-7. Linear regressions of eye score on age for workers
exposed to microwave radiation and controls
(from Cleary and Pasternack 1966. Figure 3).
12-
11-
10-
9-
8-
7-
o>
8
-------
The survey was later extended to six other installations
with results reported by Appleton in 1973. The
exposure of military personnel was classified as
"likely" vs. "unlikely"; the latter group served as
controls. Masking procedures were used for the
examining ophthalmologists; that is, they were not
aware of the exposure classification of subjects. The
same team of examiners performed all tests, except at
one location, to minimize interobserver variation. The
same three end points used in the 1972 study were
also used in the 1973 study. Older age groups
demonstrated a trend of greater opacities among
exposed personnel, but since the numbers in some
groups were small, the validity of this result is
questionable.
Odland (1973) reported results of a survey of ocular
anomalies in personnel from eight military installa-
tions. The population consisted of 377 exposed
individuals and 320 controls. Exposure conditions
were not specified. Exposed personnel were defined
as individuals whose primary duties involved the
operation or maintenance of radar equipment. The
selection criterion for controls was duty that did not
permit actual or potential exposure to radar, although
the actual work assignments were not stated.
Medical histories were taken, and ophthalmic
examinations were performed in a manner which
masked the exposure classification of the individuals.
The frequency of occurrence of lens anomalies was
similar in the two groups; however, the frequency of
anomalies between control and exposed groups was
different for individuals who had a family history of
diabetes, nontraumatic cataract, glaucoma, or
defective vision. Lens changes were noted in 29
percent of the exposed individuals with such a history
vs 17 percent in the controls with a family history of
eye problems. No statistical tests were applied to any
of the reported frequency distributions.
Shacklett et al. (1975) reported eye examinations of
817 military and civilian personnel. There were 477
persons with a history of microwave exposure and
340 controls without exposure drawn from eight U.S.
Air Force bases between November 1971 and
December 1974. The authors stated that detailed
work histories were recorded (including time spent
with different types of equipment), but information on
typical exposure settings was not given. Local unit
commanders selected the subjects by using criteria
established by the examining team. Standard
diagnostic criteria were established. The same
ophthalmologists performed all examinations and
were not aware whether a subject was considered as
exposed or a control. No differences were noted
between the two groups in the frequency of opacities,
vacuoles, and posterior subcapsular iridescence.
Differences in results were reported as not being
statistically significant, but the type of statistical test
was not stated. An age-dependent increase in lens
changes was noted in both groups.
The study by Siekierzynski et al. (1974b) discussed
earlier also compared lens opacities in the two
exposure groups (< 0.2 mW/cm2 and 0,2 to 6
mW/cm2). Ophthalmologic examinations were
performed. Lens translucency was assessed with a
slit lamp after pupil dilatation and according to criteria
established for five grades. No differences were
reported between the exposure groups nor within the
groups for duration of exposure.
5.10.4 Congenital Anomalies and Reproductive
Effects
In 1965 Sigler era/, reported a history of occupational
exposure to radar and more military service among
fathers of children with Down's Syndrome. The
association with radar exposure was an ancillary
observation; this study was specifically directed
toward examination of the relationship between
ionizing radiation exposure and Down's Syndrome. A
case-control approach was used, and 288 children
born with Down's Syndrome in Baltimore between
January 1946 and October 1962 were identified for
inclusion in the study. The investigators selected
controls by matching each case of Down's Syndrome
with another normal birth for (1) hospital of birth, (2)
sex, (3) date of birth, and (4) maternal age at birth of
child. Of the original 288, 216 matched pairs were
available for final analysis. Eliminations occurred for
various reasons such as non-cooperation or
equivocal diagnoses. Occupational histories and
other data were obtained by interview of the parents.
The fathers of the children with Down's Syndrome
had more military service experience than control
fathers, but the difference was not statistically
significant. A more frequent history of radar exposure
was reported by case fathers; this difference was
statistically significant. Exposure to radar occurred
primarily in job assignments as radar operators or
technicians. (Some radar operators may be exposed
to only low levels if the place of operation is distant
from the power-generating equipment or the micro-
wave source.)
Cohen et al. (1977) extended the study. The case
series was expanded to include 128 additional
verified cases and their matched pairs born through
1968. To serve as an independent replication,
essentially the same procedures were applied along
with the following expansions: (1) more extensive
questions on microwave/radar exposure and military
service, (2) validation of exposure histories by
searching of armed service records, and (3)
chromosomal studies. The previously noted differences
disappeared in the extended analysis (Table 5-34).
Results of the cytogenetic analyses are not yet
available.
The authors stated that although the extended study
did not confirm excess radar exposure among Down's
case fathers, the possible relationship of such
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Table 5-34.
Case Seriest
Paternal Radar Exposure Before Conception of
Index Child (from Interview and/or NAS)"
Down's Cases Controls
No.
No. %
1. Current Exposed 20 15.7 27 21.3
Exposure Known 127 100.0 127 100.1
2. Original Exposed 36 18.6 30 15.2
Exposure Known 194 100.1 198 100.0
3. Combined Exposure 56 17.4 57 17.5
Exposure Known 321 99.9 325 100.0
•Data are from Cohen et at. 1977.
t1, 128 pairs; 2, 216 pairs; 3, 344 total pairs.
exposure to increased risk of Down's offspring cannot
completely be ruled out. They added further that the
most challenging aspect of the investigtion was the
definition of radar "exposure." In discussing
explantions for lack of confirmation of a radar
exposure factor (if one does exist), the authors offer
several possibilities. As mentioned above, inaccurate
exposure estimates could distort results. The role of
maternal factors in Down's Syndrome is so important
that paternal factors could be masked. It was also
suggested that detecting a paternal relationship in a
retrospective study of Down's cases may be difficult.
If radar exposure does pose some increased health
risk to the fathers, the most highly exposed males
may have poor survivorship or an increased risk of
germinal tissue damage. This factor could result in
elimination of such men from reproductive experience.
It was further suggested that a prospective approach
might then prove more fruitful. Although not
discussed by the authors, radar equipment and
military occupational specialties could have changed
over time in such a way as to lower risk. It has also
been suggested that since microwave-generating
equipment, especially of an older vintage, may have
emitted more ionizing radiation than modern
equipment, the ionizing radiation presents the actual
risk factor, with microwave radiation possibly
operating as a covariable.
Lancranjan era/. (1975) studied 31 adult males with a
mean age of 33 years and a mean exposure of 8 years
(a range of 1 to 17 years) to electromagnetic fields
that "frequently were in the range of tens to
hundreds of //W/cm2." The frequencies were
defined as microwaves of wavelengths between 3 and
12 cm and frequencies between 10,000 and 3,600
MHz. No details on the RF source(s) were provided. A
group of 30 men of similar mean age and no known
exposure to microwaves served as a control group for
the analysis of spermatic fluids and hormones.
Statistical analysis of the results showed no
differences in urinary content of 17 ketosteroids (as
an indirect measure of Leydig cell function) or total
gonadotropin between the exposed and controls.
Slight but statistically significant decreases were
reported for exposed personnel in the number of
sperm per milliliter of semen, percent of motile sperm
in the ejaculate, and the percent of normal sperm.
The goal of this study was application of objective
measures to assess the subjective reports of
decreases in libido or of other sexual disturbances.
This goal was accomplished, but the exposures are
poorly defined, and the number of men evaluated was
very small. Spermatogenesis improved in two-thirds
of the subjects after cessation of exposure. The
investigators felt this supported an argument for
microwave influence on the observed alterations. But
the values obtained by the semen analyses for both
exposed and control groups might be considered to be
low-normal or below normal values.
Kallen et al. (1982) examined the pregnancy outcome
of 2018 Swedish women who were certified
physiotherapists at the time of pregnancy during
1973 to 1978. There were 2043 infants born,
including 25 pairs of twins. To identify the mothers
and the births, the investigators linked data from
computerized national registers of certified physio-
therapists, of deliveries, and of major congenital
malformations. It is likely that use of these record
systems resulted in reasonably complete ascertain-
ment of the study population.
Overall, this cohort had a better than expected delivery
outcome as measured by eight different end points.
All measures of infant health were near or below the
expected national values, which were adjusted for
age and parity distribution, as well as hospital of
delivery, to control for diagnostic variability.
To examine whether a "healthy worker" effect may
have been operating in this group and to obtain more
detailed work histories, a nested case-control study
was also conducted. The cases were defined as
infants with a major malformation plus all perinatal
deaths. Two controls per case were selected,
matched for maternal age, parity, and date of delivery-
After elimination of ineligible women, 33 cases and
63 controls remained. A work history questionnaire
was mailed to the study group, and the response rate
was 93 percent.
Of several end points explored, the only positive
finding was a higher frequency of shortwave
equipment use among the women with a dead or
malformed infant than among the control physiother-
apists. This difference was statistically significant in
both unmatched and matched pair analyses. Use of
ultrasound equipment followed a similar pattern but
was not statistically significant. The authors stressed
that exposure to the two types of equipment was
heavily associated. Information on wbrk with X rays
was not reported, although questions on X rays were
included in the questionnaire. Measurement of the
radiation fields in the work environment was not
performed in conjunction with the health study.
Furthermore, no information was presented on
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shortwave radiation levels typical of the various
physiotherapy work environments or on the types of
equipment most commonly used in Sweden.
5.10.5 Unresolved Issues
There are some general issues surrounding the use
and applicability of epidemiological research
methods to study the effects of environmental agents,
including RF radiation. Examples of such issues
include the ability of epidemiological studies to detect
low-level risks, to separate the effects of multiple
causes, and to identify and control confounding
factors. Moreover, specific problems are common in
the current epidemiologic literature on RF radiation
that limit the ability to draw inferences from this body
of data and its usefulness in establishing environ-
mental exposure limits for the general population.
These problems are briefly discussed below.
5.10.5.1 Exposure Assessment
It is difficult to determine actual exposure and dose
for individuals, and even for groups; that is perhaps
the largest single problem in epidemiological studies
on RF radiation. In general, there are no continuous
surveillance programs in the workplace that could
yield data for use in epidemiological studies. It is a
formidable task to reconstruct RF-radiation exposure
data for health studies that are begun after exposure
has taken place. The study by Robinette and
Silverman (1980) is a good example of attempts to
deal with the difficulties of retrospective exposure
assessment, e.g., two approaches (job type vs. Hazard
Number) were used, and an exposure gradient was
obtained with the Hazard Number which simultane-
ously considered the RF sources and the length of
service assignment. Despite these efforts, the
estimates remain those of potential rather than
actual exposures. In many of the other studies, the
levels and frequencies of exposure are not known, not
estimated, or not reported. Also, in studies of military
populations, information relevant to exposure
conditions might be classified. When well-developed
exposure data are not available, it is difficult to
analyze possible dose-response relationships, to
interpret the significance of the findings, and to use
the data in establishing protective exposure limits.
5.10.5.2 Documentation and Methods
Another problem in the RF radiation literature on
human beings relates to documentation of methods
and procedures. Degree of detail in reporting seems
to be a major difference between studies done in the
U.S. and those conducted in other countries. The
paper "Guidelines for Documentation of Epidemio-
logic Studies" (Epidemiology Work Group 1981)
suggests the types of topics that are useful to
document when reporting an epidemiologic study,
especially one used to support regulatory decisions
These major elements include a statement of
background and objectives, methods of selection and
characterization of study and comparison subjects,
data collection procedures, and analysis. Few reports
on human beings exposed to RF radiation adequately
include such necessary information. It is frequently
difficult to tell whether certain research methods
were not applied or simply not reported. For example,
the criteria for selecting controls are frequently not
stated, but controls are often said to be comparable in
all respects except exposure; analyses or data to
support such statements may not be supplied. Also,
common practices such as development of standard-
ized rates or use of procedures to control confounding
variables, e.g., age ajdustment, are usually not
reported. Statistical power is rarely evaluated or
discussed, but it is difficult to estimate power if the
underlying prevalence or incidence of the disease
under study is not well known, especially for some of
the conditions and symptoms, e.g., functional
disturbances, studied in relation to RF radiation
exposure.
5.10.5.3 Health End Points: Design and
Populations
Another issue is the medical significance of any
changes that may be induced by exposure to RF
radiation. For example, the studies on ocular effects
usually have examined a subclinical end point, e.g.,
lens opacities, which may not necessarily be an early
marker or risk factor for cataractogenesis and visual
problems (Silverman 1979). Further, most studies
present only single measures at one point in time; the
study populations have not been followed long
enough to permit development of longitudinal data
upon which to base a determination of whether
symptoms and subtle changes lead to disability or
disease. A similar concern surrounds the problematic
information on functional changes and nervous
system effects reported in some of the Eastern
European literature. The potential for neurological or
behavioral effects has not been thoroughly and
rigorously evaluated, and standardized questionnaires
and more objective medical measurements need to
be used in studies on these effects.
Most studies concern occupational groups of
relatively young healthy males. It cannot be
presumed that sensitivity, or lack thereof, to RF-
radiation exposure would be the same in the general
population as in working groups. The general
population is more diverse, with the full range of
ages, sexes, races, and other factors that could
influence health status or the development of
disease. To resolve this issue, specific exposed
populations could be identified and evaluated if such
research appeared feasible.
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5.10.5.4 Summary
Serious methodological problems in the human
studies literature make results equivocal. These
problems are not necessarily insurmountable. But at
present, the data on human beings exposed to RF
radiation are not adequate nor sufficiently developed
to be very useful in determining exposure limits for
the general population.
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Section 6
Summary and Conclusions
Joe A. Elder
This document presents a critical review of the
literature on the biological effects of RF radiation with
the objective of determining the relation between
biological effects and exposure to RF radiation in
terms of (1) absorbed dose rate (SAR) and (2)
increased body temperature. In Sec. 3, the interaction
of RF radiation with biological systems is discussed,
and in Sees. 4 and 5, research reports are reviewed
for the presence or absence of biological effects of RF
radiation. The major conclusions or generalizations
that can be drawn from these three sections are now
presented. In addition, the biological effects of RF
radiation are discussed in relation to SAR and to
increased body temperature in an attempt to analyze,
synthesize, and consolidate the available information
from this multidisciplinary field into a coherent
picture.
6.1 Major Conclusions and
Generalizations
1. RF radiation is a form of nonionizing electromag-
netic radiation of very low photon energies and
frequencies (0-3000 GHz), as distinguished from the
very high photon energies and frequencies associated
with ionizing electromagnetic radiation, e.g., X and
gamma rays. Included in the RF-radiation spectrum
are AM and FM radio, UHF and VHP TV, radar, and
microwave communication frequencies. The frequency
range of concern in this document is 0.5 MHz to 100
GHz, which includes nearly all the significant sources
of population exposure except 60-Hz electrical power
systems. However, there is very little information on
effects in human beings at any of these frequencies
and limited data on responses of animals exposed at
frequencies above 10 GHz and below 10 MHz; most of
the animal research is concentrated in the range of
900 MHz to 3 GHz.
2. RF-energy absorption by biological systems is a
complex function of frequency and the dimensions,
orientation, and dielectric properties of the absorber
and the complexity of the incident radiation fields.
Resonant frequencies (and their related wavelengths)
for an absorber are those at which maximum RF
energy is coupled into the absorbing system.
Resonance occurs when the long dimension of the
absorber is approximately 0.4 times the wavelength
of the incident RF radiation, if the object is located in
free space. Under these conditions, the whole-body
resonant frequency range for humans (from adults to
infants) is approximately 30 to 300 MHz. In this
document, whole-body average specific absorption
rate (SAR) is used to normalize the rate of energy
absorption across the frequency range, 0.5 MHz to 100
GHz, and to quantitate the relation between biological
effect and dose rate of RF radiation. SAR is the mass-
normalized rate at which the energy of an electro-
magnetic field is coupled into an absorbing body; the
units of SAR are watts per kilogram (W/kg).
3. High level RF radiation is a source of thermal
energy (e.g., microwave ovens) that carries all of the
known implications of heating for biological systems.
At a given incident field strength, maximal heating
occurs at the resonant frequency (D'Andrea et al.
1977). In general, the data are consistent with the
hypothesis that the SAR required to raise body
temperature of laboratory animals decreases as body
mass increases.
4. In most of the animal studies that report a biological
effect of RF radiation, exposures occurred at ambient
temperatures of 20 to 25°C and relative humidities of
50 to 70 percent. At more thermally stressful
conditions, e.g., higher ambient temperature and the
same or higher relative humidity, the experimental
results show that lower SARs cause a similar
biological effect. For example, Rughefa/. (1974)found
that the lethal dose of 2450-MHz radiation for mice
was inversely related to the temperature-humidity
index (Figure 4-22). Gage (1979b) showed that a
2450-MHz exposure at 22°C resulted in a reduced
behavioral response rate in rats at 3 W/kg, but that
similar exposures at 28°C caused reduced rates at 1,2
and 3 W/kg.
5. No consistent biological effect has yet been found
with molecular and subcellular systems exposed in
vitro to RF radiation other than effects occurring at
SARs that cause general temperature increases.
Conclusions regarding effects of in vitro exposure of
higher-order biological systems, such as single cells
and brain tissue, are given below.
6. The electrophysiological properties of single cells,
especially the firing rates of neurons in isolated
preparations, may be affected by RF radiation at SARs
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as low as 1 W/kg in a manner different from
generalized heating.
7. In general, no changes in chromosomes, DNA, or
reproductive potential of RF-exposed animals have
been reported and corroborated in the absence of
significant rises of temperature. Similarly, RF
radiation does not appear to cause mutations or
genetic changes in bacterial test systems unless
temperatures well above the normal physiological
range are produced.
8. Effects on the hematologic and immunologic
systems have been reported at SARs > 0.5 W/kg;
however, there is a lack of convincing evidence for
RF-radiation effects on these systems without some
form of thermal involvement. Some of the reported
effects of RF radiation on the hematologic and
immune systems are similar to those resulting from a
stress response involving the hypothalamic-hypo-
physeal-adrenal axis or following administration of
glucocorticoids. In those few cases where the
reversibility of RF radiation effects on the hematologic
and immunologic systems has been examined, the
effects have proved to be transient.
9. RF radiation is teratogenic at high SARs (> 15
W/kg) that approach lethal levels for the pregnant
animal. High maternal body temperatures are known
to be associated with birth defects. There appears to be
a threshold for the induction of experimental birth
defects when a maternal rectal temperature of 41 to
42°C is reached. Any agent capable of producing
elevated internal temperatures in this range,
including RF radiation, is a potential teratogen.
10. Reduced fetal mass seems to occur consistently
in rodents exposed during gestation to teratogenic
levels of RF radiation, or at SARs somewhat less than
those which cause death or malformation.
11. There is evidence that exposure of rodents during
gestation to RF radiation may cause functional
changes later in life. For example, Johnson et al.
(1978) observed lower body weight at weaning and in
young adult rats exposed at 2.5 W/kg for 20 h/day
during 19 days of gestation, and Chernovetz et al.
(1975) found increased postnatal survival of mice
exposed at 38 W/kg for 10 min during gestation.
12. Permanent changes in reproductive efficiency
have been directly associated with RF-radiation
exposures that caused temperatures in animal testes
greater than 45°C. At temperatures of 37 to 42°C
mature sperm may be killed with a temporary loss of
spermatogenic epithelium. Irradiation of rats at an
SAR of 5.6 W/kg, which produced a core temperature
of 41 °C, resulted in temporary infertility.
13. Neurons in the central nervous system (CNS) of
experimental animals have been reported to be
altered by acute high-level and by chronic low-level
exposures (> 2 W/kg). Pulsed RF radiation may have
a potentiating effect on drugs that affect nervous
system function. Some of the early reports of RF-
radiation effects on the blood-brain barrier (BBB) at
SARs < 2 W/kg have not been substantiated by later
investigations.
14. An increased mobilization of calcium ions occurs
in brain tissue exposed in vitro to RF radiation,
amplitude modulated at frequencies recorded in the
electroencephalogram (EEC) of awake animals. The
response appears to be based on the intensity of the
electric field within the tissue, which can be related to
SAR; the lowest effective SAR in in vitro samples is
estimated to be 0.0013 W/kg> Calcium-ion efflux is a
nonlinear effect in terms of both AM frequency and
field intensity; that is, the response occurs at specific
frequencies and electric field strengths. The
physiological significance of this effect has not been
established.
15. Some types of animal behavior are disrupted at
SARs that are approximately 25 to 50 percent of the
resting metabolic rates of many species. For example,
changes in locomotor behavior in rats occur at an
SAR of 1.2 W/kg, and alterations in thermoregulatory
behavior in squirrel monkeys occur at an SAR of 1
W/kg. Decreases in other operant or learned
behavioral responses during exposure have been
found at an SAR of 2.5 W/kg in the rat and at 5.0
W/kg in the rhesus monkey. The reported behavioral
alterations appear to be reversible with time.
16. Changes reported in endocrine gland function
and blood chemistry are similar to those observed
during increased thermoregulatory activity and heat
stress, and are generally associated with SARs > 1
W/kg. Exposures of sufficient intensity to produce
whole-body heating produce an increase in heart rate
similar to that caused by heating from other sources.
Changes in whole-body metabolism have been
reported following exposures at thermal levels (~ 10
W/kg), and brain energy metabolism is altered at
levels as low as 0.1 W/kg following irradiation of the
exposed surface of the brain of anesthesized animals.
17. A single acute exposure of the eye to high-
intensity RF radiation, if applied for a sufficient time,
is cataractogenic in some experimental animals. In
the rabbit, the animal most often used in ocular
studies, the cataractogenic threshold for a 100-min
exposure is 150 m W/cm2 (138 W/kg peak absorption
in the lens). The cataractogenic potential of
microwave radiation varies with frequency; the most
effective frequencies for cataracts in the rabbit eye
appear to be in the 1 - to 10 GHz range. Cataracts were
not produced in primates exposed acutely to RF-
radiation conditions that caused cataracts in lower
mammals such as the rabbit. The absence of
cataracts in the primate is attributed to the different
facial structure that caused a different pattern of
absorbed energy in the eye. No cataracts have been
reported in rabbits after whole-body, far-field RF-
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radiation exposures, even at near-lethal levels (SAR
= 42 W/kg for 15 min). No data at present support a
conclusion that low-level, chronic exposure to
microwave radiation induces cataracts in human
beings, although some studies have associated
ocular-lens defects with microwave radiation
exposure.
18. Pulsed RF radiation in the range 216 to 6500 MHz
can be heard by some human beings. The sound
associated with the "RF hearing" varies with pulse
width and pulse-repetition rate and is described as a
click, buzz, or chirp. The threshold for human
perception of this effect is approximately 40/uJ/cm2
(incident energy density per pulse). The most
generally accepted mechanism for the RF-auditory
sensation is that the incident pulse induces a
minuscule but rapid thermoelastic expansion within
the skull, which results in a pressure wave that is
conducted by the bone to the cochlear region of the
ear.
19. For the broad range of frequencies between 0.5
MHz and 100 GHz, cutaneous perception of heat and
thermal pain may be an unreliable sensory mechanism
for protection against potentially harmful RF-
radiation exposure levels. Many frequencies deposit
most of their energy at depths below the cutaneous
thermal receptors.
20. There is no convincing evidence that exposure to RF
radiation shortens the life span of human beings or
experimental animals or that RF radiation is a primary
carcinogen (cancer inducer); however, (1)fewstudies
have used longevity or cancer incidence as end
points, and (2) human studies have lacked statistical
power to exclude life shortening or cancer. There is
evidence from one group of investigators that chronic
exposure to RF radiation (SAR = 2 to 3 W/kg) resulted
in cancer promotion or co-carcinogenesis in three
different tumor systems in mice; the incidence of
cancer was comparable to that observed in mice
exposed to chronic stress conditions only.
21. Human data are currently limited and incomplete
but do not indicate any obvious relationship between
prolonged low-level RF-radiation exposure and
increased mortality or morbidity, including cancer
incidence.
The prospects for revision and refinement of the
major conclusions and generalizations stated above
are considerable because of our limited knowledge of
(1) effects of most frequencies in the range 0.5 MHz to
100 GHz; (2) effects of chronic low-level exposures on
human beings and laboratory animals; (3) which
segments of the population are most sensitive; (4) the
influence of ambient environmental conditions and of
potential synergistic interaction with other agents;
(5) the implication of nonhomogeneous RF-energy
deposition; (6) the existence and significance of
frequency-specific effects and power-density
windows; and (7) the physical mechanisms of
interaction at low exposure levels, including field-
specific phenomena.
6.2 Specific Absorption Rate
Reports on the biological effects of RF radiation
usually specify the frequency and power density of
the field applied to the biological system. Individually
or together, these parameters do not provide a
reasonable correlate with biological effects because
RF-energy absorption is known to depend on the
relation between wavelength and absorber size and
orientation. However, when frequency and power
density are combined with a knowledge of absorber
size and dielectric property, an estimate of SAR can
be made. The whole-body average SAR is currently of
limited use because it is an estimate of absorbed
energy averaged over the whole-body mass. It does
not address the existence of localized areas of
increased energy deposition in exposed biological
systems, nor the considerable differences between
species in their capacity to regulate a given energy
burden. However, work is currently under way to
extend the usefulness of this concept in both areas.
The SAR is currently the parameter used most
frequently to describe the energy absorbed by a
biological system exposed to RF radiation. In the
discussion below, whole-body average SAR is used as
a correlate for the observed biological responses.
The data cited in the preceding sections show that
acute whole-body exposure of laboratory animals at
SAR values > 30 W/kg is lethal. For example,
Chernovetz et al. (1977) reported that a 20-min
exposure (2450-MHz) at 31 W/kg was lethal to 23
percent of the rats. Appleton et al. (1975) found that
3000-MHz exposures at 42 W/kg for 30 min or 70
W/kg for 15 min were lethal to rabbits. A shorter
exposure (15 min) at 42 W/kg caused acute ocular
changes, but no cataracts, and cutaneous burns
around the eye (see Table 5-15). During a 15-min
exposure at 14 W/kg, rabbits showed signs of acute
heat stress and struggled out of the field. Localized
exposure to very high intensity RF radiation can result
in burns, as shown by Kramar et al. (1978), who
reported second- to third-degree burns on the face of
rhesus monkeys exposed for 22 min to 2450-MHz
radiation that produced an SAR in the eye of ~ 115
W/kg.
Brief exposures (< 5 min) of the whole body to high
intensities result in significant biological damage, as
shown by Rugh (1976a)and Hugh era/. (1975), who
irradiated pregnant mice at SAR values near 100
W/kg and found birth defects, increased embryonic
and fetal resorptions, postnatal weight decrements,
and reduced survival upon re-irradiation of the
offspring of mice exposed during pregnancy.
Laboratory animals have generally been found to be
affected by SARs in the 10- to 30-W/kg range, even
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when the exposures have been short (minutes to
hours). Fetotoxic effects in mice exposed at 22 W/kg
have been reported by Berman et al. (1978). Some
components of the immune system appear to react
with an increased response, whereas others
demonstrate diminished responses. Components
reported to increase are PMN levels (Kitsovskaya
1964; Michaelsoh et al. 1964; Lappenbusch et al.
1973; Liburdy 1977), splenic lymphocytes (Wiktor-
Jedrzejczak et al. 1977a,b,c; Sulek et al. 1980),
lymphocyte response to mitogen stimulation (Huang
and Mold 1980; Wiktor-Jedrzejczak era/. 1977a,b,c),
and lymphocyte transformation to the lymphoblast
stage (Huang et al. 1977). Decreases are reported
in the primary antibody response to sheep red blood
cell (SRBC) (Wiktor-Jedrzejczak et al. 1977a,b,c), the
CPU for the erythroid granulocyte-macrophage series
in bone marrow (Huang and Mold 1980), lymphocyte
traffic from lung to spleen (Liburdy 1980), and
circulating lymphocyte levels (Lappenbusch et al.
1973; Liburdy 1977). Roszkowski et al. (1980)
reported a general immunosuppressive effect at 35
W/kg; they found an increase in lung cancer colonies
and an inhibition of contact sensitivity to oxazlone in
mice.
Some biological end points appear to be unaffected
even at 10 to 30 W/kg. Examples are postnatal
survival, adult body weight, and longevity (Guillet and
Michaelson 1977; Spalding et al. 1971).
In contrast to the results of animal studies, in vitro
studies at 10 to 30 W/kg have shown few effects on
the irradiated systems if temperature is properly
controlled, e.g., no mutation induction in bacteria
(Blackman et al. 1976; Corelli et al. 1977; Dutta et al.
1979a, 1980), no effects on enzyme activities (Ward
et al. 1975; Bini et al. 1978; Allis and Fromme 1979),
no effects on the physical characteristics and
structure of biomolecules such as nucleic acids and
proteins (Allis 1975; Allis et al. 1976; Corelli et al.
1977), and no change in lymphocyte transformation
(Smialowicz 1976). Notable exceptions are Ismailov's
(1971, 1977, 1978) reports that the human RBC
exhibits increased electrophoretic mobility, K+ efflux,
Na* influx, and hydrogen exchange at SARs between
5 and 45 W/kg; and Seaman and Wachtel's (1978)
observation of a decreased firing rate of Aplysia
pacemaker neurons at SARs as low as 1 W/kg.
The majority of the experimental studies that met the
criteria for inclusion in this document employed SARs
< 10 W/kg. Many of these studies are differentiated
by observed "effects" (without regard to biological
significance) or "no effects," and arranged within
these two groupings by decreasing SAR values in
Tables 6-1 and 6-2.
Biological variables that do not appear to be sensitive
to RF radiation at < 10 W/kg include organ weight,
litter size, teratology and growth (Table 6-1).
Physiological systems and parameters that appear to
be sensitive include behavior, the central nervous
system, and hematology and immunology (Table 6-2).
In Table 6-2, several positive findings at SARs < 10
W/kg are listed for a number of biological variables.
A comparison of Table 6-1 with Table 6-2 reveals that
many reports of "no effects" occur in the same
biological systems (e.g., behavior and hematology/
immunology) over a similar SAR range. Negative
findings are important to define the lower exposure
limits of biological effects and the sensitivity of
specific biological end points; however, in general,
they cannot displace the reports of positive findings
that are the principal concern in a review of the
biological effects of RF radiation.
It seems appropriate at this point to cite the
conclusions of the subcommittee that developed the
rationale for the recently published ANSI RF-
radiation (0.3 MHz to 100 GHz) exposure guidelines
(ANSI 1982). The subcommittee completed its
review of the literature in February 1979. Note that
about half of the reports on behavior shown in Tables
6-1 and 6-2 were published prior to 1979. The ANSI
subcommittee concluded the following:
The most sensitive measures of biological effects
were found to be based on behavior.
The whole-body-averaged SARs associated with
thresholds of reversible behavioral disruption were
found to range normally between 4 and 8 W/kg in
spite of considerable differences in carrier
frequency (600 MHz to 2.45 GHz), species (rodents
versus primates), and mode of irradiation (cavity,
waveguide, and plane wave).
Because of the paucity of reliable data on chronic
exposures, the subcommittee focused on evidence
of behavioral disruption under acute exposures,
even that of a transient and fully reversible
character. The assumption is that reversible
disruption during an acute exposure is tantamount
to irreversible injury during chronic exposure.
The concensus remained that reliable evidence of
hazardous effects is associated with whole-body-
averaged SARs above 4 W/kg.
Other significant effects in laboratory animals which
occur at SARs of 4 to 8 W/kg are:
1. Temporary sterility in male rats exposed at an SAR
= 5.6 W/kg for 4 h/day for 20 days (Berman et al.
1980).
2. Bradycardia in rats after whole-body exposure
(SAR = 6.5 W/kg) (Phillips et al. 1975b). Exposure
of the head of the rabbit at an SAR of 3 W/kg
caused tachycardia (Birenbaum et al. 1975).
Potentially significant biological effects that have
been reported at SARs < 4 W/kg include the
following:
6-4
-------
Table 6-1. Selected Studies Reporting
Biological Variable
'No Effects" at SARs < 10 W/kg Grouped by Biological Variable
Relevant Studies
SARs
Growth
(Food, Water Intake)
Behavior
Mortality/Life Span
Hematology/lmm unology
Mutations/Chromosomal
Aberrations
Teratology
Litter Size
Organ Weight
Blood Chemistry
Fertility
Hormones
Neurotransmitter Levels
Metabolic Rate
Cardiovascular System
Stavinoha et al. (1975)
McAfee et al. (1973)
Kaplan (1981)
Michaelson et al. (1978)
Johnson et al. (1978)
Lovely et al. (1977)
D'Andrea et al. (1979)
D'Andrea et al. (1976)
Moe era/. (1976)
Mitchell etal. (1977)
Sanza and de Lorge (1977)
Gage(1979a)
Scholl and Allen (1979)
de Lorge (1976)
Lovely etal. (1977)
Robert! era/. (1975)
Schrotefa/. (1980)
Thomas etal. (1979)
Kaplan (1981)
Johnson etal. (1978)
Spaldingef a/. (1971)
Smialowicz et al. (1981 a)
Smialowicz etal. (19796)
Liburdy(1980)
Smialowicz (1981 a)
Spa Iding etal. (1971)
Djordjevic et a/ (1977)
Blackman et al. (1975, 1976)
McLees et al. (1972)
Bermanera/. (1980)
Johnson et al. (1978)
Bermanera/. (1978)
Michaelson et al. (1978)
Johnson etal. (1978)
Michaelson et al. (1978)
Mikolajczyk(1976)
Wangemann and Cleary (1 976)
Berman etal. (1980)
Mikolajczyk(1976)
Parker (1973)
Lu etal. (1977)
Milroy and Michaelson (1972)
Merritt etal. (1976)
Ho and Edwards (1977a,b)
Phillips et al. (1975b)
6.3
6.0-8.0
3.4
2.5-10.0
2.5
1 .0-2.5
1.0-2.5
5.0-6.0
3.9
2.3
2.1-4.7
0.3
1.6
1.1-1.4
1.0
0.2-8.3
0.2
0.2
3.4
2.5
1.7
10
>4.0
3.8
2.0-3.0
1.7
1.0
0.08-7.5
1.3
0.9
2.5
2.0-8.1
2.5-10.0
2.5
2.5-10.0
1 .0-2.0
0.8
1 .0-2.0
1 .0-2.0
2.0-6.5
2.5
0.25-2.5
3.0
5.5
4.5
1. The decrease in behavioral response rates cited in
ANSI (1982) were based on studies done at
ambient temperatures of 20 to 25°C. Gage
(1979b) has shown that similar changes in
behavior occur at lower SARs when exposures are
conducted at higher ambient temperature; that is,
at 22°C the effective SAR was 3 W/kg, whereas at
28°C SARs of 1 and 2 W/kg were effective.
2. Although RF radiation does not appear to be a
primary carcinogenic agent (cancer inducer),
there is evidence from one laboratory that RF
radiation acts as a cancer promoter or co-
carcinogen in three different tumor systems in
mice at an SAR of 2 to 3 W/kg (Szmigielski et al.
1980, 1982).
3. A decrease in the number of Purkinje cells in the
brain of rats exposed at an SAR of 2 W/kg was
reported by Albert et al. (1981 a).
4. Endocrine gland function and blood chemistry
changes are similar to those observed during heat
stress and are generally associated with SARs>1
W/kg (Sec. 5.7.1).
6-5
-------
Table 6-2. Selected Studies with Reported
Biological Variable
'Effects" at SARs < 10 W/kg Grouped by Biological Variable
Relevant Studies
SARs
Behavior
Central Nervous System
Hematology/lmmunology
Hormones
Drug Potentiation
M utations/Chromosome
Aberrations
Neurotransmitter Levels
Fertility
Clinical Chemistry
Cardiovascular System
Gordon (1983a)
Gordon (1983b)
deLorge(1976)
Moeeta/ (1976)
Gage(1979a)
de Lorge and Ezell (1980)
D'Andrea et at. (1980)
Mitchell etal. (1977)
Gage(1979b)
Thomas etal. (1975)
D'Andrea et a/. (1979)
Stern etal. (1979)
Thomas et at. (1976)
Rudnevef a/. (1978)
Adair and Adams (1980a,b)
Schrot et al. (1980)
Frey and Feld(1975)
Albert and DeSantis (1975, 1976)
Switzer and Mitchell (1977)
Albert (1979b)
Albert et al. (1981 a)
Seaman and Wachtel (1978)
Albert and Kerns (1981)
Sanders et al. (1980)
Goldstein and Sisko (1974)
BaranskM 19726)
Blackman et al. (1979, 1980a,b)
Takashima et al. (1979)
Sulekera/ (1980)
Smialowicz et al. (1979a, 1982)
Liburdy(1979)
Michaelson et al. (1964)
Huang and Mold (1980)
Huang et al. (1977)
Djordjevic and Kolak (1973)
Deichmann et al. (1963)
McRee et al. (1980a)
Czerski (1975)
Szmigielski et al. (1975)
Baranski(1971)
Prince et al. (1972)
Lu etal. (1977)
Lotz and Michaelson (1978)
Mikolajczyk (1976)
Edelwejn (1968)
Thomas and Maitland (1979)
Manikowska et al. (1979)
Merritt et al. (1977)
Berman et al. (1980)
Wangemann and Cleary (1976)
Kaplan et al. (1971)
Phillips etal. (1975b)
Birenbaum etal. (1975)
7.0
5.3
5.0
3.6
27
2.5-4.9
2.5
2.3
2.0
1.4-1.5
1.2
1.1
1.1
1.0
1.0
0.7
0.4
5.0-12.5
2.3
2.0
2.0
1.0
0.9-2.0
0.1
0.1-0.3
0.4-2.5
0.0013
0.0001
5.0-11.8
5.0-7.0
4.6
4.0-6.0
3.6-10.0
2.3-30.7
2.0
1.5-2.2
1.5
0.5-0.8
0.5
0.5
0.4-2.0
5.0
3.0-12.8
1.0-2.0
1.0
0.2
0.05-5.0
6.0
5.6
1.6-4.0
8.0
6.5
3.0
5. Effects on the hematologic and immunologic
systems occur at SARs > 0.5 W/kg and appear to
resu It from some form of therma I i nvolvement due
to absorbed RF energy (Sec. 5.2).
6. Changes in cellular energy metabolism in the rat
brain have been reported at an SAR =0.1 W/kg;
the data support the conclusion that the effect is
frequency specific (Sanders et al. 1980).
7. Results of studies of amplitude-modulated (AM)
radio-waves, particularly AM frequencies near or
at 16 Hz, have shown changes in calcium-ion
efflux from chick brain tissues in vitro. The effect
6-5
-------
has been shown to be frequency and intensity
specific and to occur at SARs as low as 0.0013
W/kg (Blackman et at. 1979, 1980a,b). In 1984
Dutta et al. reported that 16-Hz AM microwave
radiation caused changes in calcium-ion efflux
from human brain cells in culture at an SAR of 0.5
W/kg.
Human data are limited and not useful for developing
a quantitative relation between effect and SAR;
however, two recent studies of physiotherapists
suggest two potentially significant health effects
associated with work with RF equipment. The first is
heart disease (primarily ischemic) in males; (Ham-
burger et al. 1983) the second is pregnancy outcomes
in female physiotherapists (Kallen et al. 1982). Both
studies are considered to be exploratory, and neither
provides quantitative data on the RF radiation levels
in the work environment, so that SAR values cannot
be estimated.
In summary, the data currently available on the
relation of SAR to biological effect show evidence for
biological effects at an SAR of about 1 W/kg. This
value is lower by a factor of 4 than 4 W/kg, the value
above which reliable evidence of hazardous effects
was found by ANSI (1982) following a review of the
literature in February 1979. The above conclusion is
based on:
1. the findings that more thermally stressful
conditions result in lower threshold SARs for
behavioral changes similar to those changes
determined by ANSI (1982) to be the most
sensitive measures of biological effects
2. the effects on endocrine gland function, blood
chemistry, hematology, and immunology that
appear to result from some form of thermal
involvement due to absorbed RF energy
3. data from one laboratory showing that RF
radiation can act as a cancer promoter or co-
carcinogen and results from another laboratory
describing changes in brain cellularity.
The experimental evidence suggests that the central
nervous system is particularly sensitive to RF
radiation. Two other areas of research that may prove
to be highly significant are calcium-ion efflux and
brain energy metabolism.
6.3 Core Temperature
Heating is the least controversial explanation for
most RF-radiation effects, and it is appropriate to
examine the biological effects in relation to an
increase in body temperature in the range of 0 to 6°C
above normal. The average rectal (core) temperature
is approximately 37.0°C (98.6°F) for human beings
and ranges from 36 to 38°C for most mammals
(Schmidt-Nielsen 1979). In general, the lethal
temperature is approximately 6°C above the average
core temperature (cf. Table 4-2). Prolonged elevation
of core temprature at 5°C above normal (42CC -
107°F) is associated with heat stroke and brain
lesions; the temperature 41,2°C (106.2°F) occurs m
only 1 of 1000 humans during fever (Folk 1974) With
RF-radiation exposures, even brief periods (1 5 to 20
min) at core temperatures of 41.5 to 42 5°C in rats
can result in increased fetal resorptions, decreased
fetal body weights (Chernovetz et al. 1977), and
significant hemolysis and K" efflux in red blood cells
of adult rats (Peterson et al. 1979). In healthy young
men whose mean body temperature was increased to
41 °C by RF-radiation exposure for up to 3 h, sperm
numbers had decreased by 60 percent by 40 to 60
days after treatment (MacLeod and Hotchkiss 1941).
At this core temperature, temporary infertility in male
rats has also been reported (Berman et al. 1980)
Berman et al. (1981 (showed that when RF-radiation
exposure produced a maternal colonic temperature of
<41°C in the pregnant rat, no effects were detectable
in the fetus; O'Connor (1980) reached a similar
conclusion. The mouse fetus is apparently more
sensitive to increased maternal body temperature
than is the fetal rat. Berman era/. (1978) reported that
a 0.8°C temperature differential between exposed
and sham-irradiated dams produced a 10-percent
decrease in the body mass of the exposed mouse
fetus.
Several RF-radiation-induced effects have been
reported for other stages of life in various animal
species at core temperature increases of 1 to 3°C.
These effects include an increased response of the
adrenal glands in irradiated infant rats (Guillet and
Michaelson 1977); increased serum glucose and
blood urea nitrogen (BUN) levels in adult rabbits
(Wangemann and Cleary 1976); increases in
circulating neutrophils.and T and B lymphocytes in
spleens of mice, along with a decrease in circulating
lymphocytes (Liburdy 1977, 1979); changes in
lymphocyte circulation between bone marrow,
spleen, liver, and lung similar to that produced by
stress-related steroids (Liburdy 1980); increased
responsiveness of lymphocytes to mitogen stimulation
in monkeys (Prince et al. 1972); increased white blood
cell (WBC) count and decreased S9Fe uptake in mice
(Rotkovska and Vacek 1975); decreased exploratory
activity of rats (Hunt et al. 1975); decreased vigilance
in monkeys (de Lorge 1976); and work stoppage in
rats (D'Andrea et al. 1977).
RF-radiation exposures that produced core temperature
increases of 1 to 2°C are reported to be associated
with decreased serum thyroxine and increased
corticosteroid levels (Lu era/. 1977). Michaelson era/.
(1964) found decreased lymphocyte, neutrophil, and
eosinophil levels and hemoconcentration at tempera-
tures of 1.0 to 1.7°C above normal in dogs. In
association with a temperature rise of 1.0°C in
irradiated rats, Djordjevic and Kolak (1973) observed
5-7
-------
increases in RBC. hematocrit, and hemoglobin which
may also be a case of hemoconcentration. Pazderova-
Vejlupkova and Josifko (1979) reported decreases in
the hematocrit, WBC, and lymphocyte numbers in
rats at a temperature change of only +0.5°C.
As a general rule, exposures that produce a core-
temperature rise of £ 0.5-C do not cause detectable
effects on reproduction, fetal weight, growth,
development, hematological and immunological end
points, hormonal levels, and clinical blood chemistry
(Berman et al. 1978, 1980; Johnson et at. 1978;
Michaelson et al. 1978; Guillet and Michaelson
1977; Djordjevic et al. 1977; Smialowicz eta/. 1979b;
Milroy and Michaelson 1972, Lovely et al. 1977;
Wangemann and Cleary 1976).
In most of the animal studies that report a biological
effect of RF radiation, the exposures occurred at
ambient temperatures of 20 to 25°C and relative
humidities of 50 to 70 percent. At more thermally
stressful conditions, e.g., higher ambient temperature
and the same or higher relative humidity, the
experimental results show that lower SARs will cause a
similar biological effect. In other words, it is
reasonable to expect that all the above biological
effects described in Sec. 63 that are associated with
an increase of core temperature > 0.5°C will occur
also at lower SARs if the combination of RF radiation
exposure and ambient conditions result in a similar
core-temperature increase.
In Sec. 6.2, the biological effects relative to SAR were
presented, and the important conclusions from ANSI
(1982) relative to hazardous levels of RF radiation
were discussed. In this section, it is instructive to
use the threshold limit value (TLV) for deep-body
temperature of workers as an introduction to a
discussion of temperature changes in human beings
exposed to RF radiation. The TLV of the American
Conference of Governmental Industrial Hygienists
(1983) states that workers should not be permitted to
continue their work when their deep-body tempera-
ture exceeds 38°C , that is, 1 °C above the average
normal temperature for adult human beings. One
may conclude therefore that exposure to an
environmental agent such as RF radiation that may
cause a 1°C rise in core temperature should be
considered hazardous to relatively healthy individuals.
The application of this reasoning to the general
public, which varies in health status, age, etc., is
discussed below.
There are few data on the RF-radiation exposure
conditions that cause core temperature changes of 0
to 1 °C in human beings. One of the first attempts to
consider the addition of RF energy as a thermal load in
a model of man was done by Guy et al. (1973), who
later used a thermodynamic model of the human
body to determine increase in temperature (Guy et al.
1978). They reported that an exposure of 4 W/kg at
79 MHz (resonant frequency for an adult human
being in free space) for about two hours caused the
hypothalamic temperature to rise 1°C. If no unusual
hot spot occurred in the hypothalamic area, one could
assume that the temperature within the head was a
good estimate of core temperature, that is, the core
temperature rose about 1&C also. Using a mathema-
tical model of the human body, Spiegel etal. (1980a)
predicted than an 80-MHz exposure (Ta = 30CC, RH =
30 percent) at an SAR - 2.3 W/kg would produce a
1 ~C rise in core temperature; and SAR of 1.4 W/kg
resulted in a 0.5'C rise in core temperature. In their
report, in which they examined the relation of
biological effects to increase in body temperature.
Tell and Harlen (1979) concluded that whole-body
exposure of human beings to 3 W/kg at resonant
frequencies would raise a resting individual's rectal
temperature by about 1 °C for exposure durations of
the order of 1 h or more. In summary, the results of
Guy et al. (1978), Spiegel et al. (1980a), and Tell and
Harlen (1979) show that SARs of 1 to 4 W/kg for short
durations (1 h) produce significant increases in
human body temperature at ambient temperatures of
25 to 30°C It is reasonable to conclude that increases
in body temperature are likely to occur at lower SARs
if exposure takes place under more thermally
stressful conditions, e.g., higher ambient tempera-
ture and/or higher relative humidity.
Data from experimental studies with primates are in
good agreement with the results of the modeling
experiments described above. In 1976, de Lorge
found that a 2450-MHz exposure of the rhesus
monkey for 1 h (Ta = 21 to 24°C; RH = 70 percent) at an
SAR of 2.2 to 2.9 produced a temperature rise of
0.5°C; an SAR of 4.3 W/kg caused an increase of
1 °C. Exposure of the rhesus monkey to 225 MHz, a
frequency close to resonance, at only 1.2 W/kg (Ta =
24°C) caused a 0.5 to 0.6°C rise in rectal temperature;
at 1290 MHz, an SAR of 3 W/kg caused a similar
temperature rise (Lotz 1982; Lotz and Podgorski
1982). In these two studies, the ability of the animals
to dissipate heat may have been compromised
because of various factors in the experimental
design.
Two additional points must be given serious
consideration.
1. When a measurable increase in body temperature
occurs, it can be interpreted as an indication that
the body is under some stress. Exposure to RF
radiation at SARs below those that cause an
increase in core temperature may activate the
heat-dissipating thermoregulatory mechanisms
of the body to maintain core temperature within
the normal range.
2. Under many conditions of RF exposure, some
regions of the body will probably experience an
increase in temperature due to localized RF-
energy absorption while the core temperature
6-8
-------
remains near normal (Guy et al. 1978; Spiegel et
al. 1980a). For example, Spiegel et al. (1980a)
showed that an SAR of 1.4 W/kg produced a
3.6°C rise in temperature of the thigh while the
core temperature rose only 0.5°C.
Consideration is now given to the health impact of the
thermal extremes that can exist in the U.S. during
summer months. During the period 1952-67, heat
waves occurred in five different years. Ellis (1972)
examined the Vital Statistics Reports of the U.S.
Public Health Service for these years and drew the
following conclusions:
1. During the five heat-wave years 1952-55 and
1966, excess deaths due to heat-aggravated or
heat-precipitated illness during the heat wave
were conservatively estimated to be at least 10
times those to be expected in this category in
the General Mortality Tables.
2. In either June or July there were excess numbers
of deaths due to vascular accidents of the central
nervous system in 1952-55 and 1966, and similar
but smaller excess numbers of diabetic deaths in
1952, 1954, 1955, and 1966.
3. Excess deaths from arteriosclerotic and degene-
rative heart disease, including coronary disease,
were observed in 1955 and 1966, and there was
an excess of deaths from hypertensive heart
disease in May, June, or July in each of the heat-
wave years but not in 10 of the other 11 years.
4. Infants below 1 year of age are the most heat-
illness-prone age group below 50 years of age;
adults above 50 years are more heat-illness-
prone than infants and become progressively
more so with advancing age.
The evidence indicates that exposure of human
beings at frequencies in the resonant region at an
SAR of approximately 1 W/kg produces significant
changes in body temperature under some environ-
mental conditions. This conclusion should not be
interpreted as conservative because, as stated above:
1. when an increase in body temperature occurs, it
can be interpreted as an indication that the body is
under some stress;
2. under many conditions of RF exposure, it is very
likely that some regions of the body increase in
temperature due to localized RF-energy absorption
while the core temperature remains near normal;
3. the general population has groups of individuals
particularly susceptible to heat.
6.4 Summary
The review of the currently available literature on RF
radiation provides evidence that biological effects
occur at an SAR of about 1 W/kg; some of them may
be significant under certain environmental conditions.
This value was derived from two perspectives; (1) the
relation of biological effects to SAR (dose rate) and (2)
the relation of biological effects to increased body
temperature caused by absorption of RF energy.
6-9
-------
-------
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Glossary
ABSORPTION The irreversible conversion of electro-
magnetic energy into other forms of energy as a result
of interaction with matter. See SPECIFIC ABSORPTION
and SPECIFIC ABSORPTION RATE.
ACCLIMATION A physiological change, occurring
within the lifetime of an organism, which reduces the
strain caused by experimentally induced stressful
changes in particular climatic factors.
a-HELIX A conformation found in protein molecules
where the amino acid chain turns in a helical pattern
with weak chemical bonds (hydrogen bonds) forming
between successive turns in the helix.
AMES TEST A standard test for mutagenic potential
of various agents performed with specialized strains
of bacteria.
ANECHOIC CHAMBER A chamber lined with material
that absorbs RF radiation; an RF-exposure system
free of scattered and reflected radiation.
ANGULAR MOMENTUM The quantity of motion of a
rotating body - directly proportional to the angular
velocity of the rotating body.
ANTENNA A device for radiating or receiving radio
waves.
ANTENNA REGIONS The distinction between
electromagnetic fields far from and those near to the
antenna. The regions are usually classified into three
zones: near (static) zone, intermediate (induction)
zone, and far (radiation) zone. The zones are spatially
located by drawing spheres of different radii around
the antenna. The radii are approximately r < ^ for the
near zone, ^ < r(^) for the intermediate zone, and r >
h for the far zone. Note that -A is the wavelength of the
electromagnetic field produced by the antenna. In the
far zone the field components (E and H) lie transverse
to the direction of the propagation, and the shape of
the field pattern is independent of the radius at which
it is taken. In the near and intermediate zones the field
patterns are quite complicated, and the shape is, in
general, a function of the radius and-angular position
(azimuth and elevation) in front of the antenna.
ATHERMAL EFFECT (NONTHERMAL EFFECT) Any
effect of electromagnetic energy on a body that is not
a heat-related effect.
ATTENUATION A general term used to denote a
decrease in magnitude of RF transmission from one
point to another.
AUTOLYSIS The decomposition of an organ or tissue
by its own enzymes.
AVERAGE POWER W The time-average rate of
energy transfer:
= 1/(t2-ti)/,t2W(t)dt
For radar calculations, average power W = peak
power x pulse width x pulse repetition frequency.
BASES Biochemcial compounds, either purine or
pyrimidines, that are ring structures containing
carbon and nitrogen and which are capable of weak
bonding to each other.
/3-SHEET A conformation found in protein molecules
where two or more portions of amino acid chains line
up side-to-side, with weak hydrogen bonds forming
between adjacent chains.
BIOPOLYMER A polymeric substance formed in a
biological system, e.g., DNA, proteins.
BLASTOGENIC RESPONSE The transformation of
small lymphocytes into large morphologically
primitive blast-like cells capable of undergoing
mitosis; this phenomenon can be induced in cultured
cells by a variety of agents, including mitogens as well
as antigens, to which the cell donor has been
previously immunized.
BLOOD-BRAIN BARRIER A functional concept to
explain the observation that many substances
transported by blood readily enter other tissues but do
not enter the brain. The barrier functions as if it were
a continuous membrane lining the brain vasculature.
BURSA OF FABRICUS A lymphoidal organ in the
hindgut of birds that influences B cell development.
CALCIUM EFFLUX The release of calcium ions from a
sample into a surrounding solution.
CALORIE The amount of heat necessary to raise the
temperature of one gram of water 1 °C. One calorie
equals 4.184 joules.
CARCINOMA Any of the various types of malignant
neoplasm derived from epithelial tissue, occurring
more frequently in the skin, bronchi, stomach, and
prostate gland in men, and in the breast, cervix, and
skin in women.
CATARACTOGENIC Giving rise to the formation of a
cataract, an opacity in the crystalline lens of the eye.
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CHEMOSIS Excessive edema of the ocular conjunc-
tiva.
CHROMOSOMES Large complex biochemical struc-
tures, containing nucleic acid (DNA) and proteins,
which can be visualized in some cells by certain light
microscopy techniques.
CIRCULARLY POLARIZED If the electric field is
viewed as a point in space, the locus of the end point
of the vector will rotate and trace out an ellipse once
each cyle.
COLONY-FORMING UNIT (CPU) Colonies of bone
marrow or blood cells arising from a single progenitor
cell when grown in vitro or in vivo.
COMPLEX DIELECTRIC PERMITTIVITY The character-
ization of electrical parameters of materials at the
macroscopic level.
CONFORMATION The spatial distribution of the parts
of a macromolecule in relation to each other, i.e., how
a chain of amino acids folds on itself to form a protein.
CONTINUOUS WAVE (CW) Electromagnetic fields
that vary sinusoidally in time; that is, those fields
which oscillate at a single frequency.
COUNTER-CURRENT HEAT EXCHANGE The heat
exchange between blood flowing in opposite
directions at different temperatures, e.g., adjacent
arteries and veins.
CORE TEMPERATURE The temperature near the
center of the body; usually measured through the
rectum.
CRITICAL TEMPERATURE, LOWER The ambient
temperature below which the rate of metabolic heat
production of a resting thermoregulating animal
increases by shivering and/or nonshivering thermo-
genic processes to maintain thermal balance.
CRITICAL TEMPERATURE, UPPER 1. The ambient
temperature above which thermoregulatory evapor-
ative heat loss processes of a resting thermoregulating
animal are recruited. 2. The ambient temperature
above which there is an increase in metabolic rate
due to a rise in the core temperature of a resting
thermoregulating animal.
CYTOSIS Increase in number of cells, e.g., leukocy-
tosis, increase in the total number of circulating
leukocytes.
DEBYE A unit for dipole moment equal to the dipole
moment of a charge distribution of one positive and
one negative charge, each equal in magnitude to the
charge of an electron separated by 1 A (10"10m).
DECIBEL (dB) A unit expressing the logarithmic ratio
of two powers or voltages. One tenth of a Bel.
DENSITOMETRY The measurement of exposure to an
RF field; usually expressed in units of milliwatts per
square centimeter.
DEPTH OF PENETRATION For a plane wave electro-
magnetic field incident on the boundary of a good
conductor, the depth of penetration of the wave is that
depth at which the field strength of the wave has been
reduced to 1 /e or approximately 37% of its original
value.
DIELECTRIC MATERIAL A class of materials that act
as electric insulators. For this class the conductivity is
presumed to be zero, or very small. The positive and
negative charges in dielectrics are tightly bound
together so that there is no actual transport of charge
under the influence of a field. Such material alters
electromagnetic fields because of induced charges
formed by the interaction of the dielectric with the
incident field.
DIPOLE A molecule (or other structure) having the
effective centers of positive and negative charges
separated.
DIPOLE MOMENT A quantity describing the strength
of a particular dipole:
"d*=/vp(r)"r*d7
where the dipole (d) is the integral of the charge
distribution (p(T)) times the vector distance (rf from a
designated origin over the entire space containing the
charge distribution (v).
DNA Deoxyribonucleic acid; the chemical which
makes up the genes, the basic unit of heredity.
DNA MELTING CURVE Characteristic loss of helical
structure and separation of the strands of a DNA
molecule when temperature is raised.
DOSIMETRY The measurement of the absorbed dose
or dose rate by an object in a radiofrequency field;
usually expressed as watts per kilogram or joules per
kilogram.
DUTY FACTOR (CYCLE) The product of the pulse
duration and the pulse repetition frequency.
ELECTRIC FIELD STRENGTH The force on a stationary
unit positive charge at a point in an electric field. This
force may be measured in volts per meter (V/m).
ELECTROMAGNETIC RADIATION (EMR) Energy in
the form of electric and magnetic fields.
ELECTROMAGNETIC WAVE A wave characterized by
variations of electric and magnetic fields. Electro-
magnetic waves are categorized as radio waves, light
rays, etc., depending on the frequency.
ELECTROPHORETIC MOBILITY The ability of a cell or
macromolecule to move in response to a constant
electric field.
ELECTROSTRICTIVE FORCE Force exerted by an
electrostatic field that causes the elastic deformation
of a dielectric.
ELLIPSOID SHAPE A surface, all plane sections of
which are ellipses or circles.
G-2
-------
ENZYME KINETICS (ACTIVITY) Measure of how
rapidly an enzyme catalyzes a chemical reaction.
EPITHELIOMA Carcinoma derived from squamous
cells (scale-like cells) or from the basal and adnexal
cells (accessory cells) of the skin.
ERYTHROPOIESIS The production of red blood cells.
EUKARYOTE An organism composed of one or more
complex cells containing chromosomes that are
segregated from the rest of the cell by a nuclear
membrane. This distinction is in contrast to bacteria,
which have less complex DNA structure distributed
throughout the cell volume.
EXCITATION The absorption of energy by a molecule
or other structure.
FAR FIELD REGION See antenna regions.
FEVER A pathological condition in which there is an
abnormal rise in core temperature. The extent of the
rise is variable. The temperature rise in an individual
may be considered as fever when it is greater than the
mean standard deviation for the species in basal
conditions.
FIELD-INDUCED MIGRATION The physical movement
of charged bodies under the influence of an
electromagnetic field.
50TH PERCENTILE For a large set of measurements
arranged in order of magnitude, the 50% percentile is
the value such that 50% of the measurements are
less than that value and 50% are greater.
FINITE DIFFERENCE TECHNIQUE The approximation
of differentials by their finite difference; e.g., dy/dx ~
Ay/Ax.
FIRST-ORDER DIFFERENTIAL EQUATION A differen-
tial equation of order one (only single-order
derivatives are included in the equation).
FREQUENCY The number of sinusoidal cycles made
by electromagnetic radiation in one second; usually
expressed in units of hertz.
GIGAHERTZ (GHz) One billion cycles per second.
HERTZ (Hz) One cycle per second.
HISTOPATHOLOGY The department of pathology
concerned with minute structure, composition, and
function of diseased tissues; microscopic pathology.
HOMEOTHERMY The pattern of temperature regula-
tion in a warm-blooded species in which the cyclic
variation in core temperature, either nychthemerally
or seasonally, is maintained within arbitrarily defined
limits (±2°C) despite much larger variations in
ambient temperature.
HUMORAL Relating to the extracellular fluids of the
body, i.e., blood and lymph. In immunology, the name
ascribed to immune mechanisms leading to antibody
products.
HYPERTHERMIA The condition of a temperature-
regulating animal when the core temperature is more
than one standard deviation above the mean core
temperature of the species in resting conditions in a
thermoneutral environment.
HYPOTHERMIA The condition of a temperature-
regulating animal when the core temperature is more
than one standard deviation below the mean core
temperature of the species in resting conditions in a
thermoneutral environment.
INSENSIBLE WATER LOSS The sum of the water lost
by diffusion through the skin and water lost in
breathing, and excluding any water excreted.
IN UTERO Within the uterus or womb.
IN VITRO Within glass; observable in a test tube.
IN VIVO Within the living body.
INFINITE SLAB A piece of material that has an infinite
cross section but finite thickness.
IONIZING ELECTROMAGNETIC RADIATION Electro-
magnetic radiation of high frequency, short wave-
lengths, and high photon energy which, when it
interacts with matter, causes the removal of
electrons from atoms, e.g., x-rays and gamma rays.
KILOHERTZ (kHz) One thousand cycles per second.
LATENT HEAT OF VAPORIZATION The quantity of
heat released (or absorbed) in the reversible process
of evaporation (or condensation) of unit mass of liquid
(or vapor) under isobaric and isothermal equilibrium
conditions.
LOSSY CAPACITOR A capacitor containing a
dielectric material with a loss tangent above 0.1.
MACROMOLECULE A molecule, such as a protein or
a nucleic acid, that has a molecular weight greater
than a few thousand.
MEGAHERTZ (MHz) One million cycles per second.
METABOLIC RATE See resting metabolic rate.
M ETASTABLE A state that is not stable but wi II exist for
a long period of time.
MICROWAVES A particular segment of the RF
radiation spectrum with a frequency range of 300
MHz to 300 GHz.
MITOGEN A substance that stimulates lymphocytes
to proliferate independently of any specific antigen.
MODULATION The process of varying the amplitude,
frequency, or phase of an RF carrier wave.
MULTILAMELLAR VESICLES Phospholipid bilayers
that form a series of concentric closed spherical
structures somewhat analogous to the layers of an
onion; these structures are commonly used as
models for studying membrane properties.
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MYELOPOIESIS The formation of bone marrow and
the cells that arise from it.
NEUROTRANSMITTER A chemical substance that
transmits nerve impulses across a synapse.
NEAR FIELD REGION See antenna regions.
NONIONIZING RADIATION (NIR) Electromagnetic
radiation of low frequency, long wavelength, and low
photon energy, unable to cause ionization (i.e., to
remove an electron from an atom); e.g., RF radiation.
NONTHERMAL Not related to heat.
NUCLEIC ACIDS Biochemical compounds, consisting
of one or more subrings of a base, a sugar, and a
phosphate group. When subrings are covalently
bonded to each other, forming a chain, the bond
occurs between the sugar and the phosphate, with
the base off to the side. In DNA (q.v.), two such
chains are weakly attached to each other through
contact of their bases, which form the rungs of a
ladder, while the sugar and phosphate groups form
the sides of the ladder. The bases associate with each
other only if their chemical structure is compatible,
i.e., complementary. There are four such bases
commonly found in DNA. The sequence of these
bases provides the information necessary to make
other biochemical molecules.
OPERANT CONDITIONING The process of rewards
and reinforcements by which specific behaviors are
learned.
ORGANOGENESIS The development or growth of
organs, especially embryologic.
OSMOTIC FRAGILITY The tendency of a cell
membrane to break because of a large imbalance of
ion concentration inside and outside the cell.
PARABOLIC REFLECTOR One of the most widely
used microwave antennas, consisting of a metal disk
whose surface forms a circular parabola.
PARAMETER Any of a set of physical properties
whose values determine the characteristics or
behavior of something.
PHAGOCYTOSIS The engulfing of microorganisms,
other cells, or foreign bodies by phagocytes.
PENIA Reduction in the number of cells; e.g.,
neutropenia, reduction in the number of polymorpho-
nuclear neutrophiles.
PERITONEAL Relating to the peritoneum, which is
the serous sac lining the abdominal cavity and
covering most of the viscera therein contained.
PHILIA Increase in number of cells; e.g., neutrophilia,
increase in number of neutrophiles.
PHONON A particle of mechanical vibrational (sound)
energy.
PHOTON A particle of electromagnetic energy.
PHOSPHOLIPID BILAYER A double-layered sheet of
phospholipid molecules arranged so that the hydrophi-
lic (water-liking) part of the molecules associate with
water and the hydropholic (water-disliking) part of the
molecules associate with each other and avoid
contact with water; this structure is the basis for
biological membranes.
PLASMID Short piece of DNA that normally codes for
one of a few proteins and can often be transferred to
another cell; it is usually separate from the cell's
major DNA, which carries the information for
reproducing the cell.
PLANE WAVE An electromagnetic wave in which the
electric and magnetic field vectors lie in a plane
perpendicular to the direction of wave propagation.
POIKILOTHERM A cold-blooded animal; an ectotherm;
an animal with little or no control of its body
temperature.
POIKILOTHERMY The pattern of thermoregulation of
a species exhibiting a large variability of core
temperature as a proportional function of ambient
temperature.
POLARIZABILITY A linear coefficient that quantitates
the change in the magnitude of the dipole moment
(q.v.) of a molecule or any other structure in response
to an electric field, i.e.,
"d*=crE*+c£
where or is_the polarizability, E is the applied electric
field, and 87 is the dipole moment when there is no
applied field.
POWER DENSITY Magnitude of the Poynting vector at
a point in space, in power per unit area (watts per
square meter). For plane waves E2 is simply related to
power density, and it is the quantity measured by a
survey meter when the sensing element is sensitive
to the square of the magnitude of the electric fields;
i.e., P = EV3770, in mW/cm2.
PROLATE SHPEROID An approximately spherical
object that is elongated in the direction of a line
joining the poles; similar to a football.
PUPA The second stage in the development of an
insect, between the larva and the imago.
Qio The ratio of the rate of a physiological process at a
particular temperature to the rate at a temperature
10°C lower, when the logarithm of the rate is an
approximately linear function of temperature.
RADIATION The transfer of energy from one body to
another through an intervening medium.
RADIOFREQUENCY RADIATION See RF radiation.
RESONANCE A small electrical stimulus at a given
frequency that produces a large amplitude response
in the system at the same frequency.
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RESONANT FREQUENCY That frequency which
produces resonance in a system; typically those
frequencies whose wavelengths are integral multiples
of the body's length.
RESPIRATORY CONTROL RATIO. A measure of
mitochondria! activity and integrity; the rate of
utilization of oxygen in the presence of adenosinedi-
phosphate (ADP) divided by the rate of utilization of
oxygen in the absence of ADP.
RESTING METABOLIC RATE (RMR) The metabolic
rate of an animal which is resting in a thermoneutral
environment but not in the postabsorptive state. The
relationship of RMR (W/kg) to body mass, M (kg), is
RMR = 3.86M"024 Basal metabolic rate (BMR) is the
rate of energy production of an animal in a rested,
awake, fasting, and thermoneutral state.
RF RADIATION Radiofrequency radiation; nonionizing
electromagnetic radiation in the frequency range 0 to
3000 GHz.
ROOT MEAN SQUARE (RMS) Certain electrical
effects are proportional to the square root of the mean
value of the square of a periodic function (over one
period). This value is known as the effective value or
the root-mean-square (RMS) value since it is derived
by first squaring the function, determining the mean
value of this squared value, and extracting the square
root of the mean value to determine the end result.
SARCOMA A tumor, usually highly malignant,
formed by proliferation of poorly differentiated cells; a
malignant connective tissue neoplasm.
SCHEDULE OF REINFORCEMENT Also called
reinforcer schedule. The specification of the way in
which reinforcers are assigned to particular
responses within an operant-class or classes.
Examples include: the fixed ratio schedule, in which
the last of a constant, specified number of responses
is reinforced; the fixed interval schedule, in which a
constant, specified period of time must elapse before
a response is reinforced; the differential reinforce-
ment of low rate schedule, in which a response is
reinforced only if at least a specified period of time
has elapsed since the last response.
"SILK" Polyester material used in the silk-screen
graphic process.
SPECIFIC ABSORPTION The absorbed energy in the
tissue, in joules per kilogram (J/kg). See also
SPECIFIC ABSORPTION RATE.
SPECIFIC ABSORPTION RATE (SAR) The rate at
which energy is absorbed in the tissue, in watts per
kilogram: SAR =a£i2/p, where a = tissue conductivity
at irradiation frequency, Et = rms electric field
strength in the tissue, and p = tissue density (kg/m3).
SPECIFIC HEAT (c) The quantity of heat required to
raise the temperature of unit mass of a substance by
SPONTANEOUS BEHAVIOR Unlearned or natural
responses to a stimulus.
SQUARE LAW The output of a device is proportional
to the square of the input to the device.
SUBSTRATE The molecule upon which an enzyme
catalyzes a chemical reaction.
SURVEY INSTRUMENT A portable instrument
capable of measuring the strength of electric and
magnetic fields.
SYNGENEIC Individuals of a species that are
genetically identical at all relevant transplantation
loci.
TEMPERATURE, AMBIENT (Ta) The average tem-
perature of a gaseous or liquid environment (usually
air or water) surrounding a body, as measured
outside the thermal and hydrodynamic boundary
layers that overlay the body.
TEMPERATURE, CORE The mean temperature of the
tissues at a depth below that which is affected directly
by a change in the temperature gradient through
peripheral tissues. Mean core temperature cannot be
measured accurately, and is generally represented by
a specific core temperature, e.g., that of the rectum
(Synonym: TEMPERATURE, DEEP BODY.)
TEMPERATURE-HUMIDITY INDEX A means of
estimating the heat stress caused by variations in
temperature and humidity.
TEMPERATURE REGULATION The maintenance of
the temperature or temperatures of a body within a
restricted range under conditions involving variable
internal and/or external heat loads. Biologically, the
existence of some degree of body temperature
regulation by autonomic or behavioral means.
TEMPERATURE REGULATION, AUTONOMIC The
regulation of body temperature by autonomic (i.e.,
involuntary) responses to heat and cold which modify
the rates of heat production and heat loss (i.e., by
sweating, thermal tachypnea, shivering, and
variations in peripheral vasomotor tone and basal
metabolism).
TEMPERATURE REGULATION, BEHAVIORAL The
regulation of body temperature by complex patterns
of responses of the skeletal musculature to heat and
cold which modify the rates of heat production and/or
heat loss (e.g., by exercise, change in body
conformation, and in the thermal insulation of
bedding and (in man) of clothing, and by the selection
of an environment which reduces thermal stress).
TERATOLOGY That division of embryology and
pathology which deals with abnormal development
and congenital malformations.
THERMAL EFFECT In the biological tissue or system,
an effect that is related to heating of the tissue
through the application of electromagnetic fields,
and that can occur through other forms of heating.
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THERMOGRAM A recording of temperature distribu-
tion over a surface or in a material as measured at the
surface.
THERMOGENIC LEVELS Power densities of RF
radiation which produce measurable temperature
increase in the exposed object.
THERMOGRAPHY A technique for detecting and
measuring variations in heat emitted by various
regions of the body.
THERMONEUTRAL ZONE (TNZ) The range of ambient
temperature within which metabolic rate is at a
minimum, and within which temperature regulation
is achieved by nonevaporative physical processes
alone.
THERMOREGULATION See temperature regulation.
TRANSDUCE To convert one form of energy into
another form, e.g., from heat to electrical current in a
thermocouple.
TWIN-WELL CALORIMETRY The technique used to
determine the absorbed RF dose or dose rate by
comparing the excess heat in an RF-exposed system
to an identical unexposed system in a comparison
well.
VIGILANCE The degree of attentiveness or watchful-
ness. Vigilance is often investigated by measuring the
number of times the occurrence of an infrequent
event is correctly detected. In some experiments
objective measurements are made of the times the
subject looks for occurrence of the infrequent event.
Called observing responses, these responses may be
required to allow observation of the infrequent event.
WAVE A disturbance that moves through a medium.
WAVEGUIDE A transmission line comprised of a
hollow conducting tube within which electromagnetic
waves may be propagated.
WAVE, TRANSVERSE ELECTRIC (TE) In a homogen-
eous, isotropic medium, an electromagnetic wave in
which the electric field vector is everywhere
perpendicular to the direction of the propagation.
WAVE, TRANSVERSE ELECTROMAGNETIC (TEM) In
a homogeneous isotropic medium, an electromagnetic
wave in which the electric and the magnetic field
vectors are everywhere perpendicular to the direction
of propagation.
WAVE, TRANSVERSE MAGNETIC (TM) In a homo-
geneous isotropic medium, an electromagnetic wave
in which the magnetic field vector is everywhere per-
pendicular to the direction of the propagation.
WAVELENGTH The distance between points of
corresponding phase of a periodic wave of two
constant cycles. The wavelength A is related to the
phase velocity v and the frequency by A = v/f.
WHOLE-BODY IRRADIATION Pertains to the case in
which the entire body is exposed to the incident
electromagnetic energy or the case in which the cross
section (physical area) of the body is smaller than the
cross section of the incident radiation beam.
G-6
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APPENDIX A
Science Advisory Board
Subcommittee on the Biological Effects of Radiofrequency Radiation
Charles Susskind, Ph.D.
Chairman, Radiofrequency Health Effects Sub-
committee
College of Engineering
University of California, Berkeley
Berkeley, CA 94720
Eleanor Adair, Ph.D.
John B. Pierce Foundation Laboratory
290 Congress Avenue
New Haven, CT06519
Barbara Chang, M.D.
Chief, Hematology/Oncology Section
V.A. Medical Center
Augusta, GA 30910
Stephen Cleary, Ph.D.
Department of Physiology
Medical College of Virginia
Virginia Commonwealth University
Richmond, VA 23298
Carl Durney, Ph.D.
Department of Electrical Engineering
University of Utah
Salt Lake City, UT84112
Arthur Guy, Ph.D.
Bioelectromagnetics Research Laboratory
Department of Rehabilitation Medicine
University of Washington
Seattle, WA 98195
Steven Horvath, Ph.D.
Institute of Environmental Stress
University of California
Santa Barbara, CA 93106
Abraham Lilienfeld, M.D.
The Johns Hopkins University
School of Hygiene and Public Health
615 N.Wolfe Street
Baltimore, MD 21205
Solomon Michaelson, D.V.M.
Department of Radiation Biology and Biophysics
University of Rochester School of Medicine and
Dentistry
602 Elmwood Avenue
Rochester, NY 14642
Mary Ellen O'Connor, Ph.D.
Department of Psychology
University of Tulsa
600 S. College Avenue
Tulsa, OK 74104
Charlotte Silverman, M.D.
(Committee consultant/liaison)
Food and Drug Administration
National Center for Devices and Radiological Health
12721 Twinbrook Parkway
RockviMe, MD 20852
A-}
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APPENDIX B
Authors
Ernest N. Albert1
Joseph S. Ali
JohnW. Allis
Ezra Berman
Carl F. Blackman
Daniel F. Cahill2
Joe A. Elder
Michael I. Gage
Christopher J. Gordon
Doreen Hill3
William T. Joines4
James B. Kinn
William P. Kirk5
Charles G. Liddle
James R. Rabinowitz
Ralph J. Smialowicz
Ronald J. Spiegel
Claude M. Weil6
U.S. Environmental Protection Agency
Office of Research and Development
Office of Health Research
Health Effects Research Laboratory
Research Triangle Park, NC 27711
'Department of Anatomy
The George Washington University
Medical Center
Washington, DC 20037
"Also with Department of Electrical Engineering
Duke University
Durham, NC 27706
Current Addresses:
2Carolina Power and Light Company
Harris Energy and Environmental Center
Route 1, Box 327
New Hill, NC 27562
3Office of Radiation Programs
U.S. Environmental Protection Agency
Washington, DC 20460
5Three Mile Island Field Station
U.S. Environmental Protection Agency
100 Brown Street
Middletown, PA 17057
6Boeing Company, BMAC 41 -08
P.O. Box 3707
Seattle, WA 98124
B-1
« U.8.aoV0MMENTFMNTMa OFFICE 1H4 - 759-102/107M
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Environmental Protection
Agency
Center for Environmental Research
Information
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