Title: Microwave frequency electromagnetic ﬁelds (EMFs)
produce widespread neuropsychiatric effects including
Author: Martin L. Pall
Reference: CHENEU 1334
To appear in:
Received date: 13-4-2015
Revised date: 1-8-2015
Accepted date: 9-8-2015
Please cite this article as: Pall, M.L.,Microwave frequency electromagnetic ﬁelds
(EMFs) produce widespread neuropsychiatric effects including depression, Journal
of Chemical Neuroanatomy (2015), http://dx.doi.org/10.1016/j.jchemneu.2015.08.001
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Page 1 of 25
Microwave frequency electromagnetic fields (EMFs) produce widespread
neuropsychiatric effects including depression
Martin L. Pall
Professor Emeritus of Biochemistry and Basic Medical Sciences
Washington State University
638 NE 41
Ave., Portland, OR 97232-3312, USA
Non-thermal microwave/lower frequency electromagnetic fields (EMFs) act via voltage-
gated calcium channel (VGCC) activation. Calcium channel blockers block EMF effects
and several types of additional evidence confirm this mechanism. Low intensity
microwave EMFs have been proposed to produce neuropsychiatric effects, sometimes
called microwave syndrome, and the focus of this review is whether these are indeed well
documented and consistent with the known mechanism(s) of action of such EMFs.
VGCCs occur in very high densities throughout the nervous system and have near
universal roles in release of neurotransmitters and neuroendocrine hormones. Soviet and
Western literature shows that much of the impact of non-thermal microwave exposures in
experimental animals occurs in the brain and peripheral nervous system, such that
nervous system histology and function show diverse and substantial changes. These may
be generated through roles of VGCC activation, producing excessive
neurotransmitter/neuroendocrine release as well as oxidative/nitrosative stress and other
responses. Excessive VGCC activity has been shown from genetic polymorphism studies
to have roles in producing neuropsychiatric changes in humans. Two U.S. government
reports from the 1970’s-80’s provide evidence for many neuropsychiatric effects of non-
thermal microwave EMFs, based on occupational exposure studies. 18 more recent
epidemiological studies, provide substantial evidence that microwave EMFs from
cell/mobile phone base stations, excessive cell/mobile phone usage and from wireless
smart meters can each produce similar patterns of neuropsychiatric effects, with several
of these studies showing clear dose-response relationships. Lesser evidence from 6
additional studies suggests that short wave, radio station, occupational and digital TV
antenna exposures may produce similar neuropsychiatric effects. Among the more
commonly reported changes are sleep disturbance/insomnia, headache,
depression/depressive symptoms, fatigue/tiredness,dysesthesia, concentration/attention
dysfunction, memory changes, dizziness, irritability, loss of appetite/body weight,
restlessness/anxiety, nausea, skin burning/tingling/dermographism and EEG changes. In
summary, then, the mechanism of action of microwave EMFs, the role of the VGCCs in
the brain, the impact of non-thermal EMFs on the brain, extensive epidemiological
studies performed over the past 50 years, and five criteria testing for causality, all
collectively show that various non-thermal microwave EMF exposures produce diverse
Page 2 of 25
Key Words: Excessive calcium effects; oxidative/nitrosative stress; low-intensity
microwave electromagnetic fields
Chemicals having roles:
Nitric oxide (NO)
Oxido nitrite (peroxynitrite)
Microwave syndrome (Hocking, 2001; Johnson Liakouris, 1998), a combination of
various neuropsychiatric symptoms originally described in persons with occupational
exposures to microwave frequency EMFs, has been disputed largely because of the lack
of an apparent mechanism for generating these symptoms. It is reported to often include
such symptoms as fatigue, headache, insomnia, dysesthesia (impaired sensation),
irritability, lack of concentration and other symptoms (Hocking, 2001; Johnson
Liakouris, 1998). Similar but more extensive combinations of symptoms have been
reported following occupational exposures in two U.S. government reports from the
1970s/1980s (Naval Medical Research Institute Research Report, 1971; Raines, 1981)
and following environmental exposures as described in two more recent reviews
(Khurana et al, 2010; Levitt and Lai, 2010).
The goal here is not just to review the epidemiology, however, but more importantly to
consider the issue of possible physiological mechanism(s). Hennekens and Buring
(1989), on p. 40 in their textbook Epidemiology in Medicine state "The belief in the
existence of a cause and effect relationship is enhanced if there is a known or postulated
biologic mechanism by which the exposure might reasonably alter risk of developing
disease." It is of critical importance therefore to assess possible biological mechanism
before considering the epidemiological evidence.
Accordingly, this paper considers the mechanism by which low intensity microwave
EMFs impact the cells of our bodies, how that mechanism may be predicted to impact the
nervous system, evidence for such impact from experimental animal studies, genetic
polymorphism evidence for that mechanism acting in humans to produce
neuropsychiatric effects and finally, the epidemiological evidence for such effects in
human populations with repeated low level microwave EMF exposure. Consideration of
each of these types of evidence influences the overall interpretation presented in this
Microwave/lower frequency EMFs act to activate voltage-gated calcium channels
In 24 different studies reviewed earlier (Pall, 2013) and two additional studies (Li et al,
2014; Lisi et al, 2006), microwave and lower frequency low intensity EMF effects were
blocked or greatly lowered by calcium channel blockers, agents thought to be specific for
blocking voltage-gated calcium channels (VGCCs). In these 26 studies, a total of 5
Page 3 of 25
distinct types of channel blockers were used, with each type having a distinct structure
and binding to a distinct site, such that it is essentially certain that these must be acting by
blocking VGCCs, which is their only known common property. In each of these 26
studies, each of the responses studied, were blocked or greatly lowered by calcium
channel blockers, showing that VGCC activation has roles in producing a wide variety of
EMF effects. There is a large literature on changes in calcium fluxes and in calcium
signaling following microwave EMF exposure (partially reviewed in Walleczek 1992;
Adey 1993); each of these, including calcium efflux changes, can be explained as being
due to VGCC activation, again suggesting a widespread role of VGCC activation in
producing biological responses to EMFs. Pilla (2012) showed that pulsed microwave
field exposure, produced an almost instantaneous increase in calcium/calmodulin-
dependent nitric oxide (NO) signaling, providing strong evidence that these fields can
produce an almost instantaneous VGCC activation. It is likely, that these EMFs act
directly on the voltage sensor of the VGCCs to produce VGCC activation (Pall, 2015)
with the voltage sensor being exquisitely sensitive to these EMFs because of its physical
properties and location in the plasma membrane.
EMFs have been proposed to act to produce a wide variety of responses in the cell, via
downstream effects of VGCC activation (Pall, 2013, 2014, 2015), including elevated
intracellular calcium [Ca2+]i, excessive calcium and nitric oxide signaling and also
excessive peroxynitrite, free radicals and oxidative stress.
VGCC activation has been shown to have a universal or near-universal role in the release
of neurotransmitters in the brain and also in the release of hormones by neuroendocrine
cells (Berridge, 1998; Dunlap et al, 1995; Wheeler et al, 1994), with such release being
produced by calcium signaling. There are high densities of diverse VGCCs occuring in
neurons throughout the nervous system. Both the high VGCC density and their function
in neurotransmitter and neuroendocrine release throughout the nervous system suggests
that the nervous system is likely to be highly sensitive to low intensity EMFs.
Genetic Polymorphism Studies
Genetic polymorphism studies are powerful tools for looking at the roles of specific
proteins in human populations. In Table 1, a series of genetic polymorphism studies have
been performed that show that an allele producing increased expression of the gene
encoding the channel of the main L-type VGCC in the brain, produces diverse
neuropsychiatric effects. These studies clearly show that excess L-type VGCC activity
can cause neuropsychiatric effects. They also predict, therefore, that increased VGCC
activity produced by microwave EMFs may be able to also produce widespread
Table 1 Influence of Genetic Polymorphism of the CACNA1C in Producing
Diverse Neuropsychiatric Effects
Citation Genetic Polymorphism Changes produced by allele of gene
Review: The polymorphism Is associated with
Page 4 of 25
2012 producing Increased
increased susceptibility to bipolar disorder,
“depression, schizophrenia, autism spectrum
disorders, as well as changes in brain function
and structure in control subjects who have no
diagnosable psychiatric illness.”
Bigos et al,
Associated with increases in both bipolar
disorder and schizophrenia
Krug et al,
Negatively influences language production on a
Krug et al,
Influences episodic memory and retrieval
Produces impaired facial emotion recognition
Tesli, et al,
Produces increased activation of the amygdala
during emotional processing
al, 2011 Polymorphism
Associated with attention deficits including
alerting, orienting and executive control of
Histological and Functional Changes in Central Nervous System (CNS) and Peripheral
Nervous System ((PNS) in Animals Exposed to Microwave EMFs
The most extensive literature on histological and functional changes in animals is from
the Soviet literature from the 1950s/1960s with additional Western literature from the
same time period. Both Soviet and non-Soviet literature were reviewed in an English
language Publication by Tolgskaya and Gordon (1973). This publication is, therefore,
the main focus of this section. That publication was divided into thermal and non-
Page 5 of 25
thermal exposure studies, with the non-thermal studies which occupy the majority of the
text (pp. 53-137) being of sole interest here.
Table 2 Histological and Functional Changes in Brain Function in Animals
following Exposure to Non-Thermal Microwave EMFs
Observations including page numbers Comment from Author
The majority of the histological changes seen following
non-thermal exposures, occurred in the nervous system,
despite its being only about 2% of the tissue mass in
rodents; this suggests that the nervous system is highly
sensitive to such exposures. Elsewhere (p.129,136), it
is suggested that the nervous system is the most
sensitive tissue, followed by the heart and the testis,
among all of the tissues of the body. The most severe
histological changes produced by these non-thermal
EMF exposures occur in the nervous system (p. 136).
High CNS sensitivity to EMFs
is predicted by the high density
of VGCCs that occur in
neurons throughout the
nervous system, plus the
VGCC role in neurotransmitter
and neuroendocrine release.
Pulsed fields were more active than non-pulsed fields
in producing histological changes (p. 71,97) Pulsed fields have often been
found to be more biologically
active than are non-pulsed
fields in many different studies
from many countries (Pall,
2015, Panagopoulos et al,
2013; Belyaev, 2015)
Nervous system regions impacted by non-thermal
microwave and lower frequency fields include: cortex,
diencephalon including the hypothalamus and
thalamus, hippocampus, autonomic ganglia, sensory
fibers, pituitary gland including neurohypophysis
Neuroendocrine changes seem to undergo change over
increased time of exposure. Neurosecretion in the
hypothalamus and in the pituitary each go through a
complex sequence over time, where EMF exposure
initially produces increased hormone secretion but
where over time, the neurosecretory cells become
“exhausted”, leading to lowered secretion and in some
cases cell death (pp.77-96).
Elevated [Ca2+]i stimulates
hormone secretion. However
when such elevated [Ca2+]i
occurs over extended time
periods it is highly damaging
to the cell, leading in some
cases to apoposis; thus this
time course of action should
not be surprising.
Histological changes include boutons/argyrophilia,
smaller neurons, vacuole formation in neuroendocrine
cells, bead-like thickening along dendrites
Spines near the ends of dendrites become deformed and
with still more sessions of irradiation, disappeared
Page 6 of 25
entirely (p.70). Sensory neurons, following exposures,
developed changes characteristic of irritation, with
“marked tortuosity of the nerve fibers.” Many
histological changes are seen in the hypothalamic cells
(p.87-92) as their neuroendocrine function becomes
impacted. Histological changes were found even with
exposures that produced no apparent functional
Many histological and functional changes are reported
to initially be reversible, following cessation of
exposure, but progressively become irreversible with
longer exposure. (p.64,72,74). Paralleling the
development of irreversibility, it is found that
“Repeated exposure leads to gradual increase in
severity of observed changes.” … including
“increasingly severe disturbance of conditioned reflex
activity in the animals, changes in responses of
animals particularly sensitive to acoustic stimulation…
.” (p. 104)
If this is also true in humans,
then claims that there cannot
be non-thermal effects, claims
which act to prolong
exposures, may be causing
irreversible damage to many
EEG changes (p. 55,60,102), including seizure activity
following sensory provocation Lai, 1997 has an extensive
review of EEG changes in
animals following non-thermal
microwave EMF exposures
Neurodegeneration is reported in a number of places in
this review (p.72,83,117).
Synaptic connections in regions of the brain are
disrupted (p.65-74, 97,113,121,136), and at the
extreme, some neurons are completely asynaptic (p.73).
Synaptic connections are
known to be disrupted in
autism; could this suggest that
autism may be generated by
EMF exposure? No doubt, we
need much more evidence on
“after prolonged and repeated irradiation with low-
intensity centimeter waves, with no elevation of the
body temperature and when the animal’s condition
remained satisfactory, changes were nevertheless found
in the sensory fibers of the skin and viscera in the form
of irritation phenomena. These findings concur with
the view in the literature that the receptor system as a
whole and, in particular its preterminal portions are
highly sensitive.” P.76. This description is similar to
what is reported to occur in electromagnetic
hypersensitivity (EHS). Other such studies are
described and include cumulative changes over time,
that may also explain changes reported in EHS
One wonders whether almost
60 years ago, the Soviet
literature may have already
described a possible animal
model for EHS. None is
known to exist today, and
because of that, EHS studies
are severely constrained.
Clearly one needs to be
skeptical about this
interpretation, but it is of great
importance that this be further
Page 7 of 25
These were all derived from the Tolgskaya and Gordon,1973 review and page numbers
listed are page numbers from that document. All refer to changes produced by non-
thermal exposures in the nervous system of experimental animals, with most being in
This discussion scrolls down through Table 2.
The majority of the histological changes seen in these mostly rodent studies, are seen in
the nervous system, despite its being less than 2% of the rodent cell mass. There are
statements made that the nervous system, both central and peripheral, is the most highly
sensitive tissue to these non-thermal microwave and lower frequency EMFs. Following
the nervous system in sensitivity are the myocardium and the testis; myocardial cells are
known to have very high densities of VGCCs with especially high densities in the
pacemaker cells and the testis is known to have high densities specifically of the T-type
VGCCs. Pulsed EMFs are more active in producing histological changes in the brain
than are non-pulsed fields, in two studies reviewed; there is a much larger literature
showing that in most cases pulsed fields are more biologically active (Pall, 2015,
Panagopoulos et al, 2013, Belyaev, 2015).
A wide variety of brain and peripheral nervous system tissues show histological changes
following non-thermal exposures. Among the important tissues impacted are the
hypothalamus and pituitary gland, where both show similar patterns of changes in
neuroendocrine activities. There Is an initial increase in neuroendocrine activity (this
may be produced directly by VGCC stimulation of secretion), followed over time by
“exhaustion” of neuroendocrine activity (this may be produced by tissue damage
produced from long term intracellular calcium [Ca2+]i elevation).
There are widespread histological changes produced in neuronal and neuroendocrine
tissues. These were repeatedly reported to be largely reversible on cessation of EMF
exposure. They become, however, irreversible when exposure is extended in time. There
are changes in EEG activity, which may be an easily measurable monitor of neurological
In a summary statement, Tolgskaya and Gordon, 1973 state “This does not confirm the
view,so widely held in the past among Soviet investigators and still maintained to a large
extent even at the present time in the West, that the action of microwaves is entirely
While there were many studies of brain impact of non-thermal EMFs performed in the
1950s/60s that make the information content of Tolgskaya and Gordon, 1973 quite high,
there is also a substantial recent literature on brain effects of non-thermal microwave
EMF exposures (see, for example: Ammari et al, 2008a; Ammari et al, 2008b; Bas et al,
2009; Brillaud et al, 2007; Carballo-Quintás, et al, 2011; Eberhardt et al, 2008; Dasdag et
al, 2009 & 2012; Grafström et al, 2008; Kumlin et al, 2007; López-Martín, 2006;
Mausset-Bonnefont et al, 2004; Odacia et al, 2008; Rağbetli, et al, 2010; Salford et al,
2003; Sonmez et al, 2010).
Page 8 of 25
Older Epidemiological Reviews and Other Related Studies
Two U.S. Government reports each listed many apparent neuropsychiatric effects of
microwave/radiofrequency EMFs and a third recognized the role of non-thermal effects
on our bodies, but had only a little consideration of neuropsychiatric effects.
The earliest to these was a Naval Medical Research Institute (NMRI) Research Report
(1971) which listed 40 apparent neuropsychiatric changes produced by non-thermal
exposures:, including 5 central/peripheral nervous system (NS) changes, 9 CNS effects, 4
autonomic system effects, 17 psychological disorders, 4 behavioral changes and 2 misc.
effects. This NMRI report also provided a supplementary document listing over 2300
citations documenting these and other effects of microwave exposures in humans and in
The Raines (1981) NASA report reviewed extensive literature based on occupational
exposures to non-thermal microwave EMFs, with that literature coming from U.S.,
Western European and Eastern European studies. There are no obvious differences in the
literature coming from these different regions. Based on multiple studies, Raines (1981)
reports 19 neuropsychiatric effects to be associated with occupational
The Bolen (1994) report put out by the Rome Laboratory of the U.S. Air Force,
acknowledged the role of non-thermal effects of microwave EMFs on humans. This
report states in the Conclusion section that “Experimental evidence has shown that
exposure to low intensity radiation can have a profound effect on biological processes.
The nonthermal effects of RF/MW radiation exposure are becoming important measures
of biological interaction of EM fields.” Clearly Bolen (1994) rejects the claim that only
thermal effects occur. Bolen (1994) discusses a specific non-thermal neuropsychiatric
effect, where anesthetized animals are awakened when the head is irradiated with
microwave EMFs. This suggests a similar mechanism to that acting in humans where
such EMFs produce insomnia (see below).
Specific Epidemiological Studies on Neuropsychiatric Effects of Microwave EMFs
There are 26 different epidemiological studies described in Table 3. Although 4 of these
only studied a single neuropsychiatric effect, 22 of these each provide substantial
evidence for the pattern described in the earlier U.S. reports, that a wide range of
neuropsychiatric effects are produced by exposure to various non-thermal microwave
frequency EMFs. Perhaps the most important of these 26 is the Santini et al, 2003 study
of people living near cell phone base stations.
Table 3: Neuropsychiatric Symptoms Apparently Produced by Exposure to
Various Electromagnetic Fields
Citation EMF exposure Apparent neuropsychiatric symptoms
Page 9 of 25
et al, 2007 Living near mobile
phone base station Significant increases in neuropsychiatric
complaints included: headache, memory
changes, dizziness, tremors, depressive
symptoms, sleep disturbance; attributed to
effects of EMFs on the human nervous
Meo, 2004 Mobile phone use Higher prevalence of fatigue, headache,
dizziness, tension and sleep disturbance;
the authors conclude that mobile phone use
is a risk factor for developing these
Altpeter et al,
2000 Short-wave broadcasting
tower, ranging from 6.1
to 21.8 MHz
Sleep disruption shown to occur, correlated
with exposures and apparent increase over
time; short term suppression of melatonin
shown, based on melatonin increases during
a 3 day period when the tower was turned
et al, 2004 Living near cell phone
base station EMFs Sleep disturbance, irritability, depression,
blurred vision, concentration difficulties,
nausea, lack of appetite, headache, vertigo
et al, 2012 Living near mobile
phone base stations Dose response relationships for sleep
disturbance, irritability, depression, blurred
vision, concentration difficulties, nausea,
lack of appetite,
Chu et al, 2011;
Also Chia et al,
et al 2000
Mobile phone use Headache during prolonged mobile phone
use or within an hour following such use,
with pain occurring on the ipsilateral side of
the head; similar observations obtained in
each of the 3 studies in column 1; see also
2013 Smart meter EMF
exposure 14 common new symptoms (both severe
and moderate) among those exposed and
symptomatic, 13 apparent neuropsychiatric:
Insomnia, tinnitus, pressure in the head,
concentration difficulty, headaches,
memory problems, agitation, dizziness,
fatigue, skin tingling/burning, involuntary
muscle contractions, eye/vision problems,
numbness; These ranged in prevalence
from 63% to 19% of those experiencing
symptoms, such that most symptomatic
people experienced multiple symptoms
Dasdag et al,
1992 People working in MW
broadcasting or at a
These groups suffered from headache,
fatigue, irritability, stress, sleepiness, loss of
appetite, loss of hearing
Page 10 of 25
Leeper, 1978 People working in
radiofrequency EMFs Headache, eyestrain, dizziness, disturbed
sleep, daytime sleepiness, moodiness,
mental depression, memory impairment,
muscle and/or cardiac pain, breathing
difficulties, increased perspiration,
difficulty with sex life
Eger & Jahn,
2010 Living near mobile
phone base station Neuropsychiatric symptoms, with most
showing dose-response relationships:
depression; headache; cerebral symptoms;
dizziness; disorders of optical and acoustic
sensory systems; sleep disturbance; skin
changes; with the exception of dizziness, all
of these had p<0.001
Study of personnel in
U.S. embassy in
Moscow exposed to
Statistically significant increases in
neurological (peripheral nerves and
ganglia), dermographism (skin responses),
irritability, depression, loss of appetite,
concentration difficulties, peripheral gangia
and nerve dysfunction
2008 Excessive mobile phone
use Complaints of headache, fatigue, impaired
concentration, memory disturbance,
sleeplessness, hearing problems
Children living near a
Radio Location Station,
Memory dysfunction, attention dysfunction,
lowered motor function, slowed reaction
time, lowered neuromuscular endurance
2014 Exposure to wireless
smart meter radiation in
The most frequent symptoms to develop
after smart meter radiation exposure were
insomnia, headache, tinnitus, fatigue,
cognitive disturbances, dysesthesias
(abnormal sensation), dizziness
Navarro et al,
2003 Living near cell phone
base station Statistically significant dose response
relationships for fatigue, irritability,
headache, nausea, loss of appetite, sleep
disorder, depressive tendency, feeling of
discomfort, difficulty of concentration, loss
of memory, visual disorder & dizziness
Oberfeld et al,
2004 Living near cell phone
base station Statistically significant dose-response
relationships for headache, fatigue,
irritability, loss of appetite, visual disorder,
nausea, sleeping disorders, dizziness, poor
concentration, memory loss
Oto et al, 1994 Occupational exposure
of 25 workers to either
broadcasting (10) or to
1062 KHz me
10 neuropsychiatric changes were assessed,
all showing statistically significant changes
compared with controls: Somatization*,
obsessive compulsivity*, interpersonal
sensitivity, depression, anxiety*, hostility*,
Page 11 of 25
wave broadcasting (15) phobic anxiety*, paranoid ideation,
psychoticism*, sleeping disturbance.
1974 Occupational exposure
to microwave radiation,
including at <.07
Heaviness in head*, fatigue*, irritability*,
sleepiness, memory loss*, cardiac pain*,
dermographism (skin sensitivity)*,
* significant increase with time of exposure
Salama et al,
2004 High cell (mobile)
phone use Most common effects were headache, ear
ache, sense of fatigue, sleep disturbance,
concentration difficulty, face burning
sensation. The first three of these had very
high statistical significance for correlation
with extent of cell phone use.
Santini et al,
2003 Living near cell phone
base stations Each of the following neuropsychiatric
symptoms showed statistical significant
dose-response relationships: nausea, loss of
appetite, visual disturbance, irritability,
depressive tendencies, lowered libido,
headache, sleep disturbance, feeling of
Schüz et al,
2009 Mobile phone use Found a small, statistically significant
increase in migraine and vertigo. Also
found an apparent lowered occurrence of
Alzheimer’s, other dementia, Parkinson’s
and epilepsy – these latter were interpreted
as being due to perhaps early symptoms of
the developing diseases lowering
probability of acquiring a mobile phone
al, 2008 Use of mobile phone
among adolescents Increased mobile phone use was associated
with increases in tiredness, stress, headache,
anxiety, concentration difficulties and sleep
Thomée et al,
2011 High mobile phone use High mobile phone use was associated with
statistically significant rises in stress and
sleep disturbance, with somewhat weaker
association with depression
Selsam C, et al.
Digital TV signaling Constant headaches, pressure in head,
drowsiness, sleep problems, tightness in
chest, shortness of breadth, depressive
mood, total apathy, loss of empathy,
burning skin, inner burning, leg weakness,
pain in limbs, stabbing pain in various
organs, weight increase
Page 12 of 25
There are three recent studies on the generation of headache during or shortly following
long mobile phone calls (listed under Chu et al, 2011 in Table 3). The timing of
development of these headaches and the finding that they occur on the ipsilateral side of
the head, the side receiving much higher EMF exposure during the call, both argue
strongly that these headaches are caused by the long mobile phone calls. Such causality
was concluded earlier by Frey, 1998 based on earlier studies and is now still more
Criteria for Assessing Causality In Epidemiological Studies
It is important to consider the different criteria that allow one to judge whether a cause
and effect relationship is justified by the studies listed in Table 3 and the individual
studies cited in Raines, 1981. There are five such criteria that should be considered in
making that judgment (See pp.39-43 in Hennington and Buring, 1987):
Strength of Association: Is there a strong correlation between exposure and the
neuropsychiatric symptoms? There clearly is for several studies cited in Raines, 1981.
One example is the Dwyer and Leeper, 1978 study (see Table 3) where there is a large
increase in symptoms and where that increase is greater with longer occupational
exposure. Another example is the Lerner, 1980 study of 1300 microwave workers,
where workers with relatively low exposure levels had an approximate doubling of
neurological complaints and where those with substantially higher exposure levels had an
approximate tripling of neurological complaints over controls. Sadcikova, 1974 found
that 7 of 8 neuropsychiatric symptoms studied, showed a statistically significant rise in
prevalence with longer occupational exposure (see Table 3). Sadcikova, 1974, also found
that microwave workers had increases of 3 to over 10-fold in: feeling of heaviness in the
head; tiredness; irritability; sleepiness; partial loss of memory; and skin sensitivity.
There is also a strong association where important new exposures occur – this is clearly
the case with all of the studies of people living near cell/mobile phone base stations,
listed in Table 3 and also with the two studies of people who become exposed to radiation
from smart meters. The studies listed in Table 3 under Chu et al, 2011 (see also Chia et
al, 2000; Oftedal et al 2000) are of a special type. Here people making very long (over 1
h.) cell/mobile phone calls develop headaches an hour or more following the initiation of
the long call. So these occur within a specific time range following initiation of these
long calls, such that headache would only occur very infrequently in that time frame by
chance. So here again, there is a strong association. While there is no question that many
of these studies show high strength of association, it is also clear that it is becoming
progressively more difficult to do these studies. As exposures become almost universal
in countries around the world, it is getting difficult if not impossible to find good negative
controls. There may be a similar problem in doing animal studies, such that it may be
necessary to raise animals in Faraday cages in order to avoid exposures that would
otherwise occur as a consequence of our near ubiquitous EMFs.
Biological credibility is extremely strong here, with three aspects of the biology
predicting that these low intensity fields cause widespread neuropsychiatric effects. This
was discussed above and is reconsidered in the following section.
Page 13 of 25
Consistency within the different epidemiological studies and with other types of studies:
The epidemiological studies listed in Table 3 and also those showing neuropsychiatric
effects that were cited in Raines, 1981 have been performed in many different countries
with different cultures. They have been performed in multiple countries in Western
Europe, Eastern Europe, the Middle East and in East Asia, as well as in the U.S. and
Australia. They are, therefore, not limited to one or two cultural contexts. This is
deemed, therefore, an important indicator of causality. We also have a surprising
consistency of apparent neuropsychiatric effects of different fields, including various
occupational exposures and exposures to cell/mobile phone base stations, exposure to the
phones themselves, exposure to smart meter pulses, and other EMFs (see Table 3).
Pulsation patterns, frequencies and exact intensities may produce various biological
responses (Pall, 2015, Panagopoulos et al, 2013, Belyaev, 2015) so it is a bit surprising
that we have as much consistency as we do have across different types of exposures. We
also have consistency with the biology discussed in the previous section. Because
elevated VGCC activity produced by genetic polymorphism (Table 1) produces diverse
neuropsychiatric effects, it is not surprising that elevation of VGCC activity produced by
microwave EMF exposure apparently also produces diverse neuropsychiatric effects.
Similarly because non-thermal EMF exposures produce widespread changes in brain
structure and function in animals (Tolgskaya and Gordon, 1973), it is not surprising that
the neuropsychiatric symptoms, which are produced as a consequence of brain
dysfunction are produced by such EMFs.
Time sequence: It is clear that the all of these effects follow exposure in the various
studies that have been published. In some studies, it is also clear that longer occupational
exposure times produce increased symptom prevalence. These include Dwyer and
Leeper, 1978 and Baranski and Edelwejn, 1975. These observations all support a causal
relationship between exposure to EMF and the development of neuropsychiatric
Dose-response relationship: It is assumed, here, that biological effects have a positive
correlation with the intensity of the apparent causal stressor. This is not necessarily true
of EMF effects, because it has been shown that there are “window effects” where specific
intensities have larger biological effects, than do either lower or higher intensities (Pall,
2015, Panagopoulos et al, 2013, Belyaev, 2015). Nevertheless, where different
intensities were studied in these epidemiological studies, they do show the dose-response
relationship assumed here including Altpeter et al, 2000; Dwyer and Leeper, 1978; Eger
and Jahn, 2003; Lerner, 1978; Navarro et al, 2003; Oberfeld et al, 2004; Salama et al,
2004; Santini et al, 2003; Thomée et al, 2011. Thus these data do fit well to the assumed
dose-response relationship, found in most causal roles. The Altpeter et al, 2000 study
showed a special type of evidence for causality: during a 3-day period when the
broadcasting tower was turned off, the melatonin levels recovered to near-normal levels.
The studies of headache occurrence on prolonged cell/mobile phone calls (typically well
over one hour) listed under Chu et al, 2011 in Table 3 also suggest the assumed dose-
response relationship (see also Chia et al, 2000; Oftedal et al 2000 and earlier citations
listed in Frey, 1998). Because such headaches only occur with prolonged cell/mobile
Page 14 of 25
phone calls, these studies also provide evidence for a dose-response relationship because
low doses are ineffective. Furthermore these same studies provide evidence for such a
dose-response relationship from another type of observation. Because the headaches
occur predominantly on the ipsilateral side of the head which receives much higher EMF
exposure intensity, rather than on the contralateral side of the head, which receives much
lower intensities, this provides an additional type of evidence for the predicted dose-
While the evidence is convincing that the various neuropsychiatric apparent
consequences of microwave EMF exposure are in fact caused by such exposures, there
may be somewhat more controversy about another EMF-neuropsychiatric linkage. Havas
et al (2010) have reported a similar list of neuropsychiatric symptoms in electromagnetic
hypersensitivity (EHS) patients. They found that each of the following symptoms were
common in EHS: poor short term memory; difficulty of concentration; eye problems;
sleep disorder; feeling unwell; headache; dizziness; tinnitus; chronic fatigue; tremors;
body pain; difficulty speaking; tingling sensation in feet or hands; difficulty writing;
difficulty walking; migraine. The similarity of these symptoms to the most commonly
found symptoms following non-thermal microwave EMF exposures (Table 3), suggests
that EHS is a genuine sensitivity to EMFs. In the bottom row in Table 2, sensitivities
were found in rodent studies following non-thermal exposure, that suggest a possible
animal model for the study of EHS. Each of these EHS-related issues needs to be
followed up experimentally.
Discussion and Conclusions:
In the previous section, each of the five criteria for assessing whether an epidemiological
association is causal were considered. Those five are (Hennekens and Buring, 1989): 1.
Strength of association; 2. Biological credibility; 3. Consistency; 4. Time sequence; 5.
Dose-response relationship. Each of these five provide strong support for causality such
that the combination of all five provide compelling evidence for causality. Low-intensity
microwave frequency EMFs do cause diverse neuropsychiatric symptoms. While each of
these five is important here, the one that is most important is the criterion of biological
Three related sets of biological observations each predict that low-intensity microwave
EMFs produce widespread neuropsychiatric effects:
1. Such EMFs act via activation of VGCCs, acting through the VGCC voltage
sensor which is predicted to be exquisitely sensitive to these EMFs (Pall, 2015).
VGCCs occur in high densities throughout the nervous system and have essential
roles throughout the nervous system in releasing neurotransmitters and
neuroendocrine hormones. These properties predict, therefore, that these low
intensity non-thermal microwave EMFs cause widespread changes in the nervous
system, causing, in turn, diverse neuropsychiatric effects.
2. Elevated VGCC activity, produced by an allele of the CACNA1C gene which
encodes the channel of the main L-type VGCC in the brain, produces various
Page 15 of 25
neuropsychiatric effects (Table 1). This predicts, that low intensity non-thermal
microwave frequency EMFs which also produce elevated L-type and other VGCC
activity, therefore produce widespread neuropsychiatric effects.
3. Studies reviewed in the Tolgskaya and Gordon, 1973 publication (Table 2) have
shown that the cells of the mammalian nervous system show high sensitivity to
various non-thermal microwave and lower frequency EMFs, being apparently
more sensitive than any other organ in the body of rodents. These studies predict
that the human nervous system is likely to be similarly sensitive to these EMFs,
predicting, therefore, widespread neuropsychiatric effects in humans.
We not only have biological credibility but more importantly, each of these distinct but
interrelated biological considerations predicts that low-intensity, non-thermal microwave
EMFs produce widespread neuropsychiatric effects. That common prediction is verified
by extensive data summarized in citations provided by the Naval Medical Research
Institute Research Report, June 1971, data provided by The Raines, 1981 NASA report,
and by 26 epidemiological studies summarized in Table 3.
The most commonly reported neuropsychiatric symptoms from these studies are
summarized in Table. 4.
Table 4. Commonly Reported Neuropsychiatric Symptoms following Microwave
Symptom(s) Numbers of studies
Sleep disturbance/insomnia 17
Depression/depressive symptoms 10
Dysesthesia (vision/hearing/olfactory dysfunction) 10
Concentration/attention/cognitive dysfunction 10
Memory changes 8
Loss of appetite/body weight 6
Skin tingling/burning/inflammation/dermographism 6
A total of 22 different studies described in Table 3 were used for data for this table, but
not 4 others that only assessed a single neuropsychiatric end point. The Altpeter study
which only assessed sleep disturbance/melatonin depletion and the three studies listed
under Chu et al which only assessed headache occurrence following long cell phone calls,
listed in Table 3 were not included. Because many of the studies only assessed from 3 to
7 specific symptoms, it is not surprising that the numbers of studies reporting a specific
Page 16 of 25
symptom fall far below 22. Where several symptom descriptions were included under
one heading, such as dysesthesia, if a study had more than one of these symptom
descriptions, it was only counted once.
All the symptoms listed in Table 4 should be considered established parts of microwave
syndrome (Hocking, 2001; Johnson Liakouris, 1998). Even if the statistical significance
in each study was of the lowest statistical significance (p<.05) one would expect only 1
positive study to occur at random out of the 22 studies included here. Because many
individual symptoms were not surveyed in many individual studies, the expectation is
substantially lower than that. Each of these, having shown positive results in 5 or more
studies, are highly unlikely, therefore, to have occurred by chance. Stong statistical
significance is also seen for individual neuropsychiatric effects reported to have p<0.001
in the Eger and Jahn, 2010 and Otto et al, 1994 studies (see Table 3).
EEG changes may well be part of microwave syndrome, as well. While none of the
studies described in Table 3 measured EEGs, six studies of human occupational exposure
cited in the Raines, 1981 showed EEG changes (Baranski and Edelwejn, 1975; Bise,
1978; Dumanskij and Shandala, 1974; Lerner, 1980; Hauf and Weisinger, 1973;
Sheppard and Eisenbud,1977). Murbach et al, 2014 cited 10 human studies in support of
their statement that “The most consistently reported effects (of mobile phone use) in
various studies conducted by different laboratories are changes in the
electroencephalogram (EEG) power spectrum.” Three recent studies (Lustenberger et al,
2013; Schmid et al, 2012a,b) and several earlier studies cited in Wagner et al (1998) have
each shown EEG changes in sleeping humans exposed to non-thermal pulsed microwave
fields. Two recent studies showed EEG changes in persons exposed to Wi-Fi fields
(Maganioti, 2010; Papageorgiou, 2011). Lai, 1997 described 8 animal studies showing
changes in EEG patterns in animals exposed to non-thermal EMFs and three additional
animal studies were described in Tolgskaya and Gordon, 1973. With the exception of the
6 studies cited in the second sentence in this paragraph, all of these are direct
experimental studies which are not, therefore, susceptible to the questions of causality
that can be raised about epidemiological studies. It is the author’s view that future
studies should consider studying EEG changes as an objectively measurable assessment
of brain physiology and that before and after increased exposure studies should be
considered when a new EMF source is to be introduced into human populations. While
such studies must be done carefully, given the complexity of EEGs, even very small
numbers of individuals may produce highly statistically significant results in well
designed studies analyzed with paired t-tests.
One of the citations from the previous paragraph, Bise, 1978 reviewed earlier studies of
low level microwave frequency exposures in humans and concluded that such EMFs
produced the following neuropsychiatric effects: headache, fatigue, irritability, dizziness,
loss of appetite, sleepiness, sweating, difficulty of concentration, memory loss,
depression, emotional instability, dermographism, tremor, hallucinations and insomnia.
The strong similarity of this list from 37 years ago and the list in Table 4 should be noted.
The Bise, 1978 list is based on occupational exposure studies whereas the current list in
Table 4 is based primarily on EMF exposures from cell/mobile phone base stations, from
Page 17 of 25
heavy cell phone usage and from smart meters, three types of exposures that did not exist
in 1978. The strong similarity between the Bise, 1978 list and the current one 37 years
later alone produces a compelling argument that the 11 neuropsychiatric effects found on
both lists are caused by exposure to multiple types of low-intensity microwave EMFs.
The pattern of evidence is compelling in support of the earlier statement of Levitt and Lai
(2010) that “The primary questions now involve specific exposure parameters, not the
reality of complaints or attempts to attribute such complaints to psychosomatic causes,
malingering or beliefs in paranormal phenomena.”
We can barely imagine how the combinations of neuropsychiatric effects, including those
in Table 4, will influence human behavior and social interactions, now that the majority
of the human populations on earth are exposed to ever increasing intensities and diversity
of microwave frequency EMFs. You may recall that three of the occupational exposure
studies cited in (Raines, 1981 showed increasing prevalence of neuropsychiatric
symptoms with years of exposure to consistent patterns of EMF exposure intensities
(Dwyer and Leeper, 1978, Sadcikova, 1974 and Baranski and Edelwejn, 1975). With
ever increasing exposures in human populations, we have no idea what the consequences
of these ever increasing exposures will be.
The author declares no conflict of interest.
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