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Repeated Wi-Fi studies show that Wi-Fi causes oxidative stress, sperm/testicular damage, neuropsychiatric effects including EEG changes, apoptosis, cellular DNA damage, endocrine changes, and calcium overload. Each of these effects are also caused by exposures to other microwave frequency EMFs, with each such effect being documented in from 10 to 16 reviews. Therefore, each of these seven EMF effects are established effects of Wi-Fi and of other microwave frequency EMFs. Each of these seven is also produced by downstream effects of the main action of such EMFs, voltage-gated calcium channel (VGCC) activation. While VGCC activation via EMF interaction with the VGCC voltage sensor seems to be the predominant mechanism of action of EMFs, other mechanisms appear to have minor roles. Minor roles include activation of other voltage-gated ion channels, calcium cyclotron resonance and the geomagnetic magnetoreception mechanism. Five properties of non-thermal EMF effects are discussed. These are that pulsed EMFs are, in most cases, more active than are non-pulsed EMFs; artificial EMFs are polarized and such polarized EMFs are much more active than non-polarized EMFs; dose-response curves are non-linear and non-monotone; EMF effects are often cumulative; and EMFs may impact young people more than adults. These general findings and data presented earlier on Wi-Fi effects were used to assess the Foster and Moulder (F&M) review of Wi-Fi. The F&M study claimed that there were seven important studies of Wi-Fi that each showed no effect. However, none of these were Wi-Fi studies, with each differing from genuine Wi-Fi in three distinct ways. F&M could, at most conclude that there was no statistically significant evidence of an effect. The tiny numbers studied in each of these seven F&M-linked studies show that each of them lack power to make any substantive conclusions. In conclusion, there are seven repeatedly found Wi-Fi effects which have also been shown to be caused by other similar EMF exposures. Each of the seven should be considered, therefore, as established effects of Wi-Fi.
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Environmental Research
journal homepage: www.elsevier.com/locate/envres
Wi-Fi is an important threat to human health
Martin L. Pall
Washington State University, 638 NE 41st Avenue, Portland, OR 97232-3312, USA
ARTICLE INFO
Keywords:
Electromagnetic eld (EMF)
Brain impact
Testis/sperm count and quality
Impact of pulsation and polarization
Activation of voltage-gated calcium channels
Wi-Fi or WiFi
ABSTRACT
Repeated Wi-Fi studies show that Wi-Fi causes oxidative stress, sperm/testicular damage, neuropsychiatric ef-
fects including EEG changes, apoptosis, cellular DNA damage, endocrine changes, and calcium overload. Each of
these eects are also caused by exposures to other microwave frequency EMFs, with each such eect being
documented in from 10 to 16 reviews. Therefore, each of these seven EMF eects are established eects of Wi-Fi
and of other microwave frequency EMFs. Each of these seven is also produced by downstream eects of the main
action of such EMFs, voltage-gated calcium channel (VGCC) activation. While VGCC activation via EMF inter-
action with the VGCC voltage sensor seems to be the predominant mechanism of action of EMFs, other me-
chanisms appear to have minor roles. Minor roles include activation of other voltage-gated ion channels, calcium
cyclotron resonance and the geomagnetic magnetoreception mechanism. Five properties of non-thermal EMF
eects are discussed. These are that pulsed EMFs are, in most cases, more active than are non-pulsed EMFs;
articial EMFs are polarized and such polarized EMFs are much more active than non-polarized EMFs; dose-
response curves are non-linear and non-monotone; EMF eects are often cumulative; and EMFs may impact
young people more than adults. These general ndings and data presented earlier on Wi-Fi eects were used to
assess the Foster and Moulder (F&M) review of Wi-Fi. The F&M study claimed that there were seven important
studies of Wi-Fi that each showed no eect. However, none of these were Wi-Fi studies, with each diering from
genuine Wi-Fi in three distinct ways. F&M could, at most conclude that there was no statistically signicant
evidence of an eect. The tiny numbers studied in each of these seven F&M-linked studies show that each of
them lack power to make any substantive conclusions. In conclusion, there are seven repeatedly found Wi-Fi
eects which have also been shown to be caused by other similar EMF exposures. Each of the seven should be
considered, therefore, as established eects of Wi-Fi.
1. Introduction
Wi-Fi (also known as WiFi or WLAN) is a wireless network involving
at least one Wi-Fi antenna connected to the internet and a series of
computers, laptops and/or other wireless devices communicating
wirelessly with the Wi-Fi antenna. In this way, each such wireless
communication device can communicate wirelessly with the internet.
All the studies reviewed here were of Wi-Fi using the 2.4 GHz band,
although there is also a 5 GHz band reserved for possible Wi-Fi use.
Telecommunications industry-linked individuals and groups have
claimed that there are no and cannot possibly be any health impacts of
Wi-Fi (Foster and Moulder, 2013;Berezow and Bloom, 2017). However
with Wi-Fi exposures becoming more and more common and with many
of our exposures being without our consent, there is much concern
about possible Wi-Fi health eects. This paper is not focused on anec-
dotal reports but rather on 23 controlled, scientic studies of such
health-related eects in animals, cells including human cells in culture
and in human beings (Table 1).
Each of the eects reported above in from 2 to 11 studies, have an
extensive literature for their occurrence in response to various other
non-thermal microwave frequency EMFs, discussed in detail below.
These include (see Table 1)ndings that Wi-Fi exposures produce im-
pacts on the testis leading to lowered male fertility; oxidative stress;
apoptosis (a process that has an important causal role in neurodegen-
erative disease); cellular DNA damage (a process causing cancer and
germ line mutations); neuropsychiatric changes including EEG changes;
hormonal changes.
The discussion here focuses on those Wi-Fi eects which have been
found by multiple Wi-Fi studies and have been previously conrmed by
non-thermal exposures to other microwave frequency EMFs. The 1971/
72 U.S. Oce of Naval Medical Research study (Glaser, 1971) reported
the following changes related to testis or sperm: 1. Decreased testos-
terone leading to lowered testis size. 2. Histological changes in testi-
cular epithelial structure. 3. Gross testicular histological changes. 4.
https://doi.org/10.1016/j.envres.2018.01.035
Received 22 September 2017; Received in revised form 20 January 2018; Accepted 23 January 2018
For submission to the Wireless Radiation and Health special issue of the journal Environmental Research.
E-mail address: martin_pall@wsu.edu.



Decreased spermatogenesis. Glaser (1971) also reported a total of 35
neurological/neuropsychiatric eects of non-thermal EMF exposures,
including 9 central nervous system eects, 4 autonomic system eects,
17 psychological disorders, 4 behavioral changes and EEG changes. It
also reported 7 types of chromosomal aberrations several of which are
known to be caused by chromosomal double stranded DNA breaks, 8
types of endocrine changes, and cell death (what we now call apop-
tosis). Glaser (1971) also provided over 1000 dierent citations each
reporting various types of non-thermal microwave frequency EMF ef-
fects. Consequently, the existence of 5 types of Wi-Fi eects, each
supported by multiple Wi-Fi studies were already well-supported as
general non-thermal EMF eects back in 1971, 47 years ago: eects on
the testis and sperm production, neurological/neuropsychiatric eects,
endocrine eects, attacks on cellular DNA and increased apoptosis/cell
death.
The 146 page review published by Tolgskaya and Gordon (1973)
found that in studies of histological changes in rodents, the three most
sensitive organs in the body to non-thermal microwave EMFs were the
nervous system (including the brain), followed closely by the heart and
the testis. They also reported changes in neuroendocrine tissues and
increased cell death in multiple tissues. Thus those pre-1973 rodent
studies already showed that other EMFs caused 4 of the repeated, re-
cently documented Wi-Fi eects: changes in testis structure/function,
neurological eects, increased cell death (possibly via apoptosis) and
endocrine eects. Findings from our longer list of EMF reviews of non-
thermal eects are summarized in Table 2.
Each of the 7 Wi-Fi eects found in 211 studies (Table 1), have also
been found to be caused by other microwave frequency EMFs, in a
much larger literature (Table 2). From 10 to 16 reviews extensively
document each of these seven eects as general microwave frequency
eects (Table 2). These are, therefore, general eects produced by such
EMFs. Each of these 7 repeatedly found Wi-Fi eects should, therefore,
be considered established Wi-Fi eects. The author is not aware of any
genuine Wi-Fi studies on these 7 eects that reported no statistically
signicant evidence of eect.
Each of these 7 is very serious: Oxidative stress has causal roles in
most chronic human diseases; cellular DNA damage can cause cancer,
thus producing a partial explanation for EMF cancer causation; because
such DNA damage occurs in sperm cells (Atasoy et al., 2013; Avendaño
et al., 2012; Akdag et al., 2016; Adams et al., 2014; Liu et al., 2014;
Asghari et al., 2016), such damage is highly likely to produce mutations
that impact future generations; calcium overload is highly likely to be
the cause of each of these various other eects, as discussed below;
apoptosis has central roles in neurodegenerative diseases; the neu-
ropsychiatric eects are almost certainly caused by the impact of EMFs
on brain structure which is extensively documented and, in my opinion,
produces many impacts (Pall, 2016b). A recent meta-analysis shows
major lowering of sperm counts and sperm quality in many countries
around the world, with declines of over 50% in all advanced technology
countries (Levine et al., 2017). The senior author of this study suggested
that this eect alone may lead to human extinction (No authors listed,
2017). Given the major impact of EMF exposures on sperm count and
quality in human and in animal studies, the pattern of evidence on male
fertility is very worrying.
One thing needs to be claried, here, however. In the two studies on
calcium overload following Wi-Fi exposure, such overload was mea-
sured a substantial time period following exposure. Overload was
shown to be caused, to a substantial eect, by increased TRPV1 re-
ceptor activity (Çiğand Nazıroğlu, 2015; Ghazizadeh and Nazıroğlu,
2014). The TRPV1 receptor is known to be activated by oxidative stress.
It is my view, discussed in detail below, that there is a central me-
chanism that acts to produce excessive intracellular calcium im-
mediately following EMF exposure and that the oxidative stress/TRPV1
activation is secondary.
We have then, major impacts of non-thermal EMF exposures on both
of the most important intercellular regulatory systems in the body, the
nervous system and the endocrine systems. We have major impacts on
what may be the most important intracellular regulatory system, the
calcium regulatory system. And we also have non-thermal EMFs at-
tacking the DNA of our cells, putting our biological inheritance at great
risk. As living organisms, EMFs attack each of the most important
functions that go to the heart of our human complexities.
Despite all of these clear and important, non-thermal eects, and
the fact that there was substantial evidence for many of them already
known before 1973, our current U.S. and international safety guidelines
are still based on considering only thermal eects.
2. Wi-Fi and other wireless communication EMFs are pulsed,
leading to larger biological impacts; These EMFs are also
polarized, also producing larger eects; Dose response curves are
often both non-linear and non-monotone
There are three patterns of EMF action, each of which is very im-
portant and each of which is almost universally ignored by the
Table 1
Summary of health impacts of Wi-Fi EMF exposures.
Citation(s) Health Eects
Atasoy et al. (2013);Özorak et al. (2013);Aynali et al. (2013);Çiftçi et al. (2015);Tök
et al. (2014);Çiğand Nazıroğlu (2015);Ghazizadeh and Nazıroğlu (2014);Yüksel
et al. (2016);Othman et al. (2017a, 2017b);Topsakal et al. (2017)
Oxidative stress, in some studies eects lowered by antioxidants
Atasoy et al. (2013);Shokri et al. (2015);Dasdag et al. (2015);Avendaño et al. (2012);
Yildiring et al. (2015);Özorak et al. (2013);Oni et al. (2011);Akdag et al. (2016)
Sperm/testicular damage, male infertility
Papageorgiou et al. (2011);Maganioti et al. (2010);Othman et al. (2017a, 2017b);
Hassanshahi et al. (2017)
Neuropsychiatric changes including EEG; prenatal Wi-Fi leads to post-natal neural
development, increased cholinesterase; decreased special learning; Wi-Fi led to greatly
lowered ability to distinguish familiar from novel objects, changes in GABA and
cholinergic transmission
Shokri et al. (2015);Dasdag et al. (2015);Çiğand Nazıroğlu (2015);Topsakal et al.
(2017)
Apoptosis (programmed cell death), elevated apoptotic markers
Avendaño et al. (2012);Atasoy et al. (2013);Akdag et al. (2016) Cellular DNA damage
Saili et al. (2015);Yüksel et al. (2016);Topsakal et al. (2017) Endocrine changes incl.: Catecholamines, pancreatic endocrine dysfunction, prolactin,
progesterone and estrogen
Çiğand Nazıroğlu (2015);Ghazizadeh and Nazıroğlu (2014) Calcium overload
Aynali et al. (2013) Melatonin lowering; sleep disruption
Othman et al. (2017a) MicroRNA expression (brain)
Othman et al. (2017a) Abnormal postnatal development
Çiftçi et al. (2015) Disrupts development of teeth
Saili et al. (2015) Cardiac changes, blood pressure disruption; erythrocyte damage
Lee et al. (2014) Growth stimulation of adipose stem cells (role in obesity?)
M.L. Pall 

telecommunications industry and industry-linked organizations. The
most extensively reviewed of these is that pulsed EMFs are usually
much more biologically active than are non-pulsed (also known as
continuous wave) EMFs of identical frequency and similar average in-
tensity (Osipov, 1965; Pollack and Healer, 1967; Creighton et al., 1987;
Grigor'ev, 1996; Belyaev, 2005, 2015; Markov, 2007; Van Boxem et al.,
2014; Pall, 2015b; Panagopoulos et al., 2015b). This pattern of action is
particularly important because all wireless communication devices,
including Wi-Fi (Panagopoulos et al., 2015b; Maret, 2015) commu-
nicate via pulsations and are likely to be particularly dangerous as
consequence of this. Panagopoulos et al., 2015b have argued that the
more pulsed they are, the more damaging EMFs will be and while this
may still be questioned, it may well be a roughly applicable general-
ization.
It is also true that articial EMFs are polarized and this makes ar-
ticial EMFs particularly dangerous (Belyaev, 2005, 2015;
Panagopoulos et al., 2015a). Polarized EMFs put much larger forces of
electrically charged chemical groups than do non-polarized EMFs
(Panagopoulos et al., 2015a), an observation that is relevant to the
main mechanism of EMF action in living cells discussed below.
It has often been found that there are windows of exposure where
specic intensity ranges produce maximum biological eects, which
drop ogoing to both lower or higher intensities (Belyaev, 2005, 2015;
Pall, 2015b). It can be seen from this that dose-response curves are
often both non-linear and non-monotone whereas industry linked
groups often assume a linear and therefore monotone dose-response
curve.
3. EMF eects are often cumulative and irreversible
One question that has been raised about the eects of these low-
intensity EMFs producing biological eects is are they cumulative? I am
aware of three dierent types of evidence for cumulative eects. Three
of the human occupational exposure studies from the 1970's reviewed
in Raines (1981), showed that eects increased substantially with in-
creasing time of exposure to a particular type and intensity of EMF.
The impacts of such EMFs on animal brains were reviewed in
Tolgskaya and Gordon (1973) and discussed in Pall (2016b). Initially
exposures over period of 12 months produced relatively modest
changes in structure of the brain and the neurons and when exposures
ceased, most of the structural changes disappeared that is the changes
were largely reversible. However more months of exposure produced
much more severe impacts on brain and neuronal structure and these
were irreversible (Tolgskaya and Gordon, 1973; Pall, 2016b).
Magras and Xenos (1997) put pairs of young mice into cages on the
ground at two locations each with somewhat dierent exposures within
an antenna park. The exposure levels at both sites were well within
safety guidelines, so if the safety guidelines have any biological re-
levance, there should have been no apparent eects. It takes about 30
days for mice to go through gestation. At the higher level exposure, the
pairs produced one litter of lower than normal size, and a second litter
with lowered numbers of progeny; after that they were completely
sterile or had extremely low fertility (Magras and Xenos, 1997). At the
other site, the mating pairs produced four litters, with decreasing
numbers of progeny over time followed by complete sterility. In both
groups, the mating and possible subsequent gestatation for the fth
possible litter were performed under conditions of no EMF exposure,
but the fertility eects were not reversed; therefore fertility eects may
become irreversible, suggesting a similar pattern to the brain related
eects of EMFs. It should be noted that Özorak el al (2013) showed that
Wi-Fi exposure impacted animal reproduction and that (Atasoy et al.,
2013; Shokri et al., 2015; Dasdag et al., 2015; Avendaño et al., 2012;
Yildiring et al., 2015; Oni et al., 2011; Akdag et al., 2016) suggest this
as well from the Wi-Fi impacts on testis structure and sperm production.
Mutation accumulation produced by cellular DNA damage is likely
to be both cumulative and irreversible, as well, because later mutations
are highly unlikely to reverse previously occurring mutations.
We have therefore reason to think that such eects as brain damage
to animal brains, neuropsychiatric eects in humans, reproductive
dysfunction in mice and mutational eects, are each cumulative. Those
same eects may be completely or largely irreversible. One thing that
this should tell us is that the short-term Wi-Fi studies shown in Table 1
may greatly underestimate the damage Wi-Fi may do over much longer
time periods. Given the fact that Wi-Fi has been placed in most schools,
hotels, restaurants, coee shops, commercial aircraft and airports as
well as in many homes and that Wi-Fi hot spots are becoming in-
creasingly common in cities around the world, we should expect mas-
sive cumulative Wi-Fi eects in many people. A second tentative in-
ference is that false assurances of safety on the part of industry are
likely to lead to much more severe eects on people exposed to Wi-Fi or
other EMFs; rather than leading them to protect themselves or their
children by avoiding exposures or demanding that others stop non-
voluntary exposures, they are likely to avoid protective changes or be
prevented from doing such protective changes. A third inference is that
these eects may be among the more dicult ones for us to attribute to
EMF exposure. We are much more aware of eects that occur rapidly
than those that take months or years before they become readily ap-
parent.
Table 2
Reviews of Non-thermal Eects of Microwave Frequency EMFs Similar to Those Found in Multiple Wi-Fi Studies.
Non-thermal eects Citations
Cellular DNA damage Glaser (1971);Yakymenko et al. (1999);Aitken and De Iuliis (2007);Hardell and Sage (2008);Hazout et al. (2008);
Phillips et al. (2009);Ruediger (2009);Makker et al. (2009);Yakymenko and Sidorik (2010);Batista Napotnik et al.
(2010);Yakymenko et al. (2011);Pall (2013, 2015b);Asghari et al. (2016);Pall (2018)
Changes in testis structure, lowered sperm count/
quality
Glaser (1971);Tolgskaya and Gordon (1973);Aitken and De Iuliis (2007);Hazout et al. (2008);Desai et al. (2009);Gye
and Park (2012);Nazıroğlu et al. (2013);Carpenter (2013);Adams et al. (2014);Liu et al. (2014);Houston et al. (2016);
La Vignera et al. (2012);Makker et al. (2009)
Neurological/neuropsychiatric eects Glaser (1971);Tolgskaya and Gordon (1973);Raines (1981);Lai (1994);Grigor'ev (1996);Hardell and Sage (2008);
Makker et al. (2009);Khurana et al. (2010);Levitt and Lai (2010);Consales et al. (2012);Carpenter (2013);Pall
(2016b);Belyaev et al. (2016);Sangün et al. (2016); Kaplan et al. (2016)
Apoptosis/cell death Glaser (1971);Tolgskaya and Gordon (1973);Raines (1981);Yakymenko et al. (1999);Batista Napotnik et al. (2010);
Yakymenko and Sidorik (2010);Pall (2013, 2016b);Asghari et al. (2016);Sangün et al. (2016)
Calcium overload Adey (1981, 1988);Walleczek (1992);Yakymenko et al. (1999);Gye and Park (2012);Pall (2013, 2015a, 2015b, 2016a,
2016b)); Asghari et al. (2016)
Endocrine eects Glaser (1971);Tolgskaya and Gordon (1973);Raines (1981);Hardell and Sage (2008);Gye and Park (2012);Hardell and
Sage (2008);Makker et al. (2009);Pall (2015b);Sangün et al. (2016);Asghari et al. (2016)
Oxidative stress, free radical damage Raines (1981);Houston et al. (2016);Hardell and Sage (2008);Hazout et al. (2008);Desai et al. (2009);Yakymenko and
Sidorik (2010);Yakymenko et al. (2011);Consales et al. (2012);La Vignera et al. (2012);Nazıroğlu et al. (2013);
Yakymenko et al. (2015);Pall (2013, 2018);Dasdag and Akdag (2016);Wang and Zhang (2017)
M.L. Pall 

4. Wi-Fi and other EMFs may be particularly damaging to young
people
Most arguments that have been made that microwave frequency
EMFs may be much more damaging to young children have centered on
the much smaller skulls and skull thickness in young children, in-
creasing the exposure of their brains to EMFs (Gandhi and Kang, 2001;
Gandhi et al., 2012). However there are other arguments to be made.
EMFs have been shown to be particularly active in producing eects on
embryonic stem cells (Lee et al., 2014; Belyaev et al., 2009; Markovà
et al., 2010; Czyz et al., 2004; Xu et al., 2016; Bhargav et al., 2015;
Odaci et al., 2008; Uchugonova et al., 2008; Wang et al., 2015; Teven
et al., 2012). Because such stem cells occur at much higher cell densities
in children, with stem cell densities the highest in the fetus and de-
creasing with increasing age (Belyaev et al., 2009; Markovà et al.,
2010), impacts on young children are likely to be much higher than in
adults. The decreased DNA repair and increased DNA damage following
EMF exposure strongly suggest that young children may be increasingly
susceptible to cancer following such exposures (Belyaev et al., 2009;
Markovà et al., 2010; Czyz et al., 2004). EMF action on stem cells may
also cause young children to be particularly susceptible to disruption of
brain development (Xu et al., 2016; Bhargav et al., 2015), something
that may be relevant to autism causation. These are all very proble-
matic issues and we cannot rule out the possibility that there are other
problematic issues as well. Redmayne and Johansson (2015) reviewed
the literature showing that there are age-related eects, such that
young people are more sensitive to EMF eects. It follows from these
various ndings that the placement of Wi-Fi into schools around the
country may well be a high level threat to the health of our children as
well being a threat to teachers and any very sensitive fetuses teachers
may be carrying, as well.
5. How do EMF exposures lead to non-thermal health impacts?
The author found the answer to this question in the already pub-
lished scientic literature (Pall, 2013). That study showed that in 24
dierent studies [there are now a total of 26 Pall (2015b)], eects of
low-intensity EMFs, including microwave frequency and also extremely
low frequency EMFs, static electrical elds and static magnetic elds
could be blocked by calcium channel blockers, drugs that are specic
for blocking voltage-gated calcium channels (VGCCs). There were 5
dierent types of calcium channel blockers used in these studies, each
thought to be highly specic, each structurally distinct and each
binding to a dierent site on the VGCCs. In studies where multiple ef-
fects were studied, all studied eects were blocked or greatly lowered
by calcium channel blockers. These studies show that EMFs produce
diverse non-thermal eects via VGCC activation Pall (2013, 2014,
2015a, 2015b, 2016a, 2016b)) in many human and animal cells. In
plant cells, EMFs activate somewhat similar calcium channels and
produce somewhat similar eects on oxidative stress, cellular DNA
damage and calcium signaling (Pall, 2016a). Furthermore, many dif-
ferent eects shown to be produced in repeated studies by EMF ex-
posures, including the eects discussed above, can be produced by
downstream eects of VGCC activation, via increased [Ca2+]i, as
discussed in detail below.
Before leaving this issue, it is important to discuss why the VGCCs
are so sensitive to activation by these low-intensity EMFs. The VGCCs
each have a voltage sensor which is made up of 4 alpha helixes in the
plasma membrane, with each such helix having 5 positive charges on it,
for a total of 20 positive charges (Pall, 2015b). These voltage sensor
helixes are each called S4 helixes because each is the fourth helix in a
distinct multi-helix domain. Each of these voltage sensor charges is
within the lipid bilayer part of the plasma membrane. The electrical
forces on the voltage sensor are very high for three distinct reasons
(Pall, 2015b, 2015a, 2016a). 1. The 20 charges on the voltage sensor
make the forces on voltage sensor 20 times higher than the forces on a
single charge. 2. Because these charges are within the lipid bilayer
section of the membrane where the dielectric constant is about 1/120th
of the dielectric constant of the aqueous parts of the cell, the law of
physics called Coulomb's law, predicts that the forces on those charges
will be approximately 120 times higher than the forces on charges in
the aqueous parts of the cell. 3. Because the plasma membrane has a
high electrical resistance whereas the aqueous parts of the cell are
highly conductive, the electrical gradient across the plasma membrane
is estimated to be concentrated about 3000-fold. The combination of
these eects means that comparing the forces on the voltage sensor
with the forces on singly charged groups in the aqueous parts of the cell,
the forces on the voltage sensor are approximately
20 ×120 ×3000 = 7.2 million times higher (Pall, 2015b). The physics
predicts, therefore, extraordinarily strong forces activating the VGCCs
via the voltage sensor. It follows that the biology tells us that the VGCCs
are the main target of the EMFs and the physics tells us why they are the
main target. Thus the physics and biology are pointing in the same
direction.
There are also additional ndings pointing to the voltage sensor as
the direct target of the EMFs. In addition to the VGCCs, there are also
voltage-gated sodium, potassium and chloride channels, with each of
these having a voltage sensor similar to those found in the VGCCs. Lu
et al. (2015) reported that voltage gated sodium channels, in addition
to the VGCCs were activated by EMFs. Tabor et al. (2014) found that
Mauthner cells, specialized neurons with special roles in triggering
rapid escape mechanisms in sh, were almost instantaneously activated
by electrical pulses, which acted via voltage-gated sodium channel
activation to subsequently produce large [Ca2+]i increases. Zhang
et al. (2016) reported that in addition to the VGCCs, potassium and
chloride channels were each activated by EMFs, although these other
voltage-gated ion channels had relatively modest roles compared with
the VGCCs in producing biological eects. Each of these three studies,
the Lu et al. (2015) study, the Tabor et al. (2014) study and the Zhang
et al. (2016) study used specic blockers for these other voltage-gated
ion channels to determine their roles. The Tabor et al. (2014) study also
used genetic probing to determine the role of the voltage-gated sodium
channels. Lu et al. (2015) also used whole cell patch clamp measure-
ments to measure the rapid inux of both sodium and calcium into the
cell via the voltage-gated channels following EMF exposure. Sodium
inux, particularly in electrically active cells, act in the normal phy-
siology to depolarize the plasma membrane, leading to VGCC activation
such that the voltage-gated sodium channels may act primarily via in-
direct activation of the VGCCs. In summary then, we have evidence that
in animal including human cells, seven distinct classes of voltage-gated
ion channels are each activated by EMF exposures: From the Pall (2013)
review, four classes of voltage-gated ion channels were shown from
calcium channel blocker studies, to be activated by EMFs, L-type, T-
type, N-type and P/Q type VGCCs. In this paragraph we have evidence
that three other channels are also activated, voltage-gated sodium
channels, voltage-gated potassium channels and voltage-gated chloride
channels. Furthermore the plant studies strongly suggest that the so
called TPC channels, which contain a similar voltage sensor, are acti-
vated in plants allowing calcium inux into plants to produce similar
EMF-induced responses (Pall, 2016a). One can put those observations
together with the powerful ndings from the physics, that the electrical
forces on the voltage-sensor are stunningly strong, something like 7.2
million times stronger than the forces on the singly charged groups in
the aqueous phases of the cell. Now you have a stunningly powerful
argument that the voltage sensor is the predominant direct target of the
EMFs.
There is one additional nding that should be discussed here. In a
study published by Pilla (2012), it was found that pulsed EMFs pro-
duced an instantaneousincrease in calcium/calmodulin-dependent
nitric oxide synthesis in cells in culture. What Pilla (2012) showed was
that following EMF exposure, the cells in culture, must have produced a
large increase in [Ca2 + ]i, this in turn produced a large increase in
M.L. Pall 

nitric oxide synthesis, the nitric oxide diused out of the cells and out of
the aqueous medium above the cells into the gas phase, where the nitric
oxide was detected by a nitric oxide electrode. This entire sequence
occurred in less than 5 s. This eliminates almost any conceivable in-
direct eect, except possibly via plasma membrane depolarization.
Therefore that the pulsed EMFs are acting directly on the voltage sen-
sors of the VGCCs and possibly the voltage-gated sodium channels, to
produce the [Ca2 + ]i increase.
Why is it that the VGCCs, acting via calcium inux, seem to be much
more important in producing EMF eects than are the other voltage-
gated ion channels? Probably for three reasons: 1. Ca
2+
ions under
resting conditions in cells have about a 10,000-fold concentration
gradient driving them into the cell, and over a million-fold electro-
chemical gradient also driving them into the cell. Because of this, one
can have huge calcium inuxes upon channel activation. 2. [Ca2 + ]i
produces many important regulatory eects, such that over activation
of those eects can have very large pathophysiological consequences. 3.
Sustained elevation of [Ca2+]i produces major cell damage.
6. How can the Wi-Fi eects be produced by EMF triggered VGCC
activation?
Can the various eects produced by Wi-Fi and by other microwave
frequency EMFs be produced by the downstream eects of VGCC acti-
vation? In order to determine that, one needs to consider the various
downstream eects of VGCC activation, summarized in Fig. 1 and how
these are likely to produce each of the eects of Wi-Fi and other mi-
crowave frequency EMFs. Let's consider Fig. 1.
As shown in the top left section of Fig. 1, microwave and lower
frequency EMFs act via VGCC activation to produce increases in in-
tracellular calcium [Ca2+]i. All of the downsteam eects of VGCC
activation considered in Fig. 1 are produced by elevated (often ex-
cessive) [Ca2+]i.
Just to the right of [Ca2+]i in Fig. 1, you will see that elevated
[Ca2+]i produced increases in nitric oxide (NO) synthesis. This is be-
cause two of the three types of enzymes producing NO are calcium-
dependent. There is an NO signaling pathway that goes through in-
creased cGMP and increased protein kinase G activity. Protein kinase G
can act by raising the activity of the transcriptional regulatory factor,
Nrf2, to produce the therapeutic eects produced by EMF exposures
(Pilla, 2013; Pall, 2014; Pall and Levine, 2015).
High levels of NO can bind to heme groups on cytochromes (up-
permost section, Fig. 1) inhibiting cytochrome oxidase, the terminal
oxidase in the mitochondria, inhibiting ATP synthesis. NO can also
inhibit cytochrome P450s involved in steroid hormone synthesis, low-
ering levels of estrogen, progesterone and testosterone (sex hormones).
The main pathophysiological eects of EMF exposures are produced
via excessive calcium signaling (lower left) and the peroxynitrite
pathway (lower right). Peroxynitrite levels are elevated because both
NO and superoxide are elevated by increased [Ca2+]i with NO and
superoxide reacting with each other to form peroxynitrite. Peroxynitrite
and its CO
2
adduct, can break down to produce reactive free radicals,
hydroxyl radical, carbonate radical and NO
2
radical which produce
oxidative stress. These various oxidants act to produce greatly elevated
NF-kappaB activity, leading to inammation. All of this biochemistry
and physiology is well-accepted and widely known with a single ex-
ception: The role of protein kinase G in raising Nrf2 has only recently
been reviewed (Pall and Levine, 2015).
The ways in which these mechanisms can produce each of the seven
eects produced by Wi-Fi, as well as other microwave frequency EMFs,
are described in Table 3.
It can be seen from Table 3, that there are plausible mechanisms by
which each of those seven eects can be produced by VGCC activation
via known pathways. Given the complexities of biology, the mechan-
isms described in Table 3 may, in some cases, be over simplied.
There is one other nding, not related to the Wi-Fi ndings, that is
included in Table 3. A question that was raised in review of the paper
was whether the heat shock stress elevation found following EMF ex-
posure in many studies, could be produced by VGCC activation. As you
can see from Table 3, it can be.
7. Other proposed biophysical mechanisms
One question that can be asked is how the VGCC activation me-
chanism compares with other biophysical models of non-thermal EMF
eects. Belyaev (2015) has discussed a number of what he describes as
biophysical models which are, therefore considered here. These models
are basically theoretical models of how the weak electrical forces of the
EMFs can interact with biologically plausible structures to produce non-
thermal eects.
The rst of these Belyaev considers is Fröhlich's theory. This is
where there are coherent longitudinal vibrations of electrically polar
structures.The mechanism of Fröhlich's theory will not be considered
here (the reader is referred to Belyaev, 2015). The author considers this
to be a plausible mechanism for possible production of some non-
thermal EMF eects. However, there are no specic testable predictions
made by the theory that suggest how it could be tested, given the fact
that there may be multiple possible targets of the EMFs according to
Fig. 1. Various pathways of action by which EMF VGCC activation can produce eects produced by EMF exposure (modied, with permission from Pall, 2015b).
M.L. Pall 

Fröhlich's theory.
A second possible mechanism involves the spin state of radical pairs.
When radical pairs are generated from the breakdown of a non-radical
molecule, these radical pairs often react back with each other to form
another non-radical molecule, not necessarily identical to the original
non-radical. What is postulated by this theory is that EMFs can interact
with one or both radicals, changing their spin state and greatly lowering
their ability to react back with each other, thus generating increased
free radicals and therefore increased oxidative stress. The potential
strong point of this theory is that it provides an explanation for the
oxidative stress found following EMF exposure. However, as noted
under oxidative stress in Table 3, there are 6 studies where oxidative
stress following EMF exposure was associated with very high levels of
3-nitrotyrosine, a specic marker of peroxynitrite elevation. These
studies argue, therefore, that oxidative stress following EMF exposure is
produced by peroxynitrite elevation and is not primarily produced by
this radical pair mechanism. It follows from this that the proposed ra-
dical pair mechanism cannot even explain the properties of oxidative
stress production, let alone the various consequences of non-thermal
EMF exposure that do not involve oxidative stress. Does that mean that
the radical pair mechanism has no possible role in producing non-
thermal EMF eects? No, but it does argue there is no evidence for any
such role.
A third mechanism discussed in Belyaev (2015) is the electrosoliton
theory proposed by Brizhik and colleagues, involving a self reinforcing
solitary wave packet.Brizhik and her colleagues discussed this in the
context of reaching a threshold minimum energy state where both
charged molecules and the EMF is in a coherent state, such that charge
movement can ratchet from one state to another. This concept shows
substantial similarity to what is thought to occur in the activation of the
voltage sensor, that is discussed above. There we have four alpha he-
lixes, each designated an S4 helix and with each S4 helix having 5
positive charges, with the 4 S4 helixes together making up the voltage
sensor. Most of those positive charges are 3 amino acid residues apart
from each other, such that the closest charged residues stick out from
the helix pretty much on the same side of the helix. Three of those
positive charges are electrostatically attracted to negative residues on
other helixes thought to be in xed positions. What is thought to
happen in activation is that there a ratcheting of the S4 helixes toward
the extracellular space, ratcheting such that the negative charges are
now bound to a positive charge 3 residues away from the one that was
previously bound. The ratcheting also produces some turning of the S4
helix. This needs to occur several times on each of the four S4 helixes to
open the channel and allow calcium ions to ow. While I dont com-
pletely understand the Brizhik electrosoliton model, it may well be
relevant to our understanding the VGCC activation, because the me-
chanism of the voltage sensor is similar to what Brizhik and her col-
leagues propose to occur in the electrosoliton model. Both the elec-
trosoliton model and the voltage sensor activation mechanism involve
both charge movements and ratcheting. In order to test these biophy-
sical models one needs to have a specic mechanism where it may
apply and where such tests can be done. In the case of the voltage
sensor of the VGCCs, these tests have already been done.
These models are basically theoretical models of how the weak
electrical forces of the EMFs can interact with biologically plausible
structures to produce non-thermal eects. Their theoretical support is
their strong point. They are weak, however, in providing any compel-
ling evidence that they have causal roles in producing non-thermal
Table 3
How Eight Established Eects of Wi-Fi and Other EMFs Can Be Produced by VGCC Activation.
EMF eect Probable mechanism(s)
Oxidative stress Produced by elevated levels of peroxynitrite and the free radical breakdown products of peroxynitrite and its C0
2
adduct. Four studies of EMF exposure, cited in Pall (2013) showed that oxidative stress following exposure was
associated with major elevation of 3-nitrotyrosine, a marker of peroxynitrite, thus conrming this interpretation.
Two other studies each found 3-nitrotyrosine elevation, both following 35 GHz exposures (Sypniewska et al.
(2010);Kalns et al., 2000).
Lowered male/female fertility, elevated spontaneous
abortion, lowered libido
Both the lowered male fertility and lowered female fertility are associated with and presumably caused by the
oxidative stress in the male and female reproductive organs. Spontaneous abortion is often caused by
chromosomal mutations, so the germ line mutations may have a causal role. Lowered libido may be caused by
lowered estrogen, progesterone and testosterone levels. It seems likely that these explanations may be greatly
oversimplied. One mechanism that may be important in lowered fertility is that VGCC activation and
consequent high {Ca2+]i levels is known to have a key role in avoiding polyspermy. Consquently, if this if
triggered before any fertilization of an egg has occurred, it may prevent any sperm from fertilizing and egg.
Neurological/ neuropsychiatric eects Of all cells in the body, the neurons have the highest densities of VGCCs, due in part to the VGCC role and [Ca2+]
i role in the release of every neurotransmitter in the nervous system. Calcium signaling regulates synaptic
structure and function in 5 dierent ways, each likely to be involved here. Oxidative stress and apoptosis are both
thought to have important roles. Lowered sleep and increased fatigue are likely to involve lowered nocturnal
melatonin and increased nocturnal norepinephrine.
Apoptosis Apoptosis can be produced by excessive Ca2+ levels in the mitochondria and by double strand breaks in cellular
DNA; it seems likely that both are involved following EMF exposure. A third mechanism for triggering apopotosis,
endoplasmic reticulum stress (see bottom row in this Table), may also be involved.
Cellular DNA damage Cellular DNA damage is produced by the free radical breakdown products of peroxynitrite directly attacking the
DNA [see Pall (2018) for discussion].
Changes in non-steroid hormone levels The release of non-steroid hormones is produced by VGCC activation and [Ca2+]i elevation. The immediate
eects of EMF exposures is to increase hormone release and to raise, therefore, hormone levels. However many
hormone systems become exhaustedas a consequence of chronic EMF exposures. The mechanism of exhaustion
is still uncertain, but it may involve oxidative stress and inammation.
Lowered steroid hormone Steroid hormones are synthesized through the action of cytochrome P450 enzymes; activity of these hormones is
inhibited by binding of high levels of nitric oxide (NO) leading to lowered hormone synthesis.
Calcium overload Produced by excessive activity of the VGCCs; secondary calcium overload is produced by oxidative stress
activation of TRPV1, TRPM2 and possibly some other TRP receptors, opening the calcium channel of these
receptors.
Heat shock protein induction There is a large literature showing that excessive [Ca2+]i induces very large increases in heat shock proteins.
This is thought to be produced by complex calcium signaling changes involving the endoplasmic reticulum,
mitochondria and the cytosol and also involving excessive [Ca2+]i producing increasing protein misfolding
(Garbuz, 2017;Park et al., 2014;Krebs et al., 2011). It should be noted that some calcium is essential for proper
protein folding in the endoplasmic reticulum such that only excessive calcium leads to misfolding and consequent
endoplasmic reticulum stress.
M.L. Pall 

changes in cells in culture or in whole animal (or human) studies. They
are also weak because they do not provide stated explanations for the
range of EMF eects that have been documented.
Belyaev (2015) discusses microwave hearing in this context. He
discusses the ndings showing that people can hear microwave elds
that are pulsed, including pulsed low intensity EMFs. While there is no
doubt that these are very interesting observations on what are clearly
non-thermal eects, they do not provide a biophysical model explaining
how microwave hearing may occur. It is important, therefore to ask
whether such microwave hearing could be caused by VGCC activation.
It has been shown that hearing involves the activation of the VGCCs
(Joiner and Lee, 2015). Furthermore, various otolaryngological condi-
tions, including tinnitus, involve excessive VGCC activity, such that the
calcium channel blocker, nimodipine is useful in their treatment
(Monzani et al., 2015). These ndings tells us that microwave hearing
may be produced by VGCC activation. Consequently, microwave
hearing may be interpreted as providing further support for the VGCC
mechanism.
Following microwave hearing, Dr. Belyaev (2015) discusses plasma
membrane and ion models. Here the VGCC mechanisms t into the
scheme, as do the other voltage-gated ion channels and the plant TPC
channels, all discussed above as being activated by their voltage sensor
following EMF exposures.
Finally, Dr. Belyaev (2015) discusses possible direct eects of EMFs
on DNA, possibly leading to changes in chromatin structure and/or
nuclear structure. There is a literature showing that aqueous solutions
of DNA absorb microwave EMFs much more eciently than do iden-
tical solutions not containing DNA. This clearly shows that DNA has a
high absorbance of the EMFs, Furthermore, there are studies showing
such dissolved DNA, when it absorbs such EMFs, undergoes structural
changes as measured by biophysical techniques. All of this suggests that
DNA is a plausible potential target for the EMFs. The problem is what
are the predicted eects of such changes in DNA structure in living cells
and organisms? Dr. Belyaev spends almost a page and a half in his paper
discussing various possible models of interactions of DNA or of chro-
matin with EMFs. But again, how do we test any of these in living cells
to demonstrate a role of such DNA or chromatin changes in producing
any specic or general biological eects? Given the extraordinary
complexity of living cells and organisms, there are only two powerful
ways of demonstrating causal roles in such living cells and organisms.
These are to use genetics or to use specic pharmacological agents. The
extraordinary power of each of these approaches comes from the fact
that these approaches allow researchers to vary one variable at a time
out of the thousands of interacting variables in a living cell, allowing us
to ask does that specic variable have a causal role in determining a
specic response. But these two approaches can be used when specic
proteins have specic roles, not when you are looking at the role of
DNA structural changes, Fröhlich's theory, radical pair mechanisms or
electrosoliton models. Fortunately the VGCC mechanism does allow this
approach by studying various classes of calcium channel blockers, so
here we do have hard data on widespread causal roles of VGCC acti-
vation in producing EMF eects.
8. Two other models for producing non-thermal eects
With the possible exception of the electrosoliton model, the author
does not nd any of the models discussed by Dr. Belyaev (2015) to have
substantial evidence for roles in producing EMF eects. There are two
other models which may be more compelling, each of which either
produces increased [Ca2+]i.
Six studies have supported the view that calcium cyclotron re-
sonance, has a role in producing biological eects produced by certain
specic frequencies which can interact with Ca
2+
ions to produce a cy-
clotron-like resonance (Foletti et al., 2010;Gaetani et al., 2009;De
Carlo et al., 2012;Lisi et al., 2008;Pazur and Rassadina, 2009;Pazur
et al., 2006). In each case, the eects involved a very specic frequency
which produces the calcium cyclotron resonance and in three studies,
these frequencies were shown to produce increases in [Ca2+]i levels.
In the De Carlo et al. (2012) study, the calcium channel blocker nife-
dipine was shown to greatly lower the apparent calcium cyclotron re-
sonance eect. This nding strongly suggests that the calcium cyclotron
resonance can feed Ca
2+
ions into the VGCCs, thus increasing the ow
of Ca
2+
ions through the VGCCs into the cell following EMF exposure.
The frequencies studied here for cyclotron resonance, one was close to
7 Hz and the other was close to 50 Hz, are both in the extremely low
frequency range and consequently are not relevant to microwave fre-
quency eects. The nding that only very specic calcium cyclotron
resonance frequencies produce these eects is the main evidence for
this mechanism.
It is now well established that there is a magnetoreception me-
chanism found in many animals that can detect and respond to the very
low intensity geomagnetic eld. This has been most studied in bees and
in birds, both of whom use it for navigation. This has been suggested to
involve tiny particles of magnetite which occur in bacterial, animal and
plant cells, including human cells. Kirschvink (1992) rst proposed a
model of how such a mechanism might act. He proposed that magnetite
particles may be tethered through a microtubule and/or microlament
or perhaps other bers to a mechanosensitive channel, such that tiny
magnetic forces could open the mechanosensitive channels, allowing
cation ow into the cells. It is still uncertain what mechanosensitive
channel or channels might be involved, but most of the candidates are
channels that allow both sodium and calcium to ow into cells. Hsu
et al. (2007) suggested that such magnetite particles were linked in
honeybees to an undened calcium channel, such that magnetic eld
exposure produces increases in [Ca2+]i. The worm Caenorhabditis
elegans had been shown to have a geomagnetic orientation system.
Vidal-Gadea et al. (2015) found that certain specic neurons in C.
elegans which may be geomagnetic sensory neurons, very low intensity
geomagnetic elds could produce increases in [Ca2+]i in those specic
neurons, even when they had no synaptic inputs, suggesting that these
neurons themselves acted as geomagnetic sensors.
Cadiou and McNaughton (2010) reviewed the literature on a mag-
netite-based magnetoreception system in birds and its role in avian
migration. They also reviewed ndings on neurons found in the tri-
geminal nerve of birds, where magnetic elds as low as 200 nT can
activate specic neurons. Trains of action potentials are produced by
magnetic elds, plateauing in the region of 20100 mT. Latency in a
study presented by Cadiou and McNaughton (2010) was about 4 s, but
other studies have reported latencies of about 2.5 s. Therefore these are
rapid eects. Cadiou and McNaughton (2010) also discuss possible roles
mechanosensitive channels, including a model similar to that proposed
by Kirschvink (1992) and also three other models, each involving dif-
ferent ways of coupling forces on magnetite to opening of a channel.
Magnetoreception has also been reported to occur in a mammal, the
mole-rat (Wegner et al., 2006). There are also studies of magnetic
compass orientation in salmonids, newts, sea turtles and other rodents.
There is evidence in Drosophila, that a magnetic structure attached to
cryptochrome is involved in magnetoreception, as opposed to magne-
tite.
The two mechanisms described in this section have minor roles,
only acting, as far as we can tell, in very specic situations. The calcium
cyclotron resonance mechanism only acts with a few specic fre-
quencies in the extremely low frequency range. The magnetoreception
mechanism only acts, as far as one can tell, on detecting the weak
geomagnetic elds and only acts, as far as one can tell, in certain spe-
cic neurons. It is possible that this view may change with regard to the
magnetoreception mechanism but what is clear is that the VGCC me-
chanism is vastly more important than either of these mechanisms,
acting in diverse cell types and acting to provide responses to a very
wide frequency range and even to static electrical elds and static
magnetic elds. Because static magnetic elds only place forces on
moving electric charges, this produced a puzzle on how they can
M.L. Pall 

activate the VGCCs. Pall (2013) suggested that the solution to that
puzzle is that the plasma membrane of animal cells is often moving,
such that the charges in the voltage sensor are also moving and can,
therefore, have forces placed on them by the static magnetic elds.
These static magnetic elds, activating the VGCCs can be relative low
intensity but probably must be much higher intensity than the extra-
ordinarily weak geomagnetic elds. The reader is referred to Lu et al.
(2015) for empirical information from an important static magnetic
eld study, where those static magnetic elds activate both VGCCs and
voltage-gated sodium channels.
9. Foster and Moulder on Wi-Fi
The Foster and Moulder (2013) paper argues that there are no and
cannot be any health eects of Wi- Fi. The rst 7½pages of the paper
are, however, largely irrelevant to that issue. These pages discuss such
issues as predicted peak power output, incident power density and the
FCC and international safety guidelines. They also discuss specic ab-
sorption rate (SAR) values, a measure of heating. Because it is now
established, as discussed above that thermal eects are not the relevant
mechanism of non-thermal eects and that VGCC activation is the main
mechanism of such eects, this whole section is irrelevant. Foster and
Moulder (2013) discuss the issue of biological eects, praising 7 studies
listed in table 4 of their paper as having well-characterized exposure
systemsof well dened SARS values, reporting that there were no
eects in the rats or mice in those 7 studies. Those 7 studies are Laudisi
et al. (2012),Sambucci et al. (2010),Aït-Aïssa et al. (2010, 2012, 2013)
and Poulletier de Gannes et al. (2012, 2013). The rst two studies come
from one research group and the other ve from another, albeit with
some shared personnel.
Six or those seven studies (Sambucci et al., 2010; Aït-Aïssa et al.,
2010, 2012, 2013; Poulletier de Gannes et al., 2012, 2013) used an
exposure system described by Wu et al. (2009) that is important here
and that was claimed to produce a near uniform exposure. Laudisi et al.
(2012) used a somewhat similar exposure system of Ardoino et al.
(2005), albeit another one that is also claimed to produce near uniform
exposures. The important features here of the Wu et al. (2009) exposure
system need to be examined in the light of the fact that, as discussed
above, articial EMFs are polarized with the polarization producing
much larger biological eects than natural non-polarized EMFs
(Belyaev, 2005, 2015; Panagopoulos et al., 2015a). The probable im-
portant feature of these polarized EMFs is that they put much larger
forces on electrically charged groups (Panagopoulos et al., 2015a);
since such forces are central to VGCC activation via the voltage sensor,
as discussed above, they are likely to be central to the production of
most biological eects. Let's examine Wu et al. (2009) with that issue in
mind. It uses a large chamber surrounded by 1 mm aluminum mesh
wire mesh to provide reections of the EMFs. The chamber in which
animals are exposed on a platform at its center, is also surrounded by
antennae in all 6 directions (up, down, all four horizontal directions)
such that each antenna is broadcasting with one polarization is opposed
(at 180°) by another broadcasting with the 180° opposite polarization,
as well as by four other antennae, broadcasting with 90° dierent po-
larization in each of the four possible directions. This produces a eld
that is more like a non-polarized EMF rather than the usual polarized
articial EMF. This move toward non-polarization is further ex-
acerbated by the aluminum wire reverberation system whose reec-
tions will generate vast numbers of reections of dierent polarity, like
a non-polarized EMF. The consequences of this is that the structure of
this exposure system is clearly very dierent from that seen in Wi-Fi or
any other articially produced EMF that we may be exposed to, with
biological eects produced via electrical forces being vastly less. Con-
sequently this exposure system is not only inherently dierent from
genuine Wi-Fi, it is predicted to be inherently less active than genuine
Wi-Fi, regardless of what EMFs are being fed into the 6 antennae.
There is a second type of consequence of using such reverberation
exposure systems. Because of the many reverberations occurring, the
path lengths of dierent photons reaching a specic point in the ex-
posed tissue, will often be quite dierent from each other, such that the
phase of the EMFs produced will also be quite dierent from each other.
This leads to the possibility of destructive interference and thus a
second mechanism which is predicted to lead to substantial decreases in
the intensity of the exposures. Because exposures are usually predicted
by groups using such exposure chambers without considering such
destructive interference, rather than being measured, the actual ex-
posures may be substantially lower than are the predicted exposures.
Both the polarization eect and the possible dierence between pre-
dicted exposure and actual exposure were considered in an earlier
study.
Vian et al. (2006), using a dierent reverberation exposure
chamber, discussed in Fig. 1 of that paper, how the various re-
verberations lead to the initial polarized EMF being converted to a non-
polarized or at least, less polarized EMF. They also on p. 69 if that paper
compared the predicted with the measured amplitude and found that
the measured amplitude was only 78% of the predicted amplitude.
These ndings suggest that both of the lowered polarization and de-
structive interference discussed in the previous two paragraphs can
have substantial roles in lowering biological responses produced when
using such reverberation exposure chambers.
Laudisi et al. (2012) used a dierent exposure system, that of
Ardoino et al. (2005) where the vast majority of the exposure is pro-
duced from reections oa long cylindrical surface in a TEM cell,
where the curvature of the cylinder will also produce a largely non-
polarized EMF and dierent reverberation paths and consequent de-
structive interference, may both be expected to occur. Consequently the
predicted low biological activity of EMFs produced by the Wu et al.
(2009) system may be expected to also occur from this TEM exposure
system Ardoino et al. (2005). It is not possible to study biological eects
of EMFs from Wi-Fi, cell phones or any other important exposures using
such exposure systems because of the polarization changes they pro-
duce from the original polarized EMFs and because of destructive in-
terference.
Let's now shift to the issue of the important role of pulsations in
producing biological eects and ask whether the EMFs fed into the
antennae have pulsation patterns similar or dierent from genuine Wi-
Fi. Poulletier de Gannes et al. (2012) used a non-pulsed (continuous
wave) as did Wu et al. (2009), an EMF which will have, therefore, much
lower biological eects that genuine Wi-Fi with its myriad of pulsations
(Maret, 2015). The other 6 studies (Laudisi et al., 2012; Sambucci et al.,
2010; Aït-Aïssa et al., 2010, 2012, 2013; Poulletier de Gannes et al.,
2013) used computers with Wi-Fi cards. Such Wi-Fi cards are designed
to communicate with genuine Wi-Fi antennae, but are used here to
communicate with each other, using two such computers to generate
Wi-Fi. How the EMFs so generated compare with the pulsations of
genuine Wi-Fi is a complete mystery and none of these papers provide
any information to allow the reader to make such a comparison. It
follows that these studies (Laudisi et al., 2012; Sambucci et al., 2010;
Aït-Aïssa et al., 2010, 2012, 2013; Poulletier de Gannes et al., 2013) are
not studying genuine Wi-Fi, even before the eects of the reverberation
chamber and the reader is left with no evidence to compare these ori-
ginal EMFs with genuine Wi-Fi. In summary, then none of the EMFs
used in these studies are genuine Wi-Fi, with them diering from
genuine Wi-Fi in three dierent ways: the antenna locations produce a
substantial dierence from genuine Wi-Fi regarding EMF polarization
and this is further exacerbated by the eects of the aluminum mesh
reverberation producing further lowering of any polarization; dier-
ences in path lengths of dierent photons produce substantial de-
structive interference; the initial EMF fed into the antennae diers
substantially from genuine Wi-Fi, with the main concern here being due
to the issue of pulsation patterns and biological eects.
Let's shift now to the claim made by Foster and Moulder (2013) that
there were no eects found in any of these 7 studies. Rothman et al.,
M.L. Pall 

Modern Epidemiology, 3rd Edition is a highly respected source of in-
formation, cited over 18,500 times according to the Google Scholar
database. It states (p. 151, bottom) that: A common misinterpretation
of signicance tests is that there no dierence between two observed
groups because the null test is not statistically signicant, in that P is
greater that the cutofor declaring statistical signicance (again,
usually .05). This interpretation confuses a descriptive issue (whether
two observed groups dier) with an inference about the super-
population. The signicance test refers only to the superpopulation, not
the observed groups. To say that the dierence is not statistically sig-
nicant means only that one cannot reject the null hypothesis that the
superpopulation groups are the same; it does not imply that the two
groups are the same.It follows that the claim of no eectthat Foster
and Moulder (2013) make about each of these 7 studies in Table 4 of
their paper is false because one can never legitimately make such a
claim; one can at most claim that there were no statistically signicant
dierences.
However there are other reasons to reject those claims that need to
be considered for each of these 7 studies. Each of these 7 studies fails to
provide raw numerical data, the lack of which is problematic, given the
other aws that follow. 1). Laudisi et al. (2012) nds in Table 2, that
two T cell populations are statistically signicantly dierent in pre-
natally exposed mice vs sham controls: DP and CD4SP cells are sig-
nicantly aected by exposure in mice at 26 weeks after birth; CD4SP
cells are aected in female mice at 5 weeks after birth (P < .02 in each
case). Furthermore in each of the measurements in Laudisi et al. (2012),
only 11 or 12 mice were studied, tiny numbers. It follows that claims in
Foster and Moulder (2013) that there were no eects are false or mis-
leading for 3 distinct reasons: You can never make such claims even in
large studies; there were 3 comparisons each of which showed statis-
tically signicant eects; this study was done with tiny numbers of
animals being compared and thus had extremely low statistical power.
2). Sambucci et al. (2010) also had a tiny numbers, with 11 or 12 per
group studied in Table 2, from 6 to 35 studied in Table 3 and 6 to
12 studied in Table 4. The claims of no statistically signicant eects in
Figs. 2, 3, 4 and 5 are based on the tiny numbers in Table 3, are
therefore, based on studies with very low statistical power. 3). The rst
part of the Aït-Aïssa et al. (2010) paper focused on GFAP values, a
measure of gliosis, which is a risk factor for glioma formation. The
groups studied in Fig. 4 of Aït-Aïssa et al. (2010) range from 3 to 10, so
again we have tiny numbers and the authors report that none of the
exposures, SAR= .08, = .4. or = 4 W/Kg produced statistically sig-
nicant changes according to their statistical calculations. As in the
other studies, no raw data are provided but Fig. 4 provides bar graph
information which includes median values for each of the 10 dierent
regions of the brain in these rats, control rats and also rats exposed
either pre-natally or both pre-natally and post-natally. For 5 of those
brain regions, M4, CA1, CA2, CA3 and DG, the median values are high
enough that one can see which are higher and which are lower from the
graph. It appears to this author that the median values go up from the
sham exposures to the lowest intensity (= .08), that they drop going to
the next intensity (= .4) and that they go up going to the highest in-
tensity studies (= 4). You may recall (see above) that there are certain
windows of exposure that give the highest biological response but with
both lower and higher intensities giving lower responses. It follows that
the complex apparent dose-response curve of Aït-Aïssa et al. (2010),
can be explained by these window eects. The question is whether any
such apparent changes are statistically signicant? I did, therefore a
Chi-square analysis of these data, to determine statistical signicance,
using both the only prenatal and both prenatal and postnatal exposures
(see Fig. 4 in Aït-Aïssa et al., 2010). Those data show that in 10 out of
10 cases, the median value increased going from sham to .08
(P < .002.). Similarly, in 10 out of 10 cases, the median value drops
going from .08 to .4 (P < .002). However in 8 out of 10 cases, the
median value increases going from .4 to 4 (P < .07), falling just short
of statistical signicance. The median values increased with exposure,
comparing the sham values with the values at 4 (P < .02). It follows
from this, that three of the comparisons show statistically signicant
changes, and the fourth falls just short of statistical signicance. Does
this mean that that we should conclude that Wi-Fi can cause gliosis and
thus possibly gliomas? No, but only because they did not study Wi-Fi. It
should be noted, however that the long-term eects on the brain from
pre-natal exposures may be relevant to autism causation.
4). Poulletier de Gannes et al. (2012) also suered from tiny num-
bers in their study, with 12 to 15 rats studied in each group in Fig. 1,
only 5 females in each group in Table 1, 12 to 15 rats in each group in
both Table 2 and Table 3.5). Aït-Aïssa et al. (2012) also suers from
tiny numbers of rats in the various studies. It used from 9 to 12 preg-
nant female rats in each group to attempt to assess EMFs impact of
reproduction; it used 9 to 12 juvenile rats to determine if EMFs act to
change antibody production; it used 9 to 12 young rats to determine
whether EMFs impact growth over time. These tiny numbers mean that
failure to nd statistical signicant changes has very low power to
support any inferences. 6). Aït-Aïssa et al. (2013) had similar problems
with tiny numbers, 6 to 12 in Fig. 5, 5 to 11 in Fig. 8 and 6 to 12 in
Fig. 9. 7). Poulletier de Gannes et al. (2013) also suers from tiny
numbers. Fig. 1 groups each had 12 males or females and there were
also groups of 12 studied in Table 1, Fig. 2 and Table 2. Regarding, the
authors give no information regarding statistical signicance or lack
thereof; rather they only state that the values of these groups were
similar, without providing a denition of similar. However in
comparing the values of testis weight and epididymis weight at 4 W/Kg
exposure vs sham control, they provided values for the mean and
standard error of the mean (SEM). It is usually the case that when the
mean values dier by more than 2.4 times the SEM, the dierence is
statistically signicant. Here the testis weight, comparing sham with
4 W/Kg, values diered by 3.18 times the SEM and the epididymis
weight diered by 3.40 times the SEM, each arguing strongly for sta-
tistical signicance. This raises the question of why the authors failed to
provide their P values?
An additional aw of these 7 supposed Wi-Fi studies is that they
each studied exposures of 2 h per day, 5 days per week except for one
that only studied one hour per week, 5 days per day. Given that many
people are exposed to Wi-Fi elds for 5, 6, 8 or more hours per day, this
is another factor which argues that these studies may have been set up
to minimize any eects seen.
To sum up the other aws:
1. The 6 antennae of the reverberation chamber used in 6 out of 7
studies, minimized probable eects produced through the arrange-
ment of the antennae in such a way as to greatly lower the polar-
ization of the EMFs.
2. The use of 1 mm aluminum wires to produce the reverberation re-
ections, further decreases such polarization, again lowering prob-
able eects. These structures are clearly very dierent from those
found in genuine Wi-Fi, emphasizing the point that these are not
genuine Wi-Fi studies, because of 1 and 2 here.
3. Dierences in path lengths for dierent photons, produced by re-
verberation produce substantial destructive interference.
4. Furthermore the EMFs fed into the antennae are not genuine Wi-Fi
either. It follows from this that claims that these are studies of
genuine Wi-Fi made by both the authors of these individual studies
and by Foster and Moulder (2013) are false.
5. The claims made by Foster and Moulder (2013) that there are no
eects produced are also false; the most that may be legitimately
concluded is that there is no statistically signicant evidence of ef-
fects.
6. Each of the 7 studies used only tiny numbers of animals in each
group studied, such that lack of statistical signicance, because of
the low power of these studies, drastically limits the drawing of
inferences.
7. Finally, 3 out of 7 had evidence of statistically signicant eects,
M.L. Pall 

with each of these being ignored by Foster and Moulder.
Funding
This research did not receive any specic grant from funding
agencies in the public, commercial or not-for-prot sectors.
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... To increase the bandwidth of Wi-Fi, the frequency of radio waves has to be increased, which will ultimately be dangerous for human health. Moreover, regular usage of Wi-Fi will affect human health [8][9]. ...
...  A white LED and RGB LED can convey data at a speed of 1Gbps and 3.4 Gbps respectively, which is far higher than the existing speed.  It is a free band and does not require any license  As lights are present everywhere including the street, availability of light sources is not an issue and common people can use it at a low cost by creating each light source as a channel [7,9,[24][25][26]. ...
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Every social being need communication for a better life. Exponential growth is taking place in Wi-Fi connections and data transfer now a days. The 5G technology for data transfer, Li-Fi(Light Fidelity) invented by Prof. Harald Haas in 2011 is a wireless networking technology by means of LED light using the principle of Visible Light Communication. Recent research shows that by 2022, 74zetta bytes of data will be generated. As data volume goes up exponentially and generating demand for electromagnetic spectrum, which will cause damage to human as well as animal health. In such situations, Li-Fi performs well to get data quickly and the applications of Li-Fi include hospitals, under water communication, Schools, Military operations, Business and many more. Also the situations where transmission of radio frequencies is hazardous such as chemical plants or petroleum plants, data transmission can be replaced by Li-Fi technology instead of using Wi-Fi. This paper reviews the Li-Fi technology and lists out the advantages and limitations which will help for further research.
... Most of the studies reviewed were conducted on rodents. [73] Santini et al. (2018) in their review article on the effect of RF-EMF on female fertility, did find a correlation between depletion of antral follicles and its exposure in rodents. No human studies were reported. ...
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Infertility has got to be a broadly concerned social issue these days, in which the malefactor cannot be overlooked. Numerous studies have shown that electromagnetic pulse (EMP) radiation may have seriously damaging effects on reproductive health, through nonthermal effects and oxidative stress. Molecular hydrogen, a selective hydroxyl radical scavenger, explains the protective effects against many diseases closely associated with oxidative damage, such as ionizing radiation (IR). We sought to characterize the beneficial effects of molecular hydrogen on the male reproductive system in a rodent EMP exposure model. The 8-week-old male Sprague-Dawley rats were exposed to EMP (peak intensity 1000 kV/m, pulse edge 20 ns, pulse width 200 ns, 1 Hz, and 200 pulses), with or without hydrogen-rich water. The pathological structure of the testis, the rate of apoptosis of the testis, the serum testosterone level, the sperm parameters, and the activity of the antioxidant enzymes of the testis were measured. Then, transcriptomic and untargeted metabolomic analyses were applied to uncover the underlying mechanism. Exposure to EMP increased testicular apoptosis rate and apoptosis protein level, decreased sperm viability and motility, decreased serum testosterone levels, and diminished testicular antioxidant capacity. Molecular hydrogen-alleviated damage decreased the testicular apoptosis rate and apoptosis protein level, increased sperm motility, increased serum testosterone levels, and improved antioxidative capacity. Omics results showed that molecular hydrogen has a strong influence on metabolic pathways, and EMP affects mainly oxidative phosphorylation, TNF signaling pathways, and cytokine-receptor interactions. The mechanism of molecular hydrogen’s effect may be related to the reversal of some metabolite levels. These observations warrant molecular hydrogen as an innovative approach for potential protection against EMP.
... The Panagopoulos model has been further applied and promoted by Pall [34], who has reviewed and summarised the main biological effects from RFR into seven distinct types: nervous system effects, hormonal system effects, oxidative stress damage, DNA damage, elevated levels of programmed cell death, lowered fertility, and calcium overload [35]. Pall has concluded that Each of these 7 repeatedly found Wi-Fi effects should, therefore, be considered established Wi-Fi effects (p. ...
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page:423 Big Data Analytics for Large Scale Wireless Body Area Networks; Challenges, and Applications
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Children are exposed to various kind of non-ionizan radiation in their daily life involuntarily. The potential sensitivity of developing organism to the effects of radiofrequency (RF) signals, the higher estimated specific absorption rate (SAR) values of children and greater lifetime cumulative risk raised the scientific interest for children's vulnerability to electromagnetic fields (EMFs). In modern societies, children are being exposed to EMFs in very early ages. There are many researches in scientific literature investigating the alterations of biological parameters in living organisms after EMFs. Although the international guidelines did not report definite, convincing data about the causality, there are unignorable amount of studies indicating the increased risk of cancer, hematologic effects and cognitive impairment. Although they are less in amount; growing number of studies reveal the impacts on metabolism and endocrine function. Reproductive system and growth look like the most challenging fields. However there are also some concerns on detrimental effects of EMFs on thyroid functions, adrenal hormones, glucose homeostasis and melatonin levels. It is not easy to conduct a study investigating the effects of EMFs on a fetus or child due to ethical issues. Hence, the studies are usually performed on virtual models or animals. Although the results are conflicting and cannot be totally matched with humans; there is growing evidence to distress us about the threats of EMF on children.
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Mobile phone usage has become an integral part of our lives. However, the effects of the radiofrequency electromagnetic radiation (RF-EMR) emitted by these devices on biological systems and specifically the reproductive systems are currently under active debate. A fundamental hindrance to the current debate is that there is no clear mechanism of how such non-ionising radiation influences biological systems. Therefore, we explored the documented impacts of RF-EMR on the male reproductive system and considered any common observations that could provide insights on a potential mechanism. Among a total of 27 studies investigating the effects of RF-EMR on the male reproductive system, negative consequences of exposure were reported in 21. Within these 21 studies, 11 of the 15 that investigated sperm motility reported significant declines, 7 of 7 that measured the production of reactive oxygen species documented elevated levels and 4 of 5 studies that probed for DNA damage highlighted increased damage, due to RF-EMR exposure. Associated with this, RF-EMR treatment reduced antioxidant levels in 6 of 6 studies that studied this phenomenon, while consequences of RF-EMR were successfully ameliorated with the supplementation of antioxidants in all 3 studies that carried out these experiments. In light of this, we envisage a two-step mechanism whereby RF-EMR is able to induce mitochondrial dysfunction leading to elevated ROS production. A continued focus on research which aims to shed light on the biological effects of RF-EMR will allow us to test and assess this proposed mechanism in a variety of cell types.