Wi-Fi is an important threat to human health #WakeUp 😈💩👎

Wi-Fi is an important threat to human health

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https://www.researchgate.net/publication/323998588_Wi-Fi_is_an_important_threat_to_human_health

Article (PDF Available) in Environmental Research 164:405-416 · March 2018 with 5,507 Reads 

DOI: 10.1016/j.envres.2018.01.035Cite this publication

Martin L Pall

36.15

Washington State University

Abstract

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.

Various pathways of action by which EMF VGCC activation can produce effects produced by EMF exposure (modified, with permission from Pall, 2015b).

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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 field (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 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 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

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.

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 effects. This paper is not focused on anec-

dotal reports but rather on 23 controlled, scientific studies of such

health-related effects in animals, cells including human cells in culture

and in human beings (Table 1).

Each of the effects 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)findings 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 effects which have been

found by multiple Wi-Fi studies and have been previously confirmed by

non-thermal exposures to other microwave frequency EMFs. The 1971/

72 U.S. Office 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

☆

Decreased spermatogenesis. Glaser (1971) also reported a total of 35

neurological/neuropsychiatric effects of non-thermal EMF exposures,

including 9 central nervous system effects, 4 autonomic system effects,

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 different citations each

reporting various types of non-thermal microwave frequency EMF ef-

fects. Consequently, the existence of 5 types of Wi-Fi effects, each

supported by multiple Wi-Fi studies were already well-supported as

general non-thermal EMF effects back in 1971, 47 years ago: effects on

the testis and sperm production, neurological/neuropsychiatric effects,

endocrine effects, 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 effects: changes in testis structure/function,

neurological effects, increased cell death (possibly via apoptosis) and

endocrine effects. Findings from our longer list of EMF reviews of non-

thermal effects are summarized in Table 2.

Each of the 7 Wi-Fi effects found in 2–11 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 effects as general microwave frequency

effects (Table 2). These are, therefore, general effects produced by such

EMFs. Each of these 7 repeatedly found Wi-Fi effects should, therefore,

be considered established Wi-Fi effects. The author is not aware of any

genuine Wi-Fi studies on these 7 effects that reported no statistically

significant evidence of effect.

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 effects, as discussed below;

apoptosis has central roles in neurodegenerative diseases; the neu-

ropsychiatric effects 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 effect 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 clarified, 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 effect, 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 effects, 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 effects.

2. Wi-Fi and other wireless communication EMFs are pulsed,

leading to larger biological impacts; These EMFs are also

polarized, also producing larger effects; 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 Effects

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 effects 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 artificial EMFs are polarized and this makes ar-

tificial 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

specific intensity ranges produce maximum biological effects, which

drop offgoing 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 effects are often cumulative and irreversible

One question that has been raised about the effects of these low-

intensity EMFs producing biological effects is are they cumulative? I am

aware of three different types of evidence for cumulative effects. Three

of the human occupational exposure studies from the 1970's reviewed

in Raines (1981), showed that effects 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 1–2 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 different 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 effects. 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 fifth

possible litter were performed under conditions of no EMF exposure,

but the fertility effects were not reversed; therefore fertility effects may

become irreversible, suggesting a similar pattern to the brain related

effects 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 effects as brain damage

to animal brains, neuropsychiatric effects in humans, reproductive

dysfunction in mice and mutational effects, are each cumulative. Those

same effects 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, coffee 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 effects 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 effects 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 effects may be among the more difficult ones for us to attribute to

EMF exposure. We are much more aware of effects that occur rapidly

than those that take months or years before they become readily ap-

parent.

Table 2

Reviews of Non-thermal Effects of Microwave Frequency EMFs Similar to Those Found in Multiple Wi-Fi Studies.

Non-thermal effects 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 effects 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 effects 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 effects 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 effects, such that

young people are more sensitive to EMF effects. It follows from these

various findings 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 scientific literature (Pall, 2013). That study showed that in 24

different studies [there are now a total of 26 Pall (2015b)], effects of

low-intensity EMFs, including microwave frequency and also extremely

low frequency EMFs, static electrical fields and static magnetic fields

could be blocked by calcium channel blockers, drugs that are specific

for blocking voltage-gated calcium channels (VGCCs). There were 5

different types of calcium channel blockers used in these studies, each

thought to be highly specific, each structurally distinct and each

binding to a different site on the VGCCs. In studies where multiple ef-

fects were studied, all studied effects were blocked or greatly lowered

by calcium channel blockers. These studies show that EMFs produce

diverse non-thermal effects 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 effects on oxidative stress, cellular DNA

damage and calcium signaling (Pall, 2016a). Furthermore, many dif-

ferent effects shown to be produced in repeated studies by EMF ex-

posures, including the effects discussed above, can be produced by

downstream effects 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 effects 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 findings 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 fish, 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 effects. 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 specific 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 influx of both sodium and calcium into the

cell via the voltage-gated channels following EMF exposure. Sodium

influx, 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 influx into plants to produce similar

EMF-induced responses (Pall, 2016a). One can put those observations

together with the powerful findings 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 finding that should be discussed here. In a

study published by Pilla (2012), it was found that pulsed EMFs pro-

duced an “instantaneous”increase 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 diffused 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 effect, 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 influx, seem to be much

more important in producing EMF effects 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 influxes upon channel activation. 2. [Ca2 + ]i

produces many important regulatory effects, such that over activation

of those effects can have very large pathophysiological consequences. 3.

Sustained elevation of [Ca2+]i produces major cell damage.

6. How can the Wi-Fi effects be produced by EMF triggered VGCC

activation?

Can the various effects produced by Wi-Fi and by other microwave

frequency EMFs be produced by the downstream effects of VGCC acti-

vation? In order to determine that, one needs to consider the various

downstream effects of VGCC activation, summarized in Fig. 1 and how

these are likely to produce each of the effects 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 effects 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 effects 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 effects 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 inflammation. 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

effects 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 effects 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 simplified.

There is one other finding, not related to the Wi-Fi findings, 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

effects. 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 effects.

The first 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 effects. However, there are no specific 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 effects produced by EMF exposure (modified, with permission from Pall, 2015b).

M.L. Pall 

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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 specific 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 effects? 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 fixed 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 flow. While I don’t 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 specific 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 effects. 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 Effects of Wi-Fi and Other EMFs Can Be Produced by VGCC Activation.

EMF effect 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 confirming 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

oversimplified. 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 effects 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 different 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

effects of EMF exposures is to increase hormone release and to raise, therefore, hormone levels. However many

hormone systems become “exhausted”as a consequence of chronic EMF exposures. The mechanism of exhaustion

is still uncertain, but it may involve oxidative stress and inflammation.

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 effects that have been documented.

Belyaev (2015) discusses microwave hearing in this context. He

discusses the findings showing that people can hear microwave fields

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 effects, 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 findings 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 fit 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 effects 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 efficiently 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 effects 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 specific or general biological effects? 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 specific 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 specific variable have a causal role in determining a

specific response. But these two approaches can be used when specific

proteins have specific 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 effects.

8. Two other models for producing non-thermal effects

With the possible exception of the electrosoliton model, the author

does not find any of the models discussed by Dr. Belyaev (2015) to have

substantial evidence for roles in producing EMF effects. 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 effects produced by certain

specific 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 effects involved a very specific 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 effect. This finding strongly suggests that the calcium cyclotron

resonance can feed Ca

2+

ions into the VGCCs, thus increasing the flow

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 effects. The finding that only very specific calcium cyclotron

resonance frequencies produce these effects 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 field. 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) first proposed a

model of how such a mechanism might act. He proposed that magnetite

particles may be tethered through a microtubule and/or microfilament

or perhaps other fibers to a mechanosensitive channel, such that tiny

magnetic forces could open the mechanosensitive channels, allowing

cation flow 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 flow into cells. Hsu

et al. (2007) suggested that such magnetite particles were linked in

honeybees to an undefined calcium channel, such that magnetic field

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 specific neurons in C.

elegans which may be geomagnetic sensory neurons, very low intensity

geomagnetic fields could produce increases in [Ca2+]i in those specific

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 findings on neurons found in the tri-

geminal nerve of birds, where magnetic fields as low as 200 nT can

activate specific neurons. Trains of action potentials are produced by

magnetic fields, plateauing in the region of 20–100 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 effects. 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 specific situations. The calcium

cyclotron resonance mechanism only acts with a few specific fre-

quencies in the extremely low frequency range. The magnetoreception

mechanism only acts, as far as one can tell, on detecting the weak

geomagnetic fields and only acts, as far as one can tell, in certain spe-

cific 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 fields and static

magnetic fields. Because static magnetic fields 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 fields.

These static magnetic fields, activating the VGCCs can be relative low

intensity but probably must be much higher intensity than the extra-

ordinarily weak geomagnetic fields. The reader is referred to Lu et al.

(2015) for empirical information from an important static magnetic

field study, where those static magnetic fields 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 effects of Wi- Fi. The first 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 specific ab-

sorption rate (SAR) values, a measure of heating. Because it is now

established, as discussed above that thermal effects are not the relevant

mechanism of non-thermal effects and that VGCC activation is the main

mechanism of such effects, this whole section is irrelevant. Foster and

Moulder (2013) discuss the issue of biological effects, praising 7 studies

listed in table 4 of their paper as having “well-characterized exposure

systems”of well defined SARS values, reporting that there were no

effects 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 first two studies come

from one research group and the other five 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, artificial EMFs are polarized with the polarization producing

much larger biological effects 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 effects. 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 reflections 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° different po-

larization in each of the four possible directions. This produces a field

that is more like a non-polarized EMF rather than the usual polarized

artificial EMF. This move toward non-polarization is further ex-

acerbated by the aluminum wire reverberation system whose reflec-

tions will generate vast numbers of reflections of different polarity, like

a non-polarized EMF. The consequences of this is that the structure of

this exposure system is clearly very different from that seen in Wi-Fi or

any other artificially produced EMF that we may be exposed to, with

biological effects produced via electrical forces being vastly less. Con-

sequently this exposure system is not only inherently different 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 different photons reaching a specific point in the ex-

posed tissue, will often be quite different from each other, such that the

phase of the EMFs produced will also be quite different 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 effect and the possible difference between pre-

dicted exposure and actual exposure were considered in an earlier

study.

Vian et al. (2006), using a different 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 findings 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 different exposure system, that of

Ardoino et al. (2005) where the vast majority of the exposure is pro-

duced from reflections offa long cylindrical surface in a TEM cell,

where the curvature of the cylinder will also produce a largely non-

polarized EMF and different 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 effects

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 effects and ask whether the EMFs fed into the

antennae have pulsation patterns similar or different 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 effects 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 effects 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 differing from

genuine Wi-Fi in three different ways: the antenna locations produce a

substantial difference from genuine Wi-Fi regarding EMF polarization

and this is further exacerbated by the effects of the aluminum mesh

reverberation producing further lowering of any polarization; differ-

ences in path lengths of different photons produce substantial de-

structive interference; the initial EMF fed into the antennae differs

substantially from genuine Wi-Fi, with the main concern here being due

to the issue of pulsation patterns and biological effects.

Let's shift now to the claim made by Foster and Moulder (2013) that

there were no effects 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 significance tests is that there no difference between two observed

groups because the null test is not statistically significant, in that P is

greater that the cutofffor declaring statistical significance (again,

usually .05). This interpretation confuses a descriptive issue (whether

two observed groups differ) with an inference about the super-

population. The significance test refers only to the superpopulation, not

the observed groups. To say that the difference is not statistically sig-

nificant 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 effect”that 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 significant

differences.

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 flaws that follow. 1). Laudisi et al. (2012) finds in Table 2, that

two T cell populations are statistically significantly different in pre-

natally exposed mice vs sham controls: DP and CD4SP cells are sig-

nificantly affected by exposure in mice at 26 weeks after birth; CD4SP

cells are affected 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 effects 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 significant effects; 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 significant effects 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 first

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-

nificant 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 different

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 effects. The question is whether any

such apparent changes are statistically significant? I did, therefore a

Chi-square analysis of these data, to determine statistical significance,

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 significance. 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 significant

changes, and the fourth falls just short of statistical significance. 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 effects on the brain from

pre-natal exposures may be relevant to autism causation.

4). Poulletier de Gannes et al. (2012) also suffered 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 suffers 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 find statistical significant 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 suffers 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 significance or lack

thereof; rather they only state that the values of these groups were

“similar”, without providing a definition 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 differ by more than 2.4 times the SEM, the difference is

statistically significant. Here the testis weight, comparing sham with

4 W/Kg, values differed by 3.18 times the SEM and the epididymis

weight differed by 3.40 times the SEM, each arguing strongly for sta-

tistical significance. This raises the question of why the authors failed to

provide their P values?

An additional flaw 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 fields 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 effects seen.

To sum up the other flaws:

1. The 6 antennae of the reverberation chamber used in 6 out of 7

studies, minimized probable effects 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-

flections, further decreases such polarization, again lowering prob-

able effects. These structures are clearly very different 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. Differences in path lengths for different 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

effects produced are also false; the most that may be legitimately

concluded is that there is no statistically significant 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 significance, because of

the low power of these studies, drastically limits the drawing of

inferences.

7. Finally, 3 out of 7 had evidence of statistically significant effects,

M.L. Pall 



with each of these being ignored by Foster and Moulder.

Funding

This research did not receive any specific grant from funding

agencies in the public, commercial or not-for-profit sectors.

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M.L. Pall 

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Citations (21)

References (126)

... In addition to the aforementioned studies, the increasing use of wireless Wi-Fi networks has prompted researchers to develop personal exposure studies to RF-EMF from this frequency band [27]. Among them, there is a summary on the state of the investigation of the possible effects of RF-EMF from the Wi-Fi network on public health [28], a review that shows seven effects of Wi-Fi in animals and human cells [29,30], and the results of a study conducted in primary and secondary schools [31]. The conclusions indicate that the registered values are below the exposure guidelines allowed by current international regulations [7]. ...

... When Pall's work was published [30], whose title is "Wi-Fi is an Important Threat to Human Health" it was interesting and worrisome, and therefore it motivated us to write a comment [29]. We really wanted to check if people using a Wi-Fi network are under threat to their health. ...

... Despite the results obtained in these studies, a large part of the population remains concerned as diseases of unknown etiology appear [53][54][55][56], which is why it is necessary to continue researching to try to respond to these concerns. When Pall's work was published [30], whose title is "Wi-Fi is an Important Threat to Human Health" it was interesting and worrisome, and therefore it motivated us to write a comment [29]. We really wanted to check if people using a Wi-Fi network are under threat to their health. ...

Georeferencing of Personal Exposure to Radiofrequency Electromagnetic Fields from Wi-Fi in a University Area

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Hussein Al-Taani

Enrique Arribas

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... Several governments have already issued caution especially for pregnant women and children while using mobile phones whereas many cancer institutes have called for further investigation. There are many strong evidence to prove that cell phone usage poses a cancer riskfor children and thus Russia, India, UK are discouraging use of mobile phones by children and France has banned marketing of cell phones to children (Kim, 2016;Prasad et al., 2017;Pall, 2018). ...

... "Massive increase in radiation in the environment due to these towers is associated with increase in the incidence of diseases such as asthma, learning disabilities, anxiety disorders, attention deficit disorder (ADD), autism, multiple sclerosis, amyotrophic lateral sclerosis (ALS), epilepsy, fibromyalgia, chronic fatigue syndrome, cataracts, hypothyroidism, diabetes, malignant melanoma, testicular cancer, heart attacks and strokes". Radiation to which a person is exposed during a phone call is 10 times morethan that on exposure to mobile towers and more adverse is the Wi-Fi radiation as mere moving through Wi-Fi enabled area equals radiation encountered on a 20 minutes phonecall (Anthony et al., 2017;Pall, 2018). ...

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Brijender Bhushan

Ankit Guleria

Pawitar Dulari

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... Nevertheless, this is a complex topic that is difficult to study both because of the nature of the subject matter and because of powerful financial interests that attempt to minimize any evidence of harm (Alster, 2015;Hertsgaard and Dowie, 2018). Some studies do in fact provide evidence that RF radiation could have negative effects on humans or other organisms (e.g., Volkow et al., 2011;Carlberg and Hardell, 2017;Zothansiama et al., 2017;Pall, 2018). Thus, as Schulson (2018) notes, "it's sobering to think of a world where the public is simply assured that everything is definitely okay-at least until a consensus forms and enough scientists get together and tell them that it's not. ...

... The most obvious problem is that it makes some highly questionable claims. For example, she asserts that testicles are "totally unharmed by phone radiation" (Chodosh, 2017), whereas the available evidence suggests that this is probably not true (Adams et al., 2014;Pall, 2018). Her claim that people could safely duct-tape their phone to their face, while clever, is also misleading. ...

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... A vast literature published over the past sixty years shows adverse effects from wireless radiation applied in isolation or as part of a combination with other toxic stimuli. Extensive reviews of wireless radiation-induced biological and health effects have been published (Kostoff andLau, 2013, 2017;Belpomme et al., 2018;Desai et al., 2009;Di Ciaula, 2018;Doyon and Johansson, 2017;Havas, 2017;Kaplan et al., 2016;Lerchl et al., 2015;Levitt and Lai, 2010;Miller et al., 2019;Pall, 2016Pall, , 2018Panagopoulos, 2019;Panagopoulos et al., 2015;Russell, 2018;Sage and Burgio, 2018;van Rongen et al., 2009;Yakymenko et al., 2016;Bioinitiative, 2012). In aggregate, for the high frequency (radiofrequency-RF) part of the spectrum, these reviews show that RF radiation below the FCC guidelines can result in: ...

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... The results of a recent study [34] showed that PTZ-induced seizures were resulted in dark neuron production in the hippocampal regions, as observed in previous studies. As well known in literature, Wi-Fi has important negative effects on human health [35,36]. On the basis of these evaluations, there are plenty of studies about long term exposure of Wi-Fi (2.45 GHz) on rat and mice [37][38][39][40][41]. Shahin et al. (2015) investigated the effect of short (15 days) and longterm (30 and 60 days) at a low-level of 2.45 GHz at MW radiation exposure on hippocampus with special reference to spatial learning and memory and its underlying mechanism in Swiss strain male mice, Mus musculus. ...

Wi-Fi decreases melatonin protective effect and increases hippocampal neuronal damage in pentylenetetrazole induced model seizures in rats

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