![Mechanisms of action for microwave EMFs leading to diverse pathophysiological responses and therapeutic responses.
Microwave/lower frequency electromagnetic fields (EMFs) act to stimulate voltage-gated calcium channels (VGCCs), increasing levels of intracellular calcium [Ca2+]i. Elevated [Ca2+]i increases nitric oxide (NO) synthesis which can act along two pathways. The NO signaling pathway, raises cyclic GMP (cGMP) levels and G-kinase activity, producing therapeutic effects. In the other pathway of action of NO reacts with superoxide to form peroxynitrite [ONOO(0)], which either before or after reaction with carbon dioxide (CO2) can break down to form free radicals, producing oxidative/nitrosative stress. The excessive calcium signaling produced by [Ca2+]i and the peroxynitrite/free radical/oxidative stress pathway each contribute to pathophysiological responses.](https://www.researchgate.net/profile/Martin-Pall/publication/275052209/figure/fig1/AS:11431281120126032@1676382516540/Mechanisms-of-action-for-microwave-EMFs-leading-to-diverse-pathophysiological-responses_Q320.jpg)
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Rev Environ Health 2015; 30(2): 99–116
*Corresponding author: Martin L. Pall, Washington State University,
638 NE 41st Ave., Portland, OR 97232-3312, USA,
E-mail: martin_pall@wsu.edu
Open Access
Martin L. Pall*
Scientific evidence contradicts findings and
assumptions of Canadian Safety Panel 6: microwaves
act through voltage-gated calcium channel activation
to induce biological impacts at non-thermal levels,
supporting a paradigm shift for microwave/lower
frequency electromagnetic field action
Abstract: This review considers a paradigm shift on
microwave electromagnetic field (EMF) action from
only thermal effects to action via voltage-gated calcium
channel (VGCC) activation. Microwave/lower frequency
EMFs were shown in two dozen studies to act via VGCC
activation because all effects studied were blocked by
calcium channel blockers. This mode of action was fur-
ther supported by hundreds of studies showing micro-
wave changes in calcium fluxes and intracellular calcium
[Ca2+]i signaling. The biophysical properties of VGCCs/
similar channels make them particularly sensitive to
low intensity, non-thermal EMF exposures. Non-thermal
studies have shown that in most cases pulsed fields are
more active than are non-pulsed fields and that expo-
sures within certain intensity windows have much large
biological effects than do either lower or higher inten-
sity exposures; these are both consistent with a VGCC
role but inconsistent with only a heating/thermal role.
Downstream effects of VGCC activation include calcium
signaling, elevated nitric oxide (NO), NO signaling, per-
oxynitrite, free radical formation, and oxidative stress.
Downstream effects explain repeatedly reported bio-
logical responses to non-thermal exposures: oxidative
stress; single and double strand breaks in cellular DNA;
cancer; male and female infertility; lowered melatonin/
sleep disruption; cardiac changes including tachycardia,
arrhythmia, and sudden cardiac death; diverse neuropsy-
chiatric effects including depression; and therapeutic
effects. Non-VGCC non-thermal mechanisms may occur,
but none have been shown to have effects in mammals.
Biologically relevant safety standards can be developed
through studies of cell lines/cell cultures with high levels
of different VGCCs, measuring their responses to different
EMF exposures. The 2014 Canadian Report by a panel of
experts only recognizes thermal effects regarding safety
standards for non-ionizing radiation exposures. Its posi-
tion is therefore contradicted by each of the observations
above. The Report is assessed here in several ways includ-
ing through Karl Popper’s assessment of strength of evi-
dence. Popper argues that the strongest type of evidence
is evidence that falsifies a theory; second strongest is a
test of “risky prediction”; the weakest confirms a predic-
tion that the theory could be correct but in no way rules
out alternative theories. All of the evidence supporting
the Report’s conclusion that only thermal effects need
be considered are of the weakest type, confirming pre-
diction but not ruling out alternatives. In contrast, there
are thousands of studies apparently falsifying their posi-
tion. The Report argues that there are no biophysically
viable mechanisms for non-thermal effects (shown to be
false, see above). It claims that there are many “incon-
sistencies” in the literature causing them to throw out
large numbers of studies; however, the one area where
it apparently documents this claim, that of genotoxic-
ity, shows no inconsistencies; rather it shows that vari-
ous cell types, fields and end points produce different
responses, as should be expected. The Report claims
that cataract formation is produced by thermal effects
but ignores studies falsifying this claim and also studies
showing [Ca2+]i and VGCC roles. It is time for a paradigm
shift away from only thermal effects toward VGCC activa-
tion and consequent downstream effects.
©2015, Martin L. Pall, published by De Gruyter.
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.
100 Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6
Keywords: calcium and nitric oxide signaling; calcium
channel blockers; low level microwave/radiofrequency
radiation; oxidative and nitrosative stress; peroxynitrite.
DOI 10.1515/reveh-2015-0001
Received January 8, 2015; accepted March 10, 2015; previously pub-
lished online April 16, 2015
Introduction
There has been a literature reporting various non-thermal
effects of microwave/radiofrequency radiation exposures
starting with the Soviet literature in the 1950s. Subse-
quently, there have been thousands of international
published studies reporting non-thermal or what are
sometimes called micro-thermal effects producing thera-
peutic responses, changes in calcium fluxes and signal-
ing, increased oxidative stress, and a wide variety other
health-related responses in humans and animal models.
Nevertheless, there has been a series of medical
reports, arguing that only thermal effects need be con-
sidered when setting guidelines or safety standards for
microwave electromagnetic field (EMF) exposures. These
have been based mainly on two types of arguments:
– That there cannot be any biophysically viable mecha-
nism for any such non-thermal effects and therefore
that reports of such effects should be viewed with
great skepticism.
– That there are many “conflicts” or “inconsistencies”
in the literature which according to these reports, jus-
tify rejection of the various thousands of publications
showing apparent non-thermal effects.
The focus of this review is to consider whether it is time for a
“paradigm shift” away from strictly thermal effects toward
non-thermal effects. Specifically, it is focused on the recent
finding that most, possibly all non-thermal effects can be
produced by microwave activation of voltage-gated calcium
channels (VGCCs). It is also focused on the 2014 Report of
the Canadian Panel of Experts on Safety Code 6 as the most
recent and therefore up-to-date summary of the evidence
supporting the strictly thermal point of view.
EMFs act via stimulation of voltage-
gated calcium channels (VGCCs)
Calcium provides an essential role in cell function,
being normally maintained at very low, circa 10–7 M
intracellular levels, but also with transient intracellular
calcium ([Ca2+]i) increases being used for widespread
and important regulatory signaling. A recent review (1),
noted that in two dozen studies, calcium channel block-
ing drugs block a wide range of electromagnetic field
(EMF) effects on cells and organisms by blocking voltage-
gated calcium channels (VGCCs which are also known
as voltage-operated, voltage-dependent or voltage-
regulated calcium channels). In most but not all cases,
L-type VGCCs were studied, but T-type, N-type and P/Q-
type channels can also have roles, as shown by channel
blockers specific for these other channels (1). In each
of these studies, calcium channel blockers blocked or
greatly lowered each of the responses studied, showing
that VGCC activation is required for low intensity fields
to produce a wide range of responses (1). Each of these
channel blockers is thought to be highly specific, such
that with two different types of L-type blockers being
used that act at different sites on the L-type VGCCs and
also one each of the T-type, N-type and P/Q type block-
ers being used, with each showing activity in blocking or
greatly lowering EMF responses, it is highly unlikely that
a non-VGCC mechanism is involved here.
VGCC activation is thought to act mainly by increas-
ing [Ca2+]i. Other considerations also support VGCCs as
a major EMF target, accounting for numerous biological
impacts of microwave exposures (1–3) at levels not pro-
ducing substantial changes in temperature.
Pilla published a very important paper, suggesting in
retrospect that these low-level fields directly activate the
VGCCs (4, see also 1–3). He showed that cells in culture
when exposed to a low intensity pulsed microwave field,
produce an almost instantaneous Ca2+/calmodulin-
dependent increase in nitric oxide (NO), occurring in < 5 s.
The NO increase is produced by the [Ca2+]i activating the
two Ca2+/calmodulin-dependent NO synthases, which can
occur almost instantaneously. These results show that the
[Ca2+]i increases must also occur almost instantaneously,
providing strong evidence that the VGCCs are directly acti-
vated by the low intensity field in this study. The known
properties of the VGCCs are discussed below, properties
that are expected to make them particularly susceptible to
activation by such low intensity fields.
In addition to calcium channel blocker studies, the
important role of VGCC activation for the biological effects
of microwave radiation at levels that do not produce meas-
ured changes in temperature is also supported by a large
number of studies, some of which were reviewed earlier
(5,6), showing that low level microwave EMF exposures
lead to measured changes in calcium signaling and/or
calcium fluxes consistent with VGCC activation. There are
Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6101
also hundreds of studies of oxidative stress responses to
low intensity field exposures, which can also be produced
by downstream effects of increased [Ca2+]i (1–3). The mode
of microwave action via VGCC activation also confirms
earlier predictions of Panagopoulos etal. (7, 8) that EMFs
may act via voltage-gated ion channel activation. The
whole issue of the biophysics of VGCCs and other voltage-
gated ion channels is discussed in some detail below.
Various frequencies, intensities and pulse patterns of
EMFs act via VGCC activation (1), including extremely low
frequency fields of 50 or 60Hz electrical wiring, micro-
wave frequency EMFs also referred to as radiofrequency
(RF), very short “nanosecond” pulses, and even static
electric or magnetic fields. Given recent global increases
in exposures to microwave/RF EMFs, the findings for
microwave EMFs create the most concerns for both human
and environmental health.
We are therefore in a situation where the paradigm of
EMF action focused solely on heating (9–13), should be
replaced by one based on VGCC activation of microwave
and other EMFs (1–3).
In addition to impacts of EMFs directly involving VGCCs,
there are a number of other related mechanisms which
should be explored. For instance, Pilla reviewed 2 studies
in which microwave EMFs increased apparent calmodulin
activation (14). Calmodulin is regulated by [Ca2+]i such that
calmodulin activation may act along with VGCC activation
in two related pathways of action discussed below.
Three other types of observations
that contradict the assumptions of
current safety standards
Current safety standards are based on the assumption that
all important biological effects of microwave and lower
frequency EMFs are due to tissue heating (thermal effects)
and that specific absorption rates (SARs) of EMFs are
therefore a measure of their ability to produce all impor-
tant biological effects. While the VGCC studies, discussed
above clearly invalidate that assumption, there are three
other distinct types of observations that also contradict
that assumption. As discussed below, an extensive scien-
tific literature reports biological microwave EMF effects
at exposure levels well within safety standards and that
therefore should not occur according to current safety
standards. Two other types of falsifying evidence are the
findings that pulsed fields are often much more biologi-
cally active than non-pulsed fields and that certain inten-
sity windows of exposure are more biologically active than
are exposures of both lower and higher intensities. These
two are each discussed in some detail immediately below.
It has been known for well over 30years that pulsed
microwave fields are often much more biologically active
than are continuous non-pulsed fields. This was shown,
for example, by Seaman and Wachtel in studies of micro-
wave exposures of Aplysia pacemaker cells (15). Pacemaker
cells have a very high density of VGCCs, suggesting that
the pulsed microwave exposures may in this study act via
VGCC activation. This was shown by Bassett etal. (16) and
by Pilla (17) both in 1974 studies of augmentation of bone
repair, that pulsed field microwaves were much more active
than continuous field microwave exposures. Both Baran-
ski (18) and Czerski (19) showed that microwave pulsed
field exposures were more active than non-pulsed fields in
terms of their impact on blood forming cells. Micro pulsed
field exposures were also more effective than non-pulsed
continuous wave (CW) fields in producing a breakdown of
the blood-brain barrier (20). Adey’s review (21) stated that
“There is evidence of interactions with radio and micro-
wave fields pulse-modulated at higher frequencies from
500 to 1500Hz and an absence of similar effects with CW
fields of the same average power density at the same carrier
frequency.” Several other studies are cited in the Adey (21)
review documenting higher biological activity of pulsed
fields than non-pulsed CW fields at identical power levels.
A recent study showing that pulsed microwave EMFs acted
via activation of L-type VGCCs (22) suggests that all these
inconsistencies of the pulsed field findings with any heating
mechanism may be due to their action in VGCC activation.
More than four decades ago, the biological impact of
non-thermal levels of pulsed fields was sufficiently well
documented that it became the basis for a number of
therapeutic applications of microwave pulses. Therapies
currently employed include a wide range of bone growth
and orthopedic rehabilitation regimens as well as some
applications to enhance the uptake of chemotherapeu-
tic agents (14). These numerous therapeutic effects are
well established to be non-thermal and operate through
increased levels of [Ca2+]i and nitric oxide (NO) signaling
(2, 14). The medical use of these pulsed fields provides
therefore prima facie evidence that such fields are often
more active in VGCC activation than are non-pulsed fields.
The greater biological activity of pulsed field expo-
sures were sufficiently well documented 30–48years ago,
such that it influenced safety standards of the 1960s and
1970s. For example, the Canadian Standards Association
48years ago in 1966, adopted lower standards [see Table 2
in ref. (23)] for occupational exposure to pulsed field expo-
sures (1 mWhr/cm2, limited to 6min exposure) in contrast
to those for continuous, that is non-pulsed exposures
102 Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6
(10mW/cm2, for which there was no time limitation). In
1974, in the United States, the American National Stand-
ards Institute (ANSI) adopted essentially identical stand-
ards as had Canada for occupational pulsed field and
non-pulsed field exposure (23). In 1970, the Czechoslo-
vakian government adopted more stringent occupational
and general public standards for pulsed field exposures
vs non-pulsed field exposures (23). Pulsed fields are, of
course, produced by any type of wireless communication
device since it is the pattern of pulsations that conveys the
information. Different devices often use different types of
pulsation patterns. However, we do not know how biologi-
cally active the different pulsation patterns are, because
this has not been systematically studied. As a result, we
cannot rationally compare the dangers of one device vs
another.
Furthermore, Barrie Trower, a retired military intel-
ligence expert from the United Kingdom, has stated that
classified research indicates that different wavelengths
vary in their biological activities as well. He reports that
the specific details about the biological impacts of vari-
ations in pulsed electromagnetic fields are classified by
multiple countries because of “national security”. Thus
much of what research appears to have been done in this
field remains unavailable to decision makers charged with
setting standards on such devices that emit pulsed elec-
tromagnetic fields.
It has been shown that there can be intensity
“windows” where biological activity is greater than
at intensities both higher and lower than the window
intensity (24–32). This again argues against a heating
mechanism as there are no known thermal dose-response
curves with similar windows. In addition, these window
effects are also found at levels where there is extremely
low heating. For example, Blackman etal. (28) state that
“Because of the extremely small increments of tempera-
ture associated with positive findings [less that 4 × 10(–4)
degrees C], and the existence of more than one productive
absorption rate (“window”), a solely thermal explanation
appears extremely unlikely”. It is (31) stated that “Since
there was no detectable temperature increase during
exposures, the recorded effects are considered non-ther-
mal”. The suggested mechanism (31) may involve a role of
voltage-gated ion channels such that “the action of exter-
nal EMF on cells is dependent on irregular gating of mem-
brane electrosensitive ion channels whenever a force on
the channel sensors exceeds the force exerted on them by
a change in the membrane potential of about 30mV which
is necessary to gate the channel normally. If in some kind
of cells there is an upper limit for this value of mem-
brane potential change, then the channel would be gated
whenever the force exerted on its sensors is within this
‘window’”. Five of these studies show effects on [Ca2+]
i fluxes (24–28), consistent with possible roles of VGCCs.
These studies provide strong evidence that these window
effects occur at levels where there is either no measured
change in temperature or extremely low heating.
Perhaps the strongest evidence for non-thermal effects
of EMFs comes from studies on animal female and human
male reproduction. This literature indicates that sperm
exposed to microwave radiation emitted by approved
mobile phones die three times faster and develop sig-
nificantly more damage to their mitochondrial DNA (33).
Studies of pregnant mice, rats and rabbits report that
prenatally exposed offspring develop significantly more
damage to their eyes, skin and liver (33) with hippocam-
pus and pyramidal cell formation are impaired as well.
In summary, four distinct types of evidence provide
contradictory information about the basic assumption
underlying current US, Canadian and International Com-
mission on Non-Ionizing Radiation Protection (ICNIRP)
safety standards that non-thermal effects do not exist:
Microwave and other lower frequency EMFs act via VGCC
activation rather than by heating; there are numer-
ous papers in the scientific literature reporting biologi-
cal effects with exposures well within safety standards
where substantial heating cannot occur. Moreover, pulsed
fields are, in most cases, more biologically active than
non-pulsed fields that produce equal heating; windows
of exposure intensities occur which are more active than
both higher and lower exposures of the same fields. While,
in general, lower intensities are safer than higher inten-
sities, this “window” effect shows that there are some
major, biologically and medically important exceptions
to this pattern. The pulsed field effects and the window
effects make it impossible to currently predict biological
activity without doing actual measurements of biological
activity of specific devices at specific exposure intensities.
The question of how to best approach and evaluate such
biological effects is discussed below.
The properties of VGCCs and other
voltage-gated ion channels may
make them uniquely susceptible to
low intensity MF activation
There has been an argument repeatedly put forth that
there cannot be a biophysically viable mechanism for
low intensity, apparently non-thermal effects. This claim
Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6103
is argued as follows [see Sheppard etal., ref. (34)]: While
they acknowledge that EMFs can exert forces on charged
groups, they argue that weak EMFs produce only weak
forces that are less than are exerted by thermal motion
produced at normal body temperature. They argue there-
fore that the only effects that can be produced by weak
EMFs would be dwarfed by a high background noise
created by random thermal motion. One of the problems
with the Sheppard argument comes from a consideration
of the structure of the voltage-gated ion channels and
how these channels detect electrical changes, which may
lead to opening the channel. The structure of the alpha-1
subunit containing the channel has been modeled and
discussed (35–38).
What can be seen is that there are four similar domains
in this protein, with each domain containing six transmem-
brane alpha helixes in it. These four domains are thought
to have been produced evolutionarily by two tandem dupli-
cations, starting with a gene encoding a protein with one
such domain. The fourth helix in each domain contains
five positively charged amino acid side chains which col-
lectively make up the voltage sensor (37, 38). It is thought
that 20 (4 × 5) charges make up the voltage sensor, each of
which must be pushed in approximately the same direc-
tion (and the right direction) at the same time in order for
the channel to open. Changes in the membrane potential
across the plasma membrane can do this, as can EMFs,
because the fields will produce forces on these different
charged groups in the same direction at a particular time.
Random thermal motion, in contrast, is random in three
dimensions and will only extraordinarily rarely produce
forces on 20 groups in approximately the same direc-
tion at the same time. So you can see the thermal motion
argument is clearly at best highly questionable when it is
applied to voltage-gated ion channels including VGCCs.
There are other issues that come into play, both influ-
encing the effects of fields on the VGCC voltage sensor. One
is that the plasma membrane has high electrical resist-
ance whereas both the aqueous extracellular fluid and
the aqueous cytoplasm, with their dissolve salts are good
electrical conductors. EMFs only traverse plasma mem-
branes with great difficulty (39, 40). Therefore, fields will
produce rapid movement of charges in the intracellular
and extracellular aqueous phases which will be blocked
by the plasma membrane such that voltage sensor will
be influenced by greatly amplified electrical forces, in a
direction perpendicular to the plain of the plasma mem-
brane. That circa 3000-fold amplification is recognized by
Sheppard etal. (34) immediately before their Conclusion
section. The only example of an integral membrane that
may be influenced in this way, that they give (34) is that
of bacteriorhodopsin, where light exposure leads to the
pumping of a proton across the plasma membrane. They
attempt to estimate the effects of voltages on the proton
pumping, by looking a the effects of voltages on the
absorption changes that occur in bacteriorhodopsin (34);
however, the cycling of bacteriorhodopsin is a complex
process (41) where the proton pumping is not rate-limit-
ing and therefore these studies give little insight into the
actual effects on proton pumping.
Bacteriorhodopsin differs from the voltage-sensor in
the VGCCs in several important ways:
– The voltage sensor has evolved to respond to voltage
changes across the plasma membrane, whereas bacte-
riorhodopsin has evolved to respond to light exposure.
– There are 20 charged groups in the VGCC voltage sen-
sor (37, 38), whereas there is one charge involved in
the bacteriorhodopsin mechanism.
– Whereas the bacteriorhodopsin has considerable
water in the center of its structure, water seems to be
excluded near the helix 4 structures that constitute
the voltage sensor.
The third way, above, is important because the force on
charged groups, as shown by Coulomb’s law, is inversely
proportional to the dielectric constant of the surround-
ing material. The charged groups of the voltage sensor are
found in the lipid region of the plasma membrane. The
dielectric constant of the lipid section of the membrane is
similar to the dielectric constant of hydrocarbon solvents
(41), whereas the water dielectric constant is about 40 times
higher than that of hydrocarbon solvents (41). The dielec-
tric constant of the extracellular fluid is 2.5–3.5 times that of
water, because of the dissolved salts (42, 43) and the meas-
ured dielectric constant of cytoplasm is quite similar to the
dielectric constant of extracellular fluid. It follows from this
that the aqueous phase where most charges exist in cells
has about 120 times the dielectric constant of the membrane
where the voltage sensor resides. Therefore, the forces on
the voltage sensor charges are on the order of 120 times
higher than the forces on most charges in the cell.
It follows from this that if one wants to compare the
forces on the voltage sensor with that produced by EMFs
on most other charged groups in the cell, the voltage
sensor forces are approximately 3000 × 120 × 20 = 7.2 million
times greater. [Please note again that the 3000 figure is
recognized by Sheppard etal. (34); 120 is the effect of the
dielectric constant and 20, the number of charges in the
voltage sensor.]
The above considerations in this section, clearly show
that Sheppard etal. (34) provide no evidence arguing for
biophysical implausibility of the VGCC voltage sensor as
104 Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6
a target of low-intensity EMFs, such that when we have
compelling empirical evidence that it is the main target,
that evidence should be taken at face value. Furthermore,
the VGCC voltage sensor is likely to be many orders of
magnitude more sensitive to EMF effects than are any non-
plasma membrane localized target. Because heating is pro-
duced by the joggling of charged/partially charged groups
almost all of which are outside the plasma membrane, the
much greater forces on the VGCC voltage sensors show
that fields 6–7 orders of magnitude lower than produce
heating may activate the VGCC voltage sensors.
Have others been influenced by somewhat similar con-
siderations? I believe it is likely that W.R. Adey was influ-
enced by the plasma membrane properties when in the
1980s he proposed that a plasma membrane protein was
the likely target of weak EMFs. Panagopoulos etal. (7, 8)
may have been influenced by these plasma membrane and
voltage sensor considerations when they decided to do
biophysical modeling on voltage gated ion channels. The
two reviewers of this paper each had some criticisms of the
Panagopoulos etal. (7, 8) modeling, and some of the things
in their papers go beyond my biophysics understanding, so
I am unable to judge. What I would say is that the modeling
studies came to three important predictions: That voltage-
gated ion channels may be targets of low-intensity EMFs,
that the VGCCs may be particularly activated because of
the mechanism of the actual calcium flux through the
channel and that pulsed fields may be more active than
non-pulsed fields. Biophysical modeling of such complex
membrane proteins as the voltage-gated ion channels is, at
best a work in progress, given their complexity.
At this point, there is much evidence implicating
VGCC activation but no apparent evidence implicat-
ing other voltage-gated ion channels in low intensity
EMF responses (1–3). Possible reasons for this should be
assessed elsewhere.
What is most needed at this point is not more biophys-
ical modeling, although that would be useful, but exten-
sive detailed information on the effects of various fields
on VGCC activation. Such information can be obtained
via the types of studies advocated below for biologically-
based safety standards.
Canadian Royal Society Expert Panel
Report on radiofrequency fields
This Royal Society Expert Panel was charged with review-
ing Safety Code 6 (2013) safety limits for exposure to
radiofrequency (primarily microwave frequency) fields,
following the charge to “advance knowledge, encourage
integrated interdisciplinary understanding and address
issues that are critical to Canadians”. The Expert Panel
Report (44) can be judged based on these charges and also
the requirements that apply to authors of all purportedly
scientific documents:
– The need to provide documentation that it has given
as objective an assessment of the science as possible;
– The need for clarity of thought and clarity of expres-
sion, such that it will be clear to the reader what the
Report is trying to say;
– The need to provide the reader of the Report with
sufficient information in the Report and in the cita-
tions provided in the Report such that the reader can
make an independent assessment of the quality of the
science;
– And perhaps most importantly, the need to follow
widely accepted principles for assessing scientific
evidence.
This paper considers both the charges to the panel and
these more generally applicable scientific principles to
judge the scientific merit of the Report.
What is in the report?
The Report is, in the author’s view, stronger on opinion
than on evidence (44). Let us consider some specifics.
The Report states that “The Panel considered an
‘established adverse health effect’ as an adverse effect
that is observed consistently in several studies with strong
methodology. With this definition in mind, the Panel
reviewed the evidence for a wide variety of negative health
impacts from exposure to RF energy, including cancer,
cognitive and neurologic effects, male and female repro-
ductive effects, developmental effects, cardiac function
and heart rate variability, electromagnetic hypersensitiv-
ity, and adverse health effects in susceptible regions of the
eye.” Despite this claim to have reviewed a broad array of
biological impacts, in fact the Report does not provide a
comprehensive review. Rather it engages, as documented
below, in what can be referred to as “cherry-picking” –
selecting studies consistent with its assumptions. More-
over, it often ignores studies that are not consistent with
its assumption that there are no biological effects except-
ing those that, in their view, may be tied to heating. Thus
the Report completely excludes many different studies on
prenatally exposed animals and those on spermatogen-
esis, on oxidative stress, changes of calcium fluxes and
Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6105
thousands of studies on therapeutic effects, all at non-
thermal levels of exposure.
The Report uses the existence of what it calls “incon-
sistent,” and others have called “conflicting” studies to
argue that conflict per se indicates a lack of established
health impact. This paper considers below whether there
are any genuine “inconsistencies” in this literature. Henry
Lai and Devra Davis have documented that “conflicting”
scientific evidence in the field of bioelectromagnetics
relating to mobile phones has been carefully cultivated
(45), an inference that may also explain the data of Huss
etal. (46). Huss etal. stated “We found that the studies
funded exclusively by industry were indeed substantially
less likely to report statistically significant effects on a
range of end points that may be relevant to health. Our
findings add to the existing evidence that single-source
sponsorship is associated with outcomes that favor spon-
sors’ products.” The panel ignores these findings and con-
siders that conflicting evidence about effects of exposure
to RF energy on cancer or other end points means that
effects are possible but are not ‘established’ in accordance
with its definition of ‘established health effects’. Simi-
larly, while the Report notes that effects of exposure to
RF energy on aspects of male reproductive function have
been found, it concludes that “the evidence has not been
established to indicate that these translate into fertility or
health effects” even when such aspects are used clinically
to assess male fertility.
The Panel reviewed “inconsistent” evidence about
effects of exposure to RF energy on cancer, concluding
that effects are possible but are not ‘established in accord-
ance with its definition of ‘established health effects’. The
Report states that the Panel’s conclusion on cancer is in
agreement with a recent report from the International
Agency for Research on Cancer (47). In fact, the Report’s
characterization of the IARC (47) position does not agree
with the IARC actual position. IARC states that “In the text,
the Working Group provides comments on those findings
that are of greatest relevance to the evaluation, e.g., risk
in the overall exposed group, patterns of change in risk
with increasing exposure (such as a monotonic increase in
risk with increasing exposure), and changes in risk with
duration of exposure or latency.” Furthermore, the Report
ignores the fact that WHO considers microwave radiation
to be a Class 2B carcinogen, and the Report also ignores
the fact that four prominent reviews on this topic (48–51)
all come to the conclusion that microwave exposures can
cause cancer. It is apparent therefore that the Panel of
Experts on Safety Code 6 has allowed its assumptions to
greatly influence its assessment here, rather than provid-
ing an objective assessment of the literature.
There are complexities here that the Expert Panel
fails to consider. For example, oxidative stress produced
by microwave EMF exposure is likely to have a role in
causation of cancer. For decades, it has been established
that low level oxidative stress can lower oxidative stress
markers below initial, pre-stress levels and protect the
body from subsequent higher level oxidative stress, a
phenomenon known as hormesis that has been recently
shown to act by raising the activity of a transcriptional
regulator, Nrf2; it has been suggested that this may
explain some observations that low level cell phone use
may lower cancer incidence via this mechanism, whereas
higher level, long-term cell phone use may produce major
elevation of cancer incidence. However, the Expert Panel
apparently considers these studies to be conflicting,
when to the contrary, these studies may raise the issue of
biological complexity and a possible U- or J-shaped dose-
response curve.
Another even clearer example where inferences of
“inconsistencies” or “conflicts” in the literature have been
misconstrued regarding the induction of single strand
breaks in cellular DNA, measured by what are known as
alkaline comet assays, a well-documented method for
such studies (1). This literature was reviewed by the author
(1), who found 19 different studies where greatly elevated
levels of such single strand breaks were found following
exposure as well as eight studies where they were not
found. However, in examining these studies in detail, it
is clear that the differences can be easily explained. For
instance, regarding in vitro studies of DNA damage, some
of the studies have used different cell types and studied
different microwave source EMFs. Thus adult lymphocytes
appear relatively resistant to EMF, while neural stem cells
are much more susceptible. Different cell types differ from
one another in how many and what types of VGCCs may
be present and they may differ as well in how the VGCCs
are regulated and so may be expected to differ widely in
terms of response. All of these studies were done using
exposures that were well within current safety standards.
Consequently, each of these 19 positive findings contra-
dict the assumptions behind the current safety standards,
assumptions that are being defended by the Expert Panel
Report, but the Report ignores all of these studies. More-
over, in two of the 19 positive studies, results were posi-
tive in some cell types but not others (1), clearly showing
that in measurements using identical methodologies, the
properties of the cells being studied are critical in deter-
mining the biological response found.
Thus the Panel has failed to take into account impor-
tant nuances regarding scientific research in this field.
It has limited considerations to what the Panel calls
106 Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6
“established health effects” defined in terms of con-
sistent responses of various cell and tissue types (44).
Where apparent conflict exists, the Panel uses its exist-
ence as proof that an effect is not established. In doing
so, the Panel fails to take into account scientific details
that account for many “inconsistent” results. Such details
are likely to include, in addition to the factors discussed
above in this section, such factors as the role of different
pulsation patterns in different types of exposures, the
presence of “window effects” providing very complex
dose-response relationships and the role of field fre-
quencies in determining biological response. In effect,
the panel dismisses science that does not comport with
their underlying assumptions that only thermal effects are
relevant.
Genotoxicity of non-thermal
microwave exposures: examples
ofinconsistency?
This inconsistency issue is central to the Report’s consid-
eration of genotoxicity of non-thermal microwave expo-
sures. This is one of the two areas (pp. 80–82) where the
Report cites substantial numbers of primary citations
(22 in this case). It lists 13 citations where studies found
genotoxicity following exposure levels, well within safety
standards. It also lists nine citations where the Report
states that no genotoxic effect was found. The Report only
cites a small fraction of the overall literature on geno-
toxicity. For example, it only cites one of the 19 studies
reviewed earlier by the author (1) on induction of single
strand DNA breaks in microwave frequency exposed
cells [that of Kesari etal. (52)]. In overall outline, the lit-
erature cited in the Report on this topic reflects fairly well
this overall much larger literature. There are, however,
a number of ways in which the Report is problematic in
dealing with this subject. The author has looked up all
22 of these studies to determine from the original papers
what the original authors stated.
Scientists often look at genotoxicity because of its
importance in carcinogenesis and this section of the
Report is part of a larger section on carcinogenesis.
However, the Panel of Experts nowhere considers that
many of the authors of these studies discuss their own
work as strengthening the case that such fields are car-
cinogenic. A second connection, to male infertility, is
also hidden in the report. Two of the positive studies
(53, 54) are falsely stated in the Report as being on
blood formation but what was actually being studied
in both of these studies was testicular sperm formation.
The positive study Liu etal. (55) which shows genotox-
icity in a spermatocyte cell line may also have implica-
tions regarding male infertility, because of the cell type
being studied. There is also a connection with male
infertility of one of the negative studies (56). This study
of effects of mobile phones, found no genotoxic effects
on human sperm, but the same group published two
earlier studies showing that other EMFs had substan-
tial effects that suggested lowered fertility as a conse-
quence of exposure. The Report cited the Falzoneetal.
(56) study but not the two earlier studies. Perhaps this
is an overreaction, but the Report seems to be hiding
studies providing substantial support for the view that
these EMFs can substantially impact male fertility and
also hiding the implications of many of these studies on
carcinogenesis.
There are other aspects of this section that are prob-
lematic. The Report listed the Franzellitti et al. (57)
study as a negative one but it is not; it reports increased
single strand DNA breaks as measured by alkaline comet
assays following exposure. The Report accurately lists
the Bourthoumieu etal. (58) study as being negative, but
that study cites other studies by the same research group
using other cell types as being positive; these positive
studies are not cited or discussed in the Report. Similarly,
the Report correctly lists two studies by Zeni, Sannino
and their colleagues as being negative for apparent geno-
toxicity; however, this same research group published 6
additional studies, with three showing positive effects,
depending on the cell type being studied. The Xu et al.
(59) study found genotoxicity in two cell types but not in
four other cell types. These studies clearly show that dif-
ferent types of cells respond differently to low level micro-
wave exposures, but for some reason, the Panel of Experts
seems unable to draw this very important conclusion. The
cell type differences are discussed above in relation to the
role of VGCCs in producing single strand breaks in cellu-
lar DNA (1). Another problematic aspect of this part of the
Report, is that it lists seven of the 13 positive studies as
studies providing evidence for “genotoxic or epigenetic”
changes but none of those seven have anything to do with
epigenetics.
We have here 13 (14 actually when the Franzellitti study
is added) studies each of which provide clear evidence
for genotoxic activity of non-thermal microwave fields
and each of which therefore falsify the heating/thermal
hypothesis underlying the Report and also falsify current
safety standards. Therefore, based on widely accepted sci-
entific standards, the heating/thermal hypothesis and the
safety standards should be rejected.
Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6107
What conclusion does the Panel draw? It concludes
that “Extensive in vitro studies have generated inconsist-
ent evidence that RF energy has genotoxic or epigenetic
potential”. There is, however, no inconsistent evidence
whatsoever. When one studies different cell types, differ-
ent fields with different pulsation patterns, and different
end points, even an elementary understanding of biology
argues that different results are likely to be obtained. This
section of the Report makes very clear on what basis the
Panel is inferring “inconsistency”. The authors of the
Report are simply looking at superficial similarities of
studies and falsely inferring that differences should be
interpreted as “inconsistencies” or “conflicts”, when they
are not inconsistent or conflicting at all. The only type
of studies that can produce clear evidence of inconsist-
ency are identical studies that produce different results.
Neither the Report nor, to my knowledge, its predecessors
have provided any examples of such identical studies.
Because this inconsistency argument underlies so much
of the Report, one can see that this argument and the
Report and also the current safety standards are each
deeply flawed.
Karl popper and how to assess
scientific evidence
What is the responsibility of the Expert Panel as a group
of scientists attempting to produce a scientifically defen-
sible Report? Probably the most influential work on this
topic comes from the famous philosopher of science Karl
Popper. In his work, Conjectures and refutations, Popper
argues that scientific hypotheses cannot be proven, but
they can be falsified (60). Thus science is to be regarded
as tentative information that can always be advanced
through further research. Falsifying information, informa-
tion that apparently falsifies a theory, is the most impor-
tant type of scientific information and needs therefore to
be considered very carefully. The next more important
type of evidence is what he calls “risky predictions” where
one makes a prediction based on a hypothesis, a predic-
tion that is not likely to be made based on any other unre-
lated hypothesis. Confirmation of such a risky prediction
provides substantial support whereas lack of confirma-
tion can again lead to falsifying the hypothesis. Finally,
there are confirmatory evidence studies where multiple
hypotheses may explain any confirmation and conse-
quently such confirmation is of low scientific significance.
When considered against the Popperian frame-
work, all of the evidence supporting the heating/thermal
hypothesis, favored by the Expert Panel (44) is of the third
type. It is widely established therefore that a scientific
assessment of this area needs to consider in detail each
apparently falsifying study and unless each of them can
clearly be shown to be deeply flawed, the inference that
should be drawn is that the heating hypothesis should be
rejected. This rejection is the one aspect of this that may
need to be modified in biology, given the inherent com-
plexity of biology. It is possible that rather than rejection,
the hypothesis needs instead to be modified in such a way
that the information no longer falsifies the new hypothe-
sis. However, in this situation where perhaps thousands of
such modifications may be needed because of thousands
of apparent falsifying studies, the difference in practice
from outright falsification by each study may be trivial. It
is clear, in any case that the Expert Panel has completely
avoided doing its scientific duty here, failing to assess
each of the thousands of apparent falsifying studies, and
opting instead, as seen above, to make specious argu-
ments. That is tragic, in my view, failing to protect the
health of many Canadians, and indeed others around the
world.
Some other aspects
Most of the Report is focused on their heating/thermal
interpretation of microwave radiofrequency effects (44).
That is, perhaps, not surprising. What is however very
surprising, is that having made such a fetish out of the
“inconsistencies” in dealing with various topics, nowhere
does the Expert Panel consider in this very large section of
the Report, the thousands of findings that clearly conflict
with their own favorite hypothesis. What sections of data
should be thrown out that may be relevant to this section?
The Panel of Experts seem to be completely oblivious that
if in its view “inconsistencies” are sufficient to throw out
many studies in one area, it should have at least a little
consistency in dealing with “inconsistencies” in the heart
of their own Report.
In the first paragraph in the conclusion section, the
Panel of Experts state that (44) “No viable biophysical
mechanism has been proposed for carcinogenic effects
for exposure below the levels of SC6 that are supported
by results in experimental systems,” citing three earlier
studies but neglecting to consider the VGCC mechanism of
microwave EMF action. The VGCC mechanism is clearly a
viable biophysical mechanism, because of the properties of
the voltage sensor located in the plasma membrane. VGCC
activation produces downstream effects including [Ca2+] i
elevation, NO elevation and peroxynitrite/oxidative stress/
108 Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6
free radical elevation (1–3), see Figure 1. It has been shown
that NO and peroxynitrite/oxidative stress/free radical ele-
vation are central to the mechanism of inflammatory car-
cinogenesis (61–64), the type of carcinogenesis that occurs
in chronically inflamed tissues and therefore causes cancer
in such tissues. It follows that it is biophysically and physi-
ologically plausible, that microwave caused VGCC activa-
tion may cause cancer via the same mechanisms shown to
cause cancer in inflammatory carcinogenesis. It has also
been shown that free radicals formed through Compton
scattering by ionizing radiation have essential roles in ion-
izing radiation carcinogenesis (65–67), providing probable
mechanistic similarities between microwave EMF carcino-
genesis and ionizing radiation carcinogenesis, as well.
There have been many arguments made by the advocates
of the heating/thermal mechanism of action, emphasiz-
ing the correct fact that the individual microwave photons
have insufficient energy to perturb the chemistry of our
bodies and they infer from this that these photons cannot
cause cancer or many other pathophysiological responses.
But what the Panel of Experts and others fail to realize is
that the microwave fields as a whole, acting through down-
stream effects of VGCC activation, lead to high densities of
intracellular free radicals (Figure 1) and can produce there-
fore similar effects on the body to those produced by ion-
izing radiation exposure. In any case, it follows from this
paragraph, that the statement, in the Report, that there is
no viable biophysical mechanism for low level microwave
exposure to cause cancer or other diseases is false, with
that falsehood apparently based on the failure of the Panel
of Experts to consider the information provided to the
panel by the author (Refs. 1 and 3).
This issue of biophysical plausibility of a mechanism
for such low intensity exposures is a terribly important
one. In the Report, there is a quote from a 2009 Health
Canada document, which authors of the Report essentially
adopt as their own [p. 78, ref. (44)]; “At present, there is no
scientific basis for the occurrence of acute, chronic and/
or cumulative adverse health risks from RF field exposure
at levels below the limits outlined in Safety Code 6. The
hypothesis of other proposed health effects occurring at
levels below the exposure limits in Safety Code 6 suffer
from lack of evidence of causality, biological plausibility
and reproducibility and do not provide a credible founda-
tion for making science-based recommendations for limit-
ing human exposures to lower-intensity RF fields (Safety
Code 6).” Whether or not this was a defensible position
in 2009, it clearly is not defensible in 2014. This issue of
biological/biophysical plausibility is a key one in consid-
ering various types of epidemiological evidence, such as
were considered in the Report, whenever the role of such
stressors in initiating disease is being considered based
on studies of groups of people. Hennekens and Buring
(68), on p. 40 in their textbook Epidemiology in Medicine
state “The belief in the existence of a cause and effect
relationship is enhanced if there is a known or postulated
biologic mechanism by which the exposure might reason-
ably alter risk of developing disease.” Consequently, all
of the epidemiological evidence considered in the Report
and elsewhere needs to be reconsidered in the light of the
biophysical and physiological plausibility of the VGCC
mechanism and downstream effects produced by VGGC
activation.
Cataract formation as claimed
effects of microwave-caused
heating
The Report presents a fairly extensive specific case,
arguing that microwave exposure produced cataract for-
mation is produced by their heating/thermal mechanism
(44). Unlike most other areas of the Report, the Panel con-
siders substantial amounts of the primary literature on
this topic. The studies discussed, provide evidence for the
third and weakest test, according to Karl Popper’s analysis
VGCCs [Ca2+]iNO
Microwave
/low freq.
EMFs
cGMP
Therapy
G-
kinase
Pathophysiological
effects
Superoxide
OO.(-)
ONOO(-)
Peroxy-
nitrite
Free
radicals
+/-CO2
Oxidative/
Nitrosative
stress
Figure 1:Mechanisms of action for microwave EMFs leading to
diverse pathophysiological responses and therapeutic responses.
Microwave/lower frequency electromagnetic fields (EMFs) act to
stimulate voltage-gated calcium channels (VGCCs), increasing
levels of intracellular calcium [Ca2+]i. Elevated [Ca2+]i increases
nitric oxide (NO) synthesis which can act along two pathways. The
NO signaling pathway, raises cyclic GMP (cGMP) levels and G-kinase
activity, producing therapeutic effects. In the other pathway of
action of NO reacts with superoxide to form peroxynitrite [ONOO(0)],
which either before or after reaction with carbon dioxide (CO2) can
break down to form free radicals, producing oxidative/nitrosative
stress. The excessive calcium signaling produced by [Ca2+]i and the
peroxynitrite/free radical/oxidative stress pathway each contribute
to pathophysiological responses.
Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6109
(60), namely that the exposures studied are mostly within
the range that produce substantial tissue heating and
may therefore produce both cataracts and lens opacifi-
cation via heating. This type of evidence is considered to
be the weakest of the three types of evidence in Popper’s
schema, because alternative mechanisms are not in any
way ruled out.
What is interesting is that there are three published
studies which argue strongly against a heating mecha-
nism for cataract formation by microwave exposures. One
of these, a study by Cleary and Mills (69), showed that in
comparison with other treatments raising lens tempera-
tures, microwave radiation “appears to exert a unique
component of thermal stress in the induction of opacifi-
cation in the mammalian lens,” arguing against a strictly
thermal mechanism. Two studies have been published
testing in effect the “risky prediction” that microwave-
induced cataracts are produced by heating. One of these
showed that neither eye-localized or whole-body hyper-
thermia to 42o produced any cataract-like opacity in the
rabbit (70). The other showed that localized eye heating
in the rabbit, producing the same temperature for the
same duration as cataractogenic microwave exposures,
produced no opacity in the rabbit eye (71). Both of these
“risky predictions” failed to confirm the prediction and
strongly suggest falsification of the hypothesis that micro-
wave-induced cataracts are produced through heating.
What is particularly disturbing about the Report is that it
fails to cite any of these three studies (44) despite the fact
that each of them has been cited by others in this context,
according to the Google Scholar database. Clearly, the lit-
erature the Expert Panel cites regarding cataract forma-
tion, which includes the second most extensive primary
literature in the Report, does not provide an objective
assessment of the scientific literature in this area.
In contrast to studies discussed in the previous par-
agraph, the equally “risky prediction” that VGCCs and
excessive [Ca2+]i have roles in such cataract formation
have produced validation of the hypothesis that micro-
wave-induced VGCC activation causes cataracts. Walsh
and Patterson (72) demonstrated that elevated [Ca2+]i in
the lens of the frog eye has a central role in cataract forma-
tion and that calcium channel blockers, which of course
block VGCC activation, can block cataract formation. In a
recent review, it was shown that excessive [Ca2+]i in the
lens of the human and mammalian eye plays a major role
in the opacification process producing cataracts and that
VGCCs can have a substantial role in this process (73).
While these studies do not directly relate to microwave
exposures, they clearly show that excessive [Ca2+]i in the
lens of the eye has essential roles in cataract formation
and that excessive VGCC activity causes cataract forma-
tion in experimental animals. Much of the action of [Ca2+]
i in cataract formation has been shown to occur through
the action of several calcium receptors that act indepen-
dently of NO. However, there is also an established role
of oxidative stress in cataract formation, and it is thought
that peroxynitrite also has a role because of the elevation
of a marker for peroxynitrite, 3-nitrotyrosine in cataracts
(74). It is likely therefore that microwaves act to produce
cataracts via calcium signaling as well as via downstream
effects involving peroxynitrite and oxidative stress (see
Figure 1). The difference in confirmation of these “risky
predictions” clearly shows that the VGCC/[Ca2+]i role in
producing cataracts is far better documented than any
possible heating role.
It can be seen from the above, that although the Cana-
dian Panel of Experts seems to argue that cataract forma-
tion is the strongest example of a strictly thermal EMF
response (44), the case for such a thermal mechanism is to
the contrary extremely weak. Their case is totally depend-
ent on ignoring both evidence that falsifies their view and
also evidence that confirms “risky predictions” of the
VGCC mechanism that is ignoring the two strongest types
of evidence. Thus the claimed role for heating being the
cause of cataract formation following microwave expo-
sure, advocated by the Expert Panel, has now been appar-
ently debunked.
Summary of the report
In summary, then each of the following failures in the
Report can be seen to be important in our rejecting its
conclusions:
– It fails to individually assess the thousands of studies
that provide evidence apparently falsifying their heat-
ing/thermal paradigm. By failing to assess studies con-
taining this most important type of evidence, as shown
by Popper (60), this failure provides more than suffi-
cient reason to reject the conclusions of the Report.
– The Report fails to provide any “risky prediction”
type evidence (the second most important type of evi-
dence) in favor of the heating/thermal hypothesis, but
such risky predictions are available supporting the
VGCC mechanism of action.
– The Report bases its conclusion on the weakest type of
evidence, evidence that some responses could be gen-
erated by heating but does not rule out other types of
mechanisms. A close examination of what the Expert
Panel considers to be the strongest case for heating,
110 Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6
that of cataract formation, shows that this is another
example of a probable VGCC mechanism, not heating.
– The Report repeatedly fails to provide an objective
assessment of the scientific literature. Because omit-
ted citations consistently have the effect of weakening
their position, it seems unlikely that these omissions
are just coincidental.
– The Report claims that there is no biophysically viable
alternative to the heating/thermal paradigm, a claim
clearly shown here to be false.
– The Report claims extensive inconsistencies (what
others have called conflicts) occur in the literature,
where what it considers “similar” studies produced
different results and it uses these claims of “inconsist-
encies” to throw out large amounts of the literature.
However, these “similar” studies are in fact, dissimi-
lar, differing in cell type being studied, the properties
of the fields being studied and/or the end point being
studied, with each of these having demonstrated roles
in determining outcome. It follows that the Report
provides no evidence for any such “inconsistencies.”
Any claims of such “inconsistencies” are at best
undocumented.
– The Report fails to use its own inconsistency argu-
ment (6 above) in the heart of the report, the part that
argues for a heating/thermal mechanism, thus failing
to be consistent in its own treatment of this issue.
– The Report fails to give the reader enough informa-
tion in the Report itself or in the citations provided to
allow the reader to assess its scientific merit.
The author is aware that similar flaws to those described
immediately above occur in earlier studies arguing for the
heating/thermal/SARs mechanism (9–13). But that only
emphasizes the fact that this whole point of view has been
on extraordinarily weak ground all along. That makes
it crucially important that safety standards on which
the health of most Canadians and indeed, most people
around the world are dependent, be examined in scien-
tifically defensible ways.
It is perhaps surprising that the case developed by the
Panel of Experts is so weak. That is especially so because
industry-funded research has been skewed in support of
the heating/thermal interpretation (45, 46), so one would
think that with a lot of industry-supported research, the
Expert Panel would have come up with some stronger
evidence.
Let me say that it is my opinion that the Panel of
Experts may not have been corrupted by industry influ-
ence, but rather it may have fallen victim to a common
affliction, that of groupthink. Groups of people each
carrying misconceptions in common, act to encour-
age their common misconceptions in other members of
the group. What was apparently lacking in the Panel of
Experts was someone who could challenge those mis-
conceptions, rather than encourage them. However the
“logic” presented in the Report provides industry with a
strategy to indefinitely prevent any true scientific stand-
ards from being used to assess safety. Industry need only
fund research that ends up making “inconsistent” con-
clusions, thus allowing all independently funded studies
to be thrown out because of these “inconsistencies” and
thus indefinitely preventing adoption of safety standards
based on genuine, independent science. It is my hope and
expectation that this was not the goal of the Expert Panel,
but it is nevertheless an apparent consequence of their
Report, if it is viewed as being scientific.
Still, it can be argued, that the Panel of Experts has
perhaps unwittingly fulfilled a very valuable function. By
clearly showing how weak their case is in 2014, the Panel
has shown that none of the more recent evidence has
substantially strengthened their case. It is still based on
a false premise (biophysical implausibility of alternative
mechanisms) and circular reasoning, it is still based on
the failure to consider large numbers of apparent falsify-
ing studies, it is still based on ignoring large amounts of
the relevant literature and it is still based on the failure to
provide the most well supported types of evidence needed
to establish biological mechanisms in medicine, just as
was true earlier (9–13). Of course, the weakness of the
Panel’s case means that the current safety standards are
based on quicksand.
How VGCC activation by microwave/
RF exposure can produce a variety
of important biological responses
Table 1 summarizes how VGCC activation may plausibly
produce a wide range of reported responses to microwave
and, in some cases, lower frequency EMF exposures. It can
be seen that a wide range of reported responses to low level
microwave exposures can apparently all be understood as
being a consequence of VGCC activation and downstream
effects of such activation that were outlined in Figure 1.
These can all be seen as “risky predictions” of the VGCC
activation mechanism produced by EMF exposures. While
these mechanisms support the inference that all of these
effects seem to be produced by VGCC activation, that
inference must be viewed as being surprising. After all,
Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6111
Table 1:Apparent mechanisms of action for microwave exposures producing diverse biological effects (see Figure 1).
Reported biologic
response
Apparent mechanism(s) Citation(s)/Comments
Oxidative stress Peroxynitrite and consequent free radical formation (–); detected via a large number of
oxidative stress markers
Single strand breaks in
cellular DNA
Free radical attack on DNA (, )
Double strand breaks in
cellular DNA
Same as above Same as above; detected from micronuclei
and other chromosomal changes
Cancer Single and double strand breaks, -nitroguanine and
other pro-mutagenic changes in cellular DNA; produced by
elevated NO, peroxynitrite
This paper and ()
Breakdown of blood-brain
barrier
Peroxynitrite activation of matrix metalloproteinases leading
to proteolysis of tight junction proteins
()
Male and female infertility Induction of double strand DNA breaks; other oxidative
stress mechanisms; [Ca+]i mitochondrial effects causing
apoptosis; in males, breakdown of blood-testis barrier
()
Therapeutic effects Increases in [Ca]i and NO/NO signaling (–; )
Depression; diverse
neuropsychiatric
symptoms
VGCC activation of neurotransmitter release; other effects?
possible role of excess epinephrine/norepinephrine ()
These were reported in occupational
exposures (); also reported in people
living near cell phone towers
Melatonin depletion; sleep
disruption
VGCCs, elevated [Ca]i leading to disruption of circadian
rhythm entrainment as well as melatonin synthesis
()
Cataract formation VGCC activation and [Ca]i elevation; calcium signaling and
also peroxynitrite/oxidative stress
This paper
Tachycardia, arrhythmia,
sometimes leading to
sudden cardiac death
Very high VGCC activities found in cardiac (sinoatrial node)
pacemaker cells; excessive VGCC activity and [Ca+]i levels
produces these electrical changes in the heart
()
although low level EMF activation of VGCCs is now well-
documented, other possible direct targets of EMFs cannot
be ruled out, targets that may produce changes that
cannot be easily explained as being caused by VGCC acti-
vation and downstream effects of such activation. When
the apparent mechanisms summarized in Table 1 are put
together with the calcium channel blocker studies and
other studies on widespread changes in calcium fluxes
and calcium signaling following microwave EMF expo-
sures, we are left without any alternative, non-VGCC target
of EMF action that currently can be studied for its role in
producing biological effects in humans.
Biologically-based EMF safety
standards
Hardell and Sage (76), the Scientific Panel on Electromag-
netic Health Risks (77) and the author (3) have called for
biologically-based EMF safety standards that are based
on genuine biologically relevant responses to low-level
microwave and other EMFs, rather than SARs. The only
approaches we have available for this based on a known
biological end point, as shown in the previous section, are
approaches based on VGCC activation. There are experi-
mental whole animal approaches based on VGCC activa-
tion (3), but my feeling is that initial studies should focus
on using cells in culture, cells that have high levels of
some VGCCs. Some such studies would use cell lines with
such high VGCC levels, such as neuroblastoma cell lines
or perhaps cell lines derived from endocrine cells with
relatively high VGCC levels. Among these cell lines should
be the neuroblastoma cell lines previously studied by
Duttaetal. (78) and shown to produce changes in calcium
fluxes in response to very low level EMF exposures. PC12
cells, a commonly used chromaffin cell line should also be
considered for such studies. In addition, it may useful to
use cardiac pacemaker cells which have very high activi-
ties of VGCCs (35) and can be derived from stem cells (79).
Two approaches suggest themselves for measuring
responses of such cells to EMF exposure: Cells in culture
could be monitored for NO production using an NO elec-
trode in the gas phase over the culture, both before and
following EMF exposure. This approach was used by Pilla
in studying effects of pulsed microwave fields (4) in trying
to understand the mechanism of microwave therapy. Pilla
found that the NO increase in such cultures on EMF field
112 Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6
exposure was almost instantaneous, using a NO electrode
in the gas phase (4). With this sort of approach, many dif-
ferent fields can be quickly and easily studied for their
ability to produce NO increases, including different fre-
quencies, pulsation patterns and possibly intensities,
with the last of these needed to analyze window effects.
Different cordless communication devices can be com-
pared for activity using several cell types. Continuous
measurements from an NO electrode can be recorded and
easily quantified, allowing accumulation of very large
amounts of data in very short time periods. Therefore,
issues such as reproducibility should be quickly resolved.
One might even be able to determine whether previous
exposures produce increased sensitivity to exposure, pos-
sibly developing a cell culture model of electromagnetic
hypersensitivity.
Another approach to such studies involves using
calcium-sensitive fluorescent probes that concentrate
into the cytoplasm of cells, allowing assessments of [Ca]i
levels with a fluorescence microscope. This may allow one
of obtain information of different types than described
in the previous paragraph. One can get information on
heterogeneity of responses at the cellular level and also
how raised [Ca]i levels may propagate over time from one
part of the cell to another. However, a limitation to this
approach may occur if the fields generated by the micro-
scope perturb the [Ca]i levels and cannot be well shielded
using a small Faraday cage that does not cage exposures
that are to be studied. It is also true that the NO electrode
studies are easier to quantify than such fluorescent probe
studies. So these two approaches are distinct from one
another and whether they will complement each other as
they develop is uncertain. It is my view that both of these
should be investigated if only to explore their strong points
and weak points but that the NO electrode approach may
be a very good place to start because it has already been
used to assess EMF effects (4) and because it allows easy
quantification.
Brief overview
Havas’ recent review (80) discusses 14 different docu-
ments prepared by international scientists (dated 2002
through 2012) expressing deep concern about various
non-thermal effects of microwave radiation exposures and
other studies have expressed similar views. W.R. Adey’s
papers (6, 21) reviewed much of the then current evidence
for many non-thermal effects of microwave radiation. But
his prescience is most clearly shown by his statement that
“Collective evidence points to cell membrane receptors
as the probable site of first tissue interactions with both
extremely low frequency and microwave fields for many
neurotransmitters, hormones, growth-regulating enzyme
expression, and cancer-promoting chemicals. In none of
these studies does tissue heating appear to be involved
causally in the responses” [italics added, from a talk at
the Royal Society of Physicians, London May 16–17, 2002,
quoted in ref. (81)]. The recent Herbert and Sage review
(81) discusses “the emergence of ever larger bodies of
evidence supporting a large array of non-thermal but pro-
found pathophysiological impacts of EMF/RFR in trans-
forming our understanding of the nature of EMF/RFR
impacts on the organism.” In a second paper (82), Herbert
and Sage state that “Our EMF/RFR standards are also
based on an outdated assumption that it is only heating
(thermal injury) which can do harm. These thermal safety
limits do not address low-intensity (non-thermal) effects.
The evidence is now overwhelming that limiting exposure
to those causing thermal injury alone does not address
the much broader array of risks and harm now clearly
evident with chronic exposure to low-intensity (non-ther-
mal) effects.” The Khurana etal. review (83) states: “The
authors reviewed more than 2000 scientific studies and
reviews, and have concluded that: (1) the existing public
safety limits are inadequate to protect public health; (2)
from a public health policy standpoint, new public safety
limits on further deployment of risky technologies are
warranted based on the total weight of evidence. A pre-
cautionary limit of 1 mW/m2 was suggested ….” The Sci-
entific Panel on Electromagnetic Field Health Risks listed
four well-documented central conclusions at the begin-
ning of their publication (77):
– Low-intensity (non-thermal) bioeffects and adverse
health effects are demonstrated at levels significantly
below existing exposure standards.
– ICNIRP and IEEE/FCC public safety limits are inad-
equate and obsolete with respect to prolonged, low-
intensity exposures.
– New biologically-based public exposure standards are
urgently needed to protect public health worldwide.
– It is not in the public interest to wait.
Canadian Panel of Experts do not cite these papers or
others providing clear and focused views that contradict
the views advocated in the Report, showing again that
the Report fails to provide an objective assessment of the
scientific literature. The current paper adds a number of
specific considerations to the needed debate:
– VGCC activation produces most, possibly even all
microwave and lower frequency EMF health-related
Pall: Scientific evidence contradicts findings and assumptions of Canadian Safety Panel 6113
responses. Each of the studies on VGCC activation or
on changes in calcium fluxes and signaling following
low level exposure clearly falsifies the thermal/heat-
ing paradigm.
– This VGCC activation mechanism by low level micro-
wave and lower frequency fields, rather than individ-
ual photons, is biophysically plausible based on the
special properties of the voltage sensor and its locali-
zation to lipid region of the plasma membrane.
– Downstream effects of VGCC activation (Figure 1) can
generate each of 13 different health effects repeat-
edly found to be produced by microwave exposure
(Table1).
– Studies document roles of pulsation in influencing
biological responses to microwave exposures, influ-
ences that are incompatible with these being produced
by heating.
– “Window” effects occur, where specific intensities of
microwave EMF exposure produce higher biological
effects than those produced by both lower and higher
intensities, observations incompatible with heating
effects.
– Thousands of studies have reported biological effects
at intensities well within safety standards, each of
which appear to falsify the heating/thermal para-
digm, none of which have been considered in this
light by the Panel of Experts, despite the scientific
requirement to do so under well-accepted scientific
principles.
– The claims in the Report that microwave induction of
cataracts is produced by heating has been tested in
three studies, each contradicting this claim; two of
them produce clear falsification, but none of these
three studies are cited in the Report. Because VGCC
activation can cause cataracts and elevated [Ca2+]i
has essential roles in producing cataracts, a VGCC
mechanism for microwave-induced cataracts is much
more strongly supported than is the claimed heating
mechanism.
– The claim in the Report of widespread “inconsistency”
in the literature is tested here through examination of
the literature cited on genotoxic effects. No inconsist-
encies were found in this literature despite the Report
claiming such. Furthermore, no identical studies are
cited anywhere in the Report showing inconsistency
of results, these being the only types of studies that
can clearly show inconsistency. Claims of widespread
“inconsistency” or “conflict” in the literature must be
viewed as, at best, undocumented.
– Each of the 8 considerations listed immediately above
clearly show that the Report fails to provide anything
resembling an objective assessment of the evidence on
biological effects of microwave EMF exposures and pro-
vides therefore no scientifically valid support for Safety
Code 6, ICNIRP or other current safety standards.
– Development of biologically-based safety standards
has been called for and approaches to using cell
culture-based tests that may be used to develop such
safety standards are discussed.
It has been clear for a long time that the heating paradigm
is indefensible and that a new paradigm is much needed.
We now have that with VGCC activation, and while VGCC
activation may not be the entire story behind the biologi-
cal actions of such EMFs in humans and other mammals,
it clearly is most of the story. It is time therefore for a para-
digm shift away from strictly thermal effects and toward a
central role for VGCC activation in the cellular response to
microwave and lower frequency EMFs.
Acknowledgments: I wish to thank Dr. Devra Lee Davis
for her many helpful suggestions. Any remaining errors in
this are, of course, my own. This paper is dedicated to the
memory of W. Ross Adey (1922–2004) whose studies in this
area were impressively prescient – someone I regret never
meeting.
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