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Posted: 30
July 2000
Evidence that Electromagnetic Radiation is
Genotoxic: The implications for the epidemiology of cancer and cardiac,
neurological and reproductive effects
Dr Neil
Cherry
June 2000
For presentations in May to NZ
Parliament
and June 2000 in Italy,
Austria, Ireland and at the
European Parliament in
Brussels.
Neil.Cherry@ecan.govt.nz
Environmental Management and
Design Division
P.O. Box 84
Lincoln University
Canterbury, New
Zealand
Evidence that Electromagnetic
Radiation is Genotoxic: The implications for the epidemiology of cancer
and cardiac, neurological and reproductive effects
Dr Neil Cherry
Lincoln University, New Zealand
June 2000
"Our frame of reference
determines what we look at and how we look. And as a consequence, this
determines what we find."
Burke J, The Day the Universe
Changed, 1985.
Introduction:
The way we perceive things determines how we
make decisions. To move from picturing ourselves as physical beings to
biological beings significantly changes our view of health and fitness.
Too much exercise and oxygen free radicals really damage our cells. To
move from biological to bioelectrical incorporates intelligence and
emotion and leads to a radically fundamental change in our way of seeing
things that it forms the basis of a new paradigm.
Principles of Approach:
This paper attempts to follow basic classical
scientific principles to counter the dismissive and biased approach of
industry and many government and international authorities, including the
WHO and ICNIRP.
The principles found to be important are that
biology reveals that brains, hearts and cells use electromagnetic signals,
charged ions, voltage-gated ion channels, ion regulated gap junctions, all
of which can be interfered with by external electromagnetic fields in
subtle but vital ways in relation to health.
A primary physical principle of resonant
absorption explains why external and internal signals that share the same
part of the spectrum, resonantly exchange energy at levels well below the
thermal threshold. This is also true for radio and TV receivers. It
involves tuned circuits and resonant absorption.
Laboratory experiments provide evidence of
effects. Replicated and/or extended studies provided confirmation and
establish an effect. Multiple studies confirm and strengthen the cause and
effect relationship.
In assessing genotoxicity, any evidence of
genetic damage, cell death or neoplastic transformation is evidence of
genotoxicity. The genetic material is fundamentally the double helix of
the DNA molecule. During the cell cycle the helix unwinds and clones
itself. They then fold themselves into the set of chromosomes that are so
large that they can be seen in powerful microscopes. In the second half of
the cell cycle the chromosomes clone themselves so that at mitosis, cell
division, each cell has a full set of chromosomes. They then unfold
themselves to form the DNA strands.
Any substance that damages DNA or chromosomes,
or changes genetic activity, is genotoxic because it is acting on the same
material, i.e. the DNA molecule. A genotoxic substance is mutagenic,
carcinogenic and teratogenic.
Strength of evidence for public health has a
classical hierarchy that has dose-response relationship at the top and
biological mechanism at the bottom, Hill (1965). This is seen by
considering Sir Austin Bradford Hill's descriptions of his 'view points'
from which the question of cause and effect is being considered. Of
dose-response he says:
"The simple dose-response curve admits of a
simple explanation and obviously puts the case in a clearer light", i.e.
cause and effect.
Sir Austin considers many other forms of
evidence from which cause and effect can be decided in the absence of a
dose-response. These include strength of association and consistency,
although he points out that the lack of strength and apparent
inconsistency, is not necessarily arguments against cause and effect. Of
biological mechanism, or plausibility, he states:
"It will be helpful if the causation we
suspect is biologically plausible. But this is a feature I am convinced we
cannot demand. What is biologically plausible depends upon the biological
knowledge of the day."
Thus biological plausibility has a low status
and dose-response has a very high status.
When epidemiological evidence is available it
should be used to set public health standards, where possible, using the
dose-response relationships. In the absence of these, the level of lowest
observed effect, with a safety margin to allow for uncertainly, the
vulnerable, the size of the population at risk, are appropriate.
Dose response relationships for epidemiological
studies of cancer are likely to be linear because of the cumulative cell
damage/repair/mistake mechanism. At very high levels approaching lethal
levels the curve become asymptotic. At very low levels, around the optimum
homeostatic levels, curves can become "U" shaped. Thus, with the great
sensitivity of the brain the neurological effects at extremely low
exposure levels might be curved.
EMR Spectrum
Principle:
It is observed that both biological effects and
epidemiological effects appear to be the same or very similar from ELF
exposure and from RF/MW exposures, including calcium ion efflux, melatonin
reduction, DNA strand breakage, chromosome aberrations, leukaemia, brain
cancer, breast cancer, miscarriage and neurological effects.
A frequently used method for falsely dismissing
evidence of effects is to consider effects in small frequency and
intensity bands. In fact, biophysics shows that the dielectric constant
decreases monotonically with carrier frequency across the EMR spectrum,
Schwan (1985). Vignati and Giuliani (1997) show that for a unit field
exposure, the induced current increases significantly as a function of
frequency, Figure 1.
The EMR Spectrum Principle predicts that
effects that are associated with ELF exposure are very probably found with
low intensity RF/MW exposure.
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Figure 1: Capacitive current density in a
toroid of human muscle tissue of unitary radius, to a unitary magnetic
induction, Vignati and Giuliani (1997).
Bawin and Adey (1976) show that a 56 V/m ELF
field induces a tissue gradient of 10-7 V/cm, whereas a 56 V/m
147 MHz signal induces a tissue gradient of 10-1 V/cm, a
million times higher. This is a large factor but smaller than that given
by Figure 1.
These biophysical observations show that the
impacts of RF/MW fields are higher than those of ELF fields of the same
external intensity. It also indicates that the impact rises with carrier
frequency. All of the EMR genetic damage effects are shown to occur with
ELF and RF/MW frequencies, including cell phone frequencies. As the high
frequencies couple more strongly with tissue, the depth of penetration
decreases.
While this paper is primarily about RF/MW
exposures, confirmation of effects is given by studies involving mixed and
ELF exposure.
The Bioelectrical nature of
biology:
The bioelectrical nature of brains, hearts and
cells is poorly appreciated but it is extremely well documented. Frey
(1993, 1995) advocates a change in mind-set from that which he describes
as the toxicological approach of treating EMR as an external disease
agent, to one that considers EMR as an intrinsic feature of cells and
bodies.
Neurological Electrical
Sensitivity:
Coherent thoughts and synchronized biological
processes involve a structured set of low frequency electrical signals
that are monitored as the electroencephalogram (EEG). Figure 2 shows the
spectrum of an awake EEG signal.
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Figure 2: A typical EEG spectrum, with the
Schumann Resonance peaks superimposed.
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Figure 3: Daytime Schumann Resonance Spectrum,
Polk (1982).
It is proven, but not well known, that human
brains detect, use and react to natural low frequency signals, the
Schumann Resonances, König (1974). They have a similar frequency range to that
of the EEG, Figure 3.
The Schumann Resonances are global signals that
radiate from tropical thunderstorms. They propagate around the world
within the cavity created by the earth and the ionosphere. The intensity
and spectrum of the Schumann Resonances vary markedly from day to night
and with solar activity. At night both the EEG and the Schumann Resonances
are dominated by very low frequencies (<5 Hz). With the coincidence of
the frequency ranges, some of the high frequency peaks and the diurnal
variation of the EEG and Schumann Resonances, it is biologically plausible
that there is a resonant interaction between, and EEG reaction to the
changing Schumann Resonance signals.
This biological plausibility is significantly
strengthened by the observation that mammal brains contain and use
phase-locked loop circuitry to detect and react to incoming ELF signals,
Ahissar et al. (1997). Hence our brains contain a highly efficient, tuned
FM receiver, Motluk (1997).
Konig (1974) reports on the results of an
experiment carried out at the Munich Transport Exhibition of 1953, Figure
4. About 49,500 people were recorded in a visual reaction time experiment.
Their reaction times were extremely highly correlated with the intensity
of the Schumann Resonance signals.
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Figure 4: Human reaction times are causally
correlated with natural variations in the Schumann Resonance Intensity,
Konig (1974). The mean Schumann intensity (Relative Schumann Intensity
=0.5) is 0.65mV/m or 0.1pW/cm2. The range is 0.2 to 1.2 mV/m
(0.01 to 0.4pW/cm2).
This result was confirmed by laboratory
experiments that showed that 10 Hz signals significantly and consistently
increase the reaction speed and 3 Hz signals slowed them down, Konig
(1974). These results were independently confirmed by Hamer (1966, 1969).
Hamer observed that human reaction times were significantly altered at
exposure levels down to 4mV/m, 4.2 pW/cm2. This is approaching
the level of the Schumann Resonance signal, which averages about 0.08mV/m,
0.1pW/cm2.
These experiments give substantial proof that
extremely small natural and artificial ELF signals interact significantly
with human brains. The signal level of this interaction is 2,000,000,000
times below the ELF standard. This standard is based on avoiding acute
shocks and not on avoiding proven neurological effects. The maintenance of
the standard is obtained by ignoring or rejecting any and all evidence
that contradicts it.
This early German research, done at the
Technical University of Munich and the Max Planck Institute, König (1974) and Wever
(1974), respectively. This gives a very strong basis for this paradigm
shift that recognizes the exquisite sensitivity of the human brain and its
regulation and synchronization by these very weak naturally occurring
signals.
Electromagnetic activity in
cells:
Cells consist of a nucleus surrounded by the
fluid cytoplasm that is contain within the cell membrane. The cell
membrane consist of a bimolecular layer which is penetrated by many
complex structures, Figure 5.
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Figure 5: A schematic diagram of the cell
membrane, showing the alpha helix of the signal transduction apparatus,
with its "Y" shaped receptors.
The outside surface of the cell membrane, its
receptors and ion channels, is negatively charged, and the inside is
positively charged. This creates a membrane potential. The negative charge
on the receptors helps to attract positively charged first messengers to
them, Figure 5. A first messenger entering its specific receptor, y-shaped
protein on the alpha-helix protein. This initiates an amplification
process that generates a cascade of second messengers into the cell. The
signal is amplified with a gain of between 100,000 and 1 million.
One of the types of structures that helps to
regulate cell activity is the voltage-gated ion channels. They act like
transistors, regulating a current flow of ions within voltage ranges,
Figure 6.
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Figure 6: Voltage-gated ion channel within the
cell membrane, acts like a transistor to control the ion current flow into
and out of the cell, Catterall (1992).
The primary cellular ion is the calcium ion
Ca2+. It is ubiquitous and carries out a host of cellular
communication and regulatory functions. It is a signal transduction first
and second messenger.
One of the first biological mechanisms to be
identified, confirmed and established is calcium ion efflux (positive and
negative), Blackman (1990). One of the early results, Bawin and Adey
(1976), is shown in Figure 7.
Calcium ions were induced to flow out of or
into cells, depending of the combination of exposure conditions. These
combinations are known as "windows" because nearby conditions have
markedly different effects. Figure 7 shows RF induced Ca2+
efflux which is associated with enhanced programmed cell death
(Apoptosis). The ELF induced and Ca2+ influx is associated with
enhanced cell survival of damaged cells, i.e. it enhances cancer.
Gap junctions are protein bridges between
cells. They are fundamental to the cell-to-cell communication that is
necessary to maintain healthy cells, Figure 8.
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Figure 7: ELF induced calcium ion efflux from
(A) an ELF modulated 147 MHz signal and (B) an ELF signal, Bawin and Adey
(1976).
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Figure 8: A Gap Junction structure, a
six-element protein bridge that allows selective molecules to pass between
cells as part of the cell-to-cell communication to coordinate cell
regulation.
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Figure 9: Gap junction flow as a function of 50
Hz magnetic field strength, Li et al. (1999).
Gap junction opening is regulated by calcium
ions and pH, Alberts et al. (1994). Li et al. (1999) observed that when a
50 Hz magnetic field was combined with the application of the cancer
promoter TPA then the gap junction flow was impaired in a significant
dose-response manner as a function of the magnetic field exposure, Figure
9. Li at al. conclude that 50 Hz fields act similarly to the cancer
promoter TPA, in closing the gap junction, and therefore 50 Hz fields may
act as cancer promoters by doing this.
As shown in Figure 1 above, RF signals couple
more strongly to cells and produce far higher induced fields than ELF
fields. Hence RF fields are much more likely to alter Gap Junction
functions at far lower intensities than ELF fields.
Given the fundamental bioelectrical nature of
cells and the ability of imposed electrical signals to alter the voltage
of the outsides of cells, the opening or closing the ion channels, is an
obvious biological mechanism for altering the nature and future of every
cell. Calcium ion efflux from pinealocytes is a plausible mechanism for
EMR induced melatonin reduction. In this, and other ways, alteration of
cellular calcium ions and melatonin reduction both strongly suggest that
EMR is likely to be genotoxic.
Cardiac Electrical
Sensitivity:
Hearts are obviously bioelectrical organs. The
electrocardiogram (ECG) is a fundamental monitoring tool of cardiologists
in diagnosing the state of the heart muscle. The heart-beat occurs as a
series of regular electrical pulses Each electric pulse initiates a
cascade of calcium ions to flood the heart muscle and cause it to
contract. Interference with this regular electrical pulse leads to heart
disease and heart attack of the Arrhythmic kind. We would therefore expect
electromagnetic radiation to cause arrhythmia and heart attack.
Genotoxicity:
Substances that damage cellular genetic
material, such as DNA and chromosomes, are called "genotoxic". Genotoxic
substances cause cancer, reproductive health effects and neurological
damage. Chromosome aberrations are visible through powerful microscopes.
Chromosomes are formed from folded segments of DNA. Damage to chromosomes
is therefore evidence of damage to DNA.
DNA is frequently damaged by natural processes,
such as oxygen free radicals. Gey (1993) comments that free radicals may
be involved in the etiology of cancer and cardiovascular diseases. In
epidemiological studies poor plasma levels of antioxidants (free radical
scavengers) are associated with increased relative risks of cancer and
ischemic heart disease. Cells have elaborate DNA repair mechanisms because
DNA stability is vital for species survival. Uncorrected DNA damage is
mutation, Alberts et al. (1994). Alberts et al. outline many DNA repair
mechanisms, including Repair Enzymes. They also outline the way apoptosis
can digest and destroy damaged cells by internal "programming" of the
process. The Immune System has B lymphocytes that produce antibody
proteins to protect against 'foreign' cells, such as mutated cells.
Natural Killer (NK) cells kill some types of tumours and some
virus-infected cells, Alberts et al.
Enhanced DNA strand breakage leads to enhanced
DNA repair. Hence enhanced DNA repair rates are also used as evidence of
DNA damage, Meltz (1995).
Many studies have shown that
radiofrequency/microwave (RF/MW) radiation and extremely low frequency
(ELF) fields cause increased DNA strand breakage and chromosome
aberrations. This has been shown in cell lines, human blood, animals and
living human beings. This means that epidemiological studies of people
exposed to electromagnetic radiation (EMR) are likely to show increased
cancer, miscarriage and reproductive adverse effects. In fact many
epidemiological studies have shown these effects, Goldsmith (1995, 1996,
1997, 1997a), Szmigielski (1991, 1996).
Two plausible biological mechanisms involving
free radicals are involved in this effect. The first involves increased
free radical activity and genetic damage as a response to exposure. The
second involves increased free radical activity and genetic damage because
of an induced reduction of a free radical scavenger, e.g. reduced
melatonin, Reiter (1994). It is clear however, that both mechanisms have
the same effect of damaging the DNA and chromosomes. Another established
biological mechanism, EMR-induced alteration of cellular calcium ion
homeostasis, Blackman (1990), is also involved in cell regulation, cell
survival and apoptosis, DNA synthesis and melatonin regulation.
Direct measurements of Chromosome
aberrations:
Direct evidence that EMR induces significant
increases in chromosome damage, with significant dose response
relationships, is evidence of a causal effect when replicated or extended
by independent laboratories.
Chromosome damage from RF/MW
exposure:
The first identified study that showed that
pulsed RF radiation cause significant chromosome aberrations was Heller
and Teixeira-Pinto (1959). Garlic roots were exposed to 27 MHz pulsed at
80 to 180 Hz. for 5 min and then they were examined 24 hrs later. The
concluded that this RF signal mimicked the chromosomal aberration produced
by ionizing radiation and c-mitotic substances. No increased temperature
was observed.
Blood samples were taken from the staff of the
U.S. Embassy in Moscow. They had been chronically exposed to a low
intensity radar signal. Significant increases in chromosome damage was
reported, Tonascia and Tonascia (1966) cited in Goldsmith (1997a).
Garaj-Vrhovac et al. (1990) noted the
differences and similarities between the mutagenicity of microwaves and
VCM (vinyl chloride monomer). They studied a group of workers who were
exposed to 10 to 50 m W/cm2 of radar produced microwaves. Some
were also exposed to about 5 ppm of VCM, a known carcinogen. Exposure to
each of these substances (microwaves and VCM) produced highly significant
(p<0.01 to p<0.001) increases in Chromatid breaks, Chromosome
breaks, acentric and dicentric breaks in human lymphocytes from blood
taken from exposed workers. The results were consistent across two assays,
a micronucleus test and chromosome aberration assay.
Chromosome aberrations and micronuclei are
significantly higher than the controls, (p<0.05, p<0.001,
p<0.0001), for each of the exposure intensity.
Garaj-Vrhovac, Horvat and Koren (1991) exposed
Chinese hamster cells to 7.7 GHz microwave radiation to determine cell
survival and chromosome damage. They assayed chromosome aberrations and
micronuclei and found that microwaves increased these in a dose response
manner, Figure 10, to levels that were highly significantly elevated
(p<0.02 to p<0.01).
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Figure 10: Chromosome aberrations in V79
Chinese hamster cells exposed to 7.7 GHz microwaves at 30
mW/cm2, Garaj-Vrhovac, Horvat and Koren (1991).
An exposure level of 30 mW/cm2 is
usually able to slightly raise the temperature over an hour. This
experiment was undertaken under isothermal conditions, with samples being
kept within 0.4° C of 22° C. The consistency of the time exposure and the survival assay at
non-thermal exposure levels, confirms that this is a non-thermal effect.
This is very strong evidence of genotoxic
effects from RF/MW exposures. When chromosomes are damaged one of the
primary protective measures is for the immune system natural killer cells
to eliminate the damaged cells. Alternatively the cells can enter
programmed cell suicide, apoptosis. Garaj-Vrhovac, Horvat and Koren (1991)
measured the cell survival rates. They found that cell survival reduced
and the cell death increased in a time dependent and exposure dose
response manner, Figure 11.
Figure 11 shows that cell death varies with
time and intensity of exposure, down to very low exposure levels. An
apparent 'saturation' at high levels also becoming evident. This is
probably because of the lethal effect of high intensity microwaves. Since
this is an isothermal experiment it raised important questions about the
reasons for the cell death as acute genetic damage which is continuously
related to microwave exposure down to non-thermal levels.
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Figure 11: Cell death percentage of Chinese
hamster cells exposed to 7.7 GHz microwaves (CW) for 30 minutes and 60
minutes in an isothermal exposure system, Garaj-Vrhovac, Horvat and Koren
(1991).
Note that the general public ICNIRP guideline
for microwaves above 2 GHz is 1 mW/cm2, and for workers is 5
mW/cm2. Even at 100 times below the public exposure guideline a
60 minute exposure kills 28% of the cells and 30 minutes kills 8 % of the
cells. Garaj-Vrhovac et al. (1992) exposed human lymphocytes and showed
that microwave radiation produced a dose response increase in chromosome
aberrations, Figure 12.
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Figure 12: The relation of total chromosome
aberrations. micronuclei and specific chromosome aberrations for each cell
in human lymphocyte cultures in the dose of microwave radiation in vitro,
Garaj-Vrhovac et al. (1992).
Having established that microwave exposure
damaged chromosomes, this research group were asked to analyze blood
samples from workers who had been exposed to pulsed microwaves generated
by air traffic control radars while they were repairing them.
Garag-Vrhovac and Fucic (1993) analysed the chromosome aberration (CA) in
6 technical staff who had experienced accidental exposure to the radar.
The initial CA percentage ranged from 3% to 33%, all being significantly
higher than unexposed people. The repair rate over time was monitored.
Figure 10 shows the man who had 33 % CA which was followed over 30 weeks
following this exposure. The repair rate follows a significant linear rate
(r=0.98), dropping from 33% to 3% over 30 weeks, 1 %/week.
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Figure 13: The time-dependent decrease in the
number of chromosome aberrations for subjects with high numbers of
chromosomal impairments, y = 0.318 - 0.010x, r=0.98. Garaj-Vrhovac and
Fucic (1993).
CA Repair rates in other workers are shown in
Figure 14.
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Figure 14: Decreases in human blood Chromosome
Aberrations over time from microwave exposed radar repair workers,
Garag-Vrhovac and Fucic (1993).
Two different rates are evident. Two at 0.6 to
1.1 %/week and two at 0.25 to 0.35 %/week. The authors note that
Sagripanti and Swicord (1986) showed that microwave radiation damaged
single-strand DNA and the Szmigielski (1991) showed that out of 29
epidemiological studies in the previous decade, 22 suggested a
relationship between various neoplasms and exposure to electromagnetic
fields.
Garaj-Vrhovac (1999) found that 12 workers
occupationally exposed to microwave had significantly increased chromosome
damage as well as disturbances in the distribution of cells over the
first, second and third mitotic divisions.
Quite independently, Maes et al. (1993) found
highly significant (p<0.001) increases is the frequency of chromosome
aberrations (including dicentric and acentric fragments) and micronuclei
in human blood exposed to 2.45 GHz microwaves to 30 to 120 minutes in
vitro. The micronuclei assay showed a dose response with time, Figure 15.
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Figure 15: Micronuclei in microwave exposed
human lymphocytes, the average of 4 donors, Maes et al. (1993). Exposure
was to 75 W/kg, 2.45 GHz microwaves pulsed at 50 Hz, under controlled
isothermal conditions
Timchenko and Ianchevskaia (1995), Balode
(1996), Haider et al. (1994) and Vijayalaxmi et al. (1997) have reported
significant chromosome aberrations from RF/MW exposures. In the Mar/Apr
1999 edition of Microwave News it is reported that Drs Tice, Hook and
McRee showed chromosome damage from all cell phones tested, all being
statistically significant and all but one highly significant with
dose-response relationships up to a factor of three increase in chromosome
aberrations.
Vijayalaxmi et al. (1997) chronically exposed
cancer prone mice to 2.45 GHz CW microwaves at an SAR of 1 W/kg for 20
hr/day, 7 days/week for 18 months. Their aim was to determine whether
microwaves were genotoxic through determining if there was significant
chromosome damage. They found highly significant increases in micronuclei
in peripheral blood, from 8 per 2000 cells in sham exposed mice to 9 per
2000 cells microwave exposed mice, and increase of 12.5 %, p<0.001.
There was a significant increase of 6.6%, p<0.025, of micronuclei in
the bone marrow. They also observed a significant 41 % increase in tumours
in the exposed mice compared to the sham exposed mice.
This was a totally unexpected result from this
group. A great deal of effort was put into playing down the implications.
They describe the increase in peripheral blood as a 0.05%, by dividing the
increase of 1 by 2000. This is not a significant increase and this is not
the right comparison. It is a deliberate attempt to disguise their true
result that shows that microwaves are genotoxic.
Multiple independent studies, in 15 papers,
show significant increases in chromosome aberrations from RF/MW exposure.
Four studies show dose-response relationships. This is more than adequate
to classify RF/MW radiation as genotoxic.
Chromosome damage from ELF
exposure:
El Nahas and Oraby (1989) observed significant
dose-response dependent micronuclei increase in 50 Hz exposed mice somatic
cells. Elevated CA have been recorded in a number of workers in electrical
occupations. In Sweden Nordenson et al. (1988) found significant CA in 400
kV-substation workers and with 50 Hz exposures to peripheral human
lymphocytes, Nordenson et al. (1984) and human amniotic cells, Nordenson
et al. (1994). Significant CA in human lymphocytes exposed to 50 Hz fields
are also reported by Rosenthal and Obe (1989), Khalil and Qassem (1991),
Garcia-Sagredo and Monteagudo (1991), Valjus et al. (1993) and Skyberg et
al. (1993). Skyberg et al. collected their samples from high-voltage
laboratory cable splicers and Valjus et al. from power linesmen.
Hence chromosome damage has been recorded from
exposes across the EMR spectrum from ELF to RF/MW exposures, in plants,
mammal and human cells, animals and human beings, and from many
independent laboratories. This confirms that EMR does damage chromosomes
and establishes EMR induced chromosome aberrations as a biological effect.
For a neoplastic cell to survive it must have an altered genetic structure
to store the damage and to hide this from the immune system so that NK
cells do not kill the neoplasm transformed cells.
Chromosome Aberrations
Conclusions:
Many studies, from independent laboratories,
have shown that ELF, RF/MW and cell phone radiation, significantly
increases chromosome aberrations in exposed cells, including cells taken
from human beings who have been exposed to EMR in occupational situations.
Even at very low intensity radar exposures that were experienced at the
U.S. Embassy in Moscow, significant increases in chromosome damage was
measured from human blood samples. This evidence shows conclusively that
across the EMR spectrum, EMR is genotoxic. Hence it is carcinogenic and
teratogenic.
Direct evidence of neoplasm in microwave
exposed cells:
Balcer-Kubiczek and Harrison (1991) observed a
significant dose response increase of neoplastic transformation in a
standard cell set (C3H/10T1/2) from a 24 hr exposure to 2.45 GHz
microwaves. The transformation was assayed after 8 weeks of exposure to a
known cancer promoter chemical TPA, Figure 16. The method was confirmed
with a positive control using X-rays. This also showed that 60Hz magnetic
fields also significantly increased neoplasmic transformation.
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Figure 16: Dose-response relationship for
induction of neoplasmic transformation in C3H/10T1/2 cells by a 24h
exposure to 2.45 GHz microwaves at the specific absorption rate (SAR) with
and without TPA post-treatment for 8 weeks, Balcer-Kubiczek and Harrison
(1991).
Direct evidence of DNA strand
breakage:
Sarkar, Ali and Behari (1994) investigated the
effect on DNA of exposures accepted a safe by the Non-ionizing Radiation
Committee of IRPA (International Radiation Protection Association - the
predecessor of ICNIRP).
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Figure 17: Densitometric analysis of the brain
DNA, a and b are control DNA, c to g are DNA from exposed animals. Peak 1
is present in both control and exposed animals while peak 2 appears only
in all of the exposed animals.
The exposure regime was a 2 hr exposure to 2.45
GHz CW microwaves at 1 mW/cm2, SAR = 1.18 W/kg. They observed
significant alterations in the DNA from rat brains and testis in the 7 to
8 kb region of the DNA in the hybridization profile and in a densitometric
analysis, Figure 17.
The Comet Assay Method:
A very advanced assay of DNA strand breakage
has been developed by Dr N.P. Singh at the University of Washington. This
is called the microgel electrophoresis or Comet Assay, Singh et al.
(1994). The Comet Assay involves migration of segments of DNA down an
electric field gradient, Figure 18.
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Figure 18: Photographs of double-strand break
DNA migration pattern of individual brain cells from rats exposed to (a)
bucking condition (0.1 mT), (b) magnetic fields of 0.1 mT, (c) 0.25 mT and
(d) 0.5 mT, Lai and Singh (1997a). The "bucking mode" is the condition to
reverse the field to cancel the magnetic fields with all else remaining
constant.
The modified microgel electrophoresis assay or
Comet Assay for single DNA-strand breaks, involves extraction of a sample
of tissue, washing it several times to remove blood, snipping the tissue
with sharp scissors to reduce the sample sizes and further washing to
remove blood. Single cell suspensions are mixed with agarose to make a
microgel on a slide that is cooled to form a gel. Slides are immersed in
an ice-cold lysing solution and then stored in the dark at 4 ° C.
DNA is closely associated with protein and RNA.
They help to fold the DNA. To release DNA from these bonds, one has to use
Proteinase K to digest proteins and RNAase A to digest RNA. Hence in the
morning the slides were treated with DNAase-free proteinase K for 2 hr at
37 ° C to
remove the bound protein from the DNA. They were then places on the
horizontal slab of an electrophoretic assembly. An electrophoresis buffer
is added and the sample is left for 20 min to allow the DNA to unwind. The
buffer includes antioxidants to counter the free radicals produced by
electrophoresis.
The electrophoresis was then carried out for 60
minutes with 0.4 V/m, 250 mA. During this process the fluid in the
assembly is re-circulated at the rate of about 100 ml/min. The negatively
charged segments of DNA migrate down the electric field gradient, forming
a comet-like tail, the mass of which is proportional to the amount of
damaged DNA material and the electric field gradient and time of exposure.
For DNA double-strand breaks the microgel
preparation is the same as above. Slides are then treated with
ribonuclease A for 2 hr and then proteinase K for 2 hr. They are then
placed in the neutral electrophoresis buffer (pH 9) for 20 mins and then
electrophorezed for 1 hr at 0.4 V/cm. For both single- and double- strand
assays the sample are stained with an intense florescent dye solution of
YOYO-1 and then examined in a vertical florescent microscope.
The proteinase K treatment is vital. It removes
the bound protein from the DNA strands. DNA and protein have the opposite
charge and so for the electric field to cause migration, the protein must
be removed. Four slides were prepared for each animal, two for single and
two for double-strand assays. Fifty representative cells were scored off
each slide, giving 100 cells scored for each of the single and
double-strand DNA breaks. Frequency distributions for the 100 assayed
cells are presented, Figure 19, and the comet tail moment calculated.
_files/Image71.gif)
Figure 19: Single- and double-strand DNA breaks
frequency distribution for percentage of cells of a given tail length from
pulsed RFR and sham exposed brain cells, from 8 animals and 100 cells per
animal, Lai and Singh (1996).
Figure 19 clearly shows significant increases
in single- and double-strand DNA breaks from the pulsed microwave exposed
animal brains compared with the sham exposed animals. The tail DNA
fragments extend out to 250 microns. The Comet tails in the Malyapa et al.
assay extend to less than 40 microns. This clearly documents how less
sensitive their method is.
Motorola Funded Counter Research on DNA
breakage:
Motorola funded Dr Joseph Roti Roti's group at
Washington University, St Louis, to replicate the Lai/Singh DNA damage
research and to extend it to cell phone frequencies. "Replication"
requires the work to be very closely following the method and conditions
of the earlier study. While both groups used 2.45 GHz microwaves for
exposure, the follow up study used a cell line (C3H/10T1/2) compared to
living rats, and they used a very different DNA damage assay based on
Olive et al. (1992) not Singh et al. (1994). This follow up study used a
much weaker fluorescent stain, an overall weaker electrophoresis field
(0.6 V/cm for 25 mins c.f. 0.4 V/cm for 60 mins) and did not use
proteinase K to separate the bound protein from the DNA strands. It is
therefore understandable why they didn't observe DNA stand breakage from
MW exposure.
_files/Image72.gif)
Figure 20: Frequency Distribution of Comet tail
lengths for 2.45GHz exposed C3H10T1/2 cells, Malyapa et al. (1998).
Differences between Lai and Singh and
Malyapa et al.:
There are five primary differences between the
Lai and Singh Comet Assay method derived from Singh at al. (1994) used at
the University of Washington and the Comet assay method used at Washington
University by Malyapa et al, derived from Olive et al. (1992).
The following factors make the Lai/Singh Assay
more sensitive than that of Malyapa et al.:
- Complete lysis using highly concentrated
salt and two detergents.
- The use of proteinase K to remove the
positively charges bound protein from the negatively charged DNA stands
so that the electrophoresis field produces more migration.
- The use of antioxidants during
electrophoresis.
- Electrophoresis for a longer time to allow
longer tails to form in the "Comet". Lai and Singh have 250 micron tails
while Malyapa et al. have 40 micro tails.
- The use of the YOYO-1 dye. YOYO-1 is
100-fold more sensitive when bound to DNA than propidium iodide.
Hence there are basic practical scientific
reasons why Lai and Singh observe EMR-induced DNA strand breaks with RF/MW
exposures, whereas Malyapa et al. don’t. Two independent laboratories have
shown that EMR, including cell phone radiation at extremely low
intensities, causes DNA strand breaks. They are Verschaeve et al. (1994)
and Phillips et al. (1998), who used the Lai/Singh method.
The Comet Assay and EMR
effects:
Drs Lai and Singh have now shown that ELF and
RF/MW radiation both cause single and double strand DNA breakage and are
associated with free radical and reduced melatonin in living exposed rats.
Lai and Singh (1995) observed a dose response increase in Single-strand
DNA breakage in the rat’s brain and hippocampus that increased
significantly after 4 hours, Figure 21. The increases in DNA single-strand
breakage after 4 hrs is highly significant, p<0.001 and they show a
dose-response relationship.
_files/Image73.gif) _files/Image74.gif)
Figure 21: DNA single-strand breakage in cells
from the rat brain and hippocampus, immediately after a 2 hr exposure to a
whole body SAR of 0.6 and 1.2 W/kg to 2.45 GHz microwave radiation, pulsed
at 500 pps. N is the number of rats studied. Lai and Singh (1995).
The assay method was extended to measure DNA
double-strand breakage. Lai and Singh (1996) reported that both continuous
wave (CW) and pulsed microwaves caused significant (p<0.01) increased
single-strand DNA breakage, and double-strand breakage, CW, p<0.05) and
pulsed, p<0.01), Figure 22.
This shows that both continuous and pulsed
microwaves cause single and double DNA strand breakage, but pulsed
microwaves cause more than continuous waves. Hence pulsed cell phone
signals and radar signals are highly likely to cause DNA damage. This has
been confirmed for radar and chromosome aberrations above and for cell
phones by Phillips et al. (1998).
_files/Image75.gif)
Figure 22: Single-strand (left) and
double-strand (right) breaks in brain cells of rat after exposure to
pulsed or continuous-wave RFR. Each bar represents data from 8 rats, Lai
and Singh (1996).
In the mean time Lai and Singh (1997)
investigated the mechanism which is involved with this genotoxic effect of
RF/MW radiation. They treated the microwave exposed rats with melatonin
and a spin-trap compound (PBN) to determine the role of free radicals.
They showed that both melatonin and PBN eliminated the microwave induced
DNA damage. Figure 23 shows the effect of melatonin for single- and
double- strand DNA breaks and Figure 24 the same for PBN.
_files/Image76.gif)
Figure 23: Effect of treatment with melatonin
for RFR-induced increase in DNA single-strand (left) and double-strand
(right) breaks in rats brain cells. Data was analysed using the one-way
ANOVA, which showed a significant treatment effect (p<0.001) for both
cases. "vehicle" involves injecting with the physiological saline without
the active substance. Lai and Singh (1997)
Lai and Singh (1997) conclude that if free
radicals are involved in the RFR-induced DNA strand breaks in brain cells,
the results of their study could have an important implication of the
health effects of RFR exposure. Involvement of free radicals in human
diseases, such as cancer and atherosclerosis, have been suggested. Free
radicals also play an important role in aging processes, Reiter, (1995).
They also point out that both melatonin and PBN can have other actions on
cells in the brain that can decrease DNA damage. Therefore further support
is necessary to interpret these results.
_files/Image77.gif)
Figure 24: Effect of treatment with PBN for
RFR-induced increase in DNA single-strand (left) and double-strand (right)
breaks in rats brain cells. Data was analysed using the one-way ANOVA,
which showed a significant treatment effect (p<0.001) for both cases.
"vehicle" involves injecting with the physiological saline without the
active substance. Lai and Singh (1997).
Phelan et al. (1992) exposed B-16 melanoma cell
line to pulsed 2.45 GHz, 100 pps, 1hr exposure SAR = 0.2 W/kg. This
resulted in changes of membrane ordering. Their data indicated that a
significant, specific alteration of the cell-membrane ordering followed
microwave exposure and that the alteration was due at least part, to the
generation of oxygen radicals. Hence there is independent support for the
generation of free radicals by microwaves, as well as the Lai/Singh
evidence that PBN and Melatonin reduce the RFR induced DNA damage.
Two other laboratories have recorded RF/MW
produced significant DNA stands breaks. Verschave et al. (1994), who used
a GSM cell phone signal to expose human and rat peripheral blood
lymphocytes, found significantly increased strand breaks at high, but
non-thermal exposure levels. Phillips et al. (1998) exposed Molt-4
T-lymphoblastoid cells the a range of cell phone radiation in the SAR
range 0.0024 W/kg to 0.026 W/kg for both iDEN and TDMA signals. Using the
basic equations, these SARs at the 813-836 MHz range [SAR = s
E2/2r , s
=1 S/m, r
=800 kg/m3, and S = E2/3.77 m W/cm2, E: the electric
field gradient in V/m and S the exposure in m W/cm2] result in 1.0 to
11.0m
W/cm2. A 2 hr exposure to these low levels of cell phone
radiation significantly increased (p<0.0001) or decreased (p<0.0001)
the DNA damage. Decreased DNA damage is evidence of increased repair that
is evidence of damage, Meltz (1995).
Hence RF/MW radiation has been confirmed to
enhance DNA damage under RF/MW exposure from radar-like and cell phone
exposures, including an exposure level which is 0.22% of the ICNIRP
guideline.
ELF Exposure and DNA strand
breakage:
Four independent laboratories have also
published data on ELF induced DNA strand breaks confirming that ELF EMR
damages DNA strands; Lai and Singh (1997a), Svedenstal et al. (1998),
Phillips et al. (1998a), and Ahuja et al. (1997). Lai and Singh (1997a)
also demonstrate the involvement of free radicals and the protective
effect of melatonin. With the evidence above that EMR reduces melatonin
this confirms that reduced melatonin causes higher concentrations of free
radicals which produce more DNA strand breaks from EMR exposure from ELF
to RF/MW frequencies. Increased DNA strand breaks will result in increased
chromosome aberrations.
Multiple evidence from independent laboratories
established that EMR from ELF to RF/MW causes DNA single- and
double-strand breaks at very low, non-thermal exposure levels. This
extends and confirms the genotoxic evidence from chromosome aberration
studies.
EMR Altered Gene Activity
There is also evidence that EMR not only can
damage chromosomes and DNA strands, but it is observed to alter cellular
calcium ions and the activity levels of proto oncogenes (cancer genes).
Blackman (1990) concluded that there was
overwhelming evidence that EMR can alter normal calcium ion homeostasis
and lead to changes in the response of biological systems to their
environment. On of these changes is altered gene transcription and
expression. The lowest published exposure level associated with
significant EMR-induced alteration of cellular calcium ions occur is
reported by Schwartz et al. (1990). It was 0.00015 W/kg in a 30 min
exposure to a 240 MHz signal modulated at 16 Hz. The medium was frog
hearts. This is equivalent to an exposure level of about 0.06 m W/cm2.
Calcium ion fluxes occur in "windows" of
exposure parameter combinations. Two studies associate EMR exposure
alteration of gene transcription with exposure windows. Litovitz et al.
(1990) identified amplitude (intensity) windows, and Wei et al. (1990)
frequency windows in the range 15 to 150 Hz. They observed a peak effect
in c-myc gene transcription at 45 Hz. Liburdy et al. (1993) show that
c-myc induction occurs in a direct sequence from calcium ion influx.
Increased c-myc gene transcripts by 50/60 Hz fields has also been
observed, Goodman et al. (1989, 1992) and Lin et al. (1994). Phillips et
al. (1992, 1993) observed time-dependent changes in the transcription of
c-fos, c-jun, c-myc and protein kinase C, from 60 Hz exposure and a linear
reduction in ras p21 expression by a 72 Hz signal. 50/60 Hz signals
altered c-jun and c-fos gene expression as observed by and Lagroye and
Poncy (1998) and c-fos expression by Rao and Henderson (1996) and
Campbell-Beachler et al. (1998). The ppSom gene is very important in human
neurological disorders, and is regulated by calcium ions Capone, Choi and
Vertifuille (1998).
Cell phone radiation (836.55 MHz) significantly
altered c-jun transcript levels, Ivaschuk et al. (1997). Cell phone
radiation significantly enhances the proto oncogene c-fos activity in C3H
10T 1/2 cells, from a 40 % (p=0.04) increase from a digital cell phone and
a 2-fold increase (p=0.001) from an analogue cell phone, Goswami et al.
(1999).
Hence proto oncogene activity is altered and
enhanced in multiple independent experiments from ELF and RF/MW exposure,
including cell phone radiation.
Immune system impairment by
EMR
Impairment of the immune system is related to
calcium ion efflux, Walleczek (1992) and to reduced melatonin, Reiter and
Robinson (1995). Cossarizza et al. (1993) showed that ELF fields increased
both the spontaneous and PHA and TPA- induced production of interleukin-1
and IL-6 in human peripheral blood. Rats exposed to microwaves showed a
significant reduction in splenic activity of natural killer (NK) cells,
Nakamura et al. (1997).
Dmoch and Moszczynski (1998) found that
microwave exposed workers had decreased NK cells and a lower value of the
T-helper/T-suppressor ratio was found. Moszczynski et al. (1999) observed
increased IgG and IgA and decreased lymphocytes and T8 cells in TV signal
exposed workers. Quan et al. (1992) showed that microwave heating of human
breast milk highly significantly suppressed the specific immune system
factors for E.Coli bacteria compared with conventional heating. Chronic,
25 year, exposure to an extremely low intensity (<0.1m W/cm2)
156-162 MHz, 24.4 Hz pulse frequency, radar signal in Latvia produced
significant alterations in the immune system factors of exposed villagers,
Bruvere et al. (1998).
EMR Reduces Melatonin in Animals and
People
DNA strand breaks, Chromosome Aberrations,
impaired immune system competence and many other biological and health
effects, are caused by reduced melatonin, Reiter and Robinson (1995).
Light-at-night and electromagnetic radiation, are proven to reduce
melatonin and hence pose significant adverse health effects.
The evidence for EMR reduction of melatonin is
summarized here. Rosen, Barber and Lyle (1998) state that seven different
laboratories have reported suppression of nighttime rise in pineal
melatonin production in laboratory animals. They show that a 50
m T, 60 Hz
field with a 0.06m T DC field, over 10 experiments, averages a 46% reduction in
melatonin production from pinealocytes. Stark et al. (1997) observed a
significant increase in salival melatonin in a group of 5 cows when the
short-wave radio transmitter at Schwarzenberg, Switzerland, was turned off
for three days, compared to 5 cows that had much lower RF exposure. Hence
there are now nine independent observations of melatonin reduction in
animals from ELF and RF exposure.
Fifteen studies from show that ELF and RF/MW
exposure reduces melatonin and enhances serotonin in people. Evidence that
EMR reduced melatonin in human beings commenced with Wang (1989) who found
that workers who were more highly exposed to RF/MW had a dose-response
increase in serotonin, and hence indicates a dose-response reduction in
melatonin. Fourteen studies have observed significant EMR associated
melatonin reduction in humans. They involve a wide range of exposure
situations. This includes 16.7 Hz fields, Pfluger et al. (1996); 50/60 Hz
fields, Wilson et al. (1990), Graham et al. (1994), Wood et al. (1998),
Karasek et al. (1998), Burch et al. (1997, 1998, 1999a, 2000), Juutilainen
et al. (2000) and Graham et al. (2000a); combination of 60 Hz fields and
cell phone use, Burch et al. (1997,1999a); VDTs ELF/RF exposures, Arnetz
et al. (1996), and a combination of occupational 60Hz exposure and
increased geomagnetic activity around 30nT, Burch et al. (1999b).
The fourteenth human melatonin reduction study
is from 6.1-21.8 MHz SW RF exposure as reported during the shutting down
process of the Schwarzenburg shortwave radio tower, Professor Theo Abelin
(seminar and pers.comm.). Urinary melatonin levels were monitored prior to
and following the closing down of the Schwarzenburg short wave radio
transmitter. This showed a significant rise in melatonin after the signal
was turned off.
Fifteen studies is sufficient to establish that
EMR reduces melatonin in people from exposures across the EMR spectrum,
and at extremely low mean exposure levels.
Genotoxicity Conclusions:
There is more than sufficient evidence of
chromosome aberrations, DNA strand breakage altered oncogene activity and
neoplastic transformation if cells to conclude that EMR across the
spectrum from ELF to RF/MW is genotoxic. This is independently confirmed
by the established biological mechanisms of calcium ion efflux and
melatonin reduction.
His is also totally independent of over a
hundred occupational groups showing elevated cancer from EMR exposure,
scores showing significantly to extremely significantly elevated cancer
incidence and mortality, and dozens of dose response relationships.
Epidemiological dose-response relationships
from RF/MW exposures:
Dose-response relationships are shown here
because they are very strong evidence of cause and effect and they give
guidance as to the exposure levels involved. It should be noted however,
that many other studies show significant increases in all of the cancer,
cardiac, neurological and reproductive effects reported here. All occur at
long-term mean exposure levels more than 100 times below the ICNIRP
guideline, and residential studies involve mean exposures more than 1000
times lower than the public exposure guideline.
The guidance given by Sir Austin Bradford Hill,
Hill (1965) shows that even a consistent non-significant relationship can
be assessed as a causal effect. When a dose response relationship is
obtained then it is very strong evidence of a causal effect.
"Classic" RF/MW studies:
Two U.S. radar exposure studies are classically
quoted as showing no effects. This is not true to the data contained in
Lilienfeld et al. (1978) and Robinette et al. (1980). Both show
significantly elevated mortality and morbidity for a range of diseases,
including cancer, cardiac and neurological diseases. Some symptoms also
occur with significant dose-response relationships.
Lilienfeld et al. (1978) report on the health
effects of staff and dependents exposed to low level radar signals during
tours of duty at the U.S. Embassy in Moscow.
Dose-response relationships as a function of
years of exposure to these radar signals are shown in Figure 25 for
Present Health Summary (p=0.05), Arthritis/Rheumatism (p=0.02), Back Pain
(p=0.04), Skin and Lymphatic disease (p=0.02) and Vaginal Discharge
(p=0.04). Figure 26 shows the dose-responses for Vascular System disease
(p=0.004) and Ear Problems (p=0.02).Hence this study suggests that chronic
exposure to extremely low intensity RF/MW radiation from radar produces a
wide range of illnesses in a dose-response manner.
_files/Image78.gif)
Figure 25: Rates of sickness increases
significantly with years of exposure, in the people chronically exposed to
low intensity radar at the U.S. Embassy in Moscow, Lilienfeld et al.
(1978).
_files/Image79.gif)
Figure 26: Rates of sickness increases
significantly with years of exposure, in the people chronically exposed to
low intensity radar at the U.S. Embassy in Moscow, Lilienfeld et al.
(1978).
Robinette et al. (1980) studied the health
effects of radar exposed naval technical personnel who had served on ships
during the Korean War. When a 5% sample of servicemen were assessed for
personal exposure in a job-matrix exposure survey, they were shown to have
a significant dose-response increase in Total Mortality and Respiratory
Cancer as a function of exposure level as assessed by the Hazard Number.
Figure 27 shows the dose-response relationships for these mortalities with
the lowest exposure range used as a reference with RR=1.0.
_files/Image80.gif)
Figure 27: Dose-response relationships of
mortality from all causes and respiratory cancer for radar exposure
assessed personnel, Robinette et al. (1980).
_files/Image81.gif)
Figure 28: Naval occupations grouped by
exposure category, showing dose response increases in mortality for all
mortality, all disease, cancer and Lymphatic/Leukaemia. Low exposure
(RM+RD), Intermediate exposure ET+FT), High exposure (AT).
Grouping occupational groups according to
exposure levels also reveals dose-response increases for Total Death, All
Disease, All Cancer and Lymphatic/hematopoietic Cancer, Figure 28. Hence
it is shown that these are not "no effects" studies. Rather they show
significant dose response increases in death, cancer and a wide range of
diseases. They also show significant increases of many mortality and
morbidity health effects.
Global Leukaemia dose response for RF/MW
exposure:
Leukaemia is frequently significantly raised in
RF/MW exposed populations. Table 1 summarizes several studies that are
ranked in mean exposure order. Military, occupational and residential
studies shows a global dose response relationship for increased adult
leukaemia and RF/MW exposure with a dose-response threshold close to zero.
When actual residential exposures are
considered, dose responses for residential cancer are also shown by Dolk
et al. (1997 a,b) and Michelozzi et al. (1998). These show a causal effect
of adult and childhood leukaemia are levels of residential exposure
involving exposure levels produced by cell sites out to over 500m.
Table 1: A summary of epidemiological studies
involving adult leukaemia mortality or incidence, ranked by probable RF/MW
exposure category.
Study Reference Exposure Leukaemia Risk 95%
Confidence
Category Type Ratio Interval
Polish Military Szmigielski (1996) High ALL
5.75 1.22-18.16
(Mortality) CML 13.90 6.72-22.12
CLL 3.68 1.45-5.18
AML 8.62 3.54-13.67
All Leuk. 6.31 3.12-14.32
Korean War Robinette et al. (1980) High
Leuk/Lymp 2.22 1.02-4.81
Radar Exposure (Mortality) AT/ET
Radio and TV Milham (1985) Moderate Acute Leuk.
3.44
Repairmen Leuk. 1.76
Amateur Radio Milham (1988) Moderate AML 1.79
1.03-2.85
(Mortality)
UK Sutton Dolk et al. (1997a) Moderate Leuk
1.83 1.22-2.74
Coldfield <=2km
North Sydney Hocking et al.(1996) Low All Leuk.
1.17 0.96-1.43
TV/FM towers ALL+CLL 1.39 1.00-1.92
(Mortality) AML+CML 1.01 0.82-1.24
Other Leuk 1.57 1.01-2.46
UK TV/FM Dolk et al. (1997b) Low Adult Leuk.
1.03 1.00-1.07
(Incidence)
Note: ALL : Acute Lymphatic Leukemia; CLL:
Chronic Lymphatic Leukaemia; AML Acute Myeloid Leukaemia; CML: Chronic
Myeloid Leukaemia; and All Leuk.: All Adult Leukaemia.
Childhood Cancer in the vicinity of the
Sutra Tower, San Francisco:
Many studies have identified elevated childhood
leukaemia for children living in the vicinity of high voltage powerlines,
Hardell et al. (1995), including a dose-response relationships, Wertheimer
and Leeper (1979), Savitz et al. (1988), London et al. (1991) and
Feychting et al. (1995). These should be sufficient for a causal
relationship.
_files/Image82.gif)
Figure29: Two early childhood leukaemia studies
show dose response relationships for the Wire Category which is the best
estimate of the long-term mean magnetic field.
Selvin et al. (1992) studied the spatial
distribution of 4 childhood cancers in relation to the Sutra Tower in San
Francisco. When measured and practical radial exposure patterns are
compared with the radial cancer rates a highly significant dose response
relationship results, Figure 30.
_files/Image41.gif)
Figure 30: The measured and estimated power
density (exposure in m W/cm2) with distance from the Sutra Tower.
Circles show measurements. The line follows measurement points and the
radial pattern of a typical UHF transmission beyond 3 km. From Hammett and
Edison (1997) and readings taken by the author in 1999.
Because of the complex nature of residential
radial broadcast tower exposure patterns, Figure 30, the chance of
confounding effects are extremely small. Thus this indicates a causal
relationships Plotting the radial residential mean exposure and the "All
Cancer" Risk Ratio gives the pattern in Figure 31. The match shows that no
other factor can explain this result than the RF exposure from the Sutra
Tower.
_files/Image83.gif)
Figure 31: The radial All Cancer Risk Ratio and
the mean residential RF exposure (times 20 to fit on the scale).
_files/Image43.gif)
Figure 32: All Cancer Risk Ratio for Childhood
Cancer as a function of estimated radial group mean personal exposure to
RF/MW radiation from the Sutra Tower, San Francisco, using the spatial
childhood cancer data presented in Selvin et al. (1992). The dose-response
relationship is extremely significant (p<0.0001).
Within the data uncertainty, the dose-response
threshold is zero. Hence RF/MW is causally associated with adult and
childhood cancer, including leukaemia with a dose-response relationship
with a zero exposure threshold.
Neurological effects:
Brains are very electromagnetically sensitive
because our sight, thoughts, memories, learning and emotions use complex
electromagnetic signals. Research in Germany in the post war period proved
that human brains detect and use extremely small natural low frequency
(ELF) EMR signals, Wever (1974), Konig (1974). Since RF/MW signals induce
higher currents in human tissues and low frequency signals it is
inevitable that we will observe neurological effects from chronic RF/MW
exposures.
Recent studies have revealed some neurological
dose response relationships for sleep disturbance, Multiple Sclerosis and
Suicide at extremely low exposures to RF and ELF exposures. Beale et al.
(1997) found significant dose response for psychological symptoms,
including anxiety and depression, living in proximity to high voltage
powerlines. This strongly confirms the sensitivity of human brains to EMR
exposure.
These studies have early roots in U.S. Embassy
in Moscow study. Lilienfeld et al. (1978), showed significant neurological
effects from chronic low level radar exposure, including Depression
(p=0.004), Irritability (p=0.009), Memory Loss (p=0.008) and Difficulty in
Concentrating (p=0.001).
These are all symptoms related to melatonin
reduction. The Korean War Study, Robinette et al. (1980) also found
increased neurological health effects from personnel who were exposed to
radar on ships during the Korean War. These symptoms between a high
exposure group (FT+AT) and a low exposure group (ET), Mental Conditions,
RR = 1.68, 95%CI: 1.13-2.50, p<0.01 and Neurological illness, RR =
1.42, 95%CI: 0.74-2.72.
Mild et al. (1998) show significant
dose-response relationships for cell phone usage and headaches, dizziness,
memory loss, discomfort, fatigue, and loss of concentration. Dose
responses were shown for both calls/day and minutes/day. Figures 33 and 34
show the minutes/day graphs for Norway and Sweden, respectively. Norway is
dominantly analogue and Sweden digital.
The analogue phones used in Norway typically
have higher SAR levels than the digital phones used in Sweden. The
sensation of warmth on an behind the ear is much stronger in Norway. The
symptoms reported in Norway are somewhat more prevalent than in Sweden.
For example, the Fatigue prevalence in Norway for more than 60 mins per
day is 28% and in Sweden it is 20%. The difference is quite marked for all
symptoms except Concentration and Memory Loss. These are the same symptoms
that have frequently been reported as "Microwave Sickness Syndrome" or
"Radiofrequency Sickness Syndrome", Baranski and Czerski (1976) and
Johnson-Liakouris (1998).
_files/Image84.gif)
Figure 33: Prevalence of symptoms for Norwegian
mobile phone users, mainly analogue, with various categories of length of
calling time per day, Mild et al. (1998).
_files/Image85.gif)
Figure 34: Prevalence of symptoms for Swedish
mobile phone users, mainly digital, with various categories of length of
calling time per day, Mild et al. (1998).
Sleep Disturbance near a Shortwave Radio
Tower, Schwarzenburg, Switzerland:
The Schwarzenburg Study, Alpeter et al. (1995)
and Abelin (1999) showed a causal relationship of sleep disturbance with
exposure to a short wave radio signal. The effect is assessed as causal
because of the significant dose response relationship, the variation of
sleep disturbance in two experiments, one involving changing the beams and
one turning the transmitter off, and the identification of significant
melatonin reduction. Professor Abelin told seminars in Christchurch that
they had measured a significant increase in melatonin after the tower
transmission was turned off permanently compared to the levels while it
was on.
Groups B, R and C are all exposed to a mean RF
signal of less than 0.1m W/cm2 and they experienced highly
significant sleep disturbance and reduced melatonin. Since sleep
disturbance, Mann and Roschkle (1995), and melatonin reduction, Burch et
al. (1997), has been observed with cell phone exposure. Hence these
observations also apply to cell phones and cell sites.
_files/Image86.gif)
Figure 35: Adult Sleep Disturbance with RF
exposure at Schwarzenburg, Switzerland, Abelin (1999).
Sleep disruption occurs in a dose-response
manner with a threshold below 0.1nW/cm2. ie. very close to
zero, Figure 36.
_files/Image87.gif)
Figure 36: Dose-response relationship for Sleep
Disturbance at Schwarzenburg with exposure in nW/cm2. Note:
1nW/cm2= 0.001m W/cm2
Multiple Sclerosis in Danish Electric
Utility Workers:
A study of 26,124 men working in Danish utility
companies were studied for their incidence of multiple sclerosis (MS) in
relation to average work-related exposure to electromagnetic fields. A
small group of 15 men were shown to have a dose-response incidence of MS
as a function of EMF exposure, Figure 37. The lowest group is used as a
reference (RR=1.0).
_files/Image88.gif)
Figure 37: Dose response relationship of
Multiple Sclerosis for a small group (N=15) of men occupationally exposed
to typical peak magnetic fields in a Danish utility company, Johansen et
al. (1999).
The authors conclude that they find no support
for the hypothesis. In fact, despite the small sample size, their data
shows very strong support for the hypothesis that EMR is associated with
adverse neurological effects at extremely low mean exposure levels.
Suicide in U.S. Electric Utility
Workers:
A very large study of men working in U.S.
electric utility companies included monitoring time weighted average ELF
exposures of 2842 people and the identification of 536 deaths from suicide
and 5348 controls. For recent exposure and 1 to 5 years of recent exposure
there were significant dose-response relationships with cumulative
exposure to electromagnetic fields. The recent exposure result is shown in
Figure 38.
This confirms the results of Perry et al.
(1981) who found a highly significant association between suicide and the
exposure to magnetic fields from High Voltage Powerlines. Baris and
Armstrong (1990) also found RF exposure shows a significant 53% increase
in suicide or British Radio and Radar Mechanics, and 156 % increase for
Telegraph radio operators.
_files/Image89.gif)
Figure 38: Dose response relationship of
Suicide after recent monitored exposure to cumulative 50 Hz magnetic
fields for men <50 years, adjusted for work, class, location and
exposure to sunlight and solvents, Wijngaarden et al. (1999).
Non-linear response for neurological effects at
extremely low exposure levels are evident in the three studies presented
here for sleep disturbance, multiple sclerosis and suicide
Brain Tumour with VDT
exposure:
Beall et al. (1997) found significant increases
in brain tumour, especially glioma, among long-term workers using
computers who are exposed to a mix of ELF and RF radiation from the VDTs.
For long-term computer users, Engineering/technical users show a
non-significant dose response, but computer programmers show a significant
dose-response relationship, Figure 39.
_files/Image90.gif)
Figure 39 Dose-response increases in brain
tumour from years of working with computers, Beall et al. (1997).
Melatonin reduction, clinical depression
(Verkasalo et al., 1997), and suicide are all significantly and/or dose
response related to EMR exposure. Along with sleep disruption and brain
tumour, this constitutes a very strong and coherent set of data supporting
a causal relationship between ELF to RF/MW exposure, including cell phone
usage, and neurological illness and death.
GABA is a primary neurotransmitter that is
involved in many neurological processes. Many neurological systems have up
to 60% of the synapses that are regulated by GABA (gamma-amino butyric
Acid). Substances that alter GABA can cause abnormal pathologies.
Kolomytkin et al. (1995) conclude that GABA systems are very sensitive to
microwaves. GABA indicator molecules are altered in a dose-response manner
by microwaves in living rat brains, Figure 40.
_files/Image91.gif)
Figure 40: Exposure related alteration of GABA
related molecules in rat brains exposed to 915 MHz microwaves, pulsed at
16 pps. Differences from controls are still significant at 10m W/cm2,
Kolomytkin et al. (1995)
Natural EMR Sensitivity of the Human
brain:
Since human brains detect and use naturally
occurring ELF signals under 1pW/cm2 then our brains can detect
and react to signals many orders of magnitude higher than this.
Interactions include resonant absorption of signals with particular ELF
signal or modulation frequency ranges, and interference with the natural
signals so that they cannot reliably perform their functions. These
functions include regulations of hormones such as melatonin and thyroid
stimulating hormone (TSH). Both of these have been shown to be reduced by
cell phone exposures. Reduced melatonin leads to increased DNA strand
breaks and chromosome aberrations. These in turn lead to cancer and
reproductive effects.
Cardiac Effects of EMR:
Hearts use natural electric pulses to produce
heart-beats. An electric pulse produces a cascade of calcium ions that
cause the heart muscle to contract. The Electrocardiogram (ECG) is used to
monitor heart activity and can detect heart disease through the altered
electrical signals. Hence it is biologically plausible that electric
signals, that are shown to interfere with artificial pacemakers, can also
interfere with the natural heart-beat. This has been shown in several
studies in relation to reduction of the heart rate variability (HRV). This
is a known risk factor for heart disease.
Satre, Cook and Graham (1998) observed
significantly reduced heart rate variability (HRV) in volunteers sleeping
in 60Hz fields. Extrinsic EMR signals interfere with hearts and cause
heart disease and death. Bortkiewicz et al. (1995, 1996, 1997) and
Szmigielski et al. (1998) found that RF exposure altered heart rate
variability and blood pressure. Forman et al.(1982) present case studies
of microwave exposed personnel with induced hypertension. Braune et al.
(1998) showed that cell phone significantly increased blood pressure.
Savitz et al. (1999) found a highly significant dose response relationship
for mortality from Arrhythmia related heart disease and heart attack
(Acute Myocardial Infarction) for exposed electrical occupations and for
individual occupations of electrician, lineman and power plant operator.
Hamburger, Logue and Silverman (1983) observed
significant dose responses for heart disease for male physiotherapists as
a function of treatments per month with microwaves, OR = 2.51 (1.09-5.78),
Trend p<0.05); shortwave, OR = 3.40 (1.56-7.39), trend p=0.005; and
Combined Microwave and Shortwave, OR = 2.88 (1.21-6.70), trend p=0.025.
This is a powerful set of epidemiological
evidence showing that EMR across the spectrum increases the incidence and
mortality from arrhythmia related heart disease and from heart attack. The
following graph shows the dose-response curve for Acute Myocardial
Infarction (Heart Attack) in electric utility workers, Figure 41.
_files/Image92.gif)
Figure 41: Acute Myocardial Infarction as a
function of cumulative exposure to 60 Hz fields in U.S. electricity
utility workers, Savitz et al. (1999).
Savitz et al. (1999) show crude dose responses
for Cardiac Arrhythmia related heart disease and a highly significant
dose-response, Figure 41, for Heart Attack.
Miscarriage in microwave exposed
Physiotherapists, United States:
Physiotherapists have been exposed to
microwaves and shortwave radiation in the course of diathermy of patients.
From a large survey group 6,684 women reported using microwave or
shortwave radiation at some time during their work history. A total of
1753 pregnancies involving first trimester miscarriage were matched to
1753 control pregnancies. This revealed a 7%, but non-significant rise in
miscarriage associated with shortwave exposure and a significant 28%
increase in first trimester miscarriage for those exposed to microwaves,
including a highly significant (p<0.005) dose response relationship,
Figure 42.
Exposure levels were based on 3 minutes
exposure per treatment to 600m W/cm2, a peak exposure level near the middle
of the reported range. This gives 0.042m W/cm2 per treatment per
month, to give a month mean dose response based on treatments per month.
_files/Image93.gif)
Figure 41: Microwave exposure associated
miscarriage for pregnant physiotherapists, Ouellet-Hellstrom and Stewart
(1993).
_files/Image94.gif)
Figure 42: ELF/RF/MW exposure from VDT usage
increases miscarriage in a dose-response manner, Lindbohm et al. (1992).
Occupational usage of computers, with their
mixed RF/ELF exposures, have also shown a dose-response increase in
miscarriage, Lindbohm et al. (1992), Figure 43.
Reproductive effects in mice has been shown in
residential RF exposures by Magras and Xenos (1997). Mice became totally
infertile after 3 generations in 1.05m W/cm2 and after 5
generations exposed to 0.17m W/cm2, Figure 44. This shows a dose-response
for RF induced infertility. Youbicier-Simo et al. (1998) showed that
mobile phone significantly increased the mortality of chicken embryos.
_files/Image95.gif)
Figure 44: Reproductive rates in two groups of
mice exposed to extremely low intensity radio signals, showing a dose
response in the time taken to achieve full infertility of 3 matings for
1.503m
W/cm2 and 5 matings for 0.168m W/cm2.
This supports the adverse reproductive effects
and very low exposure levels shown by Ouellet-Hellstrom and Stewart. And
Lindbohm et al. Youbicier-Simo et al. (1999) showed that cell phone
radiation caused more mortality of embryonic chickens showing that cell
phone radiation is significantly associated with reproductive effects.
Conclusions:
Many multiple independent laboratories have
shown the ELF and RF/MW radiation causes chromosome aberrations and DNA
single- and double-strand damage. These include many dose response
relationships and extremely low RF/MW exposure levels including cell phone
radiation. Multiple studies also show significantly altered proto
oncogenes expression and activity with ELF and RF/MW exposure. This also
includes cell phone radiation. Several studies show impairment of the
immune system health.
Since calcium ion efflux and melatonin
reduction are established biological effects of EMR exposure from ELF to
RF/MW, impair immune systems should be observed in EMR exposures. Multiple
independent evidence is available for RF exposures, down to extremely low
chronic mean levels, and many dose response relationships are established
to prove that these biological effects from EMR exposure is genotoxic.
Significant DNA strand breakage has been observed down to 1 m W/cm2,
Phillips et al. (1998), with elevated DNA damage below this. Therefore
there is extremely strong evidence that EMR across the spectrum is
genotoxic, even at very low exposure levels found in the vicinity of cell
sites, Figure 45.
_files/Image96.gif)
Figure 45: Summary of observed effects, and the
mean levels of the exposure for human studies of exposure to
electromagnetic radiation. All epidemiological studies occur below the
ICNIRP and New Zealand Standard of allowable exposure.
These genotoxic biological mechanisms strongly
support the large number of epidemiological studies that show significant
increases of cancer, neurological, cardiac and reproductive health effects
from ELF and RF/MW exposure in military, occupation, and residents
studies. Altogether they show a causal relationship from EMR exposure and
wide-spread adverse health effects. All of these adverse health effects
are shown to be significantly increased in multiple epidemiological
studies, including many with significant dose-response relationships. This
data puts the situation in a very clear light. There are causal
relationships between extremely low mean EMR exposures across the spectrum
and a wide range of serious adverse health effects.
Cell Phone Conclusions:
Cell phones will high probably increase many
neurological diseases and brain tumours over the next 10 to 20
years
Cell sites will highly probably increase
miscarriage, many cancers, many diseases, significant neurological and
cardiac diseases and death.
Thousands of cell sites being installed in
communities, are significantly raising the exposure of millions of people
to RF/MW at levels that are know to cause serious adverse health
effects.
The problems are going to increase unless
rapid, drastic and determined moves are made to reverse the trend and only
install new sites in locations that produce extremely low mean residential
exposures,
somewhat less than 10
nW/cm2 (0.01m W/cm2).
References:
Alberts, B., Bray, D., Lewis, J., Raff, M.,
Roberts, K. and Watson, J.D., 1994: "Molecular Biology of the cell". 3rd
edition, New York, Garland Publishing, 1994.
Abelin, T, 1999: Sleep disruption with exposure
to a Shortwave Radio transmission, Seminar at CRC.
Ahissar, E., Haidarliu, S. and Zacksenhouse,
M., 1997: "Decoding temporally encoded sensory input by cortical
oscillations and thalamic phase comparators". Proc Nat Acad Sci USA
94:11633-11638.
Altpeter, E.S., Krebs, Th., Pfluger, D.H., von
Kanel, J., Blattmann, R., et al., 1995: "Study of health effects of
Shortwave Transmitter Station of Schwarzenburg, Berne, Switzerland".
University of Berne, Institute for Social and Preventative Medicine,
August 1995.
Arnetz, B.B. and Berg, M., 1996: "Melatonin and
Andrenocorticotropic Hormone levels in video display unit workers during
work and leisure. J Occup Med 38(11): 1108-1110.
Balcer-Kubiczek, E.K. and Harrison, G.H., 1991:
"Neoplastic transformation of C3H/10T1/2 cells following exposure to 120Hz
modulated 2.45 GHz microwaves and phorbol ester tumor promoter". Radiation
Research, 125: 65-72.
Balode, Z., 1996: "Assessment of
radio-frequency electromagnetic radiation by the micronucleus test in
Bovine peripheral erythrocytes". The Science of the Total Environment,
180: 81-86.
Baranski, S. and Czerski, P., 1976: "Biological
effects of microwaves". Publ. Dowden, Hutchison and Ross, Inc.
Stroudsburg, Pennsylvania.
Baris, D. and Armstrong, B., 1990: "Suicide
among electric utility workers in England and Wales". Br J Indust Med
47:788-789.
Bawin, S.M. and Adey, W.R., 1976: "Sensitivity
of calcium binding in cerebral tissue to weak electric fields oscillating
at low frequency". Proc. Natl. Acad. Sci. USA, 73: 1999-2003.
Beale, I.L., Pearce, N.E., Conroy, D.M.,
Henning, M.A., and Murrell, K., A., 1997: "Psychological effects of
chronic exposure to 50 Hz magnetic fields in humans living near
extra-high-voltage transmission lines". Bioelectromagnetics, 18(8):
584-94.
Beall, C., Delzell, E., Cole, P., and Brill,
I., 1996: "Brain tumors among electronics industry workers". Epidemiology,
7(2): 125-130.
Blackman, C.F., 1990: "ELF effects on calcium
homeostasis". In "Extremely low frequency electromagnetic fields: The
question of cancer", BW Wilson, RG Stevens, LE Anderson Eds, Publ.
Battelle Press Columbus: 1990; 187-208.
Bortkiewicz, A., Zmyslony, M., Palczynski, C.,
Gadzicka, E. and Szmigielski, S., 1995: "Dysregulation of autonomic
control of cardiac function in workers at AM broadcasting stations
(0.738-1.503 MHz)". Electro- and Magnetobiology 14(3): 177-191.
Bortkiewicz, A., Gadzicka, E. and Zmyslony, M.,
1996: "Heart rate in workers exposed to medium-frequency electromagnetic
fields". J Auto Nerv Sys 59: 91-97.
Bortkiewicz, A., Zmyslony, M., Gadzicka, E.,
Palczynski, C. and Szmigielski, S., 1997: "Ambulatory ECG monitoring in
workers exposed to electromagnetic fields". J Med Eng and Tech
21(2):41-46.
Braune, S., Wrocklage, C., Raczek, J., Gailus,
T. and Lucking C.H., 1998: "Resting blood pressure increase during
exposure to a radio-frequency electromagnetic field". The Lancet, 351,
June 20, 1988, 1857-1858.
Brueve, R., Feldmane, G., Heisele, O., Volrate,
A. and Balodis, V., 1998: "Several immune system functions of the
residents from territories exposed to pulse radio-frequency radiation".
Presented to the Annual Conference of the ISEE and ISEA, Boston
Massachusetts July 1998.
Burch, J.B., Reif, J.S., Pittrat, C.A., Keefe,
T.J. and Yost, M.G., 1997: "Cellular telephone use and excretion of a
urinary melatonin metabolite". In: Annual review of Research in Biological
Effects of electric and magnetic fields from the generation, delivery and
use of electricity, San Diego, CA, Nov. 9-13, P-52.
Burch, J.B., Reif, J.S., Yost, M.G., Keefe,
T.J. and Pittrat, C.A., 1998: "Nocturnal excretion of urinary melatonin
metabolite among utility workers". Scand J Work Environ Health 24(3):
183-189.
Burch, J.B., Reif, J.S., Yost, M.G., Keefe,
T.J. and Pittrat, C.A., 1999a: "Reduced excretion of a melatonin
metabolite among workers exposed to 60 Hz magnetic fields" Am J
Epidemiology 150(1): 27-36.
Burch, J.B., Reif, J.S. and Yost, M.G., 1999b:
"Geomagnetic disturbances are associated with reduced nocturnal excretion
of melatonin metabolite in humans". Neurosci Lett 266(3):209-212.
Burch, J.B., Reif, J.S., Noonan, C.W. and Yost,
M.G., 2000: "Melatonin metabolite levels in workers exposed to 60-Hz
magnetic fields: work in substations and with 3-phase conductors". J of
Occupational and Environmental Medicine, 42(2): 136-142.
Burke, J., 1985: "The Day the Universe
Changed". Publ. Little and Co., Boston.
Campbell-Beachler, M., Ishida-Jones, T.,
Haggren, W. and Phillips, J.L., 1998: "Effect of 60 Hz magnetic field
exposure on c-fos expression in stimulated PC12 cells". Mol Cell Biochem
189(1-2): 107-111.
Capone, G., Choi, C. and Vertifuille, J., 1998:
"Regulation of the prepromsomatostatin gene by cyclic-AMP in
cerebrocortical neurons". Bran Res Mol Brain Res 60(2): 247-258.
Catterall, W.A., 1992: "Cellular and molecular
biology of voltage-gated sodium channels". Physiological Reviews 72(4):
S15-S48.
Cossarizza, A., Angioni, S., Petraglia, F.,
Genazzani, A.R., Monti, D., Capri, M., Bersani, F., Cadossi, R. and
Franceschi, C., 1993: "Exposure to low frequency pulsed electromagnetic
fields increases interleukin-1 and interleukin-6 production by human
peripheral blood mononuclear cells". Exp Cell Res 204(2):385-387.
Dmoch, A. and Moszczynski, P., 1998: "Levels of
immunoglobulin and subpopulations of T lymphocytes and NK cells in men
occupationally exposed to microwave radiation in frequencies of 6-12GHz".
Med Pr 49(1):45-49.
Dolk, H., Shaddick, G., Walls, P., Grundy, C.,
Thakrar, B., Kleinschmidt, I. and Elliott, P., 1997a: "Cancer incidence
near radio and television transmitters in Great Britain, I -
Sutton-Colfield transmitter". American J. of Epidemiology, 145(1):1-9.
Dolk, H., Elliott, P., Shaddick, G., Walls, P.,
Grundy, C., and Thakrar, B.,1997b: "Cancer incidence near radio and
television transmitters in Great Britain, II All high power transmitters".
American J. of Epidemiology, 145(1):10-17.
El Nahas, S.M. and Oraby, H.A., 1989:
"Micronuclei formation in somatic cells of mice exposed to 50 Hz electric
fields. Environ Mol Mutagen 13(2):107-111.
Feychting, M., Schulgen, G., Olsen, J.H., and
Ahlbom, A., 1995: "Magnetic fields and childhood cancer- pooled analysis
of two Scandinavian studies". European J. of Cancer, 31A (12): 2035-2039.
Feychting, M, Schulgen, G., Olsen ,J.H. and
Ahlbom, A., 1995: "Magnetic fields and childhood cancer - a pooled
analysis of two Scandinavian studies". Eur. J. Cancer 31A(12): 2035-2039.
Forman, S.A., Holmes, C.K., McManamon, T.V.,
and Wedding, W.R., 1982: "Physiological Symptoms and Intermittent
Hypertension following acute microwave exposure". J. of Occup. Med.
24(11): 932-934.
Frey, A.H., 1993: "Electromagnetic field
interactions with biological systems". FASEB J., 7: 272-281.
Frey, A.H., 1995: "An integration of the data
on mechanisms with particular reference to cancer", Chapter 2 in "On the
Nature of electromagnetic Field Interactions with Biological Systems", Ed
A.H. Frey, Publ. R.G. Landes Co. Medical Intelligence Unit, Austin, Texas.
Frey, A.H., 1998: "Headaches from cellular
telephones: are they real and what are the impacts". Environ Health
Perspect 106(3):101-103.
Garcia-Sagredo, J.M. and Monteagudo, J.L.,
1991: "Effect of low-level pulsed electromagnetic fields on human
chromosomes in vitro: analysis of chromosome aberrations". Hereditas
115(1): 9-11.
Garaj-Vrhovac, V., Fucic, A, and Horvat, D.,
1990: "Comparison of chromosome aberration and micronucleus induction in
human lymphocytes after occupational exposure to vinyl chloride monomer
and microwave radiation"., Periodicum Biologorum, Vol 92, No.4, pp
411-416.
Garaj-Vrhovac, V., Horvat, D. and Koren, Z.,
1990: "The effect of microwave radiation on the cell genome". Mutat Res
243: 87-93 (1990).
Garaj-Vrhovac, V., Horvat, D. and Koren, Z.,
1991: "The relationship between colony-forming ability, chromosome
aberrations and incidence of micronuclei in V79 Chinese Hamster cells
exposed to microwave radiation". Mutat Res 263: 143-149.
Garaj-Vrhovac, V., Fucic, A, and Horvat, D.,
1992: The correlation between the frequency of micronuclei and specific
aberrations in human lymphocytes exposed to microwave radiation in vitro".
Mutation Research, 281: 181-186.
Garaj-Vrhovac, V., and Fucic, A., 1993: "The
rate of elimination of chromosomal aberrations after accidental exposure
to microwave radiation". Bioelectrochemistry and Bioenergetics,
30:319-325.
Gey, K.F., 1993: "Prospects for the prevention
of free radical disease, regarding cancer and cardiovascular disease".
British Medical Bulletin, 49(3): 679-699.
Goldsmith, J.R., 1995: "Epidemiological
Evidence of Radiofrequency Radiation (Microwave) Effects on Health in
Military, Broadcasting, and Occupational Studies". International Journal
of Occupational and Environmental Health, 1, pp 47-57, 1995.
Goldsmith, J.R., 1996: "Epidemiological studies
of radio-frequency radiation: current status and areas of concern". The
Science of the Total Environment, 180: 3-8.
Goldsmith, J.R., 1997: "TV Broadcast Towers and
Cancer: The end of innocence for Radiofrequency exposures". Am. J.
Industrial Medicine 32 : 689-692.
Goldsmith, J.R., 1997a: "Epidemiologic evidence
relevant to radar (microwave) effects". Environmental Health Perspectives,
105 (Suppl 6): 1579-1587.
Goswami, P.C., Albee, L.D., Parsian, A.J.,
Baty, J.D., Moros, E.G., Pickard, W.F., Roti Roti, J.L. and Hunt, C.R.,
1999: "Proto-oncogene mRNA levels and activities of multiple transcription
factors in C3H 10T 1/2 murine embryonic fibroblasts exposed to 835.62 and
847.74 MHz cellular telephone communication frequency radiation". Radiat
Res 151(3): 300-309.
Graham, C., Cook, M.R., Cohen, H.D. and
Gerkovich, M.M., 1994: "A dose response study of human exposure to 60Hz
electric and magnetic fields". Bioelectromagnetics 15: 447-463.
Graham, C., Cook, M.R., Sastre, A., Riffle,
D.W. and Gerkovich, M.M., 2000: "Multi-night exposure to 60 Hz magnetic
fields: effects on melatonin and its enzymatic metabolite". J Pineal Res
28(1): 1-8.
Haider, T., Knasmueller, S., Kundi, M, and
Haider, M., 1994: "Clastogenic effects of radiofrequency radiation on
chromosomes of Tradescantia". Mutation Research, 324:65-68.
Hamburger, S., Logue, J.N., and Sternthal,
P.M., 1983: "Occupational exposure to non-ionizing radiation and an
association with heart disease: an exploratory study". J Chronic Diseases,
Vol 36, pp 791-802.
Hammett and Edison Inc., 1997: "Engineering
analysis of radio frequency exposure conditions with addition of digital
TV channels". Prepared for Sutra Tower Inc., San Francisco, California,
January 3, 1997.
Hardell, L., Holmberg, B., Malker, H., and
Paulsson, L.E., 1995: "Exposure to extremely low frequency electromagnetic
fields and the risk of malignant diseases--an evaluation of
epidemiological and experimental findings". Eur. J. Cancer Prevention,
1995 Sep;4 Suppl 1:3-107
Heller, J.H., and Teixeira-Pinto, A.A., 1959:
"A new physical method of creating chromosome aberrations". Nature, Vol
183, No. 4665, March 28, 1959, pp 905-906.
Hocking, B., Gordon, I.R., Grain, H.L., and
Hatfield, G.E., 1996: "Cancer incidence and mortality and proximity to TV
towers". Medical Journal of Australia, 165: 601-605.
Ivaschuk, O.I., Jones, R.A., Ishida-Jones, T.,
Haggren, Q., Adey, W.R. and Phillips, J.L., 1997: "Exposure of nerve
growth factor-treated PC12 rat pheochromscytoma cells to a modulated
radiofrequency field at 836.55 MHz: effects on c-jun and c-fos
expression". Bioelectromagnetics 18(3): 223-229.
Johanson C, Kock-Henriksen N, Rasmussen S,
Olsen JH. 1999: "Multiple Sclerosis among utility workers". Neurology 52:
1279-1282.
Johnson-Liakouris, A.J.. 1998: "Radiofrequency
(RF) Sickness in the Lilienfeld Study: an effect of modulated microwaves".
Arch Environ Heath 53(3):236-238.
Juutilainen, J., Stevens, R.G., Anderson, L.E.,
Hansen, N.H., Kilpelainen, M., Laitinen, J.T., Sobel, E. and Wilson, B.W.,
2000: "Nocturnal 6-hydroxymelatonin sulphate excretion in female workers
exposed to magnetic fields". J Pineal Res 28(2): 97-104.
Karasek, M., Woldanska-Okonska, M., Czernicki,
J., Zylinska, K. and Swietoslawski, J., 1998: "Chronic exposure to 2.9 mT,
40 Hz magnetic field reduces melatonin concentrations in humans". J Pineal
Research 25(4): 240-244.
Khaili, A.M. and Qassem, W., 1991: "Cytogenetic
effects of pulsing electromagnetic field on human lymphocytes in vitro:
chromosome aberrations, sister-chromatid exchanges and cell kinetics".
Mutat Res 247: 141-146.
König HL. 1974, Behavioural changes in human
subjects associated with ELF electric fields. In Persinger MA, editor. ELF
and VLF electromagnetic field effects. New York, Plenum Press.
Kolomytkin, O., Kuznetsov, V., Yurinska, M,
Zharikova, A., and Zharikov, S., 1995: "Response of brain receptor systems
to microwave energy exposure". pp 195-206 in "On the nature of
electromagnetic field interactions with biological systems", Ed Frey,
A.H., Publ. R.G. Landes Co.
Lagroye, I, and Poncy J.L., 1998: "Influences
of 50 Hz magnetic fields and ionizing radiation on c-jun and c-fos
oncoproteins". Bioelectromagnetics 19(2): 112-116.
Lai, H. and Singh, N.P., 1995: "Acute
low-intensity microwave exposure increases DNA single-strand breaks in rat
brain cells". Bioelectromagnetics 16: 207-210.
Lai, H. and Singh, N.P., 1996: "Single- and
double-strand DNA breaks in rat brain cells after acute exposure to
radiofrequency electromagnetic radiation". Int. J. Radiation Biology, 69
(4): 513-521.
Lai, H. and Singh, N.P., 1996a: "Reply to
"Comment on 'Acute low-intensity microwave exposure increases DNA
single-strand breaks in rat brain cells' ". Bioelectromagnetics 17: 166.
Lai, H., and Singh, N.P., 1997a: "Melatonin and
N-tert-butyl-a-phenylnitrone Block 60 Hz magnetic field-induced DNA
single- and double-strands Breaks in Rat Brain Cells." Journal of Pineal
Research 22:152-162.
Lai, H., and Singh, N.P., 1997b: "Melatonin and
Spin-Trap compound Block Radiofrequency Electromagnetic Radiation-induced
DNA Strands Breaks in Rat Brain Cells." Bioelectromagnetics 18:446-454.
Li, C.M., Chiang, H., Fu, Y.D., Shao, B.J.,
Shi, J.R. and Yao, G.D., 1999: "Effects of 50Hz magnetic fields on gap
junction intercellular communication". Bioelectromagnetics 20(5):290-294.
Liburdy, R.P., Callahan, D.E., Harland, J.,
Dunham, E., Sloma, T.R. and Yaswen, P., 1993: "Experimental evidence for
60 Hz magnetic fields operating through the signal transduction cascade -
effects on calcium influx and c-MYC mRNA induction". FEBS Lett 334(3):
301-308.
Lilienfeld, A.M., Tonascia, J., and Tonascia
S., Libauer, C.A., and Cauthen, G.M., 1978: "Foreign Service health status
study - evaluation of health status of foreign service and other employees
from selected eastern European posts". Final Report (Contract number
6025-619073) to the U.S. Dept of State, July 31, 1978.
Lin, H., Goodman, R. and Shirley-Henderson, A.,
1994: "Specific region of the c-myc promoter is responsible for electric
and magnetic fields". J Cell Biochem 54 30: 281-288.
Lindbohm, M-L,, Hietanen, M., Kyyronen, P.,
Sallmen, M., von Nandelstadh, P., Taskinen, H., Pekkarinen, M., Ylikoski,
M. and Hemminki, K., 1992: "Magnetic fields of video display terminals and
spontaneous abortion". Am J Epidemiol 136:1041-1051.
Litovitz, T.A., Montrose, C.J., Goodman, R. and
Elson, E.C., 1990: "Amplitude windows and transiently augmented
transcription from exposure to electromagnetic fields".
Bioelectromagnetics 11(4): 297-312.
London, S.J., Thomas, D.C., Bowman, J.D.,
Sobel, E., Chen, T.S. and Peters J.M., 1991: "Exposure to residential
electric and magnetic fields and risk of childhood leukemia". Am. J.
Epidemiology 134 (9): 923-937.
Maes, A., Verschaeve, L., Arroyo, A., De
Wagter, C. and Vercruyssen, L., 1993: "In vitro effects of 2454 MHz waves
on human peripheral blood lymphocytes". Bioelectromagnetics 14: 495-501.
Maes, A., Collier, M., Slaets, D., and
Verschaeve, L., 1996: "954 MHz Microwaves enhance the mutagenic properties
of Mitomycin C". Environmental and Molecular Mutagenesis, 28: 26-30.
Malyapa, R.S., Ahern, E.W., Bi, C., Straube,
W/L/., LaRegina, M., Pickard, W.F. and Roti Roti, J.L., 1998: "DNA damage
in rat brain cells after in vivo exposure to 2450 MHz electromagnetic
radiation and various methods of euthanasia". Radiation Research 149(6):
637-645.
Magras, I.N. and Xenos, T.D., 1997: "RF
radiation-induced changes in the prenatal development of mice".
Bioelectromagnetics 18: 455-461.
Mann, K.,and Roschkle, J, 1995: "Effects of
pulsed high-frequency electromagnetic fields on human sleep".
Neuropsychobiology, 33: 41-47.
Meltz, M.L., 1995: "Biological effects versus
health effects: an investigation of the genotoxicity of microwave
radiation". In: Radiofrequency Radiation Standards, NATO ASI Series (B.J.
Klauebberg Ed). New York, Plenum Press, 1995: 235-241.
Michelozzi, P., Ancona, C., Fusco, D.,
Forastiere, F. and Perucci, C.A., 1998: "Risk of leukamia and residence
near a radio transmitter in Italy". ISEE/ISEA 1998 Conference, Boston
Mass. Paper 354 P., Abstract in Epidemiology 9(4):S111.
Mild, K.H., Oftedal, G., Sandstrom, M., Wilen,
J., Tynes, T., Haugsdal, B. and Hauger E., 1998: "Comparison of symptoms
by users of analogue and digital mobile phones - A Swedish-Norwegian
epidemiological study". National Institute for working life, 1998:23,
Umea, Sweden, 84pp.
Milham S. 1985, Mortality in workers exposed to
electromagnetic fields. Environ Health Perspectives 62:297-300.
Milham S. 1988, Increased mortality in amateur
radio operators due to lymphatic and hematopoietic malignancies. Am. J.
Epidemiol 127(1): 50-54.
Moszczynski, P., Lisiewicz, J., Dmoch, A.,
Zabinski, Z., Bergier, L., Rucinska, M. and Sasiadek, U., 1999: "The
effect of various occupational exposures to microwave radiation on the
concentrations of immunoglobulins and T lymphocyte subsets". Wiad Lek
52(1-2):30-34.
Motluk, A., 1997: "Radio head: The brain has
its own FM receiver". New Scientist, 25 October 1997, p17.
Nakamura, H., Seto,T., Nagase, H., Yoshida, M.,
Dan, S. and Ogina, K., 1997: "Effects of exposure to microwaves on
cellular immunity and placental steroids in pregnant rats. Occup Environ
Med 54(9):676-680.
Nordenson, I., Mild, K.H., Nordstrom, S.,
Sweins, A. and Birke, E., 1984: "Clastogenic effects in human lymphocytes
of power frequency electric fields". Radiat Environ Biophys 23(3):
191-201.
Nordenson, I., Mild, K.H., Ostman, U. and
Ljungberg, H., 1988: "Chromosome effects in lymphocytes of 400
kV-substation workers". Radiat Environ Biophys 27(1): 39-47.
Nordenson, I., Mild, K.H., Andersson, G., and
Sandstrom, M., 1994: "Chromosomal aberrations in human amniotic cells
after intermittent exposure to 50 Hz magnetic fields". Bioelectromagnetics
15(4):293-301.
Ouellet-Hellstrom, R. and Stewart, W.F., 1993:
"Miscarriages among Female Physical Therapists who report using radio- and
microwave- frequency electromagnetic radiation." American J. of
Epidemiology, 138 (10): 775-86.
Perry, F.S., Reichmanis, M., Marino, A. and
Becker, R.O., 1981: "Environmental power-frequency magnetic fields and
suicide". Health Phys 41(2): 267-277.
Pfluger, D.M. and Minder, C.E., 1996: "Effects
of 16.7 Hz magnetic fields on urinary 6-hydroxymelatonin sulfate excretion
of Swiss railway workers". J Pineal Research 21(2): 91-100.
Phelan, A.M., Lange, D.G., Kues, H.A, and
Lutty, G.A., 1992: "Modification of membrane fluidity in
Melanin-containing cells by low-level microwave radiation".
Bioelectromagnetics, 13 : 131-146.
Philips, J.L., Haggren, W., Thomas, W.J.,
Ishida-Jones, T. and Adey, W.R., 1992: "Magnetic field-induced changes in
specific gene transcription". Biochem Biophys Acta 1132(2): 140-144.
Philips, J.L., Haggren, W., Thomas, W.J.,
Ishida-Jones, T. and Adey, W.R., 1993: "Effect of 72 Hz pulsed magnetic
field exposure on ras p21 expression in CCRF-CEM cells". Cancer Biochem
Biophys 13(3): 187-193.
Phillips, J.L., Ivaschuk, O., Ishida-Jones, T.,
Jones, R.A., Campbell-Beachler, M. and Haggnen, W., 1998: "DNA damage in
molt-4 T-lymphoblastoid cells exposed to cellular telephone radiofrequency
fields in vitro". Bioelectrochem Bioenerg 45: 103-110.
Phillips, J.L., Campbell-Beachler, M.,
Ivaschuk, O., Ishida-Jones, T., R.A.,. and Haggnen, W., 1998a: "Exposure
of molt-4 T-lymphoblastoid cells to a 1g sinusoidal magnetic field at 60
Hz, In: 1998 Annual Review of research on biological effects of electric
and magnetic fields from generation, delivery and use of electricity; W/L
Associates, Ltd, Frederick, MD.
Polk, C., 1982: "Schumann Resonances". In: CRC
Handbook of Atmospherics, Ed: Hans Volland. Boca Raton, Florida: CRC
Press, 111-177.
Quan, R., Yang, C., Rubinstein, S., Lewiston,
N.J., Sunshine, P., Stevenson, D.K. and Kerner, J.A., 1992: "Effects of
microwave radiation on anti-infective factors in human milk". Pediatrics
89(4):667-669.
Rao, S. and Henderson, A., 1996: "Regulation of
c-fos is affected by electromagnetic fields". J Cell Biochem 63(3):
358-365.
Robinette, C.D., Silverman, C. and Jablon, S.,
1980: "Effects upon health of occupational exposure to microwave radiation
(radar)". American Journal of Epidemiology 112(1): 39-53.
Rosenthal, M. and Obe, G., 1989: "Effects of 50
Hz electromagnetic fields on proliferation and on chromosomal alterations
in human peripheral lymphocytes untreated and pretreated with chemical
mutagens". Mutation Research 210(2): 329-335.
Reiter, R.J., 1994: "Melatonin suppression by
static and extremely low frequency electromagnetic fields: relationship to
the reported increased incidence of cancer". Reviews on Environmental
Health. 10(3-4):171-86, 1994.
Reiter, R.J. and Robinson, J, 1995: "Melatonin:
Your body's natural wonder drug". Publ. Bantam Books, New York.
Rosen, L.A., Barber, I. and Lyle D.B., 1998: "A
0.5 G, 60 HZ magnetic field suppresses melatonin production in
pinealocytes". Bioelectromagnetics 19: 123-127.
Sagripanti, J. and Swicord, M.L., 1976: DNA
structural changes caused by microwave radiation. Int. J. of Rad. Bio.,
50(1), pp 47-50, 1986.
Sarkar, S., Sher, A., and Behari, J., 1994:
"Effect of low power microwave on the mouse genome: A direct DNA
analysis". Mutation Research, 320: 141-147.
Sastre, A., Cook, M.R. and Graham, C., 1998:
"Nocturnal exposure to intermittent 60 Hz magnetic fields alters human
cardiac rhythm". Bioelectromagnetics 19: 98-106.
Savitz, D.A., Wachtel, H., Barnes, F.A., John,
E.M. and Tvrdik, J.G., 1988: "Case-control study of childhood cancer and
exposure to 60Hz magnetic fields". Am.J. Epidemiology 128: 21-28.
Savitz, D.A., Liao, D., Sastre, A., Klecjner,
R.C., and Kavet, R., 1999: "Magnetic field exposure and cardiovascular
disease mortality among electric utility workers". Am. J. Epidemiology,
149(2): 135-142.
Schwan, H.P., 1985: "Biophysical principles of
the interaction of ELF fields with living matter". Publ. Plenum Press, New
York.
Schwartz,, J.L., House, D.E., and Mealing,
A.R., 1990: "Exposure of frog hearts to CW or amplitude modulated VHF
fields: selective efflux of calcium ions at 16 Hz." Bioelectromagnetics,
11: 349-358.
Selvin, S., Schulman, J. and Merrill, D.W.,
1992: "Distance and risk measures for the analysis of spatial data: a
study of childhood cancers". Soc. Sci. Med., 34(7):769-777.
Singh, N.P., Stevens, R.E., and Schneider,
E.L., 1994: "Modification of alkaline microgel electrophoresis for
sensitive detection of DNA damage". Int. J. of Rad. Biolo. 66: 23-28.
Skyberg, K., Hansteen, I.L., and Vistnes, A.I.,
1993: "Chromosome aberrations in lymphocytes of high-voltage laboratory
cable splicers exposed to electromagnetic fields". Scandinavian Journal of
Work, Environment & Health.19(1):29-34.
Stark, K.D.C., Krebs, T., Altpeter, E., Manz,
B., Griol, C. and Abelin, T., 1997: "Absence of chronic effect of exposure
to short-wave radio broadcast signal on salivary melatonin concentrations
in dairy cattle". J Pineal Research 22: 171-176.
Szmigielski, S., 1991: International Science
Meeting, Beograd, 8-11 April 1991, p 34.
Szmigielski, S., 1996: "Cancer morbidity in
subjects occupationally exposed to high frequency (radiofrequency and
microwave) electromagnetic radiation". Science of the Total Environment,
Vol 180, 1996, pp 9-17.
Szmigielski, S., Bortkiewicz, A., Gadzicka, E.,
Zmyslony, M. and Kubacki, R., 1998: "Alteration of diurnal rhythms of
blood pressure and heart rate to workers exposed to radiofrequency
electromagnetic fields". Blood Press. Monit, 3(6): 323-330.
Timchenko, O.I., and Ianchevskaia, N.V., 1995:
"The cytogenetic action of electromagnetic fields in the short-wave
range". Psychopharmacology Series, Jul-Aug;(7-8):37-9.
Tonascia, J.A. and Tonascia, S., 1969:
"Hematological Study: progress report on SCC 31732", George Washington
University, Department of Obstectrics and Gynecology, February 4, 1969.
Valjus, J., Norppa, H., Jarventaus, H., Sorsa,
M., Nykyri, E., Salomaa, S., Jarvinen, P., and Kajander, J., 1993:
"Analysis of chromosomal aberrations, sister chromatid exchanges and
micronuclei among power linesmen with long-term exposure to 50-Hz
electromagnetic fields". Radiation & Environmental Biophysics, 32(4):
325-36.
Verkasalo, P.K., Kaprio, J., Varjonen, J.,
Romanov, K., Heikkila, K., and Koskenvuo, M., 1997: "Magnetic fields of
transmission lines and depression". Am. J. Epidemiology, 146(12): 1037-45.
Verschaeve, L., Slaets, D., Van Gorp, U., Maes,
A. and Vanderkom, J., 1994: "In vitro and in vivo genetic effects of
microwaves from mobile phone frequencies in human and rat peripheral blood
lymphocytes". Proceedings of Cost 244 Meetings on Mobile Communication and
Extremely Low Frequency field: Instrumentation and measurements in
Bioelectromagnetics Research. Ed. D, Simunic, pp 74-83.
Vignati, M. and Giuliani, L., 1997:
"Radiofrequency exposure near high-voltage lines". Environmental Health
Perspectives, 105 (Suppl 6): 1569-1573.
Vijayalaxmi, B.Z., Frei, M.R., Dusch, S.J.,
Guel, V., Meltz, M.L. and Jauchem, J.R., 1997: "Frequency of micronuclei
in the peripheral blood and bone marrow of cancer-prone mice chronically
exposed to 2450 MHz radiofrequency radiation". Radiation Research, 147:
495-500.
Vijayalaxmi, B.Z., Frei, M.R., Dusch, S.J.,
Guel, V., Meltz, M.L. and Jauchem, J.R., 1997a: "Frequency of micronuclei
in the peripheral blood and bone marrow of cancer-prone mice chronically
exposed to 2450 MHz radiofrequency radiation - a correction". Radiation
Research, 148:
Walleczek, J., 1992: "Electromagnetic field
effects on cells of the immune system: the role of calcium signaling".
FASEB J., 6: 3176-3185.
Wang, S.G. 1989: "5-HT contents change in
peripheral blood of workers exposed to microwave and high frequency
radiation". Chung Hua Yu Fang I Hsueh Tsa Chih 23(4): 207-210.
Wei, L.X., Goodman, R. and Henderson, A., 1990:
"Changes in levels of c0myc and histone H2B following exposure of cells to
low-frequency sinusoidal electromagnetic fields: evidence for a window
effect". Bioelectromagnetics, 11(4): 269-272.
Wertheimer, N. and Leeper, E.,1979: "Electrical
wiring configurations and childhood cancer". Am. J. Epidemiology 109:
273-284.
Wever R. 1974, ELF-effects on Human Circadian
Rhythms. In: Persinger MA editor. ELF and VLF Electromagnetic Field
Effects. New York, Plenum Press. p 101-144.
Williams, G.M., 1996: "Comment on 'Acute
low-intensity microwave exposure increases DNA single-strand breaks in rat
brain cells' "by Henry Lai and Narendra P. Singh. Bioelectromagnetics 17:
165.
Wilson, B.W., Wright, C.W., Morris, J.E.,
Buschbom, R.L., Brown, D.P., Miller, D.L., Sommers-Flannigan, R. and
Anderson, L.E., 1990: "Evidence of an effect of ELF electromagnetic fields
on human pineal gland function". J Pineal Research 9(4): 259-269.
Wood, A.W., Armstrong, S.M., Sait, M.L.,
Devine, L. and Martin, M.J., 1998: "Changes in human plasma melatonin
profiles in response to 50 Hz magnetic field exposure". J Pineal Research
25(2): 116-127.
Youbicier-Simo, B.J., Lebecq, J.C.,and Bastide,
M., 1999: "Mortality of chicken embryos exposed fto EMFs from mobile
phones". Presented at the 20th Annual meeting of the
Bioelectromagnetics Society, St Pete Beach, FL, June
1999.
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