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Cherry on safe exposure levels :
Dr. Neil Cherry - Lincoln University - 25/4/2000
INTRODUCTION:
1.1
Background to this critique
There is a strong push from the WHO and the
ICNIRP of harmonize national RF/MW exposure standards by individual states
adopting the ICNIRP Guideline. This would be a good thing if the ICNIRP
Guideline was set at an exposure level that provided sound protection of public
health. The evidence presented here shows that the ICNIRP Guideline exposure
level is set many orders of magnitude too high to accomplish this. It is based
on the preconceived and long held view of Western Government Authorities that
the only possible and only established biological effect of RF/MW exposure is
tissue heating. This is referred to here as the RF-Thermal View. This view has
been intransigently maintained in the face of compelling laboratory and
epidemiological evidence of adverse health effects that would have had a
chemical declared carcinogenic, neuropathogenic, cardiogenic and teratogenic for
humans many years ago.
This critique was originally written when the New Zealand Ministries of Health and Environment proposed to adopt the ICNIRP Guideline as the Public Health Standard for Cell Site exposures. At the same time the New Zealand RF Standards Committee was proposing to use the ICNIRP Guideline as the New Zealand RF/MW Standard.
ICNIRP is the International Commission on Non-Ionizing Radiation Protection. The ICNIRP RF/MW guideline and scientific assessment was published in Health Physics, Vol. 74 (4): 494-522, 1988. This is the primary source document for this critique and will be referred to as ICNIRP (1998).
The ICNIRP (1998) assessment of effects has been reviewed against the research literature cited and other published research. It is found that both the basic approach of ICNIRP and its treatment of the scientific research have serious flaws. The ICNIRP assessment is determined to maintain the RF-Thermal View and it rejects or omits all evidence that conflicts with this view. This may be termed "Constructive Dismissal" for a preconceived concept is used to inappropriately dismiss all evidence that challenges it.
ICNIRP is particularly
dismissive of epidemiological evidence because all existing studies involve
nonthermal exposures. Hence accepting the validity of these studies would
directly challenge the RF-Thermal View. In this way the approach to dealing with
health effects from non-ionizing radiation was developed to follow a completely
different method than for toxic chemicals, drugs or air pollution. Both the
approach of ICNIRP and the assumptions made are severely scientifically
challenged in this report.
Overview of this
report:
Public health protection standards for toxic substances, chemicals,
drugs, air pollution, ionizing radiation are set by WHO, IARC, E.U., U.S. EPA
and the U.K. Royal Commission on Environmental Pollution primarily using
epidemiological evidence and secondarily using animal evidence. WHO and ICNIRP
base non-ionizing radiation protection standards on a single biological
mechanism, Tissue Heating. They systematically reject or ignore all
epidemiological and animal evidence of non-thermal effects, for which there is a
large body.
The history and basis of the RF-Thermal View which dominates
ICNIRP, WHO, and national authority approaches, is documented and summarized. It
will be shown that throughout the post-War period scientific research and
leading biological and medical scientists have challenged the RF-thermal
assumptions. They present very strong evidence, amounting to proof, that
biological systems intrinsically use EMR for body, organ, hormone and cellular
functions and regulation, and that extrinsic EMR interferes with these at
extremely low exposure levels. These biological effects do not involve heat but
do involve non-linear, non-equilibrium resonant interactions between ELF
oscillating signals.
The well documented and established nonthermal
biological effects of EMR include significant alteration of cellular calcium ion
homeostasis, reduction of melatonin and the detection of Schumann Resonances by
human and avian brains, DNA strand breakage and enhanced chromosome
aberrations.
The human health implications of these biological effects are
discussed and documented. This shows that calcium ion efflux/influx and
melatonin reduction are separately and jointly linked to DNA strand breaks,
chromosome aberrations, enhanced proto oncogene activity, impaired immune system
competence and impaired neurological and cardiac functioning. Many projects,
from independent labotories, have observed and reported that all of these
effects are significantly related to EMR exposure.
Human Biometeorology is a
whole body of research that is ignored by ICNIRP. This has provided the proof
over 30 years ago that human brains detect and use the Schumann Resonances for
synchronization of biological rhythms, i.e. as a Zeitgeber. This observation on
its own is an absolute challenge to the validity of the ICNIRP assumptions that
there are no established non-thermal biological effects.
Epidemiological
reviews by Dr John Goldsmith show that adverse health effects, such as
neurological, reproductive and cancer effects have been observed in EMR exposed
populations. Based on this, and the traditional public health protection
approach, Dr Goldsmith challenges the validity of the ICNIRP guideline and
approach.
To summarize the scientific evidence an initial set of eight
bioelectromagnetic principles are proposed and a brief summary of the scientific
research that supports them is given. They are:
EMR is intrinsic to our
bodies.
Our brains are the most electrically sensitive organs in our
bodies.
Our hearts are electrically sensitive.
Cells are sensitive to
EMR.
Our whole body acts as an aerial.
The brain is linked to organs and
cells through EMR-sensitive hormones.
The EMR Spectrum Principle.
The
Intrinsic Free Radical Principle.
These principles provide a sound and
scientifically reliable approach to assessing EMR impacts on people and animals.
They soundly challenge the ICNIRP assumptions and approach. The ICNIRP
assessment of biological mechanisms is reviewed and found to be selective,
limited and flawed. Their assessment of RF/MW effects on reproductive outcomes
is shown to be limited, misleading and flawed. The cancer assessment is shown to
be selective, misleading, inappropriate and flawed. An incorrect epidemiological
approach is consistently applied.
From the data in the studies cited (and
misused) by the ICNIRP and WHO reviews, and supported by a great deal of other
available research evidence, a public health protection standard is recommended
based on residential dose-response relationships for cancer, neurological
effects and reproductive effects.
2. Public Health
Protection Standards are based on Epidemiology:
The background to
identifying environmental factors that produce cancer will be given, along with
an example using the chemical Benzene. Then the principles of epidemiology
relating to assessment of cause and effect will be outlined and the particular
principles in the epidemiology of EMR will be discussed.
2.1 Cancer
Assessments are based on environmental epidemiology:
Public health Protection
Standards are based on Epidemiological Evidence. A primary textbook on Cancer,
De Vita, Hellman and Rosenburg (1993), states:
"In contrast to laboratory
studies, epidemiology directly evaluates the experience of human populations and
their response to various environmental exposures and host factors (the risk of
disease)".
Del Regato, Spjut and Cox (1985) introduce their medical textbook
on cancer by discussing the use of Incidence Rates in human populations as the
means of detecting human cancers. Fraumeni et al. (1993) outline the historical
role that epidemiology has played in identifying carcinogenic agents and the
range of methods which are classically used.
Setting public health standards
for environmental carcinogens is the role of the United States Environmental
Protection Agency (USEPA). Their website includes the Integrated Risk
Information System (IRIS), www.epa.gov/ngispgm3/iris/rfd.htm
www.epa.gov/ngispgm3/iris/rfd.htm, that details the procedures for carrying out
assessments and the results for a wide range of carcinogens. This is primarily
based on epidemiological assessments. Under the heading "Hazard Identification"
the following statement relates to the use of epidemiological studies:
"Human
data are often useful in quantitatively establishing the presence of an adverse
effect in exposed human populations. When there is information on the exposure
level associated with an appropriate endpoint, epidemiologic studies can also
provide the basis for a quantitative dose-response assessment. The presence of
such data obviates the necessity of extrapolating from animals to humans;
therefore, human studies, when available, are given first priority, with animal
studies serving to complement them."
An environmental epidemiologist of
considerable standing, alongside Sir Austin Bradford Hill, was Professor Abraham
Lilienfeld, of Johns Hopkins University. He was the epidemiologist responsible
for the survey of health effects at the U.S. Embassy in Moscow. In his paper
"Practical limitations of Epidemiologic methods" (Lilienfeld, 1983), Professor
Lilienfeld discussed some of the difficulties of demographic studies, including
the issue of the "ecological fallacy". In relation to his study on the staff and
dependents at the U.S. Moscow Embassy, he states:
"The problems associated
with these studies are illustrated by reviewing some of the details of the study
of effects of microwave radiation on embassy employees in Moscow. The study
population had to be reconstructed, individuals had to be located and
information on exposure status has to be obtained by questionnaire. The
relatively small size of the exposed group permitted the detection of only
fairly large relative risks. Despite these limitations, epidemiologic studies
have been remarkably productive in elucidating etiological factors. They are
necessary since 'the proper study of man is man' ".
Dr Lilienfeld describes a
classical epidemiological approach and problems. Epidemiology is complex and
difficult, but it is the best and most appropriate science for the study of the
effects of environmental exposures on human populations.
2.2 A Chemical
Example - Benzene:
An example is the carcinogenic assessment for Benzene.
Benzene is classified by the U.S.E.P.A. as a known human carcinogen (Category A)
based on "convincing human evidence as well as supporting evidence from animal
studies". At the end of the section on "Human Carcinogenicity Data", having
outlined the epidemiological evidence, the conclusion is:
"All of the
epidemiological studies referred to above have some methodological problems,
i.e. confounding exposures, lack of sufficient power, and other limitations, but
the consistent excess risk of leukaemia across all of these studies argues that
such problems could not be entirely responsible for the elevated risks of
cancer. Most of these epidemiologic studies have been reviewed in peer-reviewed
publications. They provide clear evidence of a causal association between
exposure to Benzene and ANLL. The evidence is suggestive with respect to CNLL
and CLL."
ANLL: Acute Nonlymphocytic Leukaemia.
CNLL: Chronic
Nonlymphocytic Leukaemia.
CLL: Chronic Lymphocytic Leukaemia.
The Benzene
Assessment is based on a total of 15 epidemiological papers covering 6 separate
studies, one showing a significant dose-response relationship. Several papers
found insignificantly elevated leukaemia rates. Some of these reached
significance when follow-up studies involved more cases. In summary the
dose-response data gives:
Table 1: Air concentrations at specific risk
levels:
Risk Level Concentration of Benzene
1 in 10,000 13.0 to 45.0
(g/m3
1 in 100,000 1.3 to 4.5 (g/m3
1 in 1,000,000 0.13 to 0.45
(g/m3
Figure 1: An example of standard setting using Benzene from the Royal
Commission on Environmental Pollution, Houghton (1998).
The United Kingdom,
Royal Commission on Environmental Pollution, 21st report "Setting Environmental
Standards", Houghton (1998), also shows the reliance on epidemiology in setting
such standards and outlines the procedures followed. The are very similar to the
USEPA and IARC. The Royal Commission also uses Benzene as an example, Figure
1.
There is no discussion at all in the EPA Benzene assessment, nor the Royal
Commission summary, about biological mechanisms. It is wholly sufficient that
consistent human studies, two cohort studies and one dose-response relationship
shows increases in leukaemia. A MEDLINE search reveals a large number of
cytogenetic studies showing that Benzene enhances chromosome damage in animals,
worker and human blood. None of these are cited by the EPA Assessment. The
epidemiological studies give the necessary and sufficient evidence for the
carcinogenicity assessment.
It is stated in Figure 1 that human studies were
more useful than animal studies. Most human studies involved high occupational
exposure that were probably under-estimated, making their results and
over-estimate of the risk of effects. They refer to the Expert Panel on Air
Quality Standards (EPAQS) who considered that the risk of leukaemia in workers
was undetectable when average exposure over a working lifetime is around 500
ppb. Taking into account working lifetime (77,000 hours) compared with
chronological lifetime (660,000 hours) the figure is reduced by a factor of 10.
A further factor of 10 is applied to extrapolate from fit, young to middle-aged
workers to the general population giving 5 ppb. Allowing for uncertainties in
the ambient exposure, and following the principle of keeping exposure as low as
practicable, a target standard of 1 ppb was adopted as a running annual average.
This applies an overall safety factor of 500 below the NOAEL for moderate to
highly exposed workers.
The UK report refers to the number and importance of
international conventions relating to the environment. This includes the
Maastricht Treaty that sets out the basis for the European Union's environmental
policy, which includes protecting human health. The basic procedure of human
health risk characterization is to compare the estimated human dose (EHD) of a
given substance with either the no observed adverse effect level (NOAEL) or the
lowest observed adverse effect level (LOAEL). The NOAEL is the greatest
concentration of a substance that produces no observed adverse effect. The LOAEL
is the lowest concentration of a substance, found by experiment or observation,
that causes any adverse alteration of morphology, functional capacity, growth,
development, or life-span, which is distinguishable from control organisms of
the same species and strain.
For the epidemiology of human populations the
NOAEL approach involves the search for the study with the highest exposure that
shows no adverse effect, with no studies that do show elevated risks below it.
Then a safety factor is applied to take into account the uncertainties, the
susceptibilities, and size of the exposed populations. The LOAEL approach uses
dose-response relationships to determine the lowest threshold for the
observation of an adverse effect. In using the epidemiological studies, careful
consideration of bias and confounding is undertaken and then the Bradford Hill
viewpoints are used to guide consideration of the likelihood of cause and
effect, Figure 2.
In Figure 2, Houghton (1998), uses the term "criteria" and
in the final quote the term "feature". The word "viewpoint" was very carefully
chosen by Sir Austin Bradford Hill. They are points from which to view the
evidence and not criteria that must the achieved. This is the importance of the
note at the bottom of Figure 2. These are not criteria, they are viewpoints with
either greater or lesser strength from which we can decide "is there any other
way of explaining the set of facts before us, is there any other answer more
likely than cause and effect. Epidemiology does not provide "scientific truth".
It provides a weight of evidence that must be considered in an informed fashion,
and decisions made with incomplete facts.
Figure 2: A summary of the
Bradford-Hill viewpoints for deciding on cause and effect from epidemiological
evidence, Houghton (1998).
2.3 The Bradford Hill Guidance:
It is also an
absolute prerequisite that the exposure takes place prior to the effect
occurring (temporality). This is the only viewpoint that could be termed a
"criteria".
2.3.1 Viewpoints NOT criteria:
Expert witnesses who appear in
court and at hearings for companies assess the epidemiological evidence using
what they call the "Bradford Hill Criteria", Black (1998), Elwood (1999) or the
"Hill Criteria", Moulder (2000). Dr Moulder states that "The Hill criteria
should be viewed as a whole; no individual criterion is either necessary or
sufficient for concluding that there is a causal relationship between exposure
to an agent and a disease." This is an approach of people who are determined to
dismiss the epidemiological evidence. It is totally inappropriate and leads to a
significant failure to protect occupational and public health
protection.
This is not the approach taken by IARC, US EPA, the U.K. Royal
Commission on Environmental Pollution, nor Sir Austin Bradford Hill himself. In
fact Sir Austin strongly opposed this approach. He states, Hill (1965):
"Here
are nine different viewpoints from all of which we should study association
before we cry causation. What I do not believe - and this has been suggested -
is that we can usefully lay down some hard-and-fast rules of evidence that must
be obeyed before we accept cause and effect. None of my viewpoints can bring
indisputable evidence for or against the cause-and-effect hypothesis and none
can be required as a sine qua non. What they can do, with greater or less
strength, is to help us make up our minds on the fundamental question - is there
any other way of explaining the set of facts before us, is there any other
answer equally or more, likely than cause and effect."
Sir Austin also
rejects strict statistical thresholds such as the 95% confidence interval. He
cites a group of cotton mill workers who persistently showed a higher incidence
of respiratory disease than similar group of unexposed workers, but the
difference was never statistically significant. He says that the evidence was so
clear-cut that no formal test could contribute anything of value to the
argument:
"No formal tests of significance can answer those questions. Such
tests can, and should, remind us of the effects that the play of chance can
create, and they will instruct us in the likely magnitude of those effects.
Beyond that they contribute nothing to the 'proof' of our hypothesis."
Hill
(1965) gives the example of respiratory sickness in workers in the cardroom of a
spinning mill where they were exposed to dust. The 30 to 60 year olds suffered
three times as much illness as other workers not exposed to the dust. The data
never reached statistical significance but Dr Bradford Hill concluded that it
was a causal effect because the evidence was so clear cut.
With EMR the usual
experience is that a small occupational group, people living near powerlines and
an electric blanket study show non-significant but elevated rates of disease or
mortality. Larger occupational groups and military personnel who experience
radar and radio exposures show significantly elevated rates of disease and
death. Attempts are then made to identify a gradient of exposure to determine
whether a dose response relationship exists. Dose response relationships and
significant dose response relationships are then identified using sub-groups who
have a graduated risk of exposure by virtue of their jobs and tasks. This builds
the picture that across the EMR spectrum similar health effects and biological
effects are observed, supporting an integrated approach to the assessment of the
data, and indicating a level of evidence that rises progressively towards the
point where we can decide that there is a causal relationship. Many years
previously we surpassed the threshold for a potential effect for a wide range of
EMR related health effects at very low level of exposure with the initial
residential and occupational studies showing elevated risks.
With the
sensitivity of the brain to electromagnetic signals it is expected that
neurological effects will be measurable from EMR exposures. There are many EMR
studies of exposed workers that show elevated by non-significant increases or
neurological effects. It is a common conclusion of the authors that the result
does not support the hypothesis that EMR is associated with neurological
disease. This is incorrect, especially if small samples are involved since tests
of statistical significant are strongly dependent on sample size. An instructive
example of this is Johansen et al. (1999). They investigated the incidence of
Multiple Sclerosis among utility workers. With 32 cases of MS diagnosed when
23.7 were expected, they found a Standardized Incidence Ratio, SIR = 1.35,
95%CI: 0.92-1.91. They then conclude: "We found no support for the hypothesis of
an association between occupational exposure to electromagnetic fields and the
risk of MS."
What would Sir Austin conclude if he looked closely at their
data? Based on only 14 cases, for low, medium and high exposures they observed
SIRs of 0.8, 1.4 and 1.6. This is a remarkable result with a biological
gradient. This "admits of a simple explanation and puts the case in a clearer
light". Actually this study provides very strong support for the hypothesis.
Along with several other studies it supports the cause and effect
hypothesis.
2.3.2 Specificity:
Specificity is valuable in situations where
a specific disease agent is observed to produce a specific disease in specific
workers exposed to a specific situation. Sir Austin says that when this occurs
it is a strong argument in favour of cause and effect. He immediately cautions
that we must not over-emphasize this characteristic because many agents are
known to produce more than one cancer or a range of illnesses. He also observed
that many diseases are produced by multiple agents. The epidemiological evidence
for EMR shows that it enhances a wide range of cancer and sickness in many body
organs, under a wide range of exposure conditions across the spectral range. Sir
Austin summarizes this with:
"In short, if specificity exists we may be able
to draw conclusions without hesitation; if not apparent, we are not thereby
necessarily left sitting irresolutely on the fence."
An application of
specificity to EMR arises when we consider which body elements are particularly
bioelectromagnetically sensitive and reactive. Our brains and hearts are
immediately identified as sensitive organs. However all cells are sensitive,
especially in the immune system and the endocrine system, through the actions of
calcium ions and melatonin.
2.3.3 Experimentation:
Experimentation is not
always possible but where it is, it is very powerful. For example, in the
Schwarzenburg Study, involving a shortwave radio tower, a significant
dose-response relationship for sleep disturbance was observed. Confirmation of
cause and effect came from turning the transmissions off for 3 days without
notifying the residents. Sleep quality improved significantly (p<0.001), with
a delay of about one day, even in the group with the lowest exposure (Group C).
This shows that even though they experienced the lowest exposure, the RF signal
was still interfering with their brains and their sleep. When the transmission
was turned off permanently, measured human melatonin levels rose significantly
(Prof. Theo Abelin Pers. Comm.). This is a biological mechanism but it was
identified after the assessment of cause and effect was concluded.
2.3.4
First Priority - Dose-Response Relationship:
In relation to dose-response Sir
Austin states:
"If the association is one which can reveal a biological
gradient, or dose-response curve, then we should look most carefully for such
evidence. For instance, the fact that the death rate from cancer of the lung
rises linearly with the number of cigarettes smoked daily, adds a great deal to
the simpler evidence that cigarette smokers have a higher death rate than
non-smokers." ... "The clear dose-response curve admits of a simple explanation
and obviously puts the case in a clearer light."
Hence a dose-response
relationship is highly indicative of a cause and effect.
2.3.5 Second
Priority - Strength of Association:
For Strength of Association Sir Austin
cites the example of John Snow's classic analysis of the cholera epidemic in
1854. He found 71 deaths per 10,000 in the group whose water came from the
Southwark and Vauxhall Company and 5 deaths per 10,000 from those using the
Lambeth Company, a factor of 14. No known biological mechanism was available at
that time but this is sufficient to decide cause and effect, especially when the
Lambeth Company water was sewage-free and the other Company's water
wasn't.
Sir Austin warns, however, not to place too much emphasis on strength
of association, for some important effects might wrongly be dismissed. He also
dismissed the requirements to achieve statistical significance as an absolute
requirement. For Dr Bradford Hill, elevated risks are important evidence to be
considered in context. A group of mill workers were consistently observed to
have elevated respiratory disease, but this never reached statistical
significance. Nevertheless it was concluded to be a causal effect.
2.3.6
Third Priority - Consistency
Consistency is a feature to be specially
considered. Has the effect been consistently observed to be associated in
different persons in different places, circumstances and times? But consistency
is not absolute. He states:
"Once again looking at the obverse of the coin
there will be occasions when repetition is absent or impossible and yet we
should not hesitate to draw conclusions."
For example, we cannot repeat the
Korean War and wait another 20 years to see if cancer and sickness is greater in
high exposure groups compared with low exposure groups. A repetition is
impossible but we can look for consistency between the Polish Military Study,
studies of RF/MW exposed electrical workers, and large population studies of
residents around high powered broadcast towers.
2.3.7 Lowest Priority -
Biological Mechanism:
Dr Bradford Hill's comments on "biological
plausibility" or "biological mechanism" place them at the lowest priority. He
states:
"It will be helpful if the causation we suspect is biologically
plausible. But it is a feature I am convinced we cannot demand. What is
biologically plausible depends on the biological knowledge of the day".
The
absence of a detailed step by step biological mechanism is not a limitation on
classifying chemicals, such as benzene, as carcinogens. A chemical that is
observed to neoplastically transform cells (e.g. the Ames Test), produces
tumours in laboratory animals and is associated with increased incidence of
cancer in exposed workers, is classified as a human carcinogen.
Just two
years ago Quinn (1997) noted that:
Although the role of ultraviolet radiation
in human skin carcinogenesis has been supported by a wealth of epidemiological
data, the mechanisms by which it leads to skin cancer are still poorly
understood."
It is accepted from the epidemiological evidence that UV
radiation is carcinogenic, causing melanoma and other skin cancers. It also
reduces immune system competence. This is a strong reason for being very
concerned about the depletion of the Ozone Layer and the formation of the "Ozone
Holes" over the Arctic and Antarctic.
2.4 ICNIRP's inappropriate reliance on
a Biological Mechanism
In setting public health protection standards,
epidemiological evidence is the strong guiding evidence. It does not need a
biological mechanism for it to be interpreted as a probable or even causal
effect. For ICNIRP to concentrate on and rely on a single biological mechanism,
Tissue Heating, is inappropriate and wrong. Large portions of official documents
are devoted to extensive discourses on SARs and determination of the thermal
threshold. This whole methodology is flawed. Health effects assessments start
with epidemiological evidence and the existence of a plausible biological
mechanism is irrelevant.
WHO, ICNIRP and their international and national
counterparts have developed a highly sophisticated system of approaches to
dismiss all epidemiological evidence and animal and cellular evidence which
conflicts with their RF-Thermal view of the world. As the epidemiological and
laboratory evidence has grown stronger and stronger, the dismissive methodology
has lost all sophistication and, as demonstrated by ICNIRP (1998), it is
blatantly selective, reductionist, biased and scientifically dishonest.
It is
selective through carefully selecting positive and negative evidence to maintain
their 'no effects' stance through a 'balance of evidence approach'.
It is
reductionist by seeking reasons, valid or not, for dismissing each study on its
own so that none are left at the end. A set of experimental and epidemiological
"criteria" have been adopted in an attempt to make the process look like good
science.
It is biased towards accepting evidence of no effects and dismissing
all evidence of effects as weak, questionable and unreliable.
It is
scientifically dishonest because it cites papers that clearly report significant
increases in cancer as showing no evidence of cancer. It deliberately chooses to
accept conclusions that claim no association between radar and health effects
when the data in the report or paper proves that this is incorrect. ICNIRP also
includes studies in its assessment that are incapable of showing effects, as
though they provide evidence that there are no effects.
This is a process of
"Constructive Dismissal" in which a pre-conceived position is defended at all
costs by inappropriately dismissing all evidence that challenges it.
The
epidemiological evidence, when appropriately assessed following the Bradford
Hill Viewpoint approach, an approach endorsed by Drs Lilienfeld and Goldsmith,
provides sufficient weight to establish cause and effect relationships between
EMR and many health effects, and to set public health standards. It is wrong in
science, and in public health protection policy terms to retain the RF-Thermal
view. ICNIRP's 1998 assessment must be rejected and urgently revised in the
light of these revelations.
2.5 Cancer Epidemiology:
The science of
epidemiology has developed to deal with complex human situations, as are found
with almost every potential disease agent, whether it is chemicals, drugs,
smoking, air pollution or ionizing radiation. Large groups of the population are
identified whose occupation, location or activity involves exposure to the
disease agent of concern. On some occasions the level of potential or probable
exposure can be reasonably well stratified to allow a dose-response comparison
to be made. In all cases, the exposure varies from day to day, week to week,
year to year, and person to person. Hence there is a frequency distribution of
hourly or daily exposures for each person and for each group. As a consequence
almost all retrospective studies deal only with potential or probable exposures.
The frequency distribution of exposures accumulates towards a mean exposure. By
judicious choice of occupational groups or residential situations the exposed
groups can be dichotomized to compare groups with higher mean exposures compared
with other similar groups who have lower or no exposure to the agent. In some
circumstances it is possible to identify a gradient of exposure which might
allow a dose-response curve to be investigated. Elevated rates of disease and
death are then considered and assessed in the light of uncertainties and the
important of the evidence for public health.
A commonly accepted model of
cancer development involves initiation, promotion and progression, Figure 3. For
cancer studies a significant time delay between initiation and the development
of malignant cancer can be many years or even several decades. When cancer does
develop it occurs in a small number of people when we are younger than 50
years.
For example in New Zealand for male brain and CNS cancer, in the 30-34
age group the incidence is near 4.4 and the mortality near 2.3 per 100,000
person years. In a city of half a million people there are about 25,000 men in
the 30-34 yr age group. This gives an annual brain tumor incidence rate of
1.1/yr. If four 30-34 yr old men develop brain tumours they won't usually be
noticed but the rate is 3.64 times average. In order to detect the influence of
a particular carcinogen, very large samples, very long periods and highly
elevated rates are necessary.
The age standardized leukaemia incidence rate
for all people is near 8/100,000 p-yr. With a population density of 800 /km2 and
population of about 2500 could live within 1 km of a tower. Over a 13 year
period this is 32,500 p-yrs giving an expected leukaemia rate of 2.6. This is
very similar to the Sutton Coldfield situation, Dolk et al. (1997a). Six
leukaemias were observed when 2.83 were expected.
Figure 3: Model of
multistage carcinogenesis. Initiation involves a single exposure to a carcinogen
that damages the nuclear DNA. Promotion involves multiple exposures at certain
intervals to agents that do not damage DNA directly. Many chemical promoters
alter cell regulation through signal transduction or gap junction alteration.
Promotion leads from benign to malignant tumours. Progression increases the
degree of malignancy, Adey (1990).
Hence studies, undertaken a few years
after exposure are very unlikely to detect any increase in cancer, even in large
populations. In small populations it is impossible because only a small
proportion of people who are exposed show increased cancer at younger ages than
about 50 to 60 years. As the total cancer rate increases with age in normal
populations, especially after 50-60 years, it becomes harder to detect the
influence of a specific carcinogen in older decadal age groups.
2.6 Exposure
Dilution:
One of the fallacious reasons used to criticize and dismiss EMR
epidemiological studies is that there is an ill defined or unknown exposure
regime between the occupational or military exposure at an early age and the
health survey data decades later. The time delay is essential to allow time for
cancer to develop. During the time between the initiating and promoting
exposures, and the collection of the health and mortality survey data, a complex
exposure regime will be experienced by every person. Rather than creating
uncertainty, it is certain what the effect of this is in large groups. The
stochastic and randomized nature of this will dilute the differences between the
groups and reduce any initial stratification or dichotomization based on the
original exposure regime. Hence any observed adverse health effects will be
significantly under-estimated. Thus, rejecting the study because of
intra-exposure uncertainty is wrong and unjustified. In fact the effects seen
can reliably be assumed to be even more elevated with higher significance than
the analysis indicates.
The exposure complexity over decades significantly
reduces the progressive exposure gradient that might have produced a
dose-response curve. Thus any observed dose-response curve for cancer will be a
very significant indication of cause and effect, even if it technically fails to
achieve p(0.05.
EMR is particularly problematic because it is ubiquitous.
Every member of society is exposed to some extent. Epidemiological method aims
to minimize the inclusion of confounding factors. Hence exposed populations are
compared with controls who are as similar in an as many respects as possible
except for the exposure. Hence similarly trained and aged military groups are
used as controls for radar exposed groups. In the Korean War Study, radar
repairers we chosen as exposed groups and radio and radar operators as the
comparison control group. Exposure surveys show that radio and radar operators
are in a moderate exposure situation that is far higher than the general public.
Hence if EMR exposure increases cancer, then the observed difference between the
operators and repairs will not be as great as the real difference between them,
and between both of them and the general male public of the same age. In
military and industrial situations the lack of a 'no exposure' group is another
significant source of exposure dilution.
A job exposure matrix can
significantly reduce the uncertainties between groups classified by job. Such a
survey was carried out in the Korean War Study. Despite this advanced exposure
analysis, the authors try to claim that the observed adverse outcomes cannot be
related to radar exposure since it was only based on potential exposure.
The
technological advancements in society have exacerbated this further. Exposures
occur from radio and TV broadcast towers, powerlines and home appliances.
Computers, portable phones, mobile phones and cell sites have significantly
raised individual EMR exposures in recent decades. Hence there is no true
"no-exposure" population. These and other similar effects are strong sources of
exposure dilution.
Residential studies are subject to dilution by
'migration'. Residential samples are diluted by exposed people leaving the area
and unexposed people arriving into the study area. This is a significant effect
because of the long periods necessary to allow for cancer to develop.
Thus
all EMR studies have an extremely high probability of significantly
under-estimating the Relative Risks.
The Korean War Study, Robinette et al.
(1980), gives a good example. They surveyed exposures in a 5% sample of the
"high exposure" repairers groups. They found frequency distributions within the
three occupational groups being studied. This resulted in distinctly different
distribution and mean Hazard Number for each occupational group that enabled a
dose-response exposure gradient to be identified. The health and mortality
survey data collected about 20 years later revealed a significant dose-response
gradient in the mortality for each of the sailors surveyed when grouped in
Hazard Number ranges. Despite 20 years of exposure dilution, the initial
exposure dichotomy using occupational group produces elevated and significantly
elevated mortality and morbidity differences 20 years later. Many of the
elevated Relative Risks don't quite reach the p(0.05 threshold. The very large
exposure dilution effect in this case is highly likely to raise them so that
they do. This is accentuated by realizing that the comparison or control group
was also regularly exposed and so this too produces its own exposure dilution
effect, artificially reducing the observed RR and its significance.
An
elevation in the rates of a wide range of sicknesses, neurological and cardiac
disease and death and cancer incidence and mortality were observed in the Korean
War Study, Robinette et al. (1980) and the Moscow Embassy study, Lilienfeld et
al. (1978). Neither the authors of these studies, nor the WHO and ICNIRP
assessors appreciate the effects of dilution for even though they found
significant effects, they sought to dismiss all evidence of adverse effects,
even when the data and appropriate interpretations strongly clash with
this.
2.7 Dr Goldsmith is critical of ICNIRP standards approach
Eminent,
internationally recognized, environmental epidemiologist, the late Dr John
Goldsmith, Goldsmith (1997c), states:
To this day, the ICNIRP makes little
use of epidemiological data, alleging that it is inconsistent and difficult to
understand."
Dr Goldsmith's own conclusions, Goldsmith (1997b), after
reviewing some of the epidemiological data on RF health effects
include:
"Available data suggest that RF radiation be considered a
carcinogenic risk, a position already taken in an internal U.S. E.P.A. document
[Cited in Sibbison (1990)], in 1990 when there was much less evidence of the
potential harmfulness of RF radiation."
Dr Goldsmith sets out guidance on how
to use epidemiological research in setting standards, Goldsmith (1992). Dr
Goldsmith was critical of approaches taken to date and identified problems
including:
Failure to consider both thermal and non-thermal effects
especially of non-ionizing radiation.
Interpretation of non-significant
results as equivalent to no effect.
Accepting the author's interpretation of
a study, rather than examining its data independently for evidence of
hazard.
Discounting data on unanticipated effects because of poor fit to
preconceptions.
Dependence on threshold assumptions and demonstration of dose
response relationships.
Choice of insensitive epidemiological indicators and
procedures.
Consideration of each study separately, rather than giving weight
to the conjunction of evidence from all available studies.
2.8 Dr Goldsmith
reviews EMR epidemiological evidence:
Professor John Goldsmith was one of the
world's most eminent environmental epidemiologists. A couple of decades ago when
the International Society for Environmental Epidemiology was formed, Dr
Goldsmith was invited to give the opening key note address to the first session
of the first conference. This illustrates the high standing that he was accorded
by the international epidemiological and public health community.
Because of
his standing, the editor a new scientific journal, the International Journal of
Occupational and Environmental Health, invited Professor Goldsmith to help to
launch the first issue of the new journal by providing a significant review
paper. The review, headed "Special Contributions" was carefully identified by Dr
Goldsmith as an "opinion piece" which reviews and summarizes the "Epidemiologic
Evidence of Radiofrequency Radiation (Microwave) Effects on Health in Military,
Broadcasting and Occupational Studies".
Goldsmith (1995, 1996 and 1997b)
reviews many epidemiological studies of radiofrequency and microwave exposures.
Many of these studies show increases of cancer and some show increases of
miscarriage and neurological effects. In all of these studies exposures
involving heating are extremely rare and mean long-term exposures are a very
small fraction of the heating threshold. Goldsmith (1995) concludes:
"There
are strong political and economic reasons for wanting there to be no health
effect of RF/MW exposure, just as there are strong public health reasons for
more accurately portraying the risks. Those of us who intend to speak for public
health must be ready for opposition that is nominally but not truly
scientific.
At present there seems to be little interest in or understanding
of epidemiologic information among regulatory bodies that should provide
protection. While we conduct epidemiologic studies as well as we possibly can,
we who are concerned with health protection and careful identification of risks
must also keep pressure on the regulatory agencies to include epidemiologic
thinking in their work."
This report continues Dr Goldsmith's work and
extends his reviews and conclusions. I strongly contend that the approach and
conclusions of ICNIRP and the WHO position is methodologically and factually
scientifically flawed. They place public health severely and demonstrably at
risk.
2.9 The Special case of Broadcast Tower Epidemiological Studies:
For
residential studies around broadcast Radio and TV towers the cause and effect
relationships can be much more decisive because to the complex nature of the
radiation patterns. For example, broadcast antennae usually focus the signal
more in one direction than another, towards the major population centres. A
cancer rate that is higher on the high emission side than the low emission side
is a first indication of a dose-response.
For example, the San Francisco City
Department of Public Health, San Francisco (1988), analysed the childhood and
adult cancer rates in the vicinity of the Sutra Tower. For childhood All Cancer,
leukaemia and brain tumour the whole San Francisco Standard Incidence Ratios
were SIR = 0.98, SIR = 1.16 and 0.90, respectively. For a community on the
western side of the tower, Sunset East, these rates were SIR = 1.47, SIR = 1.88
and SIR =1.00. For the Noe/Eureka Valley to the easy of the tower they were SIR
= 1.78, SIR = 1.94 and SIR = 2.27. Antenna patterns and measurements show higher
exposures to the east of the tower (Noe/Eureka Valley) than to the west (Sunset
East). Hence there is a dose response relationship.
The radial public
exposure pattern around broadcast towers is complex and undulating. If health
effect rates follow these complex patterns then they form significant dose
response relationships that cannot be explained by any other factor. Hence they
show a causal effect.
Radial ground level exposure levels vary with the
antenna pattern and the frequency of the carrier. The higher the frequency the
better the signal is focussed towards the horizon. The antenna elevation tilt is
crucial in determining the position and strength of the main beam when it
eventually strikes the ground several km from the base of the tower. Closer to
the tower than this the exposure pattern varies with distance as the side-lobes
intercept with the ground and the interference between the direct and reflected
beams go into and out of phase. An example of an antenna pattern with side-lobes
is given in Figure 4, for a VHF antenna.
Back
to Top
Figure 4: A
typical vertical antenna pattern for a 4-element dipole array at about 98
MHz.(VHF), Units in dB.
The side-lobes have elevation angles of 72, 57, 40,
15 and 8 degrees. For an antenna at 500 m above ground level, the ground level
side-lobe peaks occur at 160, 390, 600, 1870 and 3560 m from the base of the
tower, with significant troughs of low exposure between them. The amplitudes of
the peaks and troughs are very large because of the logarithmic nature of the dB
units. It is common to tilt the antenna pattern slightly downwards so that the
main beam is directed towards major population centres in the listening and
viewing area rather than towards the far horizon.
Figure 5a is street level
measurements around the Empire State Building for a 44 MHz VHF transmitter,
taken in 1933. These VHF signals have peaks inside 1 mile from the tower which
are repeated near 2 4, 8, and 16 miles. Beyond 10 miles the signal generally
declines as the inverse square law. Figure 5b shows the way in which VHF radial
signal patterns, and hence ground level exposure intensity peaks and troughs,
vary with carrier frequency. Figure 6 shows horizontal radiation patterns from
UHF and VHF broadcast stations.
Cancer or other health effects which follow
these complex radial patterns cannot be caused by any other confounder and hence
firmly establish cause and effect. In the North Sydney Study of Hocking et al.
(1996) there is a higher than average leukaemia rate in Lane Cove that is in the
position of Christchurch in Figure 6b, and lower than average in Willoughby,
which is north of the towers. In Sydney the major populations live to the SW of
the site. Hence it is likely that a similar antenna pattern to Figure 6b has
been used.
Epidemiologists and statisticians who are unaware of these
patterns, such as Dolk et al. (1997a,b) and Selvin et al. (1992) have made
serious errors in the interpretation of their data. In the first case they
assumed a simple inverse square law and a linear relationship in the second. In
both cases their cancer data follows a complex radial pattern which closely
approximates the radial exposure pattern.
Figure 5: Ground level radiation
pattern for (a) the 44 MHz (VHF) signal from the Empire State Building in New
York City, from Jones (1933) by merging his figures 6 and 8, and (b) a
theoretical set of antennae Antenna height 1000', receiver height 30 ', power 1
kW, Reference data for Engineers, Jordon (1985).
Figure 6: Horizontal antenna
radiation patterns showing the relative filed strength for, (a) UHF Digital TV
(linear scale) from the Sutra Tower, and (b) 99 MHz VHF for 8 dipole array
(logarithmic scale), Ouruhia transmission site, Christchurch, New
Zealand.
This indicates a significant dose-response relationship in relation
to mean exposure. The authors' weak and dismissive conclusions are favoured by
ICNIRP but their data give conclusive evidence of cause and effect between RF
radiation and cancer, especially for leukaemia, brain tumor and all cancer.
These conclusions are supported by many other studies showing significant
increases in these and other cancers in higher than average RF/MW exposures, and
by established biological mechanisms.
2.10 Residential Exposure
Factor:
There is also a significant difference between direct exposure
intensity at a residential site from the tower and personal mean exposure.
People spend time inside and out, at home and away. Hence observed health
effects need to be related to a residential exposure estimate that takes these
factors into account.
When considering cancer, the appropriate exposure
metric is the cumulative personal exposure over many years as this relates to
cumulative cell damage. The long-term cumulative exposure is the product of time
and mean personal exposure. The mean personal exposure is a combination of
indoor/outdoor and home/away times. Based on local measurements, the indoor
exposure is assumed to be 1/15th of the outdoor exposure. The away exposure is
assumed to be 1/30th of the home exposure. Taking the indoor/outdoor ratio as
20:4, the weekly home/away ratio as 108:60 and annual ratio of 44:8. This
produces a personal exposure factor or 0.136, which is rounded up to 0.15. Thus
the residential exposure factor (REF) is taken to be 15 % of the direct
exposure.
McKenzie, Yin and Morrell (1998) took readings in Sydney,
Australia, of direct roof level, street level and inside RF exposures from the
North Sydney TV Towers. At a particular house these were 3.0, 0.066 and 0.017
µW/cm², respectively. These give reduction factors of 45 and 176 for street
level and inside, showing how that the REF of 0.15 is likely to be too
high.
People who happen to live in a radial ring with very low local
exposure, will have lower mean exposures than those who live on either side of
the dip. However, since their local movements take then regularly through the
higher exposure zones, their mean exposure will be a little higher than
indicated by the estimates above. This won't be by much because of the dominance
of the inside at home period.
Cancer latencies and exposure dilution will
also reduce the size of the observed RR and its significance, under-estimating
the magnitude of any actual adverse health effects in residential
studies.
Very Close Proximity:
In residential exposure studies around
broadcast facilities the identification of associated health effects in the
immediate vicinity of the tower, inside 1 km for example, is very limited.
Limitations are produced by a very small area that is unlikely to be able to
contain a sufficiently large population to detect elevated or significantly
elevated effects. The area is smaller than 3.14 km2 because a portion of the
area is taken up with the facility itself, which often requires a very tall mast
with guy wire bracing. This means that the exposed population is quite small. In
rural areas it is very small. A further factor is the radiation pattern must
involve high powered emissions and the mix of VHF and UHF transmissions since
VHF antenna have side lobes that produce high exposures inside 1 km and UHF
antennas don't.
Hence the only circumstances that are likely to show high
cancer rates near a broadcast tower is one that combines a high population
density, a VHF signal and an RF sensitive cancer. The only place in the UK study
of Dolk et al. (1997a,b) that had a high cancer rate near the tower, was Sutton
Coldfield. It is the only high power tower in a highly populated area that had
VHF stations on it.
2.12 A more appropriate approach:
These more
fundamental considerations of method and approach, with more realistic radiation
exposure patterns and placing epidemiology well above biological effects,
strongly supports a fresh approach and significantly altered conclusions. The
WHO and ICNIRP assessments suffer from all of the problems identified by Dr
Goldsmith and Sir Austin Bradford Hill. This critique attempts to correct this
and to incorporate epidemiological evidence into processes for setting public
health protection standards.
A scientifically objective and open-minded
approach should start with an open question:
What is the epidemiological
evidence of adverse health effects, and what does this evidence suggest in terms
of potential, probable or actual adverse health effects?
3. History of the
RF-Thermal View:
A long-held Western mind-set:
ICNIRP follows a
long-held Western position that arose after the Second World War when no
epidemiological studies of radio and radar exposed populations were available.
In this situation it is appropriate to deal with the known effect of tissue
heating and to determine the levels of acute exposure which would avoid burns
and shocks. In the 1970's and 1980's time had elapsed between initial exposure
and the potential development of chronic health problems. Studies were carried
out, significant effects were observed, but the thermal mind-set was so well
established, reinforced by the Cold War politics between the U.S.A. and the
U.S.S.R. so that these results were dismissed or hidden by government officials
changing the conclusions of epidemiological studies. Through this period the
West became focussed on the single "proven" biological effect of RF/MW, Tissue
Heating.
It is demonstrable that acute high level exposure causes Tissue
Heating. Exposed people and animals had their temperature measured and it rose,
reliably and repeatably. It makes sense. Absorbed energy raises the temperature
as a function of the 'aerial' properties of the object (person), relative to the
wavelength of the electromagnetic wave.
Given the central and dominating role
of the RF-Thermal View it is important to trace its history. In the period
immediately following the Second World War, when radio and radar had come into
widespread use for the first time, there was no epidemiology to challenge the
developing view that Tissue Heating was the only possible effect. Early on there
were anecdotal, case-by-case reports of leukaemia, ocular defects, reproductive
problems, heart problems and neurological symptoms of tiredness and headache.
For example, McLaughlin (1953), Cleary and Pasternack (1966), Rosenthal and
Beering (1968), Forman et al. (1982), and Archimbaud et al. (1989). Some of
these involved quite high acute exposures. Most were relatively isolated and
they were claimed not to be confirmed to be RF/MW related.
The U.S.
Tri-Service Program:
The conviction that the only possible effect of RF/MW
exposure is tissue heating is sourced largely from the Tri-Service Program. One
of the primary aims was to determine the thermal threshold so that exposed
personnel could be protected from dangerous over heating. This is documented
through Steneck et al. (1980) and published conference proceedings from the
United States. Steneck et al. document the detailed history of the development
of the U.S. standard C95.1. They note that Dr John T. McLaughlin, a medial
consultant of the Hughes Aircraft Corporation assessed the research into the ill
effects of radar exposure. He wrote a report and sent it the military. It listed
purpura hemorrhagica (internal bleeding), leukaemia, cataracts, headaches, brain
tumors, heart conditions and jaundice as possible effects.
No weight was
given to this report and calculations proceeded to determine the heating
exposure that people could tolerate, based on their ability to deal with solar
radiation. After some basic arithmetic errors were corrected a figure of
10mW/cm² was arrived at in about 1960. This became the basis of standard C95.1
ten years later. It was supported by a large body of research that was
coordinated through the Tri-Service Program. Steneck et al. summarized this
research, pointing to the high acute exposures that were involved.
3.3 The
U.S./U.S.S.R. double standard:
In 1970 Dr Leo Inglis presented a paper to an
IEEE forum on EMR entitled "Why the double standard - a critical review of
Russian work on the hazards of microwave radiation", Inglis (1970). He notes
that a major difference between the U.S. and Soviet work was:
"In the U.S.,
the thermal effects are generally believed to be the only ones of significance;
other contentions are usually dismissed as lacking a provable basis. In the
U.S.S.R., non-thermal effects are considered the most significant and are
overwhelmingly the ones most studied."
The non-thermal effects identified by
the Soviet researchers were often referred to as the "Radiofrequency Sickness
Syndrome" or the "Microwave Syndrome". It has symptoms of functional changes in
nervous and cardiovascular systems, such as headaches, fatigue, irritability,
sleep disturbance, weakness, decreased libido, chest pains and bradychardia.
Hypotonia (muscle weakness) and related symptoms had been reported in the USSR
(Gordon, 1966), France (Deroche, 1971) and Israel (Moscovici et al., 1974).
Western scientists rejected these symptoms as "subjective". A set of them have
now been identified with cell phone usage, including a significant dose-response
relationship, Mild et al. (1998).
3.4 Determining and challenging the thermal
threshold:
The RF-Thermal View dominance is confirmed in the proceedings of
the 1974 conference on "Biological effects of Non-Ionizing radiation", held at
the New York Academy of Sciences, 12-15 February 1974, and published in Annals
of the NY Academy of Sciences, February 28, 1975. The conference chairman was Dr
Paul E. Tyler of the EMR project office in the U.S. Dept of the Navy. His
opening remarks include comments about the Tri-Service Program and the very high
levels of exposures generally used, Tyler (1975). He states:
"After I had
read and analyzed of the publications for this program (the Tri-Service
Program), I was left with the feeling that the research was conducted with the
preconceived idea that all of the effects were thermal in nature. It appears
that the protocols were designed only to determine gross thermal
effects."
"Although the Tri-Service research addressed essentially only the
problem of thermal hazard, the idea that the sole hazard was thermal became
dominant, and in the early 1960's, an air of complacency settled over this
country. At the end of the Tri-Service Program in 1960, United States research
in this area decreases to a very low level and remained there for the next
decade."
The general acceptance or complacency about the RF-thermal view was
scientifically challenged time and time again throughout this period. For
example, Dr Adey gave the introductory paper to this 1974 conference, Adey
(1975), on the effects of EMR on the nervous system. In this paper he
states:
"Even a recent review body of the World Health Organization decided
after discussion to dismiss from its concerns possible biological effects that
might occur in the absence of significant heating. It has become clear, however,
that interactions with the mammalian central nervous system can be reliably
produced by oscillating electric and electromagnetic fields without significant
heating of tissues."
It is a very strong statement to say that interactions
can be reliably produced in the CNS without the heating of tissues. Dr Adey
refers to the work of König and Wever in Germany and to work from his own
laboratory, on behavioural effects, such as changed reaction times and altered
circadian rhythms in ELF exposures. These effects were associated with induced
electric field gradients in monkey phantoms in the range 0.1 to 0.01(V/cm. The
effects were also linked to changes in EEG and significant effluxes of calcium
ions and GABA, Kaczmarek and Adey (1973). During the 1970's was as shown that
calcium ion efflux occurred at non-thermal exposure levels and was primarily
related to modulation frequency, i.e. a non-thermal, possible resonant,
biological mechanism.
Two large epidemiological studies were carried out in
the 1970's, Lilienfeld et al. (1978) and Robinette et al. (1980) in the middle
of the Cold War. These found small but significant increases in cancer, cardiac
problems and neurological symptoms. However, the authors were under strong
pressure, for a range of reasons, to not relate these results to the radar
exposure. In one case, Lilienfeld et al., the U.S. State Department case
officer, Dr Herbert Pollock, actually changed the conclusions, Goldsmith
(1996).
Tell and Harlen (1979) outline the Thermogenic properties of RF/MW.
>From a number of studies that recorded rectal temperatures under various
exposure conditions. This was to give guidance in setting RF/MW exposure
standards. The 10 mW/cm² standard was confirmed as protecting from temperature
rise of less than 1(C.
An official attempt to declare EMR carcinogenic
(1990):
In 1990 an internal review team of the U.S. E.P.A. recommended that
ELF be classified as a probable human carcinogen and RF/MW as a possible human
carcinogen. Under pressure from the Bush White House, EPA administrators changed
the conclusions of the review and the classification never became official EPA
policy, Sibbison (1990). The rationale was based on the preferred public policy
stance "We don't want to scare the public". Public health protection was not
considered as important.
3.6 U.K.'s NRPB retains the RF thermal view
(1991):
In May 1991 the United Kingdom's NRPB issued a series of reports on
EMR, which included a report on the Biological Effects of ELF, Sienkiewicz,
Saunders and Kowalczuk (1991) and the Biological Effects of RF/MW, Saunders,
Kowalczuk and Sienkiewicz (1991). This second report reviews many cell and
animal studies that used thermal exposures and produced some observable effects.
These thermal and behavioural effects were not seen when SAR's dropped below 4
W/kg. They don't find anything reliably significant in the long-term mouse study
of Guy et al. (1985) in which found a significant increase in primary malignant
tumors at an SAR of 0.4 W/kg. The U.S. E.P.A. internal review team found this
study much more relevant and used it as an important support for their
recommendation to classify RF/MW as a possible human carcinogen, McGaughy et al.
(1990). Epidemiology played no role at all in the NRPB review, which was solely
concerned with biological mechanisms. However it did play a major role in the
EPA review.
U.S. IEEE/ANSI review retains RF Thermal View (1993):
In 1993
the U.S. based IEEE published their revision of the IEEE/ANSI RF/MW standard
C95.1-1991, IEEE(1991). This report is solely about thermal biophysical
interactions that create heat and the SAR levels that will avoid dangerous
heating, burns and shocks. The assessment criteria all related to thermal
absorption mechanisms. The primary revision is a relaxation of power density
limits for all body parts except eyes and testes. This relates to a revised
calculation of the 6-min dose that produces an SAR of 0.4
W/kg.
Conclusion:
Of all the major western authorities who are responsible
for setting RF/MW exposure standards, the only body which is departed from
solely considering thermal effects, was an internal review team of the U.S.
E.P.A.. They also considered epidemiologic and animal evidence at non-thermal
levels that did involve increases in cancer. However, they were not allowed to
retain their recommended carcinogenic classification because EPA administrators
bowed to political pressure.
4. The ICNIRP and WHO
Approach in the 1990's:
Introduction:
The world Authorities, WHO and
ICNIRP, in the early and late 1990's, also retain the RF-Thermal View and
recommend guidelines based on avoiding tissue heating. They have undertaken more
comprehensive reviews that considered epidemiological and long-term animal
evidence. Their reviews of this evidence did not sway them from the RF-Thermal
View. A detailed analysis of their reviews and the research papers cited reveals
evidence of predetermination to reject any evidence that contradicted this view.
The long history of holding the RF-Thermal View has brought extensive comfort
and complacency. This is partly through the great degree of precision,
repeatability and reliability of SAR calculations and heat protection. This is
such a long-held view that it has become a mind-set. This way of thinking makes
it extremely difficult to move review teams from the RF-Thermal View to the
Public Health Protection approach. It requires a complete change of thought and
approach to move from a comfortable and well understood mechanism to the much
more complicated consideration of epidemiological data derived from complex
human situations. But, as Dr Lilienfeld reminded us:
"The proper study of man
is man".
The Constructive Dismissal Approach:
In order to maintain the
RF-Thermal View against the extremely strong evidence from epidemiology, animal
experiments and of non-thermal mechanisms, the WHO and ICNIRP assessors and
their colleagues have developed as set of dismissive methodologies. These
include:
Maintaining that the RF-Thermal view as the "consensus of science".
This allows the biological mechanism to dominate and epidemiology and animal
evidence is dismissed.
Maintaining a contrast between Ionizing radiation and
Non-ionizing radiation.
Moving the level of evidence goalpost where for a
study to become "evidence" it must first be replicated, whereas in the past each
study was evidence and to "establish" a biological effect replication was
required.
Promoting strict sets of scientific criteria which are proposed as
being necessary for reliable use of the results, e.g. the Bradford Hill
"criteria", instead of "viewpoints", and Dr Martin Meltz's 13 experimental
criteria for testing genotoxicity, Meltz (1995). In this way all non-thermal
evidence is rejected.
Citing studies which are too small and have small
follow-up periods so there is little or no opportunity for cancer to develop, as
evidence that radar exposure does not cause cancer.
Citing studies which do
show significant increases in cancer as showing no evidence of increases in
cancer.
Preferring to simply quote the conclusions of papers and reports that
state that there were no adverse effects found, while failing to recognize that
the data and analysis within the documents do show significant associations,
including significant dose-response relationships.
Dismissing epidemiological
studies on the grounds that populations and exposures are not well defined.
Lilienfeld explains that this is a difficulty but results are still relevant and
important.
Dismissing research results one by one and failing to assemble and
interpret the whole pattern of research results - the divide to conquer
approach.
All of these are demonstrated methods used by WHO and ICNIRP which
amounts to a systematic approach to wrongly dismiss evidence of effects, i.e.
Constructive Dismissal.
The evidence of a leading WHO/ICNIRP member:
In
the 1990's a major WHO review was published, WHO (1993). The latest ICNIRP
Guideline assessment has been published in 1998, ICNIRP (1998). Both of these
maintain the RF-Thermal View. A leading scientist, Dr Michael Repacholi, was
involved as the technical editor of the WHO review and in chairing both the WHO
review team and ICNIRP until April 1996. He is now is Chairman emeritus of
ICNIRP.
Insights into his mind-set, which is reflected by WHO and ICNIRP, is
seen in his evidence in a New Zealand cell site case in November 1995, the
MacIntyre Case. In this case the local residents of the suburb of Ilam, in
Christchurch, New Zealand, appealed a City Council decision to allow a cell site
to be installed on the roof of an old suburban movie theatre in the middle of
their community. The site would irradiate a number of local residences and the
local kindergarten that was about 70 m from the site.
Dr Repacholi appeared
in this case as an expert witness on behalf of BellSouth Ltd,. In sworn
testimony contained in his evidence-in-chief he states: (Note that the emphasis
on 'any' is Dr Repacholi's)
"To produce any adverse effect, RF exposure above
a threshold level must occur. This threshold level is the RF exposure needed to
increase tissue temperature by at least 1(C."
"Multiple exposures to
sub-threshold levels of RF have not been found to have any adverse health
impact."
"Exposure to RF fields has not been established to cause
cancer."
"No accumulation of damage occurs to tissues from low level
(sub-threshold) RF exposures".
"The science has also not found any evidence
for adverse health effects from repeated exposures at levels below the
threshold."
Dr Repacholi's evidence is fully consistent with the ICNIRP
conclusions outlined above and were referenced by Dr Repacholi to the
WHO/IRPA/UNEP review, WHO(1993). To back up Dr Repacholi's claim that the
RF-Thermal position was the "consensus of science", Dr Repacholi referenced WHO
(1993), for which he had a major responsibility.
4.4 Evidence vs
Established:
Around the time of this court case Dr Repacholi was supervising
a research project in Australia in which genetically modified mice were exposed
to a sub-thermal dose of a GSM cell phone signal, for two half-hour periods per
day. This gave SARs averaging 0.13 to 1.4 W/kg during the exposures, giving a
daily average range of 0.005 to 0.058W/kg. They concluded that "Lymphoma risk
was found to be significantly higher in the exposed mice than in the controls
(OR = 2.4, p=0.006, 95%CI: 1.3-4.5)."
Hence Dr Repacholi's own research
results, which were published after the NZ court case was concluded, contradict
his claims in court. In an industry-sponsored press conference in Vienna at the
time of the Vienna EMR Workshop in October 1998, Dr Repacholi stated that there
was no evidence of adverse effects from GSM cell phones. When questioned in the
Workshop about his own research results, he took the position that a scientific
experiment can only be considered as "evidence" once it has been independently
replicated. This is not the definition of "evidence" which most people and most
courts accept. A research result is "evidence". Replication is required in order
to establish a biological effect. Both the original and the replicate
experiments contribute evidence with amounts to the establishment of a
biological effect.
Two other long-term rodent studies have observed increases
of cancer in exposures involving RF/MW. Chou et al. (1992) chronically exposed
rats to a non-thermal radar-like signal, observed a significant increase in
benign tumors and highly significant increase in primary malignant tumors,
RR=3.6, 95%CI: 1.34-9.7, p=0.0036. Vijayalaxmi et al. (1997, 1998) exposed
cancer-prone mice to a 2.45 GHz continuous wave signal and observed a 41 %
increase in tumors and highly significant (p<0.01) 12.5% increase in
chromosome damage in bone marrow and blood. Hence the evidence consists of three
studies in which RF/MW radiation significantly increases cancer in rodents,
including one which also associates this with chromosome damage. The chromosome
damage is evidence of genotoxicity, the ability to damage DNA and cause
mutations and cancer.
These projects serve to illustrate one of the
fundamental problems with EMR research. While three independent laboratories
have observed increases in cancer in rodents with non-thermal RF/MW exposures,
all rodent species were different, all exposure regimes were different. One was
a GSM carrier of 900 MHz pulsed at 217 Hz for 2 periods of half an hour per day
with mean daily SAR in the range 0.005 to 0.058 W/kg. Two used 2.45 GHz carriers
but the first was pulsed at 800pps, modulated at 8 Hz, and involved 21.5 hr of
daily exposure with a daily mean SAR in the range 0.13 to 0.36 W/kg. The second
used a continuous wave exposure for 20 hr/day with a daily average SAR of
0.83W/kg.
For those, like ICNIRP, who maintain the RF-thermal view, these
projects do not provide "evidence" that RF/MW produces cancer in rodents because
every experiment has differences in animals and exposure regimes and none have
been precisely replicated.
Alternatively, taking the more traditional
scientific and legal approach, there are three studies, from independent
laboratories, which show significant increases in cancer in rodents at
non-thermal levels of exposure to RF/MW radiation. Hence there is animal
evidence to support the epidemiological evidence that RF/MW exposed populations
develop significantly higher rates of cancer incidence and mortality. Both the
animal evidence and the human evidence covers a wide range of RF/MW exposure
conditions. Across the same frequency range multiple independent laboratories
have observed significant DNA-strand breakage and enhanced chromosome
aberrations. Hence there is strong evidence that RF/MW is genotoxic, mutagenic,
carcinogenic and teratogenic in animals and people at non-thermal levels of
RF/MW exposure.
4.5 Ionizing Radiation vs Non-Ionizing Radiation?
The
history of EMR shows that it has always been treated differently from chemicals.
One reason for this is an argument related to radiation. The argument runs as
follows:
"Ionizing radiation has the photon energy to break chemical bonds
and produces free radicals in cells. These enhance the damage to DNA and other
macromolecules which increases the risk of cancer. Non-Ionizing radiation does
not have the photon energy to break bonds and produce free radicals. Therefore
non-ionizing radiation cannot damage DNA and cannot cause cancer."
Many
chemicals cause cancer, such as benzene, without involving ionization. We can
immediately note that UV-B radiation is non-ionizing but it is known to cause
cancer, particularly skin cancer. Among a number of identified mechanisms is
UV's ability to cause mutation in the tumor suppressor gene p53, Leffell (2000).
This proves that non-ionizing radiation does cause cancer and acts through
altering the p53 gene activity. This illustrates the point that cancer is caused
by both enhancing cell damage and by inhibiting cell damage repair rates and
efficiencies. UV radiation also enhances free radical formation, Collins,
Poehler and Bryden (1995) and Jurkiewicz and Buettner (1994, 1996).
There is
evidence that non-ionizing radiation dose enhance free radical activity. Phelan
et al. (1992) investigated membrane fluidity in Melanin-containing cells that
were exposed to low level microwave radiation, 1 hr at 0.2 W/kg. They
conclude:
"The data indicate significant, specific alteration of
cell-membranes was due, at least in part, to the generation of oxygen
radicals".
Lai and Singh (1997) showed that significant microwave induced
DNA-strand breakage could be eliminated through the application either of
melatonin, a natural free radical scavenger, or of PBN, a spin-trap compound.
This indicates that melatonin reduction and enhanced free radicals is a
plausible mechanism.
Hence UV-B and RF/MW non-ionizing radiation are both
associated with enhanced free radical activity in cells, either by enhancing the
free radicals or by reducing the free radical scavenger, melatonin. Thus the
effect on ionizing and nonionizing radiation can be very similar, but may
involve different mechanisms. Either way, the effect is the same. They both
produce genetic damage and are carcinogenic.
4.6 Ionization is not a
prerequisite for cancer:
Many generations of medical biologists and
toxicologists do not assume that ionization is a necessary prerequisite for
cancer producing agents, since thousands of chemicals are cancer producing
agents without the involvement of ionization. Chemicals are carcinogens, Baxter
(1995), when they:
Alter DNA, initiating cancer.
Corrupt cellular growth
control, thus acting as cancer promoters.
Act with other carcinogenic agents,
working as Co-promoters of cancer.
There is evidence that EMR acts in all of
these ways.
4.7 Examples of extreme lengths gone to retain the RF-Thermal
view:
ICNIRP and individual national authorities are so wedded to the
RF-Thermal view that they not only attempt to reject studies by claiming
weakness and inconsistencies, they also descend to use demonstrably incorrect
scientific statements.
4.7.1 ICNIRP misquotes results:
In the ICNIRP
(1998) cancer assessment the following statement appears:
"More recent
studies have failed to show significant increases in nervous tissue tumors among
workers and military personnel exposed microwave fields (Beall et al. 1996 and
Grayson 1996)."
Statistical significance is defined as p(0.05 and/or a 95%
confidence interval where the lowest side of the range is close to 1.0 or
higher. Beall et al. studied the increase in brain tumor with exposure to
computer monitors (VDTs). Beall et al.'s abstract states:
"Other results
included and elevated OR for 10 or more years of employment in
engineering/technical jobs [OR = 1.7; 95% confidence interval (CI) = 1.0-3.0] or
in programming jobs (OR = 2.8, 95%CI= 1.1-7.0). The OR for glioma for all
subjects who had accrued 5 years of programming work 10 years before each case's
death was 3.9 (95%CI = 1.2-12.4)."
The abstract reports significant increases
in brain tumors. The data in the paper show that for engineering/technical jobs
there is a dose-response for brain tumor death and years of work, p=0.07, and
for computer programming, p=0.04. Thus the paper does show significant increases
in brain tumor death from EMR exposure with dose-response increases and one
significant dose-response relationship.
Grayson (1996) investigated a large
sample (880,000 with 11.17 million p-yrs) of U.S. Air Force personnel, some of
whom were occupationally exposed to EMR and ionizing radiation, with exposure
assessed through a job exposure survey. From this very large sample only 275
were exposed to RF/MW, 94 of whom developed brain tumors. This yielded OR =
1.39, 95%CI: 1.01-1.90. This is a statistically significant result.
ICNIRP's
statement about Beall et al. (1996) and Grayson (1996) is demonstrably
scientifically wrong and misleading. It reveals a strong predetermination to
dismiss evidence of effects.
4.7.2 Recently in New Zealand a similar
situation occurred:
Late in 1998 the Royal Society of New Zealand released a
review report on radiation health effects. Being the Royal Society it was
assumed that it would be a high quality, up to date and authoritative
publication. The report was entitled "Radiation and the New Zealand Community -
A scientific Overview". The major contribution of two staff members of the
National Radiation Laboratory is acknowledged. The report contains statements
about the health effects of EMR being totally wrong and misleading, and reveal a
determination to ignore evidence of adverse health effects.
The N.Z. Royal
Society report takes the thermal view and at one key point makes the claim in
relation to ELF EMR, p67:
"Some questions have been raised with respect to
possible adverse effects of electric and magnetic fields, particularly those at
low frequencies, in connection with high voltage lines, computer terminals,
domestic appliances and wiring. However, no effects due to occupational exposure
have been reported, nor are there any indications of adverse health effects on
humans, other than from spark discharges and shock from direct contact."
It
is glaringly untrue to state that "no effects due to occupational exposure have
been reported". Many hundreds of studies have reported ELF biological and human
health effects. Three have even been carried out in New Zealand. Preston-Martin
et al. (1993) found for all brain cancer elevated risks were found for
electrical engineers (OR= 8.2, 95%CI: 2.0-34.7) and electricians (OR = 4.6,
95%CI: 1.7-12.2). Beale et al. (1997) investigated health effects near high
voltage powerlines in Auckland and found significant linear dose-response
relationships for some health and psychological variables and magnetic field
exposure. Dockerty et al. (1998) studied childhood cancers in relation to EMF
exposure. Electric blankets produced elevated adjusted rates of leukaemia (OR=
2.2, 95%CI: 0.7-6.4), CNS cancer (OR = 1.6, 95%CI: 0.4-7.1) and other solid
cancers (OR = 2.4, 95%CI: 1.0-6.1). Leukaemia risk was highest when bedroom
magnetic field was ( 0.2 µT compared with ( 0.1 µT, (OR= 15.5,
95%CI:1.1-224).
A totally independent team of Swedish medical scientists,
reviewed over 100 epidemiological papers, an over 300 studies in total,
published up to July 1994, Hardell et al. (1995). They
concluded:
"Epidemiological and experimental studies concerning extremely low
frequency electromagnetic field exposure and malignant diseases published up to
1 July 1994 were evaluated to assess the possible carcinogenicity of
electromagnetic fields and the scientific basis for environmental and
occupational standard setting. We concluded that there are possible associations
between
an increased risk of leukaemia in children and the existence of, or
distance to, power lines in the vicinity of their residence,
an increased
risk of chronic lymphatic leukaemia and occupational exposure to low frequency
electromagnetic fields and,
an increased risk of breast cancer, malignant
melanoma of the skin, nervous system tumours, non-Hodgkin lymphoma, acute
lymphatic leukaemia or acute myeloid leukaemia and certain occupations.
There
is no scientific basis for occupational or environmental standard setting for
low frequency electric or magnetic fields."
The final statement about
standards setting is based on the lack of good exposure measurement in most
occupational studies and the lack of dose response relationships in order to
determine an ELF field level which will avoid the observed association to risk
factors. The fact that the mean daily exposure of even the highly exposed
workers is a small fraction of the current standards demonstrates the gross
inadequacies of the standards and guidelines. The ICNIRP (1998) Guideline
recommends a 24-hr occupational limit of 500 µT and residential limit of 100
µT.
Many more ELF health studies have been published since July 1994. Four
laboratories have shown that ELF below 1.2 µT reduces the oncostatic protection
of melatonin in human breast cancer cells, with a threshold of around 0.1 to 0.2
µT. Also 4 laboratories have shown the ELF radiation is associated with
significant increases in DNA strand breaks. One replication is usually necessary
to confirm a biological effect. Four independent studies definitely establish a
biological effect. These biological effects are biological mechanisms which
confirm the plausibility of the epidemiological associations found in Hardell et
al. (1995), giving the classification to the level of probable or actual human
carcinogen with the addition of the post-1994 studies.
Residential powerline
studies on childhood leukaemia, such as Feychting and Ahlbom (1993), found for a
cut-off point of 0.2 µT a Relative Risk of RR=2.7 (95%CI: 1.0-6.3) and a trend
with p=0.02. For a cut-off point of 0.3 µT, RR= 3.8 (95%CI: 1.4-9.3, for the
trend p= 0.005 . By pooling data from Norwegian and Swedish studies, Feychting
et al. (1995) found a relative risk of RR=2.0 (95%CI: 1.0-4.1) for a 0.2 µT
cut-off and RR=5.1 (95%CI: 2.1-12.6) for 0.5 µT of, a significant dose response
relationship, p=0.03.
Hence it is now possible to determine that a current
threshold level for no observed effect for childhood leukaemia and breast cancer
is near 0.1 µT. This is 1000 times below the current guideline and has yet to
have a safety factor incorporated.
Thus it is grossly wrong for the report of
Royal Society of NZ to claim that "no effects have been reported from
occupational exposure" and "nor are there any indications of adverse health
effects on humans, other than from spark discharges and shock from direct
contact". This is so grossly misleading and dishonest, that it puts this
report's credibility, and that of the Royal Society of New Zealand, seriously at
risk. In coming to its conclusions the Royal Society of NZ relied heavily on the
Director of the National Radiation Laboratory, Dr Andrew McEwan.
Scientists
and the public expect much more scientific accuracy and integrity from
Government employees who advise the Minister of Health, and of the Royal
Society.
4.7.3 Canada does it a little better:
In contrast, the Royal
Society of Canada in their March 1999 report "Potential health risks of
Radiofrequency fields from wireless telecommunication devices", carried out a
detailed review of biological mechanisms. They involved current researchers in
the review team who concluded that most RF exposures used in experiments exceed
the limits set in the Canadian Safety Code 6 (SAR = 0.08 W/kg). They also
state:
"However, effects on cell proliferation, Ca2+ efflux, blood brain
barrier (BBB) permeability, behaviour and ornithine decarboxylase (ODC) activity
have all been repeated in independent laboratories. Because these effects occur
at exposures not thought to elicit thermal effects, it is likely that these
effects, even if they also occur at higher exposure levels, are non-thermal
biological effects."
This critique will show that some key non-thermal
biological mechanisms are well established by replication in many independent
laboratories. These established biological mechanisms are totally supportive of
and consistent with a large body of epidemiological evidence, which includes
many statistically significant associations and dose-response relationships. In
doing so this critique will show that the ICNIRP assessment takes a
predetermined dismissive approach that is highly selective and unscientific. It
even involves deliberate and repeated misquoting and misrepresentation of study
results. It becomes clear that the thermally based guideline is being defended
at all costs, even at the cost of putting public health severely at risk all
around the world.
5. ICNIRP's 1998
assessment of the RF/MW Guideline:
ICNIRP Review Conclusions:
The
failure to use epidemiological evidence as the primary source and animal
evidence secondarily, and the predetermination to retain of the RF-Thermal View
is seen in the conclusions of ICNIRP (1998), p507:
Data on human responses to
high-frequency EMF that produce detectable heating have been obtained from
controlled exposure of volunteers and from epidemiological studies on workers
exposed to sources such as radar, medical diathermy equipment and heat sealers.
They are supportive of the conclusions drawn from laboratory work, that adverse
biological effects can be caused by temperature rises in tissue that exceed 1(C.
Epidemiological studies on exposed workers and the general public have shown no
major health effects associated with typical exposure environments. Although
there are deficiencies in epidemiological work, such as poor exposure
assessment, the studies have yielded no convincing evidence that typical
exposure levels lead to adverse reproductive outcomes or an increased cancer
risk in exposed individuals. This is consistent with the results of laboratory
research on cellular and animal models which have demonstrated neither
teratogenic nor carcinogenic effects of exposure to athermal levels of high
frequency EMF."
ICNIRP conclusions are scientifically wrong:
The
Constructive Dismissal approach is evident. The thermally-based guideline is
retained. Apart from the statement about there being adverse effects of tissue
warming, every other statement made is scientifically challengable and
misleading.
For example: "epidemiological studies on exposed workers and the
general public have shown no major health effects associated with typical
exposure environments".
Epidemiological studies of exposed workers and the
general public have shown significant increases in major health effects,
including dose-response relationships which are indicative of a casual effect.
This includes multiple studies on miscarriage and significant dose-response
relationship between microwave exposure and first trimester miscarriage,
Ouellet-Hellstrom and Stewart (1993). Many laboratory studies on cells and
animals have demonstrated athermal carcinogenic and teratogenic effects, Chou et
al. (1992), Repacholi et al. (1997), Vijayalaxmi et al. (1997) and Magras and
Xenos (1997). These statements are demonstrably incorrect and misleading. It is
conclusions such as these that continue to put thousands of lives at risk in New
Zealand alone, and millions at risk around the world. Many occupational studies
have found significant increases in cancer, e.g. Lilienfeld et al. (1978),
Robinette et al. (1980), Milham (1985 a,b, 1988), Thomas et al. (1987), Demers
et al. (1991), Cantor et al. (1995), Szmigielski (1996), Grayson (1996), Beall
et. al. (1996). Residential studies showing significant increases in cancer from
RF/MW exposure, some of which show significant dose-response relationships
include: Hocking et al. (1996), Selvin et al. (1992), Dolk et al. (1997a,b), and
Michelozzi et al. (1998).
In the middle of the frequency spectrum, where the
ICNIRP Guideline exposure level is at its lowest, 200 µW/cm², there are
residential epidemiological studies that give dose-response relationships for
adult and childhood leukaemia with a threshold near 0.025 µW/cm². This is 8,000
times lower than the ICNIRP Guideline. In Switzerland, significant sleep
disturbance was observed at an RF exposure level of 0.0004 µW/cm², Altpeter et
al. (1995). For this RF frequency (6.1-21.8 MHz) for which the ICNIRP Guideline
is about 200-1000 µW/cm². The adverse effect occurs at a factor of 0.5 to 2.5
million times lower than the Guideline.
5.3 The ICNIRP 1998 Guideline:
By
ignoring the epidemiological evidence ICNIRP settles on a thermally-based
guideline by accepting a thermal threshold of 4 W/kg, a workers safety factor of
10 (0.4 W/kg) and a further factor of 5 for the general public (0.08 W/kg). This
is plotted in Figure 7 in terms of electric field strength and exposure
intensity, as a function of carrier frequency.
Figure 7: The ICNIRP (1998)
Guideline for public and occupational exposures as a function of carrier
frequency. On the left the units are electric field strength (V/m) and on the
right the exposure intensity ( µW/cm²). The three plateau regions above 1 kHz
are 87, 28 and 61 V/m, corresponding to 2000, 200 and 1000 µW/cm²,
respectively.
The ICNIRP methodology and use of scientific research is
blatantly incorrect. A long-held mind-set dominates the EMR radiation
authorities. It needs to be exposed and changed.
5.4 A sports analogy of the
different approaches:
5.4.1 The situation of conflict:
The primary issue
in this report is the ICNIRP retention of a thermally-based guideline in the
face of the dominant international approach which requires the use of
epidemiological evidence when setting public health protection standards. A
phrase comes to mind when reading the ICNIRP Guideline report, "They appear to
be playing their own game and making up the rules as they go along". This
analogy appears to be helpful. These two approaches are like two different
games.
5.4.2 The ICNIRP Game:
ICNIRP is playing its own game and setting
its own rules. It is the game that is played by national authorities which, as a
team, they feel very comfortable with it. The name of the team is "The Consensus
of Science". However, it involves quite a small and very select team that
includes national experts who come from national authorities who subscribe to
the rules of the ICNIRP game. In the ICNIRP game the first rule is that there is
only a tissue heating effect from RF/MW exposure. You must agree with this rule
to play the ICNIRP game. As a consequence of this rule, in the ICNIRP game, all
other biological effects are not real and any epidemiological study that shows
an effect with non-thermal exposure, must be faulty and will be rejected. In
other words, if you break this rule you are out of the game. In this game it is
fine to change the rules about acceptable significant, what is evidence, and
criteria for how a biological effect is established. In this game a study does
not provide evidence until it has been exactly replicated. You set up 13
criteria which must be achieved for an experiment to be reliable, for example
Meltz (1995). If even one criteria is breached then you can reject the findings.
Similarly the ICNIRP team uses the Bradford-Hill Criteria to criticize and
reject all epidemiological studies. One criticism, valid or not, is sufficient
to reject a whole study.
For a long time Dr Repacholi has been the captain of
the ICNIRP team, he has helped to make and change the rules. His own study shows
a significant non-thermal effect. He was able stay in the team by changing the
rules of evidence.
The Public Health Protection Game:
In the Public Health
Protection Game the first rule is that public health protection is paramount.
Standards are based on public health studies, i.e. epidemiology. Epidemiological
evidence is sufficient to set standards where there are dose-response
relationships or when studies have shown significant adverse effects a sound
study which involves exposures below those which have found effects, determines
that there is no evidence, not even an elevated risk, at that exposure level.
Then exposure associated with the lowest reported adverse effect has a safety
factor is applied to deal with the uncertainty. Avoidance action and experiment
are a vital part of this game.
Avoidance action is taken long before
scientific proof of cause and effect is reached. This is because it is
recognized that many disease agents cause sickness and death years or even
decades after the initiating exposure. Unnecessary delay is avoided and action
is taken to protect public health, once the evidence is judged sufficient under
the circumstances. A reversible adverse effect can be treated differently than
permanent damage that hastens disease and death, such as miscarriage, congenital
malformation, brain damage or cancer. The Bradford-Hill viewpoints inform this
decision-making, Hill (1965).
6. Non-Thermal
Biological Mechanisms
Veteran EMR biological researchers Dr Ross Adey, Dr
Carl Blackman, and Dr Alan Frey and eminent epidemiologist, the late Dr John
Goldsmith, cite sound evidence which totally refutes the claim that there are no
established non-thermal biological mechanisms.
6.1 Dr Ross Adey directly
challenges the thermal view:
Dr W. Ross Adey is one of the world's most
respected veteran EMR researchers. His pioneering work on neuroscience gives
deep insights into biological functions and processes. The following is the
abstract from his paper "Frequency and Power Windowing in Tissue Interactions
with Weak Electromagnetic Fields", Adey (1980):
"Effects of non-ionizing
electromagnetic (EM) fields that raise tissue temperature in general differ very
little from effects of hyperthermia induced by other means. However, fields
raising tissue temperature orders of magnitude less than 0.1(C may result in
major physiological changes not attributable to raised temperature per
se.
These weak fields have been observed to produce chemical, physiological,
and behavioral changes only within windows in frequency and incident energy. For
brain tissue, a maximum sensitivity occurs between 6 and 20 Hz. Two different
intensity windows have been seen, one for ELF tissue gradients around 10-7 V/m,
and one for amplitude modulated RF and microwave gradients around 10-1 V/m. The
former is the level associated with navigation and prey detection in marine
vertebrates and with the control of human biological rhythms; the latter is the
level of the electroencephalogram (EEG) in the brain tissue.
Coupling to
living cells appears to require amplifying mechanisms that may be based on
non-equilibrium processes, with long-range resonant molecular interactions. The
cooperative processes are now recognized as important in immune and hormonal
responses, as well as in nerve excitation. Polyanionic proteinaceous material
forming a sheet on the cell membrane surfaces appears to be the site of
detection of these weak molecular and neuroelectric stimuli."
Professor Adey
succinctly summarizes EMR research at that time. He does not claim, in the body
of the paper, that the two observed intensity windows are the only intensity
windows, but that these are intensity windows that have repeatedly been shown to
have significant effects.
In his conclusion Dr Adey directly challenges the
thermal view.
"Too many physicists and engineers cling desperately to the
thermal models as the alpha and omega of bioeffects from nonionizing
radiofrequency fields, shunning the exquisite beauty of long-range molecular
interactions and resonant processes in biological macromolecules."
In Adey
(1993) intercellular communications are described as "whispering between cells".
Dr Adey notes new work that involves free radicals:
"that may also
participate in highly cooperative detection of weak magnetic fields, 'even at
levels below thermal (kT) noise'."
The key role of resonance and tuning is
addressed.
"In recent studies (Grundler and Kaiser (1992)), they noted that
the sharpness of the tuning increases as the intensity of the imposed field
decreases; but the tuning peak occurs at the same frequency when the field
intensity is progressively reduced. Moreover, clear responses occur with
incident fields as weak as 5 picowatts/cm²."
A 5 pW/cm² signal is billions of
times below the ICNIRP guideline for GHz signals. The studies cited by Dr Adey
show the fundamental biological role of frequencies, tuning and resonance.
Kaczmarek and Adey (1973) showed that weak oscillating electric gradients, no
larger than the EEG (50-100 mV/cm), increase efflux of calcium ions and GABA
from cat cerebral cortex by almost 20%. Cellular calcium ions play many vital
roles in cell growth and development regulation. Hence the ability of EMR to
induce changes in cellular calcium ions is fundamentally important in assessing
the biological mechanisms which contribute to adverse health effects.
This
evidence that biological systems use tune frequencies which involve
electromagnetic signals on the surface of cells and between cells, even though
these signals are orders of magnitude below the thermal noise level, is quite
reasonable. Close to an AM tower where the 1 MHz signal had a strength of 100
µW/cm² it was still possible to tune into a remote AM and remote FM signals on
an ordinary radio even through their field intensity was less than 0.01pW/cm².
Resonant circuits within the radio were tuned into the carrier of the extremely
weak but easily detectable radio signal.
Calcium ion (Ca2+) efflux:
The
calcium ion (Ca2+) is one of the most important substances in cells. Ca2+ is a
first, second and third signal transduction messenger, Alberts et al. (1994),
Pahl (1999). Alberts et al. describes Ca2+ as a prominent and ubiquitous
intracellular messenger. This means that factors that induce changes of cellular
Ca2+ can cause significant changes of cells.
Adey (1979) contains evidence of
other windows for ELF induced Ca2+ efflux in chick and cat brains, e.g. 5, 10,
56 and 100 V/m (Figure 8), and other microwave intensity windows for Ca2+ influx
and efflux. The field intensity and modulation frequency were shown to be
important parameters in EMR causing Ca2+ efflux. Since extremely low SAR's
produce significant effects and the modulation frequency is critical, this is
not a thermal effect but it is a biological effect acting at the cellular level
affecting cellular functions. ELF and RF/MW signals cause Ca2+ efflux and ELF
signals don't involve tissue heating. enceH
Figure 8: The effects of
extremely low frequency fields on 45Ca2+ efflux from chick forebrain, for ELF
fields of 5, 10, 56 and 100 V/m. * : p<0.05; **:p<0.01, Bawin and Adey
(1976).
Figure 9 shows significant Ca2+ efflux with exposure intensity at
0.05, 0.1 and 1 mW/cm², but not at 2 and 5 mW/cm² with a 450 MHz carrier.
Particular higher exposures do not have the same significant effects as lower
specific exposures, indicating that this is a non-thermal mechanism.
Figure
9: Effects of changing intensity of 450 MHz field amplitude modulated 16 Hz as
efflux of 45Ca2+ from chick cerebral hemispheres. Cross-hatched bars show levels
of efflux exposed specimens in relation to control specimens (stripped bars)
tested simultaneously in the same experiments. Variance shown as SEMs **,
p<0.05., Bawin, Sheppard and Adey (1978)
Figure 10: Relative Ca2+ efflux
(positive and negative) from isolated chick cerebral hemisphere exposed to (A)
weak RF field (147 MHz, 0.8 mW/cm², 56 V/m in air), amplitude modulated at low
frequencies (abscissa) (Bawin et al. (1975) and (B) ELF electric field (56 V/m
in air) over the same modulation frequency range (Bawin and Adey (1976). The
tissue gradients differ by 106 between A and B.
It was established very early
on that an ELF signal carried on a RF carrier produced altered cellular Ca2+
fluxes, as the ELF signal on its own, but with a very much higher induced tissue
electric field gradient, Bawin and Adey (1976), Figure 10.
Adey (1979)
reviews a large body of research on the neurophysiological effects of RF/MW
radiation. This included the human biometeorological research on circadian
rhythms in human subjects isolated from sunlight and EMR; their own work on
altered monkey behaviour with a tissue gradient of 10-7 V/m and other animal
behaviour experiments. It also covered cellular evidence including Ca2+ flux
experiments on cats and chick brains. These show that ionic changes in amplitude
modulated RF/MW fields are much more related to modulation frequency than
intensity of signal. Often higher effects are seen at lower exposure intensities
than some higher intensities - in windows.
Significant effects occur in
fields that are too low to produce any detectable thermal effects. In great
frustration at the intransigence of the position held by scientists who doggedly
claim that there is only evidence of thermal effects. Professor Adey
concludes:
"Faced with the overwhelming complexity of the brain as a tissue
and as the organ of the mind, physical scientists and medical researchers alike
have all too often retreated shamelessly into classicisms and the argots of
their respective trades. Too many physicists and engineers cling desperately to
thermal models as the alpha and omega of bioeffects from non-ionizing
radiofrequency fields, shunning the exquisite beauty of long-range molecular
interactions and resonant processes in biological macromolecules."
"True
science can never be a popularity contest. The time has surely come when we
should place these scholasticisms of another age in a proper context, counting
ourselves thrice blessed at the prospect that through the use of non-ionizing
radiofrequency radiation as a research tool, the intrinsic organization of the
brain tissue, the subtleties of neuroendocrine phenomena and the broad sweep of
immunological interactions may at last be understood in terms of transductive
coupling at the molecular level."
Dr Adey was basing his insights on a
fascination with discovering how neurological tissue operated and how it was
altered in extremely low level RF/MW and ELF fields.
The current world leader
in Ca2+ efflux research is Dr Carl Blackman of the U.S.E.P.A.. Dr Blackman has
replicated and significantly extended the studies carried out by Dr Adey's group
and other groups. He and his team have produced over 2 dozen peer-reviewed
publications in this area, including several major reviews. Blackman et al.
(1989) identified multiple power density windows for Ca2+ efflux, using a 50 MHz
carrier modulated at 16 Hz. Their results, using units of mW/cm², are summarized
as follows:
Enhanced efflux 1.75 3.85 5.57 6.82 7.65 7.77 8.82
No change
0.75 2.30 4.50 5.85 7.08 8.19 8.66 10.6 14.7
The intensity window data was
considered as an example of non-linear dynamics because there appears to be no
progressive decline in the magnitude of the effects at low exposure intensities.
This data is consistent with a fractal process with a non-integer dimension that
is approximately 1.4, Blackman et al. (1989).
The lowest published RF
intensity that has been documented to produce significant Ca2+ efflux is 0.00015
W/kg from Schwartz et al. (1990). They used frog hearts, exposed for 30 mins, to
a 16Hz modulated 240 MHz RF signal. This has an exposure intensity of about 0.08
µW/cm².
Figure 11: Effect of 15 Vrms/m electromagnetic fields on the efflux
of Ca2+ from chicken brain tissue as a function of modulation frequency,
Blackman et al. (1988). The solid bars show significant alteration,
p<0.05.
Blackman's group confirmed and significantly extended the
"windows" concept of Ca2+ efflux, as well as aspects of homeostasis, involving
tissue temperature for example. Figure 11 shows how modulation frequencies out
to 510 Hz produce significant Ca2+ efflux at some frequencies, but not at other
frequencies on either side.
Blackman et al. (1990) showed the importance of
the local static magnetic field. Blackman et al. (1991) showed that Ca2+ efflux
occurred for tissue temperatures of 36(C and 37 (C and not at 35(C and 38(C.
They comment that these could be very good reasons why experimental outcomes
have been difficult to confirm in some laboratories. After reviewing the many
studies in the published literature on EMR induced Ca2+ efflux. Blackman (1990)
concludes:
"Taken together, the evidence overwhelmingly indicates that
electric and magnetic fields can alter normal calcium ion homeostasis and lead
to changes in the response of biological systems to their
environment".
Blackman (1990) concludes that calcium ion efflux/influx is an
established biological effect of EMR exposure and it changes the biological
response of cells. Because modulation frequencies are critically involved, and
low intensity exposures are observed under some circumstances to produce greater
effects than some higher exposure conditions, resonant interactive processes are
indicated and heating is definitely not involved except to establish a
homeostatic range.
At the Scientific Workshop on Biological Effects of
Electromagnetic Radiation in Vienna, October 1998, Dr Carl Blackman, U.S.
Environmental Protection Agency, presented the results of 30 years of research
into cellular calcium ion efflux and influx which is induced by pulsed and
modulated EMR. Having established that EMR acts in quite different and
consistent biological manner in a complex set of windows, Dr Carl Blackman
concluded that it makes a great deal of sense to move away from the concept that
EMR should act like a single chemical. The variable nature of the response, as
indicated by complex exposure 'windows', indicates that EMR acts like chemicals
(plural) rather than acting like a single chemical, Blackman (1998). This
addresses the concepts around 'consistency' and 'specificity'.
Since
alteration of cellular calcium ions concentration leads to many different health
effects, and since many other biological changes have been identified, it is
inappropriate to limit consideration of RF/MW exposure to single adverse health
effects.
EMR exposes the whole human body and not a single target organ. Each
organ has a different cellular structure that relies to a greater or lesser
extent in electric and magnetic factors and forces for its growth and control.
The brain, central nervous system and muscles, including the heart, make much
stronger use of electrical signals than bones for example. However, every cell
has an electric potential across its membrane and uses ions, such as calcium
ions (Ca2+), sodium ions and potassium ions. Receptors on cells are negatively
charged and ions and neurotransmitters which initiate signal transduction are
positively charged. DNA is negatively charged and the protein which is bound to
it is positively charged.
Hence, every cell can interact with EMR and EMR can
alter the growth regulation factors through alteration of the ionic
concentration within the cells and in the intracellular fluid. Some higher
functioning organs, especially the brain and CNS, are dependent on EMR for
normal operation and have been shown to be altered by externally applied EMR,
with consequent behaviour and neurological performance change, Bawin et al.
(1973).
Because the whole body is exposed to RF/MW radiation, and since the
brain and central nervous systems are electrically sensitive and active, it is
not surprising that the most frequent adverse health effects identified in
epidemiological studies are leukaemia and brain tumour. Leukaemia is a disease
of the blood and bone marrow, whole body organs.
Health implications of
induced alterations in calcium ion homeostasis:
Induced alteration of
cellular calcium ions:
of brain cells is associated with behavioural and
reaction time changes and associated EEG alterations, Bawin et al. (1978);
of
the pineal gland reduces the nocturnal production of melatonin (which increases
the cell damage throughout the body, reduces the integrity and competence of the
immune system, and hence increases the incidence of cancer and immune system
related disease and degenerative diseases of the brain, Reiter (1994) and
Walleczek (1992);
of lymphocytes reduced the competence of the immune system
making the subject more vulnerable to allergens, toxins and viruses, and to
leukaemia; and
of damaged cells alters the ratio of surviving neoplastically
transformed cells and those programmed to self destruct (apoptosis),
Balcer-Kubiczek (1995).
Cells have voltage-gated Ca2+ channels in the cell
membrane to allow the influx and efflux of calcium ions in order to regulate
cellular processes, Adey (1993).
The neurological role of Ca2+ is well
described and documented by Dr Adey. A university
text on the molecular
biology of the cell, Alberts et al. (1994), documents many cellular processes
which depend on Ca2+, including cell-cell adhesion, gap junction gating,
intracellular mediation, cyclic AMP and ATPase processes, and signal
transduction as a second messenger. Ca2+ mediate process in the hypocampus
involved with learning. They also mediate apoptosis. Chemical carcinogens, such
as the tumor promoting phorbol esters, for example TPA, act by elevating
intracellular calcium, Balcer-Kubiczek (1995).
Ca2+ mediate gene expression
processes, development and plasticity of the nervous system, activity-dependent
cell survival, modulation of synaptic strength and calcium mediated cell death,
Ghosh and Greenburg (1992). They are involved in the Ca2+-cAMP signal
transduction process that mediates several cellular functions, including
melatonin production in pinealocyte, Zurawska and Nowak (1992). Li et al. (1999)
showed that 50 Hz fields in TPA treated cells produce a significant
dose-response decrease in gap junction communication with magnetic fields of
0.2, 0.4 and 0.8 mT.
Neurological effects intimately involve Ca2+ as shown
originally by Dr Adey's group. This includes mediation of sodium ion activity in
the brain, Charpentier and Kado (1999). Walleczek (1992) reviewed the roles of
Ca2+ in the immune system including regulation of leukocytes, lymphocytes and
Natural Killer Cells, mainly through signal transduction processes. Through
their synergistic activity with cAMP, Ca2+ mediate some key hormones including
luteinizing hormone, testosterone, prolactin and Growth Hormone, Veldhuis et al.
(1984), Kotwicka and Warchol (1998), Rillema (1980), Vacher et al. (1994),
Ilondo et al. (1994), Ray and Wallis (1982), and Davis et al. (1987).
Cardiac
regulation occurs using calcium ion signaling, Reuter (1987) and Ugarte et al.
(1998). Takahashi et al. (1992) found that altered expression of Ca2+-dependent
genes are involved in end-stage heart failure.
Calcium ion influx is critical
to mitogen action, Hadden (1987). In this process Ca2+ acts directly and
indirectly through its action on calmodulin and protein kinase C to the
activation of a number of enzymatic processes. The tumor suppresser gene p53 is
regulated by Ca2+, Metcalf et al. (1999). Ca2+ also regulates the transcription
of the c-fos proto oncogene, Montminy et al. (1990), Thompson et al. (1995) and
Werlen et al. (1993). One of the key roles on Ca2+ in the carcinogenic process
is outlined by Fanelli et al. (1999) who showed a dose response relationship for
Ca2+ influx over a static magnetic field range from 60 to 600 µT. This Ca2+
influx was observed to inhibit apoptosis. Fanelli et al. stated that magnetic
fields thus might interfere with human health by altering/restoring the
equilibrium between cell death and proliferation. Indeed, they conclude, the
rescue of damaged cells may be the mechanism explaining why magnetic fields that
are not mutagenic per se are often able to increase mutation and tumor
frequencies.
Hence EMR's proven ability to induce calcium ion fluxes and to
significantly alter cellular calcium in homeostasis is a direct biological
mechanism for all of the biological effects associated with EMR exposure. Taken
together, this provides an established biological mechanism for genetic damage,
reproductive problems, cardiac disease, cancer and increased risk of viral and
bacterial infection. The key cancer mechanisms involve reduced melatonin, DNA
strand breaks, chromosome aberrations, altered proto oncogene expression and
impairment of the immune system. These have all been linked to EMR exposure
across the EMR spectrum from ELF to RF/MW.
Ca2+ have been implicated in
essentially every step of the transductive coupling of neurotransmitter
substances in effects of every step of the immunological reactions and every
step of the coupling of hormonal binding at the membrane surfaces to cellular
mechanisms, Adey (1979). Ca2+ efflux is the initial biological mechanism for
almost all of the observed significant adverse health effects of EMR exposure,
including neurological, cardiac, reproductive and cancer effects.
Biochemists
have now confirmed that RF/MW alters signal transduction, (e.g. Luben (1995),
Byus (1994)), alters melatonin and damages the immune system, as will be shown
below.
Dr Alan Frey directly challenges the RF Thermal view.
Dr Frey, an
eminent U.S. biologist, has been carry out EMR research for several decades. He
was the discoverer of "Microwave Hearing". In the introductory chapter of a book
that he edited, Dr Frey describes the historical tendency to use the
toxicological model that treats EMR as an external agent, Frey (1995). He then
refers to Burke and others who have made it clear that "our frame of reference
determines what we look at and how we look. And as a consequence, this
determines what we find." This is demonstrably true for the ICNIRP assessors. Dr
Frey than states "Theory and data show that this is the wrong model.
Electromagnetic fields are not a foreign substance to living beings, like lead
or cyanide."
"To model how em fields affect living beings, one might compare
them to the radio we use to listen to music. The em signal the radio picks up
and transduces into the sound of music is almost unmeasurably weak. At the same
time there are, in toto, strong em fields impinging on the radio. We don't
notice the stronger em signals because they are not the appropriate frequency or
modulation. Thus they don't disturb the music we hear. However, if you impose on
the radio an appropriately tuned em field or harmonic, even if it is very weak,
it will interfere with the music. Similarly, if we impose a very weak em signal
on a living being, it has the possibility of interfering with normal function if
it is properly tuned. This is the model that much biological data and theory
tell us to use, not a toxicology model."
Wever (1974) and König (1974) proved
that human brains are tuned to detect and use the Schumann Resonances that have
an intensity of the vertical electric field component of about 0.1pW/cm². This
is 2.65x1014 times lower than the ICNIRP guideline for low frequency signals,
Figure 7. Ahissar et al. (1997) demonstrated that mammal's brains contain
biochemical phase-locked loop circuits to detect the phase difference between
incoming ELF signals in the same manner as FM radio receivers.
EMR Reduces
Melatonin in Animals and People
The calcium ion efflux research demonstrates
one of the fundamental principles of EMR research. Under given specific
conditions the calcium ion efflux (positive or negative) does occur at some
combination of exposure conditions, but not at a nearby slightly different set
of conditions. This is because of the "window" non-linear nature of the effect
with respect to modulation frequency and intensity in particular. Also, one set
of conditions that produce a significant effect in one laboratory does not
produce any observed effect in another laboratory because it has a different
geomagnetic field. On the other hand, in real world situations workers or
residents are continually passing through effective and non-effective windows of
exposure.
This means that despite the great difficulties of detecting
melatonin reduction in people because of the large intra-personal differences
from day to day, and the very large inter-personal differences, on average there
is a dominance of exposure conditions that do cause calcium ion efflux and
reduced melatonin, so that it is observed to differ in most monitored
populations in the real world.
Since calcium ions in the pinealocytes are
associated with the regulation of cAMP, which in turn mediates the
transformation of serotonin to melatonin, Reiter (1994), it is postulated that
EMR's ability to alter calcium ion homeostasis will produce reductions in
melatonin over a wide range of exposure window conditions across the EMR
spectrum from ELF to RF/MW.
Light-at-night and electromagnetic radiation, are
proven to reduce melatonin and hence pose significant adverse health effects.
The evidence for EMR 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 µT, 60 Hz
field with a 0.06 µT 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 in people and a serotonin enhancement. 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 reduction in melatonin. Fourteen studies have observed
significant EMR associated melatonin reduction in humans.
They involve a wide
range of exposure situations, including 50/60 Hz fields, Wilson et al. (1990),
Graham et al. (1994), Wood et al. (1998), Karasek et al. (1998), and Burch et
al. (1997, 1998, 1999a, 2000), Jutilainen et al. (2000) and Graham et al.
(2000); 16.7 Hz fields, Pfluger et al. (1996), VDTs Arnetz et al. (1996), a
combination of 60 Hz fields and cell phone use, Burch et al. (1997), 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 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.
Hence it is
established from multiple, independent studies, that EMR from ELF to RF/MW
reduces melatonin in animals and human beings.
The health implications of
reduced melatonin:
Melatonin has many biological effects. The melatonin
receptor regulates several second messengers: cAMP, cGMP, diacylglycerol,
inositol trisphosphate, arachidonic acid, and intracellular Ca 2+ concentration
([Ca2+]j). In many cases, its effect is inhibitory and requires previous
activation of the cell by a stimulatory agent. Melatonin inhibits cAMP
accumulation in most of the cells examined, but the indole effects on other
messengers have been often observed only in one type of the cells or tissue,
until now. Melatonin also regulates the transcription factors, namely,
phosphorylation of cAMP-responsive element binding protein and expression of
c-Fos. Molecular mechanisms of the melatonin effects are not clear but may
involve at least two parallel transduction pathways, one inhibiting adenylyl
cyclase and the other regulating phosphohpide metabolism and [Ca 2+]j, Vaneeck
(1998).
Professor Russell Reiter, one of the world's leading medical
researchers into the effects of melatonin, summarizes melatonin's roles, Reiter
and Robinson (1995), as being:
Vital for healthy sleep, including lowering
the body temperature, and assisting in maintaining health sleep
states.
Reduces cholesterol, with consequent reductions is risk of
atherosclerosis and coronary heart disease.
Reduces blood pressure and the
tendency for blood clots, and hence reduces the risk of strokes.
Scavenger of
free radicals. This, along with the above factors, reduces the risk of heart
attack, cancer, viral replication. Melatonin plays a vital free radical
scavenging role in the brain where, because it is high in iron, has a high
production rate of hydroxyl radicals (OH(). Free radical damage is now known to
play a formative role in most brain disorders, including Alzheimer' disease, Lou
Gehrig's disease, multiple sclerosis and Parkinson's disease. While the Blood
Brain Barrier (BBB) denies access to most free radical scavengers, melatonin has
free access.
Enhances the effectiveness of the immune system. Specifically
enhancing the T-cells, i.e. the T-helper cells and the T-killer cells. T-helper
cells have a receptor for melatonin. When melatonin is received a cascade of
events is set in motion including stimulation of Interleukin-4 (IL-4) which then
stimulates natural killer cells (NK), B-cells, IgA, phagocytes and T-Cytotoxic
cells. The NK cells specialize in attacking cancer cells and virus infected
cells.
In Professor Reiter's book, published in 1995, he describes the
evidence that EMR/EMF does reduce melatonin as a Smoking Gun" level of proof.
That is, there is considerable scientific evidence but at that time it wasn't
sufficient for scientific proof. By considering more recent information, and the
extensive results of biometeorological research, and linking the melatonin
research to the calcium ion research, the level of proof can be seen as causal.
The multiple observations of melatonin reduction in EMR exposed populations
means that EMR exposure increases the incidence of all of the conditions
identified by Reiter and Robinson above, including immune system, cancer,
neurological and cardiac effects. Epidemiological evidence of exposed workers
and residential populations confirms that these adverse health effects do
occur.
Human Biometeorology:
Dr Ross Adey refers to the work of Wever and
König in Germany in the 1960's and 70's. The work was carried out at the Munich
Technical University and the Max Planck Institute, Adey (1981). Wever and his
colleagues constructed two isolation rooms to remove all daily time signals.
One, Room 2, as also surrounded by a Faraday Cage to exclude electromagnetic
signals, Wever (1974). The results included the fact that those in the Faraday
Cage shielded room, identical to the other room in all other respects, had
significantly longer circadian rhythms (p<0.01).
In addition, a
significant proportion (30%) of the Faraday Cage group desynchronized" while
none of the other group did (p<0.001). This involved rapid lengthening of the
circadian period from around 26-27 hours to 30 - 36 hours, Figure
12.
Long-term isolation experiments at the Max Planck Institute proved that
removing sunshine led to significantly longer mean circadian periods. Also
shielding subjects from natural and artificial EMR further significantly extends
mean circadian periods. Around 30 % of subjects desynchronized. When a weak 10
Hz signal was secretly introduced the desynchronization was removed, Figure 12.
This proved the role of the Schumann Resonances that act with sunshine as a
Zeitgeber.
From the results of the experiments involving human subjects,
their reaction times and altered circadian rhythm, the German researchers from
the Max Planck Institute conclude:
Thus, it has been proven at a high
statistical level that the artificial electric 10 cps field diminishes the
tendency towards internal desynchronization, as does the natural field."
The
desynchronization was removed through the application of a 10 Hz signal with a
peak to peak field strength of 2.5 V/m. This is equivalent to 0.83 µW/cm². The
signal the Faraday cage had removed, which was replaced by this artificial
signal, was the Schumann Resonance which has a field intensity of about 0.12
pW/cm². Hence the desynchronization was caused by the removal of a 0.1pW/cm²
signal. Wever (1974) concludes that their research gives:
Significant proof
that electromagnetic fields in the ELF range influence the human circadian
rhythms and therefore human beings."
Figure 12: Free-running circadian rhythm
of a subject living under strict isolation from environmental time cues. During
the first and third section protected from natural and artificial
electromagnetic fields, during the second and fourth sections (shaded area)
under the influence of a continuously operating 10 Hz electric field of 2.5 V/m,
Wever (1974).
The plausible biological mechanism involving local Schumann
Resonances (Type I) and sferics (Type II) signals, was proposed by König (1974).
He noted the strong similarity between the frequencies of the Schumann
Oscillation and the alpha band of the human EEG, see the Figure 13
below.
Figure 13:Electric fields from, (, the Schumann-Resonance, ((, Local
fields of about 3 Hz and the ( (10 Hz) and ( (3 Hz) human EEG channels, König
(1974).
A resonant interaction is entirely feasible. Human brains use the
same frequency bands as the weather produces. The EEG signals are
electromagnetic and so are the weather signals. Removing the Schumann
Oscillation from some individuals, removes part of their circadian control. This
confirms the interaction between human brains and the Schumann Resonance. Konig
provides independent confirmation of this interaction though a completely
different set of experiments involving human reaction times.
The Type II
signals on the left of Figure 13 are naturally occurring, locally sourced ELF
fields centred around 3 Hz. They are very similar to the EEG delta-band. König
(1974) showed that people's reaction time significantly sped up in the presence
of Type I (Schumann Resonance) signals and slowed down when Type II (Local
Sferic) signals were dominant, Figures 14 and 15.
Figure 14:The solid line
shows the reaction times of 4500 people per point, over the day in September
1953 in Munich, compared with (dashed line) the Type ( (10 Hz) signals field
intensity, König (1974).
Converting the data in Figure 14 to a dose response
relationship produces Figure 15.
Figure 15: The dose-response relationship
for human reaction time as a function of the intensity of the Schumann Resonance
signal, from König (1974).
Type (( Signals occurred on 10 occasions during
the August-September period. Figure 16 shows the inter-relation for the change
in reaction time relative to the onset of Type (( signals at time n hr. In the
hour and a half after the onset of Type (( signals the reaction times (involving
between 2000 and 3000 people), are well above average.
To confirm the
indicated results from these public measurements Konig carried out controlled
experiments with volunteers. He was able to produce slowed reaction times with 3
Hz signals and faster reaction times with 10 Hz signals, at will. This proves
that human brains detect and react to external electromagnetic signals of
extremely low intensity, including naturally occurring Schumann Resonances and
local sferics.
Polk (1982) summarizes many observations of the Schumann
Resonances. This reveals that the vertical electric field gradient is in the
range 0.06 to 0.3 mV/m/Hz-1/2 for the 8 Hz to 21 Hz frequency range. This
becomes 0.22 to 1.12 mV/m, averaging 0.67 mV/m. The field intensity (S) as a
function of electric field (E) is S = E2/3.77 µW/cm². Hence the mean Schumann
Resonance field intensity is 0.12 pW/cm².
At the same time that the Germans
were publishing their biometeorological results showing that human being's
reaction times vary with extremely low intensity naturally occurring and varying
electromagnetic fields in the ELF part of the spectrum, Professor Ross Adey and
Dr Susan Bawin were showing that altered human reaction times in ELF modulated
microwave fields was associated with altered EEG and calcium ion efflux from the
brain cells.
Figure 16: The speeding up of the reaction time of people in the
60 to 90 minutes following the onset of 3 Hz signals, from the Traffic
Exhibition in Munich in 1953, König (1974).
Hence the U.S. and German
research jointly confirm both the effect and the mechanism. Human brains detect
oscillating EMR signals at very low intensities through resonant absorption
interactions. This causes the altered reaction times and circadian rhythms
through induced changes in brain synchronization, cellular calcium ions and
reduced melatonin. The later two biological effects are shown to occur over a
wide range of exposure conditions from ELF to RF/MW and at very low exposure
intensities.
7. Bioelectromagnetic
Principles:
A more appropriate scientific approach than that taken by
ICNIRP is one that recognizes some fundamental principles concerning the nature
of biological systems and their use and interaction with EMR. Eight
Bioelectromagnetic Principles are set out below with some of the scientific
studies that support or confirm the principles.
Bioelectromagnetic Principle
1:
EMR is intrinsic to our bodies.
Intrinsic EMR signals are used for
timing regulation at all levels, from seasonal and circadian rhythms, heart
beat, cell ion oscillations, cell cycle timing, and synchronizing the EEG bands,
Adey (1980), Becker and Seldon (1985), Frey (1993), König (1974) and Wever
(1974).
Bioelectromagnetic Principle 2:
Our brains are the most
electrically active organs in our bodies.
Interference with timing leads to
arrhythmia of brain, neurological effects and diseases and brain
tumours.
Supporting Evidence:
König (1974) and Wever (1974) proved that
human brains detect local lightning signals and the globally radiated Schumann
Resonance signals by showing that these signals alter human reaction times and
regulate human circadian rhythms, at intensities around 0.1pW/cm², Polk (1982).
This work is indicative of a resonant absorption interaction between the
Schumann Resonance Spectrum and human brain waves (EEG-rhythms).
Shandala et
al. (1979) show than microwaves significantly altered the EEG of animals, Von
Klitzing (1995) shows that a GSM signal alters the EEG of human volunteers and
Mann and Roschke (1996) show sleep disturbance and EEG change from sleeping next
to a cell phone. Mild et al. show that cell phone users exhibit a significant
dose response increase in neurological symptoms, including dizziness, memory
loss, loss of concentration and headaches.
Over sixty studies identify
increases in brain tumours with EMR exposures across the spectrum; over 30 are
statistically significant and 13 have dose-response relationships, at least half
of which are significant, Section 16.3.
Several epidemiological studies show
significant increases in neurological effects and diseases in residential and
occupational EMR exposures, Amyotropic Lateral Sclerosis (ALS) and Parkinsonism,
Deapen and Henderson (1986); Suicide, Baris and Armstrong (1990), Perry et al.
(1991); Alzheimer's Disease, Sobel et al. (1995, 1996); Clinical Depression,
Verkasalo et al. (1997); Psychological symptoms, Beale et al. (1997); and ALS,
Savitz et al. (1998a,b). Beale et al. found significant dose-response
relationships for several symptoms including depression and anxiety and Johansen
et al. (1999) for Multiple Sclerosis and Savitz et al. (1998a) for ALS. Van
Wijngaarden et al. (2000) identified significant dose response increases in
suicide in electrical utility workers in relation to recent cumulative magnetic
field (60Hz) exposures. The strongest associations were for younger people
(<50 years).
7.2.2 Alzheimer's disease:
Sobel et al. (1996) found that
workers in industries with likely electromagnetic field exposure have a very
significant (p=0.006) increase in incidence of Alzheimer's disease, OR = 3.93,
95% CI: 1.5-10.6. For males the adjusted odds ratio was 4.9, 95% CI: 1.3-7.9,
p=0.01, and for females, OR = 3.40, 95% CI: 0.8-16.0, p = 0.01. They note
that:
These results are consistent with previous findings regarding the
hypothesis that electromagnetic field exposure is etiologically associated with
the occurrence of AD."
Sobel and Davanipour (1996) outline the etiological
process they hypothesize by which EMR produces Alzheimer's disease.
The first
step involves EMR exposure upsetting the cellular calcium ion homeostasis
through calcium ion efflux from cells increasing the intracellular calcium ion
concentrations. This cleaves the amyloid precursor protein to produce soluble
amyloid beta (sA().
sA( is quickly secreted from cells after production,
increasing the levels of sA( in the blood stream. sA( then binds to
Apolipoprotein E and apolipoprotein J to be transported to and across the Blood
Brain Barrier.
Over time, when sufficient sA( have been transported to the
brain, a cascade of further events lead to the formation of insoluble neurotoxic
beat pleated sheets of amyloid fibril, senile plaques, and eventually AD.
The
biological mechanism for EMR to cause Alzheimer's disease is well advanced and
entirely plausible, commencing with calcium ion efflux.
7.2.3 Sleep
disturbance:
Thus the German work in the 1960's and 1970's established that
naturally occurring EMR and EMR at extremely low levels influenced and altered
sleep, circadian rhythm and reaction times. In the 1990's German work showed the
cell phones alter the human EEG and interfere with REM sleep, Von Klitzing
(1995) and Mann and Roschkle (1996). Impairment of REM sleep is associated with
memory and learning difficulties. The Swiss research (Altpeter et al. (1995) and
Abelin (1998) - The Schwarzenburg Study) found a causal relationship between
sleep disturbance and subsequent chronic fatigue, and short-wave radio exposures
at extremely low mean levels.
The causal relationship between RF radiation
exposure and deterioration in sleep quality is identified through a significant
dose response relationship (p<0.001), Figures 17 and 18, improvements in
sleep quality which changing the direction of the beams and turning the
transmitter off, and reduced melatonin as the biological mechanism.
Figure
17: Adult Sleep Disturbance with RF exposure at Schwarzenburg, Switzerland,
Abelin (1999).
Figure 18: Dose-response relationship for Sleep Disturbance at
Schwarzenburg with exposure in nW/cm². Note: 1nW/cm²= 0.001 µW/cm²
Groups B,
R and C are all exposed to a mean RF signal of less than 0.1 µW/cm² and they
experienced highly significant sleep disturbance and reduced melatonin. Since
sleep disturbance and melatonin reduction has been observed with cell phone
exposure, Mann and Roschkle (1995) and Burch et al. (1997), these observations
also apply to cell sites. Assuming a normal sleep disturbance of 10 %, the
approximate exposure level threshold for zero additional effect is near 1
pW/cm², near the natural level for the Schumann Resonances.
As an experiment,
the transmitter was secretly turned off for three days. Sleep quality improved
in all three groups being studied. Figure 19 shows Groups A and C.
Figure 19:
Sleep disturbance in people exposed to a short-wave radio stations which was
turned off for three days, Altpeter et al. (1995), showing the highest exposed
Group A, and lowest exposed Group C.
Both Groups show a delayed improvement
in sleep of one to two days. The reduced wakening averaged over days 4 to 6
compared with days 1 to 3, for group A, and days 5 to 7 compared with days 1 to
4 for group C, are highly significantly reduced, p<0.001. Thus a significant
(p<0.001) improvement in sleep quality is associated with a measured 24 hour
mean and median exposure of 0.1 mA/m (0.4 nW/cm²).
Human melatonin was
sampled from urine in the morning. This is relatively ineffective because the
important measure is the nocturnal peak. Altpeter et al. note that Persons
reporting sleep disorders, however, tend to have lower melatonin levels." When
the decision was made to close down the transmitter permanently, melatonin
readings were taken from a large group of residents before and after the
closure. This showed a significant increase in melatonin following the closure,
Professor Theo Abelin pers. Comm - seminar).
Two herds of 5 cows each, had
salival melatonin sampled several times a day, including night-time. The
"exposed" herd as at 500 m from the tower with a mean exposure of 0.095 µW/cm².
Their mean melatonin levels were 17.7 pg/ml compared with 19.0 pg/ml for the
"unexposed" cows whose measured mean exposure as 0.00022 µW/cm². Figure 20 shows
the melatonin for these two herds during the experiment involving turning the
tower off.
Figure 20: Salival melatonin from two herds of 5 cows, one exposed
at 500 m, 0.095 µW/cm², (solid line) and one "unexposed" at 4000 m, 0.00022
µW/cm², (dashed line).
The small number of cows makes it difficult to show a
significant difference. There is a persistent phase shift in the nocturnal
melatonin peak with the exposed cows showing a delay. This reduced when the
transmitter was off but returned when it was turned on. The exposed cows have
lower mean melatonin prior to the off period. It rises progressively while the
transmitter is off and is significantly higher on the third night. It then drops
significantly when the transmitter is turned on again. This shows the "classic"
effect of EMR reduction of melatonin. The "low" exposure cow's melatonin drops
when the transmitter is turned on.
The causal relationship with human sleep
disturbance is strong evidence of a significant neurological effect of RF
radiation on people, associated with mean exposures down to less than 0.4
nW/cm². Hence, it is highly likely that cell phone users, with brain exposures
many millions of times higher than the Schwarzenburg exposure levels, will
experience significant neurological effects. The significant bovine behavioural
effects of extremely low RF exposure is confirmed by Löscher and Käs
(1998).
7.2.4 Neurological effects of cell phone usage:
In 1998 Mild et
al. (1998) survey around 11,000 cell phone users in Norway and Sweden, Figure
19. They found significant dose response relationships for a number of crucial
symptoms that had been clinically described and associated with cell phone use
by Hocking (1998).
The symptoms include dizziness, a feeling of discomfort,
difficulty with concentration, Memory Loss, Fatigue, Headache, Burning Skin and
tinglingness and tightness of the skin near the phone. The symptoms were
consistent across analogue and digital (GSM) phone users. A dominant physical
symptom was a sensation of warmth on the ear and behind the ear. These is not a
sensation which is experienced with a conventional telephone but are unique to
the cell phone which exposes the user's head to moderate to high intensities of
microwaves. It was significant that the neurological symptoms were highly
correlated to the warm sensations. The symptoms are consistent with the
Schwarzenburg symptoms. The headache symptoms were found with microwave exposure
during microwave hearing" experiments, Frey (1998).
Bioelectromagnetic
Principle 3:
Our hearts are electrically sensitive.
Supporting
Evidence:
Hearts use EMR signals that are detectable by the ECG. An electric
pulse produces a cascade of calcium ions that causes the heart muscle to
contract and produces a heart beat.
7.3.2 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. 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.
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.
Figure 21: The prevalence of
symptoms with various categories of calling times/day, A. Norway, B. Sweden,
Mild et al. (1998).
Geomagnetic Activity adverse effects:
Solar activity
alters the earth's geomagnetic field, electron concentrations in the ionosphere,
the Q-value of the earth/ionosphere resonant cavity and intensity and frequency
of the Schumann Resonance Spectrum. Since human brains an hearts are sensitive
to subtle changes in environmental electromagnetic fields, evidence of
correlations in cardiac functions and geomagnetic activity (GMA) would be
indications of human sensitivity to very small EMR signals.
Watanabe et al.
(1994) report that a 35-yr old cardiologist with a family history of heart
disease, monitored himself with a blood pressure monitor at 15-min intervals for
3 years. Systolic and diastolic blood pressure and heart rate were significantly
correlated with the 27.7 day solar cycle and with the geomagnetic disturbances.
Pikin et al. (1998) observed that blood coagulation and platelet aggregation
increased with increasing GMA. Gurfinkel et al. (1995) observed significant
alterations in capillary blood flow in heart patients, correlated with GMA.
These are biological effects that are risk factors for heart disease and heart
attack. Many studies have found significant correlations between geomagnetic
activity (GMA) and Ischemic Heart Disease and Heart Attack, for example Sitar
(1990), Villoresi et al. (1998), Stoupel et al. (1996, 1999), and Oraevskii et
al. (1998).
Hence blood pressure changes and reduction of heart rate
variability is observed with changes in GMA, working in RF/MW environments and
using a cell phone. Significant cardiac disease and death are highly correlated
with subtle changes in GMA, work in electrical industries (in a dose-response
manner).
Bioelectromagnetic Principle 4:
7.4.1 Cells are sensitive to
EMR.
7.4.2 Supporting Evidence
Cells have a voltage across their membrane,
voltage-gated ion channels through their membrane and use ions (e.g. Ca2+) for
many cell regulatory processes including signal transduction and gap junction
gate regulation. Altering the electric field on the surface of cells alters the
receptor efficiency and interferes with the voltage-gated ion
channels.
Induced alteration of calcium ion homeostasis has profound and
serious effects for every cell. Calcium ion efflux/influx is an established
biological effect of modulated EMR exposure, Blackman (1990). Cellular calcium
ions have many profound effects on cells. These include the regulation of the
neurotransmitter GABA and the neurohormone melatonin, as well as being
associated with DNA synthesis, chromosome aberrations, gene transcription and
protein expression, gap junction regulation, reaction times, immune system
competence, heart beat regulation, apoptosis, cancer, cardiac, reproductive and
neurological effects.
Bioelectromagnetic Principle 5:
7.5.1 Our whole body
acts as an aerial.
Unlike many chemicals, no particular body organ is the
target of an RF signal. The whole body acts as an aerial and electric current
flows down through our bodies to earth. Hence RF/MW radiation impacts on every
organ in our bodies.
Whole body organs such as our circulatory system and
bone marrow are sensitive to the altered electric fields and the currents
flowing through them, impairing our immune system and producing leukaemia, and
cancer and illness throughout human bodies.
Supporting Evidence:
Large
epidemiological studies, Robinette et al. (1980), Milham (1985 a,b, 1988),
Szmigielski (1996) and Dolk et al. (1997 a,b) show that diseases and cancer
across many body organs is produced by RF/MW and electrical occupational EMR
exposures. In all of these studies, and in many other epidemiological studies,
ELF and RF/MW exposures produce significant increases in leukaemia, including
residential studies with significant dose-response relationships.
7.6
Bioelectromagnetic Principle 6:
7.6.1 The brain is linked to organs and cells
through EMR sensitive hormones.
Normal brain functions are communicated to
the body through neurotransmitters (such as serotonin) and neurohormones (such
as melatonin).
Melatonin reduction (and serotonin enhancement) by EMR has
highly significant impacts on all organs and cells in our bodies, including
brains, hearts and immune systems, Reiter and Robinson (1995).
Supporting
Evidence
Natural EMR, the Schumann Resonances, are used for circadian
synchronization, using phase-locked loop biochemical circuits, Ahissar et al.
(1997). Artificial EMR interferes with these processes leading to
desynchronization of circadian and cellular rhythms, and alteration of the
timing and magnitude of the melatonin/serotonin cycle. De Seze et al. (1999)
showed that cell phone use significantly reduces the pituitary output of
Thyrotropin (thyroid stimulating hormone (TSH)). TSH is a primary regulator of
metabolic function.
Many animal studies and fourteen human studies show that
EMR significantly reduces melatonin, Section 6.5 above. This is a plausible
mechanism for cancer in all organs but especially breast cancer, immune system
impairment, SIDS, heart disease and reproductive effects such as congenital
malformation and miscarriage.
Breast Cancer:
Epidemiological studies have
shown significant increases and male and female breast cancer from exposure to
EMR from ELF to RF/MW, as with leukaemia and brain tumor. Table 2 summarizes the
studies for Female Breast Cancer.
There is a tendency for higher rates in
pre-menopausal women and those with estrogen-receptor-positive breast cancer,
and for black women. Elevated incidence and significantly elevated incidence of
breast cancer and breast cancer mortality has been found with electric blanket
use, residence near powerlines, electrical industry employment, radio telegraph
operators, and RF/MW exposure.
7.6.4 Epidemiological Studies of congenital
malformation and miscarriage:
Epidemiological studies of physiotherapists and
electrical occupations identify significant increases on congenital malformation
and miscarriage, Kallen et al. (1982), Vaughan et al. (1984), Taskinen et al.
(1990), Larsen et al. (1991), Sanjose et al. (1991), including a significant
dose-response associating first trimester miscarriage to MW exposure,
Ouellet-Hellstrom and Stewart (1993).
Hence metabolic functions, cancer and
reproductive effects are produced and alterations occur in many other hormone
regulatory functions with EMR exposure.
Table 2: Epidemiological studies of
Female Breast cancer associated with EMR exposure
Group SIR/RR/OR
95%CI/(p-value) Reference
Radio-telegraph SIR=1.5 Tynes et al.
(1996)
operators
Electrical Engineers OR = 1.73 0.92-3.29 Loomis, Savitz
and Ananth (1994)
Electrical technicians OR = 1.28 0.79-2.07
Telephone
installers OR = 2.12 1.17-4.02
repairers, line work
Electrical Workers OR
= 1.38 1.04-1.89
Radiofrequency EMR
Low Exp. White OR = 1.15 p<0.05
Cantor et al. (1995)
High Exp. White OR = 1.14 p<0.05
Low Exp. Black OR
= 1.23 p<0.05
High Exp. Black OR = 1.34 p<0.05
High Exposure ELF OR
= 1.43 0.99-2.09 Coogan et al. (1996)
Pre-menopausal OR = 1.98
1.04-3.78
Post-menopausal OR = 1.38 0.82-2.17
Computer equipment OR =1.80
1.04-3.12 [Trend p = 0.06]
operators, high Exp.
Electric Blankets, heavy
RR = 1.43 0.94-2.17 Vena et al. (1994)
use, pre-menopausal
All women OR =
1.45 1.08-1.94 "
> 2 years of use OR = 1.60 1.15-2.22 "
> 5 years of
use OR = 1.56 1.09-2.25 "
Positive Estrogen receptor RR = 1.12 0.78-1.43
Gammon et al. (1998)
aged 45 - 55 years.
Powerline, Sweden
> 0.2 µT,
men RR = 2.1 0.3-14.1 Feychting et al. (1998)
>0.2 µT, women < 50 yr RR
= 1.8 0.7-4.4
>0.01 µT, women with RR = 1.6 0.6-4.1
+ estrogen
receptor
>0.01 µT, women with RR = 7.4 1.0-178.1
+ estrogen
receptor,
aged < 60 years
Bioelectromagnetic Principle 7:
7.7.1 The
EMR Spectrum Principle.
The EMR spectrum should be treated as an integrated
whole, with biological impacts generally increasing with increasing carrier
frequency.
Supporting evidence:
Biological and epidemiological studies
show that biological effects, including calcium ion efflux, melatonin reduction,
DNA damage, and chromosome aberrations, and human health effects, including
neurological, cardiac and cancer disease and death, all have been shown to occur
from ELF exposure, exposures in electrical and military occupations, and with
RF/MW exposure.
Biophysics shows that the Dielectric Constant varies
progressively, decreasing with increasing carrier frequency, Schwan and Foster
(1980). This implies, as has been observed, Bawin and Adey (1976), and
calculated, Vignati and Giuliani (1997), that for a unit field exposure induced
tissue electric field gradients and induced tissue currents, increase with
increasing frequency.
This strongly indicates that if a biological or
epidemiological effect is observed for ELF exposures, then that effect will be
more likely to occur from RF and MW exposures. It also indicates that
epidemiological assessments can be carried out by integrating ELF and RF/MW
exposure studies. The uncertainties of mixed occupational exposures are
significantly reduced. Vignati and Giuliani suggest, in support of this
principle, that the biological effects and adverse effects observed from
powerlines could well be the result of the greater biological impact of the
lower field strength but measurable RF signals emitted by the
powerlines.
Bawin and Adey (1976) observed significant calcium ion
efflux/influx from both an ELF modulated 147 MHz signal and a pure ELF signal.
Both had an ambient electric field strength of 56 V/m but the RF signal produced
a tissue gradient of 10-1 V/cm and the ELF signal 10-7 V/cm. This implies that
the RF field could have been a million times smaller, i.e. 5.6x10-5 to produce a
tissue gradient of 10-7 V/cm that would also cause altered cellular calcium
ions. This smaller RF field has an exposure intensity of 0.83pW/cm². This is of
the same order as the intensity of the Schumann Resonance Spectrum during solar
storms, which has been shown to have adverse health effects, for example
S.I.D.S., O'Connor and Persinger (1997), Heart Attack, Oraevskii et al. (1998)
and Epileptic Seizures, Ilipaev (1978).
7.8 Bioelectromagnetic Principle
8:
The Intrinsic Free Radical Principle.
Supporting Evidence: Free
radicals
Oxygen free radicals, and other radical species, occur naturally in
human bodies, Guyton and Kensler (1993). Free radicals are highly reactive and
damage macromolecules such as DNA. Hence they provide a direct mechanism for
causing cancer. Melatonin, as a potent free radical scavenger, and our immune
system which detects and attempts to eliminate foreign cells, such as
neoplastically transformed cells, are vital parts of a well developed cell
repair system which is fundamental to health. Any factors or agents which reduce
melatonin or impair the health of the immune system is thus carcinogenic and
teratogenic.
It is the assumption of ICNIRP and those with the RF-thermal
view that non-ionizing radiation cannot directly break chemical bonds and form
free radicals, and therefore NIR cannot be genotoxic and cannot cause cancer and
reproductive effects unless the exposure levels are high enough to cause
significant tissue heating. Microwaves were observed to enhance free radicals in
cell membranes, Phelan et al. (1992).
Several independent laboratories have
observed significant genetic damage from nonthermal intensities of EMR, such as
DNA strand breaks, chromosome aberrations enhanced oncogene activity. Lai and
Singh (1997 a,b) have shown that ELF and microwave exposures involve free
radical damage of DNA-strands.
7.8.3 DNA strand breakage
The first report
that microwaves at non-thermal levels could produce single- and double-strand
DNA breaks in E. Coli in solution, was Sagripanti and Swicord (1986). A much
more advanced method, the Comet Assay", was used on brain cells extracted from
rats that had been exposed while alive by Lai and Singh (1995,1996,1997b). They
observed single and double strand breaks in a dose-response manner, and
identified the involvement of free radicals and the protective effect of
melatonin.
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. Phillps et al. (1998)
exposed Molt-4 T-lymphoblastoid cells to a number of cell phone technologies in
the exposure range SAR = 0.0024W/kg to 0.026W/kg. At both of these exposure
levels they observed significantly increased DNA damage (p<0.0001) for one
cell phone and decreased damage for three cell phone signals. Induced DNA repair
is also a sign of DNA 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 3% of the ICNIRP
guideline. Using the ICNIRP relationship of 0.08 W/kg and 450 µW/cm² for 1 GHz,
the exposure range is 13.5 to 146.3 µW/cm². Using the more basic equations [SAR
= (E2/2(, (=1 S/m, (=800 kg/m3, and S = E2/3.77 µW/cm²] results with 1.0 to 11.0
µW/cm².
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. (1998), 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 strand breaks at very low,
non-thermal exposure levels.
Answers to the Criticisms of the Lai-Singh
Results:
Attempts have been made to counter the Lai/Singh DNA results.
Motorola funded Dr Joseph Roti Roti's group at Washington University in St Louis
to 'replicate' the Lai/Singh work. Their research, Malyapa et al. (1998), did
not confirm the DNA strand breakage but it did not replicate the Lai/Singh
research. A very different assay method was used that differed in several key
aspects such that it should be much less sensitive.
Dr Narendra Singh
provided the following explanation:
"Here are the major differences between
the technique we are using and what Dr Joseph Roti-Roti is using to detect DNA
damages in cells after RF exposure in our technique, DNA is precipitated in
agarose so as even tiny pieces can become confined to a dense spot to be
visible. If a small piece of DNA is stretched out over long distance, we cannot
see it under the microscope but once it precipitates, it becomes many folds
shorter but denser and can be seen. The Motorola funded work is not doing that,
in fact only a few labs around the world are doing this. This is important for
those involved in detection of low levels of DNA damage.
We treat our samples
with proteinase K to digest proteins bound to DNA so DNA is made free to move in
electric current towards the positive pole as DNA is a negatively charged
molecule. Most proteins on the other hand are negatively charged and thus if not
removed will drag the DNA in the opposite direction, I call it a "protein drag".
The Motorola study did not use proteinase K.
We used an in vivo system where
cells have very low levels of damage to start with, animals were exposed to
radiofrequency at 2450 MHz, while Motorola used in vitro system, where cells
have high background DNA damage as the culture conditions are not as good as in
whole animals. In their study, cells were grown in culture which were exposed to
cellular phone frequency of 837 MHz.
Anyway, it is very difficult for me to
understand why when they said they wanted to replicate our data but didn't use
exactly the same methodology of our experiment. Instead, they chose to use a
much less sensitive assay to do their study."
Criticism has been raised about
the delay of 4 hours in observing the DNA breakage. Williams (1996) states that
"The presence of Single Strand DNA Breaks (SSDB) immediately after microwave
exposure is consistent with findings from other types of radiation. However, the
finding of no decrease in migration after 4 hr must be assumed to reflect no
repair of putative breaks, which again does not conform to knowledge of the
processing of DNA damage resulting from other forms of radiation."
Lai and
Singh (1996b) respond by stating that there is a known difference when short
term (seconds) of exposure are used compared with longer period (2 hr)
exposures, and that this is observed in the use of drugs, to produce different
dynamics. Dealing with the 4 hr questions they state: "However, it is not true
that maximal DNA strand breaks are always observed at the end of exposure to
radiation or chemical agents. For example, in a study by Arlett et al. (1993), a
maximal level of DNA strand breaks was observed in lymphocytes at 1 hr after
exposure to UV radiation, and a recent study by us [Singh et al. (1995)] showed
that ethanol-induced SSDB in brain cells of the rat at 4 hrs after an oral
administration." Several other explanations and examples are given to show that
the dynamics of DNA strand breakage and repair is more complex than often
assumed and there is considerable support for the feasibility of their finding
of significant SSDB 4 hrs after the 2 hr exposure to microwaves. The replication
in two independent laboratories is significant.
Malyapa et al. (1998) and
Moulder et al. (1999) claim that the DNA damage observed by Lai and Singh is
caused by the killing method: "It appears likely that the effects observed by
Lai and Singh were confounded by the euthanasia procedure or by some unknown
aspect of the animal handling of of the comet assay they used."
This is
answered by Dr Lai. He states:
"Why do we use carbon dioxide (CO2) in our
study? First, we did not euthanaze rats with CO2, we anaesthetised them. CO2 is
a well known anaesthetic agent, because it causes constriction of blood
capillaries in the brain. We use it because it decreases blood flow, thus, less
haemoglobin from red blood cells will get to brain tissue. Haemoglobin is known
to cause oxidative DNA damage. Thus, use of CO2 can actually decrease the
artefact of haemoglobin-induced DNA damage.
What we did was to place a rat in
a box containing dry-ice (CO2) for 65 seconds to anaesthetise it (the rat was
not dead yet), then we decapitated it and dissected the brain out for DNA comet
assay. Dr Singh actually insisted that I picked up the animal after CO2 by the
neck (instead of by the tail, so that the rat is up-side-down and blood can flow
to the brain), so that less blood would flow to the brain. Malyapa/Roti-Roti
misread our paper and euthanazed their rats with CO2. They basically asphyxiated
their rats by putting them in a box containing dry-ice for several minutes
(instead of 65 sec). Yes, asphyxiation is known to cause DNA damage. They also
found that the longer you waited after asphyxiation, the more DNA damage would
occurred. I also believe this is true.
But, what is unbelievable is that they
claimed that our results were caused by the 'artefact' that we 'killed' our rats
with CO2. It is so illogical. First, one has to wait longer to do assay on the
'exposed' rats (than the controls) to produce the artefact. We didn't do that.
We killed our animals one at a time. So, the time between CO2 anaesthesia and
start of comet assay was the same for each animal. Second, the order of doing
'control' and 'exposed' was at random. We didn't wait longer for the 'exposed'
animals to produce the artefact."
This discussion reveals a great deal about
the carrying out of laboratory experiments and the lengths some go to dismiss
other's results. It is important to hear the story from the researcher and I
thank Drs Lai and Singh for telling their side of the story to clarify the
issues.
7.8.4 Chromosome aberrations
In 1959 Heller and Teixeira-Pinto
(1959) showed that non-thermal pulsed RF signals could cause complex chromosomes
breaks which mimicked the effect of ionizing radiation and c-mitotic chemicals.
Hence significant chromosome aberrations (CA) produced by RF/MW have been
reported by eight independent groups: the staff at the U.S. Embassy in Moscow,
Goldsmith (1997); Garaj-Vrhovac et al. (1990a,b, 1991, 1992, 1993); Timchenko
and Ianchevskaia (1995), Balode (1996), Haider et al. (1994) and Vijayalaxmi et
al. (1997). 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.
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 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.
7.8.5 Gene
transcripts and activity
It is shown above that EMR induces alterations in
cellular calcium ion fluxes and that calcium ion fluxes mediate gene
transcription and expression. 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.
7.8.6 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 (<0.1 µW/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).
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. This evidence establishes that EMR is
genotoxic. This occurs through enhancing free radical damage by reducing
melatonin, by altering the signal transduction within cells in such a manner
that proto oncogene activity is increased, and by reducing the competence of the
immune system through both reducing melatonin and altering calcium ion
homeostasis.
Gap Junction Communication:
Cells in tissues are regulated by
a large number of processes that involve cell-to-cell communication, including
intercellular communication through gap junctions. When the natural opening of
gap junctions is impaired then cell damage and cell transformation can take
place more frequently. 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 22.
Figure 22: Gap junction flow as a
function of 50 Hz magnetic field strength, Li et al. (1999).
The EMR Spectrum
Principle predicts that these effects are probable with low intensity RF/MW
exposure.
7.10 Conclusions:
These Bioelectromagnetic Principles
scientifically sound. They are supported by a large body of reliable
internationally published peer-reviewed scientific research. They provide an
integrative link between biology, EMR interactions, biological mechanisms and
epidemiology. When considered with the supporting scientific evidence they
provide a very substantial scientific challenge to the validity of the ICNIRP
guideline.
8. The ICNIRP Guideline
is seriously flawed and unlawful in New Zealand:
Environment Court
Support:
The Environment Court (MacIntyre 1996) declared that the New Zealand
Standard (and hence the ICNIRP guideline) is not decisive" in New Zealand law
but that the Sections 5 and 3 of the RMA are the appropriate legal basis for
public exposure to electromagnetic radiation (EMR). This requires evidence to be
considered of actual and potential adverse effects. The applicant, BellSouth,
appealed the condition that restricted their emissions to 50 µW/cm², seeking to
have the then New Zealand Standard which was 200 µW/cm². In considering the
evidence before it, including evidence of actual or potential adverse effects
which occurred about 3 µW/cm², the court set a public exposure condition for a
cell site at that time and in that case of 2 µW/cm². This is 1 % of the then
allowed public exposure in NZS 6609, and 0.4% of the recently adopted NZS
2772.1:1999 and ICNIRP guideline.
The sections of the law that this is based
on are Section 5, which requires that we "Avoid, remedy or mitigate any adverse
effect of an activity on the environment." The definition of the 'environment'
in Section 2 includes 'people and communities'. The definition of 'effect',
Section 3, includes 3(d) "any cumulative effect of itself or in combination with
any other effect, regardless of scale, intensity, duration or frequency,
including (3f) "any potential effect of low probability which has a high
potential impact."
Thus the Chief Environment Court Judge, Judge Sheppard,
has accepted evidence that renders the ICNIRP guideline unlawful when evidence
is given that there are potential adverse effects below the
standard.
Additional strong reasons for rejecting the adoption of the ICNIRP
guideline in New Zealand is the position that ICNIRP is based on 'established'
effects whereas the legal evidence threshold in New Zealand is 'potential'
effects, which have already been accepted by the Environment Court. It is
grossly inappropriate for any country to adopt the ICNIRP guidelines for public
health protection because it is scientifically challengable as it is based on
serious errors and omissions.
In an earlier case for which no epidemiological
evidence was presented on adverse human health effects from power lines,
Transpower vs Rodney District Council, Judge Sheppard defined the basis of a
'potential effect' as being based on a plausible biological mechanism not mere
innuendo.
The MacIntyre case was presented with evidence of plausible
biological mechanism by Dr Richard Luben and epidemiological evidence of actual
or potential human health effects by Dr John Goldsmith, with the exposure
conditions associated with these effects being given by Dr Neil Cherry. Based on
this expert evidence the public exposure condition of 2 µW/cm² was
imposed.
Environment Court Judge's error:
In the most recent case, the
Shirley Primary School vs Telecom, a cell site case, it is submitted here that
the Judge, Judge Jackson, made errors in law and evidence by ignoring the
guidance given by Judge Sheppard, received evidence of potential or actual
effects below 2 µW/cm². This included the North Sydney study, Hocking et al.
(1997), presented by Dr Hocking, who recommended an exposure level of 0.2 µW/cm²
based on his study. It also included the sleep disturbance study from
Schwarzenburg, Switzerland, Altpeter et al. (1995) and the U.S. physical
therapist miscarriage study of Ouellet-Hellstrom and Stewart (1993).
In the
decision the Judge set out they way the court considered the evidence. "The
first general level is epidemiological studies. The second level is a study of
biological mechanisms. The levels are generally hierarchical (biological
mechanisms above epidemiology) in that they are perceived as having increasing
power in terms of establishing cause and effect." This is the reverse of the
assessment that is usually followed, as shown by the MacIntyre Case and Sir
Austin Bradford Hill, Hill (1965), IARC, USEPA and many other assessments. This
is simply stated by Dr Abraham Lilienfeld: "The proper study of man is
man".
The epidemiological evidence given in this case led the decision to
conclude that the main factors they had to balance including the first three
that were:
The very low risk, subjectively but reasonably assessed, of
adverse learning effects and/or sleeplessness from exposure of pupils at the
school to RF radiation;
A very low risk to pregnant women of
miscarriage;
The extremely low risk of exposure to RFR causing cancer, e.g.
leukaemia in humans;
Having stated this, based largely on the court's
incorrect rejection of the established existence of a biological mechanism, the
judgement allows the ICNIRP Guideline of 450 µW/cm² in this case. This there was
stronger evidence than given on the MacIntyre Case but the accepted exposure
level was 225 times higher.
The court was not shown the dose response
relationships contained in this report for each of these effects. Therefore they
did not know that with the probable exposure level of 2 µW/cm² the Risk Ratio
(RR) for childhood leukaemia would be about RR = 22 and for miscarriage about RR
= 3.5. For learning disturbance effects almost all of the children exposed to
measured levels much less than 0.32 µW/cm², showed significant adverse learning
effects and this almost all of the children at the Shirley Primary School could
be adversely effected which is not a "very low risk". Even so, Section 3(d) and
3(f) of the New Zealand Resource Management Act requires effects of any
potential low probability irreversible effects that have a high potential impact
(i.e. miscarriage, leukaemia or learning impairment) must the avoided.
Hence
this is clearly challengable as a misapplication of the provisions of the
Resource Management Act, especially in the light of earlier, more senior
guidance from Judge Sheppard.
9. The ICNIRP treatment
of Biological mechanisms:
9.1 Inappropriate reliance on a plausible
biological mechanism:
One of the primary reasons many skeptics about EMR
health effects, such as ICNIRP, use to dismiss studies that show statistically
significant effects and even dose-response relationships, is their claim of the
lack of a plausible biological mechanism. When a study reveals a significant
biological effect at nonthermal levels then groups such as the ICNIRP state that
it must be independently replicated before it can be accepted as an established
biological mechanism. Based on this criteria calcium ion efflux/influx, GABA
fluxes, melatonin reduction, DNA damage, chromosome aberrations and altered
proto oncogenes are established biological mechanisms. All have been reported
from two or more independent laboratories, most in 4 or more
laboratories.
ICNIRP RF/MW assessment of Calcium Ion Efflux:
ICNIRP cites
only three calcium ion efflux papers of the over 30 which have been published.
Two are cited as showing significant effects, Bawin et al. (1975) and Blackman
et al. (1979). One is cited as showing no effect, Albert et al. (1987).
The
overall conclusion, which applies to all biological mechanisms, including
calcium ion efflux, states:
"Overall, the literature on athermal effects of
AM electromagnetic fields is so complex, the validity of reported effects is so
poorly established, and the relevance to human health is so uncertain, that it
is impossible to use this body of information as a basis for setting limits on
human exposure to these fields".
This is a carefully and deliberately
constructed dismissal of athermal (nonthermal) effects so that epidemiological
effects can also be dismissed with the lack of a biological mechanism to justify
dismissal. In challenge and contrast to this Dr Carl Blackman, Blackman (1990)
concludes that calcium ion efflux is an established biological effect having
considered about 20 papers, section 6.2.
ICNIRP ignores most evidence of
genotoxicity:
The ICNIRP assessment totally ignores the vast literature on
DNA strand breakage, chromosome aberrations, oncogene activity enhancement,
melatonin reduction and Schumann Resonance interactions, summarized in Sections
6 and 7.
10. Reproductive
outcomes: 100kHz-300GHz
The ICNRIP Statement:
There are several major
errors and omissions in the ICNIRP (1998) assessment of reproductive effects,
ICNIRP (1998), Figure 19.
This includes misrepresentation of two studies,
inadequate interpretation of three studies and omission of several relevant
epidemiological studies and failure to cite the relevant animal studies. ICNIRP
(1998) concludes that studies involving pregnancy outcome and microwave exposure
suffer from poor assessment of exposure, small numbers of subjects and
contrasting results. All of these claims and conclusions are wrong.
10.2 The
studies of Daels (1973 and 1976):
The first claim is that there are two
extensive studies on women treated with microwave diathermy to relieve the pain
of uterine contractions during labour, with no evidence of adverse effects on
the fetus, quoting Daels (1973 & 1976). Daels (1973 (4 pages) & 1976 (2
pages)). They are very small papers on an analgesic therapy to ease the mother's
pain in delivery. They report on the subjective Apgar Score of the new-born
child. The score is the sum of indexes related to heart rate, respiratory
effort, muscle tone, reflex irritability and colour. Ten is a perfect score. The
test is carried out within 30 minutes of the exposure, 1 minute after birth.
This is a small fraction of the cell cycle time and therefore cannot detect
cellular damage.
Figure 23: The ICNIRP (1998) epidemiological assessment of
reproductive effects, p504.
These studies involve short-term microwave
heating of the uterine area for 30 to 40 minutes during labour. They recorded a
maximum neonate temperature of 37.8(C and amniotic fluid temperature of 36.5(C.
These are well within the normal range. Heating was limited to levels where the
mother felt skin heating as agreeable". Since most of the microwaves are
absorbed in the surface skin layers the fetal exposure will be extremely small,
see Hocking and Joyner (1995) below.
The Apgar Score showed that the
"microwave group" had a slightly higher mean score of 9.1 compared to 8.8 for
the "control group". A very low Apgar Score (0-3) indicates gross problems and
have been correlated with long-term problems, such as significantly lower Bayley
mental scores, Serunian and Broman (1975). Lan et al. (1991) found that low
(4-6) and very low (0-3) Apgar Scores were significantly associated with low
birth weight. In Daels the lowest Apgar Score was 7, within the normal range.
The Daels papers show that the slight, imperceptible heating of the mother
during delivery by microwave diathermy, results in a slight improvement in the
Apgar Score, attributed to the more relaxed mother because of the warming.
A
fully developed child is involved, exposed at extremely low levels for minutes
immediately prior to birth, and assessed immediately after birth. There is no
assessment of the developed pre-schooler to determine if there was any brain
damage or developmental problems that could have resulted from a small risk of
chromosome damage.
In Daels (1973) he simply states No undesirable side
effects of microwave heating of tissues are known." He references a single
study, Leary (1959) to note that overheating can be a rare complication. Thus
Daels (1973 & 1976) are neither extensive studies nor about subsequent
new-born health in the months or years following the birth and the
exposure.
It is therefore totally inappropriate and grossly misleading to
cite these as extensive studies" of the impact of microwaves on the fetus. The
exposure of the fetus is extremely low and very short. The studies are not
extensive, they do not relate to developing fetus and there is no actual
assessment of the long-term impact of the exposure on the children.
10.3
Interpretation of Physiotherapy Studies:
In assessing reproductive outcomes
from physiotherapist studies it is important to distinguish short-wave exposure
and microwave exposure, small study populations and larger study populations,
and whole pregnancy including birth outcomes, in contrast to early pregnancy
miscarriage alone. The effects of short-wave radiation are likely to be
different from microwave effects. Small sample sizes may have elevated Risk
Ratios but lack statistical significance solely by virtue of the small sample
size.
10.4 Physiotherapist Studies Cited by ICNIRP (1998):
In ICNIRP 1998
three physiotherapist studies are cited, Kallen et al. (1982), Larsen et al.
(1991) and Ouellet-Hellstrom and Stewart (1993).
Kallen and Larsen involve
small samples and short-wave exposure, and whole pregnancy post-natal outcomes.
Kallen et al. report significant increases in malformed children and perinatal
deaths for physiotherapists using RF diathermy. Larsen et al. observed very few
boys, and many more perinatal deaths, premature births and low birthweight
children for therapists using shortwave diathermy. Given these confirming
results the reviewers state however The results suggest further study is
necessary before conclusions can be drawn."
A further study was carried out.
Ouellet-Hellstrom and Stuart involves a very large sample, studies only early
pregnancy (first trimester) miscarriage and finds only microwaves to have an
effect. They observe a significant dose-response increase in first trimester
miscarriage for female therapists using microwave diathermy. Following the
Bradford Hill guidance, this is indicative of a cause and effect relationship.
In addition to Larsen et al. and Kallen et al. this additional study confirms
that RF/MW exposure of pregnant women is associated with adverse reproductive
outcomes. Despite this ICNIRP found reasons why this data is difficult to
interpret.
Several other studies were available prior to 1993 but they were
not cited by UNEP/WHO/IRPA (1993). The total available published research on EMR
associated reproductive effects was not cited by WHO (1993) nor by ICNIRP
(1998).
10.5 Case by case assessment:
10.5.1 ICNIRP
misrepresentation:
ICNIRP states that there were no statistically significant
effects on rates of abortion or fetal malformation" in Kallen et al. (1982).
This is wrong. Even though Kallen et al. involves small sample numbers they
conclude The only positive finding was a higher incidence of short-wave
equipment use among the females with dead and deformed infant than among
controls." Very few therapists were involved with microwaves. Hence Kallen et
al. associate fetal death and malformation with the use of short-wave diathermy
equipment, with p=0.03. This is a statistically significant association,
contrary to the ICNIRP claim.
Papers cited by ICNIRP:
Larsen et al.
(1991), identified 54 cases with birth problems and 146 spontaneous abortion
cases from Denmark. They found a significant increase in malformations, still
birth, low birth weight, cot death and prematurely when working with short-wave
diathermy.
Ouellet-Hellstrom and Stewart (1993) investigated early pregnancy
miscarriage among U.S. physical therapists using short-wave (27 MHz) and
microwave (915 MHz and 2.45 GHz) diathermy. The sample included 1753 case
pregnancies (miscarriages) and 1753 control pregnancies. They found no
significant increase in first trimester miscarriage amongst those using
short-wave diathermy. They found a statistically significant increase in
miscarriage in the first trimester with microwave exposure (OR= 1.28, 95%CI:
1.02-1.59) and a statistically significant dose response relationship
(p<0.005) using a dose measure of treatments per month. With more than 20
treatments per month OR = 1.59, 95%CI: 0.99-2.55. In addition to the three
studies cited in ICNIRP (1998) there are several others with are
relevant.
10.5.3 Additional Studies not cited by ICNIRP (1998):
Male
sexual functions are significantly reduced in ELF and RF/MW occupational
exposure situations.
Lancranjan et al. (1975) studied 31 young men, average
age 33 yr, with long-term (mean 8 yr) exposure to microwaves. "This
investigation showed a high frequency of libido decrease and sexual dynamic
disturbances in the framework of asthenic syndrome (70% of subjects) as well as
various alterations of spermatogenesis (p<0.001) in 74% of the subjects.
Exposures were to frequencies in the range of tens to hundreds of µW/cm², and
hence were non-thermal.
Nordstrom, Birke and Gustavsson (1983) observed a
significant decrease in "normal" pregnancies in high voltage substations in
Sweden, almost exclusively as a result of congenital malformations when the
father was a high voltage switchyard worker. Nordenson et al. (1988) measured a
significant increase in chromosome aberrations in similar workers.
A small
group (n=30) of U.S. Military personnel exposed to radar had significantly lower
(p=0.009) lower sperm counts, Weyandt et al. (1996). This confirms Lancranjan et
al.
Women exposed to ELF to RF/MW radiation experience significant changes in
reproductive functions.
Vaughan et al. (1984), studying U.S. workers, found
significantly increased risk of fetal death for last pregnancy for therapists,
RR=2.0, CI: 1.5-2.5, n=169, and for electronic technicians, RR= 1.5, CI:1.2-2.0,
n=202.
Wertheimer and Leeper (1986) found a seasonal pattern of developmental
delay and spontaneous abortion which significantly correlated with the use of
times when electrically heated beds were used. They were not able to correlate
the reproductive outcomes directly with electric field exposure. Subsequent
studies have found this, confirming this result could well be EMR
related.
Taskinen et al. (1990) in Finland, with 204 cases, found increased
spontaneous abortion with short-wave and microwave use: Note that the
statistical a significance is limited by the small sample sizes.
Electric
therapies >5/week OR= 2.0, CI: 1.0-3.9, n=17
Shortwaves>=5h/week, OR=
1.6, CI: 0.9-2.7, n= 30
Microwaves, OR= 1.8, CI: 0.8-4.1, n=13),
Stronger
associations with ultrasound and heavy lifting:
Ultrasound>=20/week, OR=
3.4, CI: 1.2-9.0, n=9
Heavy lifting, > 10 kg or patient transfers >=50
times/week,
OR=3.5, IC: 1.1-9.0, n=11
Odds ratios increased for
pregnancies > 10 weeks:
Electric therapies OR=2.2
Shortwaves
OR=2.5
Microwaves OR=2.4
Ultrasound OR=3.4
Heavy lifting OR=6.7
.
Taskinen et al. conclude Physical exertion during early pregnancy seems to
be a risk factor for spontaneous abortion. The findings raise suspicion of
potential harmful effect of shortwaves and ultrasound on the pregnancy, but no
firm conclusion can be drawn on the bases of these results alone."
However,
this study, in the context of all the other studies, is consistent and adds
considerable weight to the conclusion that there are adverse health effects from
RF/MW exposure. Taskinen at al. also found statistically significant increases
in congenital malformations in the children of mothers using shortwave therapy.
This confirms the results of Kallen et al, and Larsen et al.
Taskinen et al. (1990)
was the only Scandanavian study to have a large enough sample to investigate the
effects of miscarriage with microwaves. The sample was quite small (13),
limiting the significance of the result. The Odds Ratio was (OR= 1.8, 95% CI
0.8-4.1). Exposure to ultrasound and short-wave showed significant increases in
odds ratio for abortion after the 10th week of gestation, (OR = 3.4, p<0.01
and OR = 2.5, p<0.03, respectively). Taskinen et al. concluded: The effect of
shortwaves and ultrasound on the 'late' spontaneous abortions was significant
and increased in a dose response manner."
Sanjose et al. (1991) investigated
the incidence of low birthweight and preterm delivery in Scotland, 1981-84, in
relation to parent's occupation. They found statistically significant
(p<0.05) increases in low birth weight (RR = 1.4) and preterm delivery (RR =
1.8) for mothers who work in the electrical industry. People who work in
electrical industries" are recognized as being exposed to a wide range of EMR
giving them more than average EMR exposures.
Larsen (1991) found a
non-significant elevation in congenital malformations in a small (n=54) group of
RF exposed Danish physiotherapists, OR = 1.7, 95%CI: 0.6-4.3.
Lindbohm et al.
(1992) observed a dose-response relationship between the level of exposure to
VDTs and miscarriage. VDTs also emit RF radiation.
Exposure RR
95%CI
<0.13 µT 1.0 Reference
0.13-0.3 µT 1.9 0.9-3.9
>0.3 µT 3.4
1.4-8.6
Evans et al. (1993) compared reproductive outcomes between Magnetic
Resonance Workers and other groups. MRI workers had elevated outcomes compared
with other workers but compared with homemakers they were highly
elevated:
Outcome RR 95%CI
Miscarriage 3.22 1.74-5.97 (p=0.0001)
Early
Delivery 1.71 0.87-3.38
Low Birth Weight 1.52 0.52-4.41
Juutilainen et al.
(1993) observed a significant early pregnancy loss associated with "high"
residential 50 Hz exposures (( 0,63 µT at the front door), OR = 5.1
(1.0-25).
Savitz et al. (1996) investigated the association between maternal
occupation and pregnancy outcomes. For women using electrical equipment the
following results were found.
Any time in Pregnancy Fifth Month of
Pregnancy
Adjusted Adjusted
Symptom N OR 95%CI N OR 95%CI
Preterm
delivery 57 1.8 0.9-3.3 46 1.8 0.9-3.5
Very Low Birth Wt 36 1.5 0.9-2.3 24
1.2 0.7-2.1
Mod. Low Birth Wt 33 1.4 0.9-2.3 30 1.5 0.9-2.5
Stillbirth 54
1.2 0.8-1.7 50 1.2 0.8-1.9
Infant death 70 1.0 0.7-1.3 54 0.9
0.6-1.4
Small for Gestational 33 1.4 0.9-2.3 30 1.5 0.9-2.5
Age
The
electrical occupation was the most consistently the highest OR for these
reproductive effects. They are marginally non-significant because of the very
small sample size.
Belanger et al. (1998) conducted a prospective study (N=
2967) to evaluate the relation between spontaneous abortion and the use of
electrically heated beds. Electric blanket use was associated with increased
spontaneous abortion, OR = 1.84, 95%CI: 1,08-3.13 for unadjusted data, and OR =
1.74, 95%CI: 0.96-3.15 for data adjusted for other risk factors such as alcohol,
smoking, age and caffeine intake.
Summary and conclusions:
ICNIRP ignores
several male studies showing significant reduction in sexual function. The
ICNIRP reproductive assessment also fails to take into account 11 relevant
studies that reconfirm the conclusions of Kallen et al., Larsen et al. and
Ouellet-Hellstrom and Stewart. This shows how limited and therefore
unprofessional the ICNIRP assessment is.
The studies involving low frequency
EMR exposure reinforce and support the RF/MW exposure studies through the EMR
Spectrum Principle.
Vaughan et al. (1984), Taskinen et al. (1990), Sanjose et
al. (1991), Lindbohm et al. (1992) and Larsen (1991) are consistent with Kallen
et al. (1982) and Larsen et al. (1991) giving the conclusion that shortwave
exposure takes longer to produce effects than do microwaves. Shortwave effects
range from later pregnancy miscarriage, still birth, low birth weight, premature
birth, cot death and congenital abnormalities.
Taskinen et al. (1990) and
Ouellet-Hellstrom and Stewart (1993) confirm that microwave exposure is
associated with early pregancy miscarriage.
It is sobering to also note that
breast cancer risk is over 4 times higher for women who miscarry in the first
trimester, RR = 4.1, 95% CI: 1.5-11.3, Hadjimichael et al, (1986).
When all
the studies are taken together they form a comprehensive and compelling body of
research to show that microwave exposure of mothers leads to a significant
increase in early pregnancy miscarriage. There are two significant dose-response
relationships. They occur with those using short-wave radio and microwave
therapies and working in electrical industries, who have more late pregnancy
problems and malformed children. This amounts to a causal relationship between
EMR exposure and adverse reproductive outcomes.
10.5.6 Plausible
Mechanism:
The most likely mechanism is accumulated chromosome aberrations
and damaged cells in the placenta and fetus because biophysics shows extremely
small temperature increases can be expected from even very high RF/MW
exposures.
Calcium ion efflux lead to the survival of damaged cells that
carry their chromosome aberrations into future generations of cells. A reduction
in melatonin reduces the elimination of free radicals which enhances the
chromosome damage. Calcium ion efflux and melatonin reduction also impairs the
immune system with allows a greater population of damaged cells to survive.
Cells with damaged chromosomes are a known cause of spontaneous
abortion.
According to Sandyk et al. (1992):
The causes of spontaneous
abortion can be divided into two main categories: those arising from chromosomal
anomalies and those arising from abnormalities in the intrauterine environment.
In the following communication, we propose that deficient pineal melatonin
functions in early pregnancy may be causally related to the development of
spontaneous abortions in cases where chromosomal anomalies or structural
abnormalities of the uterus have been excluded."
Microwaves are shown to be
associated with DNA breakage in rats brains, Lai and Singh (1995, 1996, 1997b),
Sarkar et al. (1994) and Phillips et al. (1998), and to cause chromosome
aberrations, Heller and Teixeira-Pinto (1959), Garaj-Vrhovac et al. (1990, 1991,
1992, 1993), Haider et al. (1994) and others. Lai and Singh (1997b) show the
links to melatonin reduction and free radicals.
ICNIRP (1998) quotes Cohen et
al. (1977) which found no association between radar exposure and Down's syndrome
in their off-spring. They failed to mention a previous paper from the same
group, Sigler et al, (1965), which did find a significant risk from parental
radar exposure.
Sigler et al. suggested that this result, along with research
that found tissue damage in humans and laboratory animals" and a deleterious
effect of rat testis" as evidence that microwaves might be ionizing radiation,
since similar effects had been identified with exposure to ionizing radiation.
We now know that chromosome aberrations do occur in microwave exposed subjects
without the need for microwaves to be ionizing.
Flaherty (1994) presents The
effect of non ionizing electromagnetic radiation on RAAF personnel during World
War II". He found in a group of 302 surviving veterans, men had a ratio of
single to twin births of 41:1, women 38:1 and overall the ratio was 40:1. This
contrasts with the ratio in the normal Australian population of 85:1. Hence
radar exposed veterans had over twice the expected number of twins, a very
significant result.
10.6 Animal Toxicology:
ICNIRP (1998) fails to refer
to the significant research involving animal experiments on reproductive effects
when exposed to RF/MW. Results range from testicular degeneration, resorption of
the fetus and altered body weight at high but non-thermal levels of exposure to
total infertility in multigenerational studies of mice exposed to 0.168 µW/cm²
and 1.053 µW/cm², Magras and Xenos (1997). There are many animal studies showing
that RF/MW is teratogenic, that is, it causes severe reproductive problems.
Berman et al. (1982) introduce their paper by stating:
It has been repeatedly
shown that microwaves have teratogenic potential. Rats and mice have been used
almost exclusively in these studies."
Berman et al. (1982) extended the
studies to hamsters. They investigated the teratogenic potential of microwaves
on Syrian hamsters, using 2.45 GHz at power densities of 30 mW/cm² for 100
minutes daily This caused a temperature rise of 0.8 (C and significant fetal
resporptions or death (p = 0.0012), decreased fetal body weight (p=0.0001) and
decreased skeletal maturity. Averaging this over a whole day the mean exposure
is 2.08 mW/cm². Maternal toxicity was not observed, only fetal damage and death.
They conclude by comparing hamsters with mice.
In mice, SAR's of 16 or 22
mW/g caused fetal changes. Comparing these two species, we see that 16 mW/g and
above can cause decreased body weight and skeletal immaturity in mice, while
only 9 mW/g in the hamster causes similar changes. Additionally, this lower SAR
causes a significant increase in hamster fetal death (resporptions). Hamster
fetus, appears to be more susceptible to microwave radiation than the mouse,
exhibiting fetotoxic changes at lower SAR values."
Prausnitz and Susskind
(1962) exposed male Swiss albino mice to 9.27 GHz microwaves, pulsed with a 2 (s
pulse at 500 Hz, 4.5 mins per day, 5 days per week for 59 weeks with an exposure
level of 100 mW/cm². This is a thermal exposure load which would result in a
temperature rise of about 2(C. This amounts to a mean weekly exposure of 22
µW/cm².
Detailed autopsies were carried out on 60 irradiated and 40 control
mice who died during the experiment. Two adverse effects were more severe in the
exposed compared to the control animals.
(1) Testicular degeneration (atrophy
with no sperm) occurred in 29.8% (39/124) of the exposed animals and 7.1 %
(4/56) of the control animals, RR = 4.2.
(2) Cancer of the white cells or
leukosis was seen in 26.5% (39/147) of the exposed animals compared to 13.0%
(9/69) of the controls, RR= 2.04. This condition was described as monocytic or
lymphatic organ tumours or myeloid leukaemia in the circulating blood.
In
these mice significant and severe (4.2-fold) testicular damage and a 2-fold
increase in the initiation of leukaemia occurred is association with a mean
exposure of 22 µW/cm².
Testicular damage has also been found in men who have
radar exposures. Lancranjan et al. (1975) and Weyandt et al. (1996).
Although
as early as 1962 severe reproductive problems had been identified with and
exposure regime averaging 22 µW/cm² most of the research was carried out with
the incorrect assumption that if an effect was real it would be demonstrated if
the exposure was high enough. And if an effect was not detectable at extremely
high levels of exposure, there was no way that an effect would occur at low
levels of exposure.
Chazan et al. (1983) investigated the development of
murine embryos and fetuses after irradiation with 2450 MHz microwaves at 40
mW/cm². They found indications of retardation of development in the early period
of gestation in mice exposed to thermal MW fields. During the second half of
pregnancy an increase in the number of resorptions, stillbirths and internal
hemorrhages was noted. The living fetuses had lowered body mass compared to the
offsprings of sham-irradiated mice.
Berman, Carter and House (1982) also
found reduced weight in mice offspring after in utero exposure to 2450-MHz (CW)
microwaves using an exposure level of 28 mW/cm². They were exposed to for 100
minutes daily from the 6th through 17th day of gestation. This gives a mean
exposure during that period of 1.9 mW/cm². These data demonstrate that the
decreased fetal weight seen in microwave-irradiated mice (-10 %) detected in
utero and is retained at least 7 days after birth. Evidence from other published
studies is presented to show that the retarded growth is persistent and might be
interpreted as permanent stunting.
Suvorov et al. (1994) studied the
biological action of physical factors in the critical periods of embryogenesis.
The critical period in a chicken embryonic development (the 10-13 days of
incubation) is revealed under total electromagnetic radiation. EMR is a
physiologically active irritant that can influence functional state of the
brain. The increased absorption of electromagnetic energy takes place in this
incubation period. Its dynamics within 20 days of embryonic development has
phasic, up and down character.
Electromagnetic exposure (4 hours a day) in
the above mentioned period evokes a delay in embryo adaptive motor behavior
(biofeedback learning). Morphological investigation shows significant
pathological changes, specifically, destruction of share brain synapses. The
delay in embryo hatching for a day is also detected. Radiation exposure within
other periods of incubation (3-6th or 12-15th days) was not effective with
respect to formation of normal motor pattern in biofeedback experiment.
Unfortunately this paper is in Russian and no exposure levels are quoted in the
English translation of the abstract.
The Australian ABC television
investigative programme, Four Corners, claimed in a documentary on
electromagnetic health effects, that in a factory which used radiofrequency
heaters for sealing plastics, that of 17 women who worked at sealing machines,
14 had miscarried. Plastic sealers expose the operator to far higher levels that
do physiotherapy diathermy devices. In association with the concern in Australia
about the reproductive risks from plastic sealers, Brown-Woodman et al. (1989)
exposed a set of rats to a repeated exposure to 27.12 MHz EM fields for 5 weeks.
A reduction in fertility occurred as indicated by a reduced number of matings in
exposed rats compared to sham-exposed rats, and a reduced number of conceptions
after exposure. They conclude that:
"The data suggests that female operators
could experience reduced fertility, if they remain close to the console for
prolonged periods. This has particular significance for the physiotherapy
profession."
Magras and Xenos (1997) responded to health concerns among
residents living in the vicinity of an RF transmission tower in Greece, by
placing groups of mice at various locations in relation to the tower. The mice
fertility was monitored over several generations and related to the RF exposure.
Figure 10 shows the fertility rate of the two exposed groups. Where group A the
Low" exposure group (0.168 µW/cm²) became infertile after 5 generations and B
the High" exposure group (1.053 µW/cm²), became infertile after only 3
generations. This is a highly significant result because so few multi-generation
studies have been done and the effects of this study occur at extremely low
levels and the effect is total infertility.
The Greek study confirms the
Australian study, but shows that over several generations the infertility is
complete at very low levels of mean RF/MW exposure, Figure 24.
Figure 24:
Multigenerational exposure of mice to low level RF leads to complete
infertility.
10.7 Summary and conclusions about teratological animal
studies:
There is repeated evidence of RF/MW induced infertility in rodents
strongly showing that RF/MW have genetically damaged the cells of the animals.
This suggests that there could be reproductive and genetic damage in RF/MW
exposed humans. The epidemiological studies below confirm that there is, and at
very low mean levels of exposure comparable to the exposure of the mice in
Greece.
Developing sperm, embryos and fetuses are very vulnerable to damage
from toxins. At critical times in utero development damage to certain organs
occurs. With sufficient fetal or placenta damage a spontaneous abortion is
initiated. At other exposure levels and timing of damage a still birth can
result. Thermal levels of microwave exposure has produced retardation of
development if exposure is in early pregnancy, and resorptions, still births and
hemorrhages with exposure in the second half of the pregnancy.
A much lower
microwave dose was associated with significant reduction in birth weight and
permanent stunting and slowing of bone hardening. Changes in chick embryo
biofeedback learning is observed and testicular atrophy was observed with a mean
exposure to a radar-like signal averaging 22 µW/cm² over a week. Total
infertility occurred in mice after 5 weeks of exposure to 0.17 µW/cm².
Thus
in 1962 and 1997 it is been shown that chronic mean low level microwave exposure
of animals leads to very significant adverse reproductive effects in males and
females down. The effects were still significant at exposures of 22 and 0.17
µW/cm². These are close to the level of the lowest published results for calcium
ion efflux, 0.00015 W/kg (0.08 µW/cm²) Schwartz et al. (1990).
RF/MW
radiation causes significant birth and reproductive damage in exposed animals
down to very low short-term and extremely low average exposure levels.
10.8
Reproductive Health Effects Conclusions:
The ICNIRP (1998) assessment of
reproductive effects from RF/MW exposure is severely flawed. Animal studies show
that chromosome aberrations and single and double strand DNA breakage occurs
with EMR exposure, mice and rats have pregnancy, birth and fertility problems
associated with EMR exposure which are also found in exposed human populations.
There is consistency within human studies and between human studies and animal
studies. Many human studies show statistically significant adverse reproductive
outcomes. Two human studies, Lindbohm et al. (1992) and Ouellet-Hellstrom and
Stewart (1993), gave a statistically significant dose response relationship.
This study allows an exposure assessment to be carried out, along with the
multigeneration mice study, Magras and Xenos (1997).
This evidence supports a
causal relationship between EMR exposure and serious adverse reproductive
outcomes such as miscarriage, prematurely, still birth, low birth weight, SIDS
and congenital malformations.
10.9 Exposure Assessment:
Ouellet-Hellstrom
and Stewart (1993) report that the microwave exposure was primarily from
leakage, which at waist level was measured in the range 80 - 1200 µW/cm². At 15
cm from the source the highest reading was 15 mW/cm². The therapist needs to be
leaning over the patient during the therapy to receive this dose. This is highly
unlikely when the machine is turned on. Even so, this is not sufficient to cause
a surface heating of the skin in the few minutes it is likely to involve.
Hocking and Joyner (1995) show that microwaves produce very small SARs with the
uterus, in the following Figure 25.
In their table 2 Hocking and Joyner
(1995) show maximum SARs in the uterus for the conditions in Figure 11 for
short-wave (27.12 MHz) of 0.209 W/kg, for microwave (915 MHz) of 0.023 W/kg and
for microwave (2.45 GHz) of 0.000027 W/kg.
Gandhi (1990) gives the
relationship between SAR and temperature increase. The heating rate given is
0.0045 x SAR (C/min. With a maximum exposure time per treatment of 5 minutes,
and an external field intensity of 1,200 µW/cm², the heating of the fetus will
be 0.0055, 0.00062 and 0.00000073 (C, respectively. Not even at 15 mW/cm² does
the short-wave exposure can produce a detectable heating effect in the uterus
environment (0.071(C).
Figure 25: Specific absorption rate (SAR) profile
across the uterus for a small woman exposed to 1 mW/cm², from Hocking and Joyner
(1995).
Since an acute thermal mechanism can be ruled out it is appropriate
to calculate and use the cumulative average dose to determine the range of the
exposure regime.
Dose-Response Relationship for MW exposure:
It is not the
habit of therapists to stand close to the patient during the diathermy. In many
cases the therapist leaves the room while the 15 to 30 minute diathermy is
carried out. Hence a conservatively long mean exposure period of 3 minutes is
chosen to be associated with the exposure range of 80 - 1200 µW/cm², average 600
µW/cm². The dose-response relationship is expressed in terms of treatments per
month.
One treatment per month is associated with a mean monthly exposure of
0.042 µW/cm².
The results are plotted in Figure 26, showing a significant
dose response relationship with a threshold near zero exposure, The trend line
is fitted using a least squares fit.
Figure 26: Microwave exposure associated
miscarriage for pregnant physiotherapists, Ouellet-Hellstrom and Stewart
(1993).
Table 3: Estimated mean exposure ranges, from Ouellet-Hellstrom and
Stewart (1993).
No. of Exposures Odds Ratio Exposure Regime ( µW/cm²)
per
Month Mean
All pregnancies 0 1.00 0.0
<5 (2.5) 1.05 0.105
5-20
(12.5) 1.50 0.53
>20 (21) 1.59 0.88
11. Cancer
Assessment:
11.1 Laboratory Experiments:
I have only alluded to some
of the cell and animal laboratory studies to demonstrate the consistency of the
flawed scientific approach taken by ICNIRP.
The effect of microwaves
neoplastically transforming a standard mice embryo cell line, a cell line which
has been used several times in chemical carcinogen assessment are treated in the
same inaccurately dismissive manner, p507, referring to the work of
Balcer-Kubiczek and Harrison (1991). These researchers carried out a series of
very careful and extensive laboratory assessments using a standard mouse cell
line. One of their most significant results is presented below, Figure
27.
Figure 27: Dose response relationship for the induction of neoplastic
transformation of C3H/10T1/2 cells by a 24 h exposure to 2.45 GHz microwaves at
specific absorption rate indicated on the abscissa with or without TPA
post-treatment for 8 weeks, Balcer-Kubiczek and Harrison (1991).
This is a
clear and simple result. TPA is a known and widely used cancer promotor.
Together with TPA, microwaves significantly increase the number of
neoplastically transformed cells in a significant dose response manner. Dr
Balcer-Kubiczek states in a book chapter in 1995, Balcer-Kubiczek (1995):
In
1985 we published the first evidence indicative of EMF carcinogenesis at the
cellular level."
Further on Dr Balcer-Kubiczek states:
The mouse data of
Szmigielski et al. (1982) are also consistent with a general picture emerging
from our in vitro data, in that 2.45 GHz microwaves, and possibly 60 Hz magnetic
fields, seem to act as an initiator or carcinogen, rather than as a promoter of
malignant transformation."
This is a very different and much stronger view
than expressed by the ICNIRP review when it describes this work by saying: This
finding suggests that pulsed microwaves may exert co-carcinogenic effects in
combination with a chemical agent that increases the rate of cell proliferation
of transformed cells. To date, there have been no attempts to replicate this
finding, and its implications are unclear."
The use of the word may" when the
effect clearly does occur is wrong. The implication is clear if you want to see
it, which the reviewer obviously does not. In context, animal skin, when treated
with TPA or similar chemical cancer promoters, has the rate of cancer cell
formation increased by microwaves. This experiment shows that it also does
happen at the cellular level. That is, microwaves are carcinogenic at the tissue
and cellular level. It is then not surprising that epidemiological studies also
show that RF/MW increase cancer. But ICNIRP (1998) ignores and misrepresents
that evidence too.
The extensive research into Melatonin and its implications
are totally ignored.
12. Epidemiology of
Cancer:
12.1 Summary of ICNIRP's assessment:
The cancer assessment,
ICNIRP (1998) p 504, Figure 24, references one review (UNEP/WHO/IRPA 1993), WHO
(1993), and 13 papers covering 11 studies. The WHO (1993) review, is limited by
citing only 6 epidemiological studies and, by not reviewing the actual results,
contains errors, which are propagated through to the ICNIRP assessment.
In
ICNIRP (1998), only 13 papers are cited directly:
Barron and Baraff (1958):
The study group is too small (226) and the follow up period (4-13 years from
first exposure) is too short to detect cancer. Cancer is not one of the paper's
studies chosen outcomes. It is grossly dishonest and misleading to include this
paper in a cancer assessment and to cite it as showing that there are no cancer
risks from exposure to radar.
Robinette et al. (1980): Is widely claimed to
show no effects when its data does show significant adverse human health
effects, including a significant dose-response relationship for respiratory
cancer.
Lilienfeld et al. (1978): Is widely claimed to show no effects when
its data does show significant adverse human health effects, including
neurological, cardiac and cancer effects and includes a significant
dose-response relationship for rates of sickness as a function of years in
Moscow.
Figure 28: The Epidemiological assessment of cancer effects in ICNIRP
(1998).
Selvin et al. (1992): Is widely claimed to show no effects when it
was aiming to develop an epidemiological method relating to spatial clustering.
Its data does show significant adverse human health effects, including
significant dose-response relationships when radial cancer rates are related to
radial exposure measurements.
Beall et al. (1996): Is quoted by ICNIRP as
failing to show significant increases in nervous system tumours. Actually it
does show many significant increases of brain tumors, and it includes a
significant dose-response relationship between years of exposure and rates of
brain tumor for computer programmers.
Grayson (1996) Is quoted by ICNIRP as
failing to show significant increases in nervous system tumours, when it does
show a significant increase in brain tumor for RF/MW exposed
personnel.
Rothman et al. (1996a): ICNIRP acknowledges that it is still too
early to observe an effect of cancer incidence and mortality from mobile
telephone use as yet.
Rothman et al (1997b) ICNIRP acknowledges that it is
still too early to observe an effect of cancer incidence and mortality from
mobile telephone use as yet.
Szmigielski et al. (1988): finds significant
increases in cancer across the body, especially leukaemia incidence and
mortality among Polish Military personnel exposed to radio and radar. ICNIRP
says is difficult to interpret because neither the size of the population nor
the exposure levels are clearly stated. In fact the Polish Military microwave
exposure regime is presented and the group is described by the authors as large
and well controlled".
Szmigielski (1996): ICNIRP acknowledges that
Szmigielski found significant increases in leukaemia but criticizes the exposure
assessment and the description of the population. Again, the overall group
exposure regime is well described, but as in all large population studies,
individual exposures are not monitored but group exposures can be well
classified.
Hocking et al. (1996), (12.) Dolk et al. (1997a) and (13.) Dolk
et al. (1997b) are acknowledged as suggesting a local increase in leukaemia
incidence" in populations living in the vicinity of TV/FM transmission towers,
but ICNIRP calls the results Inconclusive". When the radial cancer rates are
compared with realistic broadcast transmission patterns, they form highly
significant dose response relationships and very strong evidence of a causal
relationship.
ICNIRP's overall cancer assessment conclusion that: "Overall,
the results of the small number of epidemiological studies published provide
only limited information on cancer risk."
This conclusion is mistakenly based
on flawed previous assessments, WHO (1993), failure to review the data on
effects (2, 3, and 4), incorrect claims of no significant effects when such
effects are reported (5 and 6), inappropriate dismissal of significant studies
(9 and 10) and inappropriate devaluing of residential studies (11, 12 and 13). A
systematic and independent analysis of the data in these papers reveals a
consistent and significant increase in cancer in this set of studies. Also, many
other studies exist which add considerable weight to this conclusion.
Much
more evidence of RF/MW induced cancer is available:
Zaret (1977), Lester and
Moore (1982 a,b) and Lester (1985), Milham (1985, 1988), Thomas et al. (1987),
De Guire et al. (1987), Archimbaud et al. (1989), Hayes et al. (1990), Tornqvist
et al. (1991), Maskarinec and Cooper (1993), Band et al. (1996), etc. In
addition, the reviews of Goldsmith (1995, 1996, 1997a,b) are ignored. Manyl
other papers are relevant. Occupational cancer studies identify a wide range of
exposure agents, including RF/MW in occupational groups. For example, for
"electrical, electronic manufacture and communications", such as Kaplan et al.
(1997), who found an elevated risk of brain tumour (OR=2.2 (0.5-9.3)). Cantor et
al. (1995) found significant increases in breast cancer for RF/MW exposed women
in the United States. Thus there is at least three times as many papers
available than those cited by ICNIRP.
It is a difficult and challenging task
for an individual scientist to take on and criticize the largest and most
prestigious bodies in the world, such as the WHO and the ICNIRP. However,
science not only allows this to occur, but supports and even demands a
comprehensive review of the data contained in the published material, an
inter-comparison between studies and an accurate quotation of the results and
analyses given. It also supports correction of analyses where errors are
identified, and new analyses where data suggests that more can be shown by
standard scientific methods.
The summary above gives a strong indication of
the ways in which ICNIRP have selectively used and consistently misquote the
studies they have chosen to assess. Hence the conclusions which should be drawn
are quite different than those ICNIRP arrived at. In order to substantiate the
brief claims made above this review will outline and list the detailed data
contained in the studies cited.
12.3 Data analysis and presentation
principles:
Some analysis principles are set out and then the detailed data
is presented.
A significant problem of principle is involved here. It is easy
to make a simple claim to dismiss as study of effects while it takes a
substantial presentation to correct such a misleading claim.
Simple incorrect
arguments are consistently used and internally reinforced in review after
review. Claims are simply made and to correct them requires detailed and
comprehensive scientific analysis and review.
It is easier to present biased
conclusions than to falsify data. In many studies the data shows significant
health effects which are ignored in the abstracts and conclusions.
Every
scientist is a person with a degree of subjectivity and bias. Hence science uses
principles and methods involving careful checking and peer review. Basic
scientific training makes it very difficult (though not impossible) for a
scientist to falsify data.
Analysis of data is more subject to error and bias
in its use and interpretation. Errors can be simple arithmetic errors or errors
in programming and data entry. Checking procedures are usually in place to
significantly reduce the chance of this occurring.
Subjective bias is
frequently involved in the choice and interpretation of statistics which makes
the principles of the application of statistical methods and agreed systems of
interpretation vital.
Epidemiology is the basic science of preventive
medicine and public health, and biostatistics is the quantitative foundation of
epidemiology, Jekel et al. (1996).
The test of statistical
significance:
In epidemiology it is agreed that a statistically significant
result is one which reaches the 1-in-20 or 5 % threshold for statistical
probability. In calculating the value of the statistical probability or p-value
(p), a single direction effect is tested against a one-tail distribution while a
bi-directional effect is tested against a two-tailed distribution. This requires
half the population to achieve statistical significance when searching for an
adverse effect than when the hypothesis involves the possibility of a positive
and a negative effect.
Epidemiology deals with chronic exposure of
populations whereas the ICNIRP guideline is based on acute thermal effects on
individuals. An important characteristic of epidemiology is its ecologic
perspective. People are seen not only as individual organisms but also as
members of communities in a social context.
Classical epidemiologist studies
the community origins of health problems. Classical epidemiologists are
interested in discovering risk factors that might be altered in a population to
prevent or delay disease or death.
Death is only one of the outcomes of
concern. In general many more people are made ill by a disease agent than those
who die of it. Illness has a significant personal, social and economic cost
which makes the prevention of illness a worthy goal.
Dose response
relationships are indicative of causal relationships and need to be taken very
seriously, Hill (1965).
Chronic mean exposures are much lower than acute peak
exposures. Health risks such as cancer are related to cumulative cellular damage
from inaccuracy on DNA repair processes and failure of the body to eliminate
genetically damaged cells. Hence the chronic mean exposure is the appropriate
metric for assessing health effects.
There are a large number of studies that
involve RF/MW exposures and show elevated and significantly elevated cancer
incidence and mortality. These are dismissed by WHO and ICNIRP assessors because
of the lack of a well defined exposure measurement. Dr Szmigielski confirms,
pers.comm., that even the highest acute military exposures in the Polish
Military study are nonthermal, and are associated with daily average exposures
around 1-5% of the daily peak exposure, and lifetime mean exposures about 20-30%
of the daily mean work day exposure. These chronic mean exposures are at a small
fraction of the ICNIRP guideline.
Significant increases in cancer are also
found in residential RF/MW exposures around TV/FM towers with annual mean
exposures around 15% of the direct exposure at the primary residence. Hence
there is a large body of epidemiological evidence showing significant increases
in cancer in RF/MW exposed populations whose chronic mean direct exposures of
less than 0.1 to 0.2 µW/cm², and hence involve chronic mean exposures in the
range 0.015 to 0.03 µW/cm². This firm knowledge of the actual mean exposure is
not necessary in order to revise the exposure standard when significant health
effects occur at exposure levels of less more than 1000 times below the present
standard.
13. Detailed evaluation
of ICNIRP cited papers and reports:
13.1 Barron and Baraff (1958):
"Medical considerations of exposure to microwaves (radar)"
The initial study
contained 226 radar exposed workers, and 88 in the control group. In the radar
group 37 had 5 - 13 years of exposure and 83 has 2 - 5 years. In the extended
study 109 new workers were added placing them generally in the 2-5 year group.
This is far too short a time for most cancers to appear, with latencies
typically between 8 and 30 years. An article in the same volume of the J.A.M.A.
records the initiation of a study on thousands of U.K. Radiologists, some of
whom had started work in 1920. It is stated that in 1958 it is too early to see
an increase in X-ray induced cancer and the sample is too small.
With the
working age incidence of all cancers at about 100 per 100,000 per year, over the
4 years of this study the probable number of normally occurring cancers would be
0.9. This paper cannot and does not assess cancer risk from radar
exposure.
This paper does report a high incidence of headache and
nervousness, so called subjective or neurasthenic symptoms. This is consistent
with stronger later findings, e.g. Djordevic et al. (1979), Lilienfeld et al.
(1978), Hocking (1998), Mild et al. (1998) and Frey (1998). The study also
reports significantly higher red blood cell counts, lower monocytes, elevated
white blood cell counts, and reduced eosinophils and polymorhonuclear cells in
the radar-exposed group compared with the control group. Altered blood cell
counts were also found in radar exposed groups in the U.S. Embassy in Moscow,
Tonascia and Tonascia (1976) and in radar technicians, Goldini (1990).
Barron
and Barraf did not assay for chromosome aberrations and DNA breakage. Laboratory
techniques were not as advanced in 1958 and they are now.
To include this
study in a cancer risk assessment is knowingly misleading and deceptive. This
level of bias and error is unbecoming of an international assessment of quality
and merit. This, along with several other similar examples, must bring the
scientific objectivity and professional credibility of the person or group who
produce this assessment into serious question.
13.2 Robinette et al. (1980):
"Effects upon health of occupational exposure to microwave radiation
(radar)"
13.2.1 Introduction
This is one of two epidemiological studies
which ICNIRP states "found no evidence of increased morbidity or mortality from
any cause". Both WHO (1993) and ICNIRP (1998) treat this is a large and reliable
study which shows that there are no effects from radar exposures. Actually it is
a large reliable study which does show significant health
effects.
Epidemiological studies regarding cancer are affected by the
complexities and long time scales involved in the initiation, promotion and
progression of cancer. This process can take decades from the initial cell
damage and genetic transformation of cells to the development of tumors and
malignant cancers. To some extent the individual complexities and the complex
nature of post war exposures to carcinogens over 20 years are smoothed by
considering large populations. This study involves around 40,900 sailors with
advanced technical training who served on ships during the Korean War and were
exposed to radio and radar signals. Their mortality statistics and health status
about 20 years later was obtained and analyzed for evidence of differences which
could be related to the RF/MW exposure. If the EMR exposure had caused a great
amount of initiation and/or promotion of cancer then this study has the ability
to reveal it.
An early challenge was to identify exposure groups so that the
health status of a large group with lower mean exposures could be compared with
a group that had received higher mean exposures. Comparing technical sailors
with similar age structures reduced confounding. The naval advisors recommended
that operators of radio and radar would have lower mean exposures compared with
those sailors who repaired and maintained the radio and radar equipment. Hence
the low exposure group included Radioman (RM) and Radarman (RD). The technical
people, including Electronics Technician (ET), Fire Control Technician (FT) and
Aviation Electronics Technician (AT) were placed in the high exposure
group.
A fourth technical group, Aviation Electrician's Mate (AE), a group
which is clearly involved with repairs and maintenance, was placed in the
operators group, the low exposure group. The AE group has a moderately high
mortality rate and plays the role of diluting the difference between the
groups.
The problem of high exposures for the radar and radio operators on
ships was pointed out when the preliminary results were presented to a
conference, Robinette and Silverman (1977).
13.2.2 Hazard Number
Assessment:
Amongst those who were originally allocated to the exposed group,
i.e. ET, FT and AT, around 5 % (1233 men) were randomly chosen to be assessed
for individual exposure through a job matrix estimate of their Hazard Number.
The results of this are in the following table:
Table 4: Distribution of
assessed Hazard Number for the three assumed high exposure groups, Robinette et
al. (1980).
Hazard Electronics Fire Control Aviation Electronics
Number
Technician (ET) Technician (FT) Technician (AT)
% % %
0 27.8 6.6 12.5
1
- 2000 28.3 23.4 16.9
2000-5000 20.0 31.1 17.6
5001+ 10.6 25.8
48.6
Unknown 13.3 13.1 4.3
Mean HN 1610 2870 3700
There is a clear
overlap between these groups with all groups having a large number in the 2000+
Hazard Number. There is a clear gradient in the proportion of each group with
5000+ Hazard Number.
Health survey results:
From the exposure survey there
was a group of individual for whom each person was assigned a Hazard Number that
was proportional to his exposure risk. Of those who had died, they identified 63
sailors with Hazard Number of 0, 160 with 1-5000 and 86 with 5001+. The
mortality results are presented in Table 5.
Table 5: Number of deaths from
disease and mortality ratios by Hazard Number: US enlisted Naval personnel
exposed to microwave radiation during the Korean War period, from Table 9,
Robinette et al. (1980). The Rate Ratio is calculated as the ratio of the
Mortality ratio for Hazard Number 5001+ exposure and 0 Hazard Number
exposure.
Cause of Death Hazard Number Trend
No. 0 1-5000 5001+ p-value RR
95%CI
All diseases 309 0.82 0.91 1.23 0.03 1.50 1.08-2.08
Malignant
Neoplasms 96 0.99 0.90 1.44 N.S. 1.45 0.83-2.52
Digestive Organs 20 1.49 1.14
0.78 N.S. 0.52 0.13-2.08>
Respiratory Tract 24 0.82 0.86 2.20 <0.05
2.68 0.84-8.55
Lymphatic and hematopoietic 26 1.09 1.04 1.64 N.S. 1.50
0.52-4.32
System
Other Malignant neoplasms 26 0.78 0.70 1.17 N.S. 1.50
0.52-4.32
Disease of Circulatory System 150 0.94 0.83 1.17 N.S. 1.24
0.79-1.94
Other Disease 63 0.30 1.13 1.08 N.S. 3.60 1.14-9.20
Given the
exposure dilution factors, all but digestive organs would probably have RR>2
and be significantly be increased. This small sample analysis shows a
significant dose response trend for mortality from all diseases (p=0.03) and for
Respiratory Cancer (p<0.05). This is remarkable given the exposure dilution.
The analysis also shows that for every disease cause but one there is an
elevated risk of mortality due to a range of cancers, Circulatory Disease and
Other Disease.
The mean Hazard Number for each group is calculated using a
mean hazard number of 0, 1000, 3500 and 6000 for the defined ranges. The mean
exposure estimate also shows a gradient and suggests that the best dichotomy
will be achieved by comparing AT as a high exposure group to ET as a low
exposure group. This was not done by Robinette et al. who preferred to compare
ET with the FT and AT groups combined (FT+AT). This maintains larger numbers in
the high exposure group by reduces the exposure separation.
The mortality
dose-response gradient persists when the total mortality rate is calculated for
the ET, FT and AT groups: MR (ET) = 1.0; MR(FT) = 1.29; and MR(AT) =
1.79.
Having identified that the FT and AT groups had higher hazard numbers
than the ET group, Robinette et al. combined FT + AT and compared their
mortality rates with ET, Table 6. Table 6 shows elevated mortality rates
compared with the ET group, for all causes of death listed. The text records
that they are significantly elevated for All Disease (p<0.01) and Other
Diseases (p<0.01).
Table 6: Mortality rates, Risk Ratios and Confidence
Intervals between the ET group and AT group of US enlisted personnel exposed to
microwave radiation during the Korean War.
Cause of death No.(FT+AT) ET FT+AT
RR 95%CI
All diseases 140 0.83 1.19 1.43 1.14-1.79
Malignant Neoplasms 40
0.95 1.18 1.24 0.83-1.86
Digestive Organs 8 1.10 1.19 1.08
0.44-2.65
Respiratory Tract 9 1.13 1.15 1.02 0.45-2.33
Lymphatic and
Hematopoietic 11 1.06 1.40 1.32 0.61-2.87
System
Other malignant neoplasms
12 0.68 1.06 1.56 0.72-3.37
Diseases of the Circulatory System 64 0.85 1.08
1.27 0.92-1.75
Other disease 36 0.61 1.46 2.39 1.45-3.94
Robinette et
al.'s Table 5 sets out the mortality data by cause of death for each
occupational group, giving the opportunity to compare AT rates with ET rates of
mortality. The results are shown in Table 6.
Table 7: Mortality Incidence per
1000 and Risk Ratio (AT/ET) as an indication of the high exposure (AT) to low
exposure (ET) difference.
Exposure
Low High Risk Ratio 95 % CI
Causes
of Death
All Deaths 33.7 60.5 1.79 1.52 - 2.12
Accidental Death 13.5 29.6
2.20 1.72 - 2.82
Motor Vehicle Death 6.3 6.1 0.97 0.60 - 1.59
Suicide,
Homicide, Trauma 4.4 6.1 1.38 0.83 - 2.29
Suicide 3.4 2.7 0.80 0.39 -
1.63
All Diseases 15.2 23.5 1.55 1.19 - 2.01
Malignant Neoplasms 5.0 8.2
1.66 1.06 - 2.60
Digestive and Peritoneum 1.1 1.2 1.07 0.35 -
3.21
Respiratory 1.2 2.1 1.75 0.72 - 4.25
Eye, Brain, CNS (FT/ET) 0.4 0.9
2.40 0.57 - 10.03
Skin 0.2 0.6 2.66 0.45 - 15.94
Lymphatic and
Hematopoietic 1.4 3.1 2.22 1.02 - 4.81
Circulatory System Disease 7.6 9.5
1.24 0.83 - 1.85
Digestive System Disease 0.8 2.7 3.27 1.35 - 7.89
Other
Diseases 1.6 2.7 1.71 0.78 - 3.74
In Table 5 where exposures are more
dichotomized, mortality due to Malignant Neoplasms and Lymphatic/Hematopoietic
cancers are both significantly elevated but when FT and AT are combined these
results are no longer significantly different. It is interesting too that in the
dose-response analysis using the individual's hazard number, respiratory cancer
shows a significant trend, but in these occupational group comparisons this
cancer is elevated but not significantly elevated. The comparisons between
Tables 6 and 7 clearly show the effect of dilution through combining the FT and
AT groups. Table 7 shows elevated Risk Ratios for all causes of death except
motor vehicle and suicide. Significant increases in mortality were found for All
Diseases, Malignant Neoplasms, and Lymphatic and Hematopoietic cancer. Very
significant increases were found for All Causes of death, Accidental Death and
Death from diseases of the Digestive System.
Figure 29: 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).
Figure 29 shows
that the overall mortality rates for all death, disease, cancer and
leukaemia/lymphoma, for the large occupation groups increase significantly and
in a dose response manner with radar exposure. This is similar to the 5%
exposure survey sample. The Aviation Electrician's Mate (AE) group has been
omitted because it is a repairer group included in the operator's group by the
original authors.
Morbidity Data:
Robinette et al. obtained two morbidity
data sets. The first was from the periods 1952-54 and 1956-59 for admissions to
naval hospitals. This is very close to the period of exposure and allows little
time for cancers to develop. For the immediate post-war data set the following
significant increases in sickness were identified by Robinette et
al.:
Diseases of the ears, nose and throat (p<0.01),
Acute respiratory
disease (p<0.01),
Other respiratory disease (p<0.02),
Diseases of
the urinary and male genital organs (p<0.05), and
Accidents, poisonings
and violence (p<0.001).
The second data set was from Veterans'
Administration Hospitals for the period 1963-76.
Table 8 gives a more
detailed description of the results of the later morbidity data set. It is not
inconsistent with the significant results cited by Robinette et al. but it does
show a wider range of significant adverse health effects.
In the later, to
1976, VA compensation data Robinette et al. found significantly increase in
sickness for Musculoskeletal system and other organs, including:
Loss of part
extremities, osteomyelitis and neoplasms of bone or muscle
(p<0.001);
Organs of special sense which includes eye cataracts
(p<0.05);
Respiratory system, excluding pulmonary tuberculosis
(p<0.01);
Cardiovascular system (p<0.001); and
Mental disorders,
including psychoses, psychoneurotic disorders
and so-called
"psychophysiologic disorders" (p<0.05).
Table 8: Number of
hospitalizations and hospitalization rates per 10,000 per year, in VA hospitals,
1963 -1976, by diagnosis and exposure class: US enlisted Naval personnel exposed
to microwave radiation during the Korean War period. The significance p-value is
calculate from the Mantel-Haenszel Chi-squared estimate.
High exposures
VA
diagnostic class Total ET FT + AT
No. Rate No. Rate No. Rate RR 95% CI
p-value
Infective, parasitic 42 1.5 24 1.3 18 1.9 1.46 0.79-2.69
0.26
Neoplasms, malignant 34 1.2 17 1.0 17 1.8 1.80 0.92-3.53
0.04
Neoplasms, other 26 0.9 9 0.5 17 1.8 3.60 1.60-8.08
<0.001
Allergic, endocrine system,
metabolic and nutritional dis. 77
2.8 41 2.3 36 3.8 1.65 1.05-2.58 0.01
Blood, blood-forming organs 17 0.6 5
0.3 12 1.3 4.33 1.53-12.3 0.001
Alcoholism 105 3.8 45 2.5 60 6.3 2.52
1.71-3.71 <0.001
Other mental disorders 276 10.1 166 9.3 110 11.6 1.25
0.98-1.58 0.02
Nervous system, sense org. 106 3.9 58 3.2 48 5.1 1.59
1.08-2.33 0.009
Circulatory 123 4.5 68 3.8 55 5.8 1.53 1.07-2.18
0.007
Respiratory 80 2.9 43 2.4 37 3.9 1.63 1.05-2.53 0.014
Digestive 255
9.3 132 7.4 123 13.0 1.76 1.38-2.25 <0.001
Genitourinary 82 3.0 45 2.5 37
3.9 1.56 1.01-2.41 0.02
Skin, cellular 61 2.2 33 1.8 28 2.9 1.61 0.97-2.66
0.04
Bones, organs of movement 80 2.9 36 2.0 44 4.6 2.30 1.48-3.57
<0.001
Trauma 108 3.9 53 3.0 55 5.8 1.93 1.32-2.81 <0.001
Symptoms,
ill-defined cond.,
special exams and other 151 5.5 85 4.8 66 6.9 1.44
1.04-1.99 0.007
Person-years (1000) 27.39 17.89 9.50
The Table 9 shows all
of the diagnosis groups detailed in Robinette et al. Table 12, for VA
compensation claims up to December 1976. Again the vast majority of symptoms
(apart from Nerves, and Genitourinary) are marginally significant to very
significantly greater for the higher exposed FT+AT group compared to the lower
exposed ET group. Except for "Nerves" all symptoms are elevated and some, as
also identified by Robinette et al., are significantly and highly significantly
elevated.
Table 9: Number of men receiving VA compensation and pension,
December 1976 and rates per 1000 men per year by diagnosis and exposure class,
and Risk Ratio (FT+AT)/ET, Robinette et al. Table 12.
ET FT+AT Risk Ratio
Significance
No. Rate No. Rate RR 95% CI
p-value
Diagnosis:
Musculoskeletal 115 8.8 119 16.9 1.93 1.49-2.49
<0.001
Organs of special sense 49 3.7 42 6.0 1.62 1.07-2.45
0.010
Systematic conditions 3 0.2 5 0.7 3.50 0.84-14.65 0.080
Respiratory
55 4.2 51 7.3 1.74 1.19-2.55 0.001
Cardiovascular 43 3.3 47 6.7 2.03
1.34-3.07 <0.001
Digestive 74 5.7 55 7.8 1.37 0.97-1.94
0.02
Genitourinary 31 2.4 10 2.7 1.13 0.55-2.30 0.32
Skin 83 6.3 58 8.2
1.30 0.93-1.82 0.052
Endocrine 15 1.1 11 1.6 1.45 0.67-3.16
0.86
Neurological 21 1.6 16 2.3 1.44 0.75-2.76 0.29
Nerves 15 1.1 3 0.4
0.36 0.10-1.24 0.14
Mental Conditions 51 3.9 46 6.5 1.67 1.12-2.49
0.003
Discussion of Results:
This project was conducted with the objective
of determining whether radar exposure to service personnel during the Korean War
produced health hazards. It appears evident that the authors of the study were
under pressure not to identify any adverse health effects. They identified
significant dose response increases of mortality and respiratory cancer with
exposure and many elevated and significantly elevated cancer and health
mortality and morbidity from the separated radar exposed groups. Even so, they
decided to conclude that they couldn't associate these effects to radar
exposure. Their abstract includes the conclusion:
"No adverse effects were
detected in these indices that could be attributed to potential microwave
radiation exposures during the period 1950-1954."
This is clearly not true.
Their published conclusion is expressed differently by Dr Silverman in a 1979
conference paper, Silverman (1979). She states:
"While some significant
differences among occupational groups classified by potential exposure have been
found with respect to all end points studied, the differences could not be
interpreted as a direct result of microwave exposure."
Here Dr Silverman uses
the term "direct radar exposure". She points out that no measures of actual as
opposed to potential exposure were available. Hence occupational groups
consisted of mixed exposure experiences. Dr Silverman notes the dilution effects
that this produces because the high exposure AT group contained nearly 30 % of
people with Hazard Number <2000, while the low exposure ET group had nearly
24 % who were in the >5000 category.
Dr Silverman is arguing that the
results relate to potential and not actual exposure, which conflicts with the
published paper that refuses to relate the effects even to potential exposure.
What both Dr Silverman on her own and Robinette, Silverman and Jablon together
fail to recognize and appreciate are that all dilutionary influences, by their
very nature, weaken the dichotomization and reduce the contrasts between exposed
and control groups. These data sets are strongly influenced by several
dilutionary factors.
A high exposure 'repairer group' (AE), was placed in the
'operator', low exposure control group.
All participants are more highly
exposed to radar than the average male population of the same age, Lin et al.
(1985).
Combining the FT and AT groups reduces the exposure
separation.
All of the three 'high exposure' groups contain a mixture of low,
middle and high exposure individuals.
Dilution weakens and destroys
dichotomization. Hence it is remarkable and highly significant that elevated,
significant, highly significant and dose-response differences still persisted
through to the health statistics 20 years after the war.
After discussing
this actual vs potential exposure problem, Robinette et al. (1980) stress that
while considering the data about death, other disease would have been present
which would not be reported:
Further, it is possible that effects involving
cardiovascular, endocrine and central nervous system do exist, but are
transient, disappearing with the termination of exposure or soon thereafter, or
are not perceived to be sufficiently consequential to result in admission to
hospital."
ICNIRP and the authors are wrong to conclude that this study shows
no increases in cancer from radar exposure.
This study shows that exposure to
radar (pulsed microwaves) results, several years later, in large, severe and
highly significant health problems and death across all surveyed organs,
including neurological, respiratory, endocrine, circulatory and cardiac, and
cancer morbidity and mortality. Dose response relationships show strong
relationships between radar exposure, mortality and morbidity.
13.3 U.S.
Embassy in Moscow: Lilienfeld, Tonascia, Tonascia, Libauer and Cauthen (1978).
"Foreign Service Health Status Study - evaluation of health status of foreign
service employees from selected eastern European posts"
13.3.1 The
context:
The Soviets irradiated the U.S. Embassy in Moscow for over 20 years
between 1953 and 1976 using radars. Measurements taken on the outside walls on
the upper floors at which the radar was aimed showed peak exposure values of 5
µW/cm² between 1953 and May 1975, 15 µW/cm² between June 1975 and Feb 1976.
After this it was a fraction of 1 µW/cm². Exposure lasted for 9hr/day in the
first period and 18 hr/day subsequently. Hence for over 20 years the daily
average outside exposure was 1.9 µW/cm². Inside the exposure was in the range of
10 to 50 times lower, i.e. 0.038 to 0.19 µW/cm².
Pollack (1979) confirms that
the employees and dependents were exposed to extremely low intensity radar
signals:
"The maximum intensity up to May 28, 1975, was 5 µW/cm². To achieve
a 5 microwatt exposure the individual has to stand in from of an open window
fully undressed for a full part of the working day. The characteristics of
microwaves are such that once away from the open window, inside the room, a
variety of field intensities fluctuate depending upon the wall, the furniture,
the presence of steel cabinets, and so forth. A few feet from the window, the
intensity was down to fractions of a microwatt most of the time with occasional
points there where one could measure one or two microwatts."
The employees
and dependents were studied for possible health effects from the radar exposure
by a team from the John Hopkins University under the direction of highly
respected epidemiologist, Professor Abraham Lilienfeld. Dr Lilienfeld noted that
the group was quite small and the follow-up time too short to generally identify
significant health effects such as cancer. He thus recommended that continued
health status surveillance should be carried out. This was not done. The
incidence of sickness and death were compare with the average US rates for
similar age groups for both the Moscow Embassy and other Eastern European
Embassies.
There was great pressure for the group not to identify adverse
health effects. Dr Herbert Pollack, the U.S. State Department Contract Officer
is recorded to have changed the conclusions of the report, Goldsmith (1995a,
1997). In a published conference paper Dr Pollack criticized the media and a
particular journalist, Paul Brodeur for their claims that there were blood tests
showing effects, Pollack (1979a). Pollack states: "He (Brodeur) goes on to day
that types of chromosome aberrations observed in this study are the same as
those induced by ionizing radiation in other organisms, including humans.
Obviously, no such data were available." This final claim is untrue. The
chromosome aberrations were recorded and reported by Tonascia and Tonascia
(1976) and their results are published in Goldsmith (1997), Table 13
below.
13.3.2 The key results included:
The all cause mortality rate for
Moscow males as 0.42 (0.3-0.6) and for females 1.1 (0.5-1.9). Hence males,
primarily State Department employees, were much healthier and females were as
healthy as the average U.S. residents. This is a good example of the "healthy
worker" effect. State Department selection procedures rule out a range of
unhealthy people and favour healthy people.
Table 10: Sickness rates
increased in Moscow with years of service: (Table 6.18)
Under 2 yrs 2-3 years
4 + years p-value for trend
Number of people 316 455 45
Person-years 3709
5570 568
Male Conditions (%)
Present Health Summary 5.4 9.7 16.2
0.05
Arthritis/rheumatism 4.3 6.5 8.8 0.02
Back Pain 4.0 7.7 11.8
0.04
Ear problems 3.8 5.6 14.7 0.02
Vascular system 0.8 2.7 11.8
0.004
Skin & Lymphatic 9.4 12.2 28.0 0.02
Female Conditions
(%)
Vaginal discharge 4.2 13.8 17.5 0.04
The sickness rates increased
independent of the age of arrival and faster than the influence of
aging.
Table 11: Neurological Symptoms per 1000 p-y, Male employees: (Table
6.31)
Moscow Comparison RR p-value
Depression 1.3 0.73 1.78
0.004
Migraine 1.8 0.97 1.86
Lassitude 1.2 0.78 1.54
Irritability 1.3
0.66 1.97 0.009
Nervous Disorders 1.5 0.64 2.34
Difficulty in
Concentrating 1.4 0.52 2.96 0.001
Memory Loss 1.6 0.50 3.20
0.008
Dizziness 1.2 0.85 1.41
Finger Tremor 1.3 0.71 1.83
Insomnia 1.1
0.90 1.22
Neurosis 1.3 0.76 1.71
These symptoms are consistent with the
"Microwave Syndrome" of the "Radiofrequency Radiation Sickness",
Johnson-Liakouris (1998). Mild et al. (1998) identified significant
dose-response relationships for the following symptoms from the use of mobile
phones: Memory Loss, Difficulty in Concentrating, Headache, Fatigue. Hence it is
now shown and known that RF/MW exposure from extremely low but chronic exposure
over many years, occupational exposure and cell phone use all produces
significant and consistent neurological symptoms. The Risk Ratios were quite
large but they were not quite significant because of the very small sample
numbers.
Table 12: Congenital Malformations of children after the first
tour:
Conditions Moscow Comparison RR Number of children
SMBR
SMBR
Leukaemia and cancer 1.2 0.84 1.43 1
Blood Disorders 1.7 0.42 4.05
7
Mental, Nervous Condn. 1.8 0.36 5.0 8
Behavioural Problems 1.4 0.68 2.06
7
Chronic Disease 1.1 0.88 1.25 7
Table 13: Blood samples showed a high
proportion of the staff had significantly altered red and white blood cell
counts and well above average chromosome aberrations (CA). The CA data is set
out in Goldsmith (1997), i.e.
Mutagenic Level Designator Subjects, No.
5
Extreme 0
4 Severe 6
3.5 Intermediate 5
3 Moderate 7
2.5
Intermediate 5
2 Questionable 5>
1 Normal 6
Patients with mutagenic
level of 3 and above were advised not to reproduce until 6 months after somatic
levels had returned to 2 or 1. This warning applied to 68 % of the patients in
this sample. Staff with elevated chromosome aberration rates were advised not to
have children for until six months after they had returned to near normal.
A
survey of cancer mortality rates is summarized in Table 14. This shows that
despite the extremely small sample size and the very significant exposure
dilution in the years between residence in Moscow and the survey results, there
are highly elevated and significantly elevated rates of mortality from cancer
Lilienfeld et al. shows significantly increases chromosome aberration and
cancer. This was recently also found in mice, Vijayalaxmi et al. (1997).
The
dominant cancers are brain tumor and leukaemia and reproductive organ cancer.
But this study, like the Korean War Study, confirms that extremely low level
chronic microwave exposure is associated which very significant increases in
illness and mortality in organs across the whole body, consistent with
widespread cellular chromosome damage. Significantly elevated chromosome
aberrations were measured in this case, Table 13, as well as significant
alterations in white and red blood cell counts, Jacobson (1969). This would also
be the expected result from reduced melatonin.
Table 14: Cancer Mortality
Rates:
Male employees (Table 6.37) Moscow Comparison RR
SMBR SMBR
Skin
Cancer 1.5 0.69 2.17
Benign Neoplasms 1.4 0.75 1.87
Female employees
(Table 6.38)
Malignant Neoplasm (Excl. skin) 1.7 0.63 2.86 (p=0.06)
Adult
Dependents: (Tables 7.12, 7.13)
Obs. Exp SMR (95%CI)
Live-in
All
malignant Neoplasms 5 1.5 3.3 (1.1-7.7)
Digestive Organs Cancer 1 0.26 3.8
(0.1-21.2)
Pancreas Cancer 1 0.03 33.3 (0.8-185)
Breast Cancer 1 0.4 2.5
(0.1-13.9)
Ovarian Cancer 3.0
Multiple Myeloma 1.5
Arteriolosclerotic 2
0.59 3.4 (0.4-12.3)
Heart Disease
Live-out
All malignant Neoplasms 7 3
2.3 (0.9-4.7)
Brain tumor 2 0.1 20.0 (2.4-72.2)
Lung cancer 1 0.44 2.3
(0.4-93)
All Accidents 4 1 4.0 (1.1-10.2)
Table 14: cont'd:
Obs. Exp
SMR (95%CI)
Suicide 1 0.36 2.8 0.1-15.6)
Children Living In (Table
7.16)
All Malignant Neoplasms 2 0.5 3.8 (0.5-13.7)
Leukaemia 1 0.2 5.3
(0.1-29.5)
Suicide 1 0.29 3.4 (0.0-1.6)
Children Living out
All
Malignant Neoplasms 2 0.83 2.4 (0.3-8.7)
Leukaemia 1 0.3 3.4
(0.1-18.9)
Suicide 1 0.3 3.3 (0.1-18.4)
13.3.3 Report conclusions
challenged:
It is stated by both Bradford Hill (1965) and Goldsmith (1992)
that elevated Odds and Risk Ratios are also relevant to the public health
protection basis in epidemiology,
Professor Goldsmith was closely associated
with the staff affected by the chronic radar exposure of the U.S. Embassy in
Moscow and obtained information through the Official Information Act. This
included the blood test results and minutes of meetings which record the fact
that the State Department case officer, Dr Herbert Pollack, changed the
conclusions of the final report compared with the draft report, to state that no
effects could be associated with the radar exposure, Goldsmith (1997). The data
and Dr Goldsmith show that this is not true. After reviewing this data, an
eminent epidemiologist, Professor John Goldsmith, Goldsmith (1995), referring to
a recent draft of criteria for health protection" which claims: No effect on
life span or cause of death of 1,800 employees and 3000 dependents of the U.S.
Embassy personnel", states:
To ignore these findings on the basis of No
effect on life span or cause of death" in setting human exposure standards is
wrong. In the first place the criteria are two narrow; mortality is not the only
relevant end-point. The positive or 'findings for concern' are ignored.
Increased cancer incidence among dependents is a nontrivial endpoint."
A
highly remarkable result is the dose-response relationship for a range of
sicknesses, Table 10. The results must be very highly significant to survive the
exposure dilution effect with the disease gradient intact and statistically
significant. As with Robinette et al. (1980), the data presented in the
Lilienfeld contract report is contrary to that stated in the report's stated (an
altered) conclusions. Despite the small numbers, the lack of long latency period
and dilutionary factors, the Lilienfeld data shows a significant increases
in:
Cardiac symptoms
Neurological and psychological symptoms
Altered
blood cell counts
Increased chromosome aberrations, and
Elevated cancer in
children and adults
Sickness increasing in a dose-response manner with years
of residence.
These symptoms are associated with chronic exposure to very low
intensity pulsed microwaves in the range < 0.04 to 0.2 µW/cm².
In a sense
too, the fact that the State Department case officer, Dr Herbert Pollack,
altered the conclusions, attests to the significance of this study, the results
of which would be embarrassing to the U.S. Government, both in terms of
compensation and in terms of the validity of the U.S. exposure standard.
13.4
Selvin et al. (1992): "Distance and risk measurements for the analysis of
spatial data: a study of childhood cancer" - The Sutra Tower Study, San
Francisco.
Background:
Selvin et al. (1992) is widely quoted in national
and international reviews as showing no evidence of health effects from a
powerful telecommunications tower near a human population. The ICNIRP (1998)
statement is typical when it says: Selvin et al. (1992) reported no increase in
cancer risk among children chronically exposed to microwaves radiation from a
large microwave transmitter near their homes."
Broadcast tower residential
exposure patterns:
Selvin et al. (1992) made a major error by assuming that
the public exposure varies linearly with distance from the tower. Their
conclusions were firmly based on this assumption and therefore are wrong. Radio
engineers know a great deal about broadcast antennae radiation patterns. Some
typical VHF examples are given in section 1.9 and Figures 4 to 6.
Figure 30:
Ground level exposure for a typical UHF TV broadcast signal, from an antenna
pattern from Hammett and Edison (1997), for a 2.4 MW ERP transmitter at 400m
AGL, for a flat surface.
The ground level radial pattern shows a complex of
undulating patterns whose peaks and troughs vary with the wavelength of the
signals and the height of the antennae. The transmissions from the Sutra Tower
have weak VHF and powerful UHF signals. Figure 30 shows a typical UHF signal
taken from an antenna vertical pattern in Hammett and Edison (1997). Figure 30
shows that the strongest peaks for UHF signals occur between 2 and 4 km, and the
main beam peaks outside 10 km, around 11 to 15 km from the base of the tower.
Measurements taken around the Sutra Tower are presented in Figure 31, showing
the mix of VHF and UHF broadcast stations.
The high peak close to the tower
and the peak near 1 km are from the VHF (FM radio) transmissions, as shown in
Figure 5. The peaks outside 2 km are primarily UHF signals, as shown in Figure
30.
Residential Exposure Factor:
The direct exposure measurements or
calculations need to be adjusted for epidemiological purposes because people
largely live inside and move around a great deal. The mean Personal exposure
Factor has (PEF) has been estimated as 0.15, Section 1.10. For example, the
measured outside signal at the five homes of the children who live within 1 km
of the tower and who have brain tumour, averages 1.74 µW/cm². When the PEF of
0.15 is applied this becomes 0.26 µW/cm².
Figure 31: The measured and
estimated power density (exposure in µW/cm²) with distance from the Sutra Tower.
Circles show measurements. The line follows measurement points and the radial
pattern of Figure 30 beyond 3 km. From Hammett and Edison (1997) and readings
taken by the author in 1999.
The objective of Selvin et al.:
Selvin et al.
were concerned with developing statistical data analysis techniques involved in
comparing spatial clustering with risk approach to data analysis of potential
effects from point sources of exposure. They apply their methods to the white,
childhood cancer data for children <21 years living in the vicinity of the
Sutra Tower to test the presence of clustering. An example, of the spatial
distribution for childhood leukaemia, is given in Figure 30.
13.4.5 The
results and errors in Selvin et al.:
Selvin et al. were totally unaware of
the reality of radiation patterns and simply assumed that exposure varied
linearly with radial distance. This was used to test three method of statistical
clustering in an attempt to define the exposed vs unexposed populations. These
approaches showed that peak cancer rates occurred at a radius of 1.75 km from
the tower. From their methods this defines the exposed group to be within twice
this distance, i.e. within 3.5 km. Because they assumed a linear decline in
exposure with distance from the tower they conclude: None of the three analytic
approaches indicates the presence of clustering of childhood cancers associated
with the Sutra Tower." If they knew the actual radial radiation pattern then
their conclusion would have been very different.
Figure 32: Spatial map of
white childhood (<21 years) leukaemia for San Francisco, 1973-88, from Selvin
et al. (1992).
Figure 33: All cancer for children (<21 years) from
1973-88, from Selvin et al. (1992), involving 123 cases; brain tumor (35),
leukaemia (51) and Lymphoma (37). The non-residential areas of Golden Gate Park,
the Central Business District (CDB) and Lake Merced are shown, along with the 1
km ring around the Sutra Tower.
Detailed spatial cancer incidence and
exposure analysis:
Childhood cancer rates and residential locations are given
for the period 1973-1988 by Selvin et al. (1992). A total of 123 cases of
childhood cancer were identified among 50,686 white individuals at risk under
the age of 21 years. These included 51 cases of leukaemia, 35 cases of brain
tumour and 37 cases of lymphatic cancer. Selvin et al. estimate that these
categories of cancer cover close to 50 % of all cancers. Each childhood
leukaemia case is given a residential location on a spatial map, Figure 30, the
four cancers reported are plotted in Figure 31.
It is immediately evident in
Figure 32 that there are higher childhood leukaemia rates in the eastern sector
compared to the western, northern and southern sectors. Antenna radiation
patterns and model calculations for all the antennae on the Sutra Tower, are
given by Hammett and Edison (1997). These show that readings and model
calculations give highest radiation intensities in the eastern sector. The
broadcasters aim their signals at the greatest population in the city and across
the Bay in Oakland and Berkeley. This is the first indication of a dose-response
relationship.
Figures 32 and 33 also reveal the lack of cancer and residence
in Golden Gate Park, the broad low density housing area of the Army Base, the
Presidio to the NW, a large park area and hills to shade suburbs to the SW, the
Central business district to the ENE the Lake Merced recreational area, and the
port and industrial area along the eastern coastline. These were all taken into
account when the residential population density was calculated below. In figure
32 the cluster 48-51 are residences on a western facing hill slope. They have
higher exposure levels from the Tower than the radial distance implies. They
contribute to the higher cancer rate in the 6-8 km ring compared with the 5-6 km
ring and explains some of the scatter about the dose response line.
Table 15:
Radial rings, with estimated population, Risk Ratios and Cumulative Risk Ratios,
for white childhood brain tumour, Leukaemia, Leukaemia + Lymphoma, and All
Cancer, in association with RF/MW exposure from the Sutra Tower, San
Francisco.
Distance (km) <0.99 1-1.99 2-2.49 2.5-2.99 3-3.49 3.5-3.99
4-4.49 4.5-4.99 5-5.99 6-8
Est. Population 1138 4334 3558 4489 5146 5566 4939
5386 8141 7988
Estimated personal mean dose
in µW/cm². 0.50 0.09 0.15 0.09
0.12 0.11 0.06 0.045 0.03 0.014
Symptom
Brain Tumour 11.81 2.48 3.02 1.80
2.09 1.93 1.63 1.00 0.99 1.01
Cumulative 11.81 4.42 3.87 3.18 2.88 2.66 2.49
2.26 2.02 1.86
Leukaemia 1.26 1.32 2.02 1.92 1.67 1.80 2.03 1.33 0.53
1.26
Cumulative 1.26 1.31 1.59 1.70 1.69 1.72 1.77 1.70 1.48 1.44
Leuk +
Lymph 2.47 1.08 2.63 2.08 2.54 1.85 2.27 1.56 0.57 1.05
Cumulative 2.47 1.37
1.86 1.94 2.10 2.05 2.08 2.00 1.73 1.62
All Cancer" 4.88 1.44 2.73 2.01 2.43
1.87 2.35 2.11 0.68 1.04
Cumulative 4.88 2.16 2.38 2.26 2.31 2.43 2.21 2.19
1.80 1.68
In order to calculate radial ring cancer rates a detailed map of
San Francisco was used to remove areas of ocean, park, hill shading, lakes, port
and central business district as outlined above, to make an estimate of the mean
residential population density in each ring. These factors are recorded in Table
15, which also shows the Risk Ratios for each childhood cancer group.
The
mean radial exposure regime, for this analysis, was assumed to be isotropic and
given by Figure 31. Direct exposures were reduced by a factor of 0.15 to allow
for mean residential exposure. These estimates are given in Table 15. Thus the
radial childhood cancer rates can be compared with a much more realistic radial
radiation exposure pattern. The resulting estimates are summarized in Table
15.
Figures 34 and 35 show extremely significant dose-response relationships
(p<0.0001) for Childhood brain tumor and All Cancer. The trend line passed
through zero within the uncertainty of the data.
The dose-response trend
analysis uses a least squares fit. The Mantel-Haenszel estimate of t with a
two-tailed t-test was used for the significance test. For All Cancer t = 14.05
and for Brain Tumour t = 13.70. For leukaemia (t = 3.31, p<0.01), Leukaemia
and Lymphoma combined (t = 3.81, p<0.005), Non-Hodgkin's Lymphoma (t = 1.94,
p><0.05) and Hodgkin's Lymphoma (t = 7.26, p<0.001).
Contrary to the
conclusion of Selvin et al. and ICNIRP (1998), who claim that this study shows
no evidence of adverse effects, the spatial data when related to actual radial
radiation exposure patterns forms significant linear dose-response
relationships, with All Cancer and Brain Tumour having extremely significant
dose-response relationships.
Figure 34: Brain Tumour Risk Ratio 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 linear dose-response relationship is extremely
significant (p<0.0001).
Figure 35: All Cancer Risk Ratio 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).
This results in the data in Selvin et al. (1992) show a very
highly significant dose response relationships which, when combined with other
epidemiological studies, shows a causal relationship between RF/MW exposure and
several childhood cancers, especially brain tumours, leukaemia, Hodgkin Lymphoma
and all cancer.
13.5 Beall, Delzell, Cole and Brill (1996) Brain Tumor among
Electronics Industry Workers:
ICNIRP (1998) claims that this study showed no
significant increases in nervous system tumours. This is factually wrong. The
overall results of Beall et al. (1996), as presented in their abstract is: There
was elevated ORs:
For 10 or more years of employment in engineering/
technical jobs (OR = 1.7, 95% CI: 1.0-3.0) or in programming jobs (OR = 2.8, 95%
CI: 1.1-7.0). The OR for glioma for all subjects who had accrued 5 years of
programming work 10 years before the case's death was 3.9 (95% CI:
1.2-12.4)."
These are statistically significant relationships. The subjects
were chosen and studied because of the possibility and concern that using VDTs
(Visual Display Terminals, i.e. computers) a great deal in their occupations.
VDTs expose workers to a wide range of EMR for long periods, could be related to
the increase in brain tumours. The researchers found differences between
different occupations who use VDTs in different ways.
For example, those in
manufacturing of VDTs they found OR = 0.8, while those in manufacturing VDTs who
also used them for programming, OR =1.5 (95%CI: 0.8-2.7) and those in
manufacturing VDTs who used them for information, OR = 1.3 (95%CI:
0.4-4.1).
Odd ratios for brain tumours increased with the longer times in
jobs using VDTs. After 10 years the engineering/technical jobs had an OR = 1.7
(95%CI: 1.0-3.0) and programming, OR = 2.8 (95% CI: 1.1-7.0). These show dose
response relationships, Figure 36.
Figure 36: Dose-response relationships for
brain tumor mortality from Table 3 in Beall et al. (1996). These show linear
dose-response relationships with years of using computers with the complex EMR
exposure from the VDT.
This study shows that the particular groups which use
live computers regularly have elevated Odds Ratios (increased levels of risk of
brain tumour), and significant increases after 10 years of service. For computer
programmers it is significant, p=0.04. The overall analysis, Figure 37,
comparing gliomas and all brain tumours, men, women and total groups all show
dose-response relationships but the relationship is not assessed as
statistically significant:
Figure 37: Dose-response relationships for all
brain tumors and Glioma for years of using VDTs.
The sample of men is
somewhat larger than that for women. Men show increasing risk of all brain
tumours and gliomas with the increasing work time with VDTs but women only show
an increase in the 10-19 year group. Only 4 women are in the (20yr-group. There
is a good evident reason for this. Women's employment is not usually as long as
men in these jobs.
Exposures to EMR from VDTs has decreased over the decades
with the introduction of low radiation" monitors. Measured RF/MW exposures at
the head level of a computer user, 0.5 m from the screen, have been measured at
0.1 to 5 µW/cm². Using a mean lifetime exposure factor of 0.25 , based on 0.3
for the time at/away from work and 0.8 for the time programmers are at/away from
the computer of 0.8, gives an estimated average lifetime exposure in the range
0.025 to 1.25 µW/cm². The range is of the same order of mean lifetime
residential exposure for the children in San Francisco who had a very
significant increase in brain tumour and other cancers with a dose-response
relationship.
Beall et al. (1996) does show statistically significantly
increases of brain tumours for those using VDTs in their work for more than a 2
decades. Several relationships also showed dose response increases with brain
tumours with longer periods of employment using VDTs, though the small sample
sizes limit the statistical significance, these are indicative of probable
relationship. The study is misrepresented by the ICNIRP reviewers as a study
that shows no effects.
13.6 Grayson (1996) : Radiation Exposure,
Socioeconomic Status, and Brain Tumor Risk in the U.S. Air Force: A nested
Case-Control Study".
The ICNIRP claim:
The ICNIRP (1998) paper claims that
this paper failed to show significant increases in nervous tumors". Grayson
actually shows the opposite conclusion.
13.6.2 The Context of this
Study:
Grayson acknowledges that EMFs are generally considered to be able to
promote cancer by interfering with intercellular communications but that
Balcer-Kubiczek and Harrison have observed that microwaves may act alone as
tumor initiators or as cocarcinogens. He also reviews several other
epidemiological studies which support the association between RF/MW exposure and
brain tumors. Eighteen such studies have been identified by the present author.
Grayson cites Thomas et al. (1987) who found a significant dose-response
relationship for Astrocytoma, the most common form of brain tumour, and years of
service in the electronics industry, with a co-carcinogenic relationship with
lead from solder fumes. The RF/MW exposure had the greater effect.
A study
published earlier in 1996, Grayson and Lyons (1996) investigated the incidence
of cancer in United States Air Force Aircrew. Aircrew are moderately exposed to
ELF and RF/MW during their flight times and on bases. Grayson and Lyons found
that Aircrew had significantly higher cancer rates than other USAF officers, RR
= 1.31 (95%CI: 1.11-1.54, n=342). For brain tumor the incidence was elevated, RR
= 1.20 (95%CI: 0.52-2.78, n=13), but not significantly so, largely because of
the small case sample size (n). For other cancers, cancer of the testes and
urinary bladder were significantly elevated.
Grayson notes that EMF (ELF)
studies generally found negative results or suggest a small excess risk. Sahl,
Kelsh and Greenland (1993), Tynes, Jynge and Vistnes (1994) found no increase in
brain tumor in electric utility or railway workers. Theriault et al. (1994)
found an elevated risk (OR = 1.95, 95%CI: 0.76-5.00) and Floderous et al. (1993)
a significantly increased risk (OR= 1.5, 95%CI: 1.0-2.2) in electrical
workers.
Mack, Preston-Martin And Peters (1991), Speers et al. (1988) and
Loomis and Savitz (1990) found highly significant increases; and Lin et al.
(1985), Thomas et al. (1987), Preston Martin, Mack and Henderson (1989) found
significant dose-response relationships for increased brain tumors in EMR
exposed populations. Using the EMR Spectrum Principle, this amounts to very
strong evidence which is indicative of a causal relationship.
13.6.3
Grayson's results:
Grayson carried out a job title-time-exposure matrix
utilising potential intensity scores for both ELF and RF/MW EMR exposures. Data
on ionizing radiation exposure was also available.
Although the present study
has its limitations, particularly in exposure estimation, it does suggest that
there is a small association between potential EMF exposures and brain tumor
risk among Air Force members, especially for personnel potentially exposed to
Radiofrequency/microwave EMFs."
The results for the three types of radiation
exposure, after adjustment for: Age-race-senior military rank, were:
Ionizing
Radiation OR = 0.58 95%CI: 0.22-1.52
ELF Radiation OR = 1.28 95%CI:
0.95-1.74
RF/MW radiation OR = 1.39 95%CI: 1.01-1.90
The relationship for
age-race adjusted Odds Ratios for rank were:
Rank OR = 2.11 95%CI:
1.48-3.01
Senior Rank OR = 3.30 95%CI: 1.99-5.45
The ELF and RF/MW
exposure results are consistent with the second part of the EMR Spectrum
Principle, that there are likely to be stronger effects at higher frequencies.
These results are consistent with and confirming of the studies cited above,
section 13.6.2.
The rank-related results are independent of the
exposure-related results. They raise the question of the influence of
socio-economic status, which is accurately represented by military rank. Preston
Martin (1989) and Preston-Martin et al. (1993) also find that brain tumour risk
increases with socio-economic status.
Grayson (1996) is far from a no
effects" study. Thus far consistently the ICNIRP claims are scientifically wrong
and misleading. This study does show a small but statistically significant
increase in brain tumour from RF/MW exposure.
13.7 Rothman, Chou, Morgan,
Balzano, Guy, Funch, Preston-Martin, Mandel, Seffens and Carlo (1996):
Assessment of Cellular Telephone and Other Radiofrequency Exposure for
Epidemiologic Research.
The Context:
This and the next paper, Rothman et
al. (1996 a and b), are used to imply that there is "no excess total mortality
was apparent among uses of mobile phones". This is the ICNIRP context of citing
papers, as the six above are quoted, claiming that they show no increases or no
significant increases in brain tumour or cancer. This paper, Rothman et al.
(1996a), is the description of an epidemiological study in progress about the
potential association of mobile phone use and brain tumour.
An important
feature of radiation is the contrast between ionizing and non-ionizing
radiation. The threshold for the ability of a photon to strip and electron off
an atom, forming an ion, is a photon energy or 12.4 eV or a wavelength of 100
nm, Hitchcock and Patterson (1995). By this criteria, ultraviolet radiation,
with a wavelength range of 200 to 400 nm is not ionizing radiation. However, the
spectrum in Rothman et al. (1996a) shows UV radiation as part of the ionizing
radiation segment. This may be because UV radiation is shown to produce skin
cancer and cause immunosuppression in people, Gochfeld et al. (1995). With the
assumption of many people that cancer can only be caused by ionizing radiation
and not by non-ionizing radiation, then rather than accepting that non-ionizing
UV radiation does cause cancer, they prefer to change the definition.
The
Conclusion:
ICNIRP's follow up statement is actually true: "but it is still
too early to observe an effect on cancer incidence or mortality". The latencies
of brain tumours is decades. This is not an appropriate paper to cite in a
cancer assessment because it has no evidence value for or against the incidence
of cancer in RF/MW exposure.
13.8 Rothman, Loughlin, Funch and Dreyer (1996):
Overall Mortality of Cellular Telephone Customers"
This study was prompted by
case reports of brain cancer among cellular telephone users. To evaluate the
possible effect of using cellular telephones on the risk of death they compared
the rates of mortality between mobile phone users and portable phone users. For
the cancer latency reasons above it is a very preliminary report. The authors
state:
First, they do not directly address the issue of the relationship
between cellular telephone use and brain cancer, which comprises only a small
proportion of deaths. Second, the time between exposure to radio frequency
energy from portable cellular telephones and the death endpoints that we
measured was comparatively short, and our study therefore addresses only
short-term effects."
Both mobile and portable phone users have lower
mortality rates than the general population. However, there are differences
between these two groups. This paper is a prime example of how to obscure
significant results. They conclude that for users with phone accounts at least 3
years old, portable phones produce a lower mortality risk than mobile phones, MR
= 0.86 (90% CI: 0.47-1.53). This is deliberately avoiding the alternative true
statement that mobile phone users have a higher mortality rate than portable
phone users. They also use a 90% confidence interval rather than the normal 95%.
Their data, Table 1, shows for all ages, significantly higher death rates among
cell phone users. The following is the result of a 2x2 analysis for all men, all
women and all people:
RR 95%CI p-value
For men: 1.40 1.06-1.86
0.017
For women: 1.52 0.78-2.95 0.31
All people: 1.38 1.07-1.79
0.013
Since the portable phone users are exposed to RF/MW radiation they are
not an unexposed group. Hence the difference is likely to be larger. A crude
analysis of mortality with years of phone usage showed RR = 1.35 for 2 yrs and
RR = 1.56 for 3 yrs. When adjusted for confounding, these reduced to 1.075 and
1.163 respectively. This shows that the adjusted comparative mobile phone
mortality elevation more than doubles from 7.5% to 16.3 % with the extra year of
usage.
Therefore, in the context of a cancer assessment, this paper does not
identify the cause of death and therefore is not a cancer assessment. The
authors hide the results by reversing the comparison. Overall the study does
show that for a large (256,284) 1 year sample there is a significantly higher
mortality rate among mobile phone users compared with portable phone users,
especially among older people, and increases with years of usage.
13.9
Interim Conclusions (Papers 1 - 8.):
All of the first 8 papers or reports
cited by ICNIRP with the clear intention of dismissing the possibility of cancer
being related to RF/MW exposure. All are inappropriately or incorrectly cited.
In some cases they are deliberately, misquoted and misused. In reality the
reverse of what ICNIRP claims is true. Often the data challenges the
conclusions.
Two of the papers, Barron and Baraff (1958) and Rothman et al.
(1996a) are inappropriately included when they are not giving epidemiological
results of cancer resulting from RF/MW exposure.
The remaining six reports or
papers all show statistically significant increases in mortality from RF/MW
exposure, including cancer of various body organs, especially brain tumour and
leukaemia. Three of them also show significant dose-response relationships for a
range of cancer, including respiratory cancer, Robinette et al.; Brain Tumour,
Leukaemia, Hodgkins and Non-Hodgkin's Lymphoma and All Cancer, Selvin et al.,
and Brain Tumour, Beall et al.. Lilienfeld et al. (1978) shows significant dose
response increases in a range of illnesses. Rothman et al. (1996b) shows
significantly increased mortality from mobile phone usage, increasing in a dose
response manner with years of usage.
Two of these, Lilienfeld et al. and
Selvin et al., show results with extremely low mean residential RF/MW exposures,
one moderate to low exposures from computer screens and two moderate to high
exposures from military radio and radar radiation. The residential study shows
that statistically significant increases in childhood cancer occur in a
dose-response manner. For All Cancer, Selvin et al.(1992), the threshold is near
to zero.
14. Studies acknowledged
by ICNRIP to show increases in cancer from RF/MW exposure:
In this
section there are five papers covering three studies. Szmigielski et al. (1988)
and Szmigielski (1996) cover the Polish Military Study, Dolk et al. (1997a and
b) cover the U.K. Regional TV Tower Study and Hocking et al. cover the North
Sydney Broadcast Tower Study.
14.1 The Polish Military Study:
Szmigielski,
Bielec, Lipski and Sokolska (1988): Immunologic and Cancer-Related Aspects of
Exposure to Low-Level Microwave and Radiofrequency Fields" , and
Szmigielski
(1996): Cancer morbidity in subjects occupationally exposed to high frequency
(radiofrequency and microwave) electromagnetic radiation".
ICNIRP
Dismissal:
ICNIRP's complete, comprehensive and in-depth assessment of this
project is fully quoted in the following two sentences:
There has been a
report of increased cancer among military personnel (Szmigielski et al. (1988)),
but the results of the study are difficult to interpret because neither the size
of the population nor the exposure levels are clearly stated. In a later study,
Szmigielski (1996) found increased rates of leukaemia and lymphoma among
military personnel exposed to EMF fields, but the assessment of EMR exposure was
not well defined."
This is a woefully inadequate and thoroughly
unprofessional treatment of this large and significant epidemiological study.
The ICNIRP response represents a total misunderstanding or misrepresentation of
epidemiology and the results of this study.
Cancer Epidemiology:
Most
cancer studies use data from cancer registers that cover several decades to
allow for cancer latencies These registers involve the large populations are
necessary for statistical quality and significance. Retrospective studies, such
as cohort and case control studies rarely, have records of the hourly or daily
mean exposure of every participant for the period of the register. Hence
occupational activities involving exposure to a potential disease agent is the
most common surrogate for exposure. Sometimes a job exposure matrix assessment
is undertaken of a typical sample of tasks involved in a job. This improves the
exposure assessment but it remains an estimate of potential or probable
exposure. Because of these practical limitations epidemiology is based on
careful selection of occupational groups in order to compare morbidity and
mortality rates between exposed and non-exposed or low exposure control
groups.
Hence many studies involve "electrical occupations", "power station
workers", "electric train drivers", "electric utility workers", "computer
programmers", "sewing machine operators", "TV repairmen", etc... Their cancer
and illness rates are then compared with a set of controls who are selected
because they have the same age-race-income-geographic- ... characteristics to
make them as similar as possible to the exposed people with the one exception of
the exposure.
Polish Military Exposure Assessment:
Years of service become
a reasonable estimate of cumulative exposure and thus a source of a
dose-response gradient. For some occupations the EMR exposures are intermittent
and associated with a particular activity. For example, physiotherapists using
RF/MW heating for diathermy prior to muscular manipulation. Their exposures are
generally for only a minute or two after the machine has been turned on. The
monthly number of treatments is a good measure of the cumulative monthly dose or
the monthly mean exposure.
Thus, most EMR epidemiological studies rely solely
on occupational descriptions as a surrogate for exposure. Refinements include
job exposure matrix surveys or reported exposure incidents. In this later case
any exposure radiation from an active radio antenna or radar antenna is reported
and recorded, along with the estimated level of exposure and time of exposure.
This is because strict daily limits are maintained based on cumulative dose.
This is the EMR Hygiene reporting regime. It has been used in the Polish
Military since about 1968. Hence the Polish Military Study uses one of the more
advanced exposure assessment regimes of any study published. Szmigielski (1996)
states:
"Data on exposure of personnel to RF/MW were collected from EM
military safety groups operating as health hygienic services. These groups are
responsible for measurements of RF/MW field intensities at and around service
posts where EM emitting equipment is used, repaired or serviced, and keep health
records of personnel working on these posts. The number of personnel considered
to have been exposed occupationally to RF/MW was easily established, but the
evaluation of the exposure rate appeared to be quite difficult."
Thus to be
considered as a member of the exposed group, exposure episodes were required to
be recorded. All other personnel are used as controls. This is one of the most
advanced exposed group selection criteria ever used.
Population
Description:
The data set used by Szmigielski et al. was 1971-80, and
Szmigielski (1996) updated this to use 1971-85. Szmigielski et al. state:
The
total population of career servicemen (in the Polish armed forces) was analyzed,
and a subgroup of personnel exposed occupationally to MW/RF radiation (on the
basis of service records) was developed; the E (exposed) group counted about 3 %
of the total population, the rest (97%) was considered as subjects without
exposure to MW/RFs (the NE group)."
Szmigielski (1996) explained that over
the 15 years there is a slight year to year variation in the population but it
averages 128,000 person each year with 3700 being RF/MW exposed. The data set is
somewhat larger than that used by Robinette et al. (1980) and exposure
dichotomization is significantly better. Over the 15-year data set there are
1.92 million p-yrs in the control group and 55,500 p-yrs in the RF/MW exposed
group.
Thus the Polish Military study is a very large study with a well
defined population with a high quality criteria for identifying the exposed vs
control groups. ICNIRP is wrong in its criticism and wrong to dismiss this
highly significant study.
14.1.5 The Results of Szmigielski et al.
(1988)
14.1.5.1 Health Effects Assessment:
Szmigielski at al. are acutely
aware that evidence of immunological impairment with RF/MW exposure is evidence
of increased cancer risk since the immune system is a vital part of the cellular
repair mechanism of our bodies. Hence they first review evidence that RF/MW
impairs the immune systems in cells and animals.
14.1.5.2 Cell line (In
Vitro) studies:
They found and present evidence of immunosuppression and
immunostimulation associated with RF/MW exposure of cells to a wide range of
frequencies, modulations and intensities. This is related to the hypothesis of
Professor Ross Adey and his group about the modification of calcium ion binding
at the cell membrane surface, and its flow on effects into the signal
transduction regulation of the cells. We are now aware that both calcium ion
efflux and influx occur at different combinations of RF/MW signal impacting on
the cell membrane. This is consistent with immunosuppression and stimulation
respectively.
14.1.5.3 Whole animal (In Vivo) Studies:
Short-term
exposures of experimental animals to low level RF/MW initially confused thermal
effects with non-thermal effects. Careful control of exposure and better
handling of animals found consistent transient and reversible increase
lymphocyte proliferation and function. However, that time there was not
convincing in vivo evidence of immune system impairment from short-term RF/MW
exposure, and, at that time There are no experiments in vivo involving exposure
of animals to low-frequency modulated MW with examination of the immune
functions. On the other hand, as discussed below, both the higher susceptibility
of animals to chronically exposed bacterial and viral diseases, and the data on
acceleration of development of neoplasms in mice exposed for months in
non-thermal MW fields (the two phenomena that might result from suppression of
immune functions in chronically exposed subjects) emphasize the problem of the
response to long-term low-level irradiation in MW/RF fields, and they call for
further investigation."
However, Szmigielski et al. appear to be unaware of
Shandala et al. (1983) which did find a highly significant (78%) and persistent
suppression of the immune system rats when exposed to 500 µW/cm² for 3
months.
14.1.5.4 Integrated evaluation of immunity in MW/RF exposed
animals:
Szmigielski et al. outline their own experiments in this area. They
conclude:
An overview of the available and of our own findings suggests the
existence of a biphasic reaction of the immune system to MW/RF radiations -
stimulation of the whole system (mainly humoral immunity) after a single or few
days exposures, followed by gradual, but transient, suppression of the whole
immunity with prolongation of the exposure period (up to several months) and/or
increasing power density of the fields. Stimulation and suppression of immunity
in MW/RF exposed animals both seem to be transient and inconsistent phenomena.
At low power densities the system recovers soon after exposure."
This raises
the question, what happens if exposure continues for years?
14.1.5.5 Cancer
related aspects of exposure to low-level microwave fields:
Human populations
contain a wide range of people, including those with already compromised immune
systems. The evidence that chronic exposure of animals can suppress their immune
system with some combinations of parameters of low-level microwave exposure
promoted the study of the effects of MW exposure on cancer prone mice. This was
a precursor for looking for cancer in MW exposed human
populations.
Szmigielski et al. planted cancer cell in the lungs and on the
skin of mice and chronically exposed them to non-thermal intensities of 2.45 GHz
microwaves. The tumors grew faster and the mice died earlier in the exposed
compared to the sham exposed mice. The MW exposed mice with induced skin cancer
showed 50 % died after 137 days, compared to 305 days for the sham exposed mice,
Figure 38.
Figure 38: Growth curves of 3,4-benzo-alpha-pyrene (BP) induced
skin tumour in mice exposed daily (2 hours) to 2450 MHz radiation at 10 mW/cm²
(SAR 4 W/kg) for a whole period of tumour growth. CDT50, cancer development time
for 50% of the animals.
The lung tumors which all started at near 2 x 105
viable cells. After 3 months, the control group stayed close to 2 (x 105), while
the exposed mice rose to 6 and 15 for 5 and 15 mW/cm² respectively, Figure
39.
Figure 39: Number of lung tumours (following intravenous injection of 2 x
105, viable sarcoma cells) in mice exposed during 1, 2, 3 months to 2450 MHz
microwaves (2 hours daily), at 5 or 15 mW/cm². Oc mice were treated with
nonspecific stress of overcrowding (confinement in cages with out exposure to
microwaves, as positive controls. Control: sham exposed mice).
Figure 39
shows a dose response relationship for the growth of cancer nodules as a
function of microwave exposure level.
Szmigielski et al. then showed that
microwaves on their own and with a cancer promoter, significantly enhanced
cyclic AMP activity in urine epidermis (scraped) samples in mice.
They
concluded:
On the basis of Balcer-Kubiczek and Harrison's reports, an the
above investigations of his own group, Adey (personal communication) recently
offered his own concept and initial model of the cancer-promotion process and
its influence by MW/RF fields modulated at low frequencies. The promotion
appears to relate to a distorted inward stream of signals from the cell membrane
to the nucleus (where carcinogenesis was already initiated by other factors) and
to intracellular organelles. MW/RF modulated at low frequencies may in certain
cases (depending upon modulation and time exposure)) act synergistically with
the action of promoters, activating the same membrane receptors."
Hence,
prior to presenting their human study of cancer in MW exposed military
personnel, Szmigielski et al. outline a strong evidence trail indication the
probability of cancer being found based on cellular and animal experiments,
based on immune system impairment, and synergistic activity of RF/MW with other
cancer initiators and promoters.
14.2 Polish Military Study
(1971-80):
Placing the study in context, the authors note several previously
published studies showing increases cancer (McLaughlin (1953)), in leukaemia
with radar exposure (Lester and Moore (1982)), Milham (1982) and Wright (1982),
and Vagero and Olin (1983).
They note that Robinette et al. (1980), the
Korean War Study, reported no significant differences between high and low
exposure groups, but point out:
However, when three sub-groups of the
high-exposure group were developed to provide a gradient of potential exposure,
a trend appeared for increased number of malignant neoplasms in the sub-group
rated as highly exposed."
They also refer to weakness of the Korean War study
in terms of its size and subject selection. They didn't investigate the Korean
War Study data in depth as is done here. The preliminary results of the Polish
Military Study, using the 1971-80 data set, is presented in Figure 40 and
41.
Figure 40: Cumulative yearly morbidity rate of neoplasms during 1971-80
(expressed as the number of new cases per 100,000 person years) for all ages
(20-59 years) in MW/RF exposed subjects and non-exposed subjects.
The top
histogram shows organ localization of malignancies for oral cavity; pharynx and
larynx; esophagus and stomach; colo-rectal, liver and pancreas; lungs; bones;
skin including melanoma; kidneys-urogential tract- prostate; eyes and central
nervous system; thyroid gland and other endocrine glands; hematopoietic and
lymphatic organs.
The high incidence of cancer of the hemato-lymphatic organs
allows the break down given in the lower half of the diagram. LGR: malignant
lymphogranulamatosis; LS, LM, lymphosarcomas and lymphomas; CLL, chronic
lymphatic leukemia; ALL, acute lymphoblastic leukemia; CML, chronic myelocytic
leukemia; AML, acute myeloblastic leukemia and PL, plasmocytoma (plasma cell
leukemia).
This data shows that the microwave exposed group, compared to the
low exposure group, had increased malignancies in every category of organ,
significantly increased in esophagus and stomach, colo-rectum, skin cancer
including melanoma and thyroid, and highly significant in blood and lymph
organs. Individual leukemia's which were significant were Acute Myeloblastic
leukaemia and highly significant were chronic myelocytic leukaemia and
lymphosarcomas and lymphomas.
The decadal age category results are presented
in Figure 41.
Figure 41: Cancer morbidity rates in RF/MW exposed and
non-exposed" personnel for all types of malignancies at various age
groups.
Note the largest differences at the age group 40-49 years and
statistical significance of differences for all age groups. The Chi Squared
values indicate that the differences are much more significant than p<0.01,
they are actually p<0.001. This analysis shows that RF/MW exposure initiates
earlier cancer and accelerates it in the young and middle decades, 20-49. The
difference is reduced a little in the oldest age group as the reference cancer
rate accelerates rapidly in the 50+ age group.
14.3 Polish Military Study
(1971-85):
Szmigielski (1996) is a follow-up study from the previous study,
adding a further 5 years of morbidity data. With the larger data set the
significance of the observed increases in cancer are increased. The data is
summarised in three tables, in parallel with the summary diagrams of Szmigielski
et al. (1988) above, showing morbidity of body organs, haemopoietic malignancies
and age-grouped relationships.
As in the 1988 analysis, this data shows that
RF/MW exposure increases cancer across the body with elevated Risk Ratios, and
several organs show significantly and very significantly higher cancer rates,
including Esophageal and stomach cancer, Colorectal cancer, Skin cancer, Brain
and CNS cancer and all malignancies, Table 16.
Table 16: Incidence of
neoplasms (per 100,000 subjects annually) in military personnel exposed and
non-exposed (control) to radiofrequency and microwave radiation, Szmigielski
(1996).
Localization of malignancies Incidence Incidence Risk Ratio 95% CI
p-value
(Expected) (Exposed) interval
Pharynx 1.96 2.12 1.08 0.82-1.24
N.S.
Esophageal and stomach 4.83 15.64 3.24 1.85-5.06 <0.01
Colorectal
3.96 12.65 3.19 1.54-6.18 <0.01
Liver, pancreas 2.43 3.58 1.47 0.76-3.02
N.S.
Laryngeal, lung 21.89 23.26 1.06 0.72-1.56 N.S.
Skin, including
melanomas 3.28 5.46 1.67 0.92-4.13 <0.05
Nervous system including brain
2.28 4.36 1.91 1.08-3.47 <0.05
tumour
Thyroid 1.38 2.12 1.54 0.82-2.59
N.S.
Haematopoietic system and 6.83 43.12 6.31 3.12-14.32
<0.001
lymphatic organs
All malignancies 57.60 119.12 2.07 1.12-3.58
<0.05
The Haematopoietic and Lymphatic cancers are very highly
significantly elevated and so are separated further in Table 17.
Table 17:
Incidence of haemopoietic and lymphatic malignancies (per 100,000 subjects
annually) in military personnel exposed and non-exposed (control) to
radiofrequency and microwave radiation.
Localization of malignancies
Incidence Incidence Risk Ratio 95% CI p-value
(Expected) (Exposed)
interval
Hodgkin's disease 1.73 5.12 2.96 1.32 - 4.37 <0.05
Lymphoma
(non-Hodgkin 1.82 10.65 5.82 2.11 - 9.74 <0.001
and
lymphosarcoma
Chronic lymphacytic leukaemia 1.37 5.04 3.68 1.45 - 5.18
<0.01
Acute lymphoblastic leukaemia 0.32 1.84 5.75 1.22 - 18.16
<0.05
Chronic myelocytic leukaemia 0.88 12.23 13.90 6.72 - 22.12
<0.001
Acute myeloblastic leukaemia 0.71 6.12 8.62 3.54 - 13.67
<0.001
Total 6.83 43.12 6.31 3.12 - 14.32 <0.001
In the 1988 data
analysis, three sub-categories of leukaemia and lymphoma were significantly
increased with RF/MW exposure. In this larger data set all are significantly
increased and 4 are very highly significantly increased, Lymphoma, Chronic
Myelocytic Leukaemia, Acute Myeloblastic Leukaemia and Total
leukaemia/lymphoma.
The age-group relationships show the same initiation and
advancement of the cancer rate in the exposed group. Table 18 shows that the
Risk Ratio decreases with increasing age as the unexposed cancer rate increases
due to normal aging processes. The Haemopoietic/lymphatic cancers are all highly
significantly increased in every age group.
Table 18: Incidence of neoplasms
(tumors) (per 100,000 subjects annually) in age groups of military personnel
exposed and non-exposed (control) to radiofrequency and microwave radiation,
Szmigielski (1996).
All sites:
Age Group Incidence Incidence Risk Ratio
95% Conf. p-value
(Expected) (Exposed) interval
20-29 11.62 21.11 2.33
1.23 - 3.12 <0.05
30-39 18.37 42.28 2.30 1.04 - 3.06 <0.05
40-49
84.29 161.62 1.92 0.98 - 2.84 <0.05
50-59 186.71 274.13 1.47 0.92 - 2.21
N.S.
All Ages 57.6 119.12 2.07 1.12 - 3.58
<0.05
Haemopoietic/lymphatic
malignancies
20-29 2.12 17.30 8.16 3.11
- 22.64 <0.01
30-39 3.08 26.43 8.58 3.46 - 19.58 <0.01
40-49 8.32
73.25 8.80 4.13 - 15.27 <0.01
50-59 24.13 108.62 4.47 2.56 - 6.81
<0.01
All ages 6.83 43.12 6.31 3.12 - 14.13 <0.001
14.4 Polish
Military Preliminary Prospective Study Results:
Szmigielski (1998) is a
prospective study on exposed Polish Military personnel between 1986 and 1990. He
concludes that the data suggests that cancers develop faster, with a shorter
latency period" in servicemen with occupational RF/MW exposures. He also found a
dose-response relationship with cancer rate against maximum microwave exposure.
Individual exposure monitoring places 92.8% of the exposed men in situations
where peak exposures were less than 1000 µW/cm², and 83.7 % below 600 µW/cm².
This data also includes the all cancer risk ratio for these groups of
people.
Table 19: Cancer rates as a function of typical peak exposures in a
prospective study extending the Polish Military study, Szmigielski
(1998).
Number of Men Peak Exposure Range Cancer Rate Ratio
µW/cm²
1900
(49.4%) 100-200 1.69
1320 (34.3%) 200-600 1.57
350 (9.1%) 600-1000
4.62
280 (7.2%) >1000 4.93
14.5 Simplified peak and mean exposure
regime:
Based on the Polish Military study measurements the following
simplified exposure regime has been proposed. The simplified regime could
consist of life-time means being half of annual means while working, annual mean
is 20% of the weekly working mean, the weekly peak is 10 times the weekly mean
and the monthly peak is 10 times the weekly peak. For example:
Table 20:
Estimated life-time, annual, weekly mean and weekly and monthly peak exposure
relationships.
Exposure Exposure ( µW/cm²) _
Category Life-time Mean
Annual Mean Weekly Mean Weekly Peak Monthly Peak
High 10 20 100 1,000
10,000
Medium 5 10 50 500 5,000
Low 2 4 20 200 2,000
14.6
Conclusions:
The three published papers in the Polish Military cancer
morbidity study shows that RF/MW is associated with increased cancer in many
major organs of the body, with the highest risks occurring for Leukaemia and
Lymphoma. A dose-response relationship has been found for the latest study which
is a prospective study following a large number of exposed servicemen and
monitoring their peak exposures associated with their military work.
The
significance of these studies cannot be dismissed because of exposure
uncertainties. There is a very good separation of exposed and low exposure
populations through one of the world's most advanced personnel exposure
monitoring systems. These are also one of the largest of any study thus far.
Hence the ICNIRP criticism of these studies is completely unfounded.
These
studies, when taken together with the other studies presented here, show a
causal relationship between exposure to RF/MW and sickness and death due to
cancer increases and very low, mean life-mean exposure levels. All peak
exposures are non-thermal (Szmigielski pers. comm.).
15. Residential
Studies:
15.1 Introduction
We have already seen that the residential
study in San Francisco showed-dose response related childhood cancer death,
brain tumor and leukaemia for residential exposure to low intensity microwaves
from a TV/FM tower on Mt Sutra. Szmigielski shows that the highest effect of
RF/MW exposure of military personnel is Leukaemia and Lymphoma.
ICNIRP cites
two residential studies contained in three papers, Hocking et al. (1996) and
Dolk et al. (1997a. and b.). They are described by ICNIRP as have suggested a
local increase in leukaemia incidence", but the results are
inconclusive."
ICNIRP consistently uses very simple statements to dismiss any
adverse effects. Every time a careful consideration of principles, methods,
application of epidemiological approaches and consideration of the actual data
and exposure regimes, produces a significantly different conclusion. And when
sets of studies are considered together, very strong conclusions are drawn.
These studies are no exception.
15.2 Hocking, Gordon, Grain and Hatfield
(1996): Cancer incidence and mortality and proximity to TV towers."
The Study
Context:
This study was carried out to allay public fears about siting cell
sites in residential properties in Australia, Hocking (pers. Comm.). The authors
correctly recognized that mobile phone base stations (cell sites) have not been
exposing people long enough to produce cancer because of the cancer latency
periods are long. Because of the then dominance of analogue cell phones using FM
radiation they decided to study the residents exposed to FM signals from FM
radio and TV stations around three tall towers in North Sydney. When the study
was commenced Dr Hocking was the Medical Director of the Telstra Research
Laboratory. At the time of publication Dr Hocking had become an independent
public health consultant and the paper was published with the support of his
professional colleagues.
15.2.2 The population Sample:
The cancer data
covered 9 municipalities in the north side of Sydney Harbour for the period 1972
to 1990, Figure 42.
Figure 42: Municipalities in northern Sydney and the TV
towers (numbered 1, 2 and 3). The circle has a 4 km radius and is for reference
only. Willoughby, Lane Cove and North Sydney are the inner exposed"
municipalities, Hocking et al. (1996).
The exposed population was chosen to
the three municipalities that surrounded three large TV towers, Lane Cove,
Willoughby and North Sydney. This gives an "exposed" population of 135,000. The
control group came from six surrounding municipalities, Ryde, Ku-ring-gai,
Warringah, Manly, Mosman and Hunters Hill, population 450,000, Figure 40.
The
cancer incidence (mortality) cases were adjusted for sex, age and calendar
period and resulted in 1206 (847) leukaemia cases for the total population and
134 (59) for children 0-14 years. For brain tumour the sample was 740 (606) for
the total population and 64 (30) for children.
15.2.3 Exposure
situation:
There are three towers. The frequencies involved are in the range
63 - 219 MHz and 626-633 MHz. Tower 1 has the highest TV/FM output power, 500
kW, while Tower 2 has 180 kW and Tower 3, 110 kW. The exposure of each
municipality is also a function of the horizontal radiation patterns. See
Figures 6 for example. One of the horizontal transmission patterns from North
Sydney is given in Figure 43.
Figure 43: A horizontal radiation pattern for
one North Sydney transmitter.
Figure 43 shows a 6-peak pattern with the peak
rotated towards the SW. This is appropriate to reach the largest population in
the viewing area, as for the patterns in Figure 6. The SW peak is over Lane
Cove. Most of the Lane Cove population lives with 2.5 km of the towers, Figure
40. The centre of North Sydney is on the side of the SE peak and the centre of
Willoughby is at the low point between the two northern peak which cover the
sides of Willoughby. If the exposure of the centroid was assessed this would
rank Lane Cove, North Sydney and Willoughby from high to low. This would then
produce a dose response in the adult leukaemia rates that are 16.7 (9.7-26.8),
7.1 (2.8-14.6) and 6.1 (3.0-10.8) respectively.
This suggests that the Lane
Cove population could experience the highest mean exposure and North Sydney the
second highest. Towers 1 and 2 were increased to these high powers in 1980 with
the addition of 340 kW to Tower 1 and 70 kW to Tower 2. In terms of cancer, this
is likely to influence the childhood leukaemia and brain tumor rates more than
the adult rates because of longer adult cancer latencies and their age
structure.
Two exposure estimates were cited by Hocking et al. The first
estimate is expressed as a function of radius from the centre point of the three
towers. At the center between the towers this gave 1 µW/cm². The highest
calculated exposures were between 4 to 8 µW/cm² in a narrow ring at about 1 km.
This would be a result of the VHF transmissions. These are the areas immediately
adjacent to each of the towers where few people reside. Outside this the
calculated exposure declines as an inverse square to be 0.2 µW/cm² at 4 km, the
limit of the "exposed" population, Figure 44.
Figure 44: Logarithm of the
calculated power densities (in µW/cm²) for TV signals from the three TV towers
against distance from the centre of the towers.
The second data set was a
number of actual readings taken by the Commonwealth Dept of Communications.
These were generally about 1/5th of the calculated values at any point. This is
largely explained by sheltering effects of the line-of-site signals, by hills
and buildings. It must also be remembered that the population spends a
proportion of its time inside, typically at least 10-12 hours, during which the
RF exposure will be significantly reduced. A factor of 2 is conservative and is
still likely to over estimate the mean population exposures. The results of the
calculated and measured exposures are given in Figure 44.
The lower limit at
the 4 km circle, enclosing the "exposed" population, the estimated mean
residential exposure (50% of measured) is 0.025 µW/cm² or 25 nW/cm². With the
population of greater Sydney being to the SW of the towers it is probable that
their horizontal antenna pattern is similar to Figure 6b, giving much lower
exposures to Willoughby and lower exposures to North Sydney than to Lane Cove at
the same radial distance.
15.2.4 North Sydney Study Results:
Hocking et
al. shows statistically significantly increased incidence and mortality for
total leukaemia, Lymphatic Leukaemia and Other Leukaemia for the whole
population, with Risk Ratios in the range 1.09 to 1.67 for leukaemia incidence
and 1.01 to 1.57 for leukaemia mortality. The highest relationship is for
Lymphatic Leukaemia mortality, RR = 1.39 (95% CI: 1.00-1.92), Table 21.
For
childhood leukaemia the relationships are generally stronger even though the
sample size is smaller. Significant relationships exist for Total Leukaemia and
Lymphatic leukaemia incidence and mortality.
Table 21: Rate Ratios (RR) and
95% confidence intervals (CI) for cancer incidence and mortality in the
population of the inner area compared to the outer area, adjusted for age, sex
and calendar period.
Cancer Type RR (95% CI) Cases
Incidence
Brain
Tumour 0.89 (0.71-1.11) 740
Total Leukaemia 1.24 (1.09-1.40)
1206
Lymphatic Leukaemia 1.32 (1.09-1.59) 536
Myeloid Leukaemia 1.09
(0.91-1.32) 563
Other Leukaemia 1.67 (1.12-2.49) 107
Mortality
Brain
Tumour 0.82 (0.63-1.07) 606
Total Leukaemia 1.17 (0.96-1.43) 847
Lymphatic
Leukaemia 1.39 (1.00-1.92) 267
Myeloid Leukaemia 1.01 (0.82-1.24)
493
Other Leukaemia 1.57 (1.01-2.46) 87
The strongest relationship is for
childhood lymphatic leukaemia death, RR=2.74 (95%CI: 1.42-5.27). The study found
that 59 children had died from having leukaemia when the expected number was
25.43, an excess of 33.6 deaths. For childhood lymphatic leukaemia 39 children
died when 14.2 were expected, an excess of nearly 25 children, Table 22.
The
authors searched diligently for confounding factors, including social economic
factors, air pollution (benzene), ionizing radiation, migration, hospitals, high
voltage power lines and local industries. None affected the relationships found.
They investigated the possibility of clustering and found that no significant
heterogeneity was found (p=0.10 for incidence and p=0.13 for
mortality).
Table 22: Rate Ratios (RR) and 95% confidence intervals (CI) for
cancer incidence and mortality in childhood (0-14 years) in the population of
the inner area compared to the outer area, adjusted for age, sex and calendar
period.
Cancer Type RR (95% CI) Cases
Incidence
Brain Tumour 1.01
(0.59-2.06) 64
Total Leukaemia 1.58 (1.07-2.34) 134
Lymphatic Leukaemia
1.55 (1.00-2.41) 107
Myeloid Leukaemia 1.73 (0.62-14.81) 9
Other Leukaemia
1.65 (0.33-8.19) 8
Mortality
Brain Tumour 0.73 (0.26-2.10) 30
Total
Leukaemia 2.32 (1.35-4.01) 59
Lymphatic Leukaemia 2.74 (1.42-5.27)
39
Myeloid Leukaemia 1.77 (0.47-6.69) 11
Other Leukaemia 1.45 (0.30-6.99)
9
15.2.5 North Sydney Study Critique:
McKenzie, Yin and Morrell (1998)
produced a very useful critique of Hocking et al. (1996).
They carried out an
analysis cancer rates of more of the municipalities in the Sydney metropolitan
area. They also showed that socio-economic status is a risk factor for acute
lymphoblastic leukaemia (ALL) in N.S.W. The concentrated of ALL because this was
found by Hocking et al. to be the most elevated childhood cancer in the vicinity
of the North Sydney TV towers. McKenzie et al. also undertook a number of
exposure calculations in an attempt to characterize the mean exposure for each
of municipalities.
Their calculations used a simple inverse square formula
that does not produce side lobes, which elevated VHF and UHF signals do produce.
These side-lobes influence ground level exposures out to beyond 4 km, Figure 5.
They are also unaware of horizontal radiation pattern differences. They
highlighted the role of shadowing as a source of lower measured values compared
with calculated values. They showed with measurements at a particular location
how the exposure varies from direct exposure on the roof (3 µW/cm²), in the
garden on the street (0.066 µW/cm²) and inside the home (0.017 µW/cm²). This
verifies the factors used for the mean exposure estimates made in section
2.10.
Using these 'representative' calculated exposures for each
municipality, McKenzie et al. plotted the total childhood ALL incidence as a
function of their calculated exposure, Figure 45. The second diagram shows the
improvement if Willoughby is reduced to its more probable mean exposure
level.
Figure 45: A dose-response relationship for total childhood cancer in
Sydney, Australia, from McKenzie, Yin and Morrell (1998), with the 95%
confidence intervals added. RFR exposure is the calculated exposure at the
geographic centroid of each municipality. The right hand diagram shows the
effect of moving Willoughby to 0.3 µW/cm² to adjust for the horizontal radiation
pattern.
Hocking et al. (Hocking, Gordon and Hatfield (1999)) reject the
substance of the criticisms of McKenzie, Yin and Morrell, concluding:
"In
summary, we consider that the second look at our study had important
deficiencies regarding post hoc analysis of data. Their conclusion that their
analysis 'casts doubt on the apparent association between childhood incidence of
acute lymphoblastic leukaemia and television RFR' is not justified. If anything,
their analysis confirms our own finding of a modest association, which warrants
further study."
In this report the contention is that the conclusion could be
even stronger than seen by Hocking et al. The calculated exposure used by
McKenzie et al. does not take into account the very much higher power being
radiated from Tower 1. When this is noted, Lane Cove has the highest calculated
mean exposure, North Sydney is next, closely followed by Willoughby. These
ignore the horizontal patterns in Figure 6b, Figure 43. If in Figure 45,
Willoughby was moved to 0.3 µW/cm² then the results form an even stronger
dose-response relationship than is shown by their original assumptions. The
error of not taking into account the radiative power of each tower is
significant.
The North Sydney Study shows significant increases in adult and
childhood leukaemia incidence and death. When realistic estimates of the mean
exposure of each municipality is used, a dose-response relationship results.
Measurements confirm that the estimates of the mean population exposure at the 4
km ring, the outer edge of the 'exposed population', is about to 25
nW/cm².
15.3 United Kingdom Regional TV Tower Study:
Dolk, Shaddick,
Walls, Grundy, Thakrar, Kleinschmidt and Elliott (1997): Cancer Incidence near
Radio and Television Transmitters in Great Britain: 1. Sutton Coldfield
Transmitter".
Dolk, Elliott, Shaddick, Walls, and Thakrar (1997): Cancer
Incidence near Radio and Television Transmitters in Great Britain: 2. All High
Power Transmitters."
15.3.1 The Study Context:
Dr Helen Dolk and her
colleagues responded to concerns about a cluster of seven cases of leukaemia and
lymphoma who were patients of a Birmingham GP, Dr Mark Payne, and who lived near
the Sutton Coldfield Transmitter. They obtained data from the cancer registry
and found a high incidence of adult leukaemia near the tower, which declined
with distance. They assumed that this was a dose-response relationship that was
following an inverse square law for exposure decline with distance from the
transmitter. Before they published this result they decided to extend the study
to 20 other regional TV towers throughout the United Kingdom.
At these
individual sites, and for all the 20 sites combined, the adult leukaemia rate
was found to be low near the tower, rose to form a broad variable peak between
about 1 km and 5 km, and then declined with distance. Over all distance it
didn't follow an inverse square law and therefore it failed to confirm the
result found at Sutton Coldfield, Figure 46. Thus Dolk et al. (1997b) concludes
that the follow-up study "at most gives very weak support to the Sutton
Coldfield findings." ICNIRP accepts this conclusion and states that the results
of these U.K. studies "are inconclusive".
Figure 46: Cumulative radial adult
leukaemia patterns for the 21 site UK study, Dolk et al.
There are two types
of radial transmission signals and two types of radial cancer patterns:
Type
A : UHF signals that are low near the tower, rise to a broad peak between 2 and
6 km and then decline with distance, Figure 30.
Type B: VHF signals have a
peak within 1 km and decline with distance in an undulating fashion, Figure
5.
For a high cancer rate to be detectable near a tower three factors are
necessary:
There must be a large population. This requires a high population
density because there is only a small area within 1 km radius of the tower and a
high proportion of this is likely to be the open field in which the tower itself
is sited.
There needs to be a high radiation exposure for the radiation to be
able to elevate the cancer rate. This occurs for the lower frequency, VHF, FM
signals, Figure 5, Figure 31.
The cancer type needs to be RF-radiation
sensitive to assist in raising the cancer incidence above the background level.
Leukaemia and Lymphoma are very RF-sensitive cancers, Szmigielski (1996), Milham
(1985, 1988), Hocking et al. (1996).
These factors completely explain these
results. Sutton Coldfield is the only tower that has these three factors. All
other towers lack at least one factor and therefore cannot show a high cancer
rate near the tower. In fact they all follow a Type A pattern which is a dose
response relationship of cancer rate as a function of mean exposure. This for
all radial cancers outlined in the Tables they follow a dose response
relationship appropriate to their radiation patterns.
15.3.2 Sutton Coldfield
Cancer Study Results:
For adult cancers the results are presented in the
following two tables. These tables show two radial cancer patterns:
Type A:
For All Cancer, Non-Hodgkin's Lymphoma, Skin Melanoma and Bladder cancer the
cancer rates are low near the tower, rise to a complex broad peak between 1 km
and 10 km. The skin melanoma drops faster than all the others. This is typical
of UHF radiation patterns, Figure 28.
Type B: Adult leukaemia has 6 people
within 1 km. This gives a high O/E ratio close to the tower. In all other
respects it is similar to the first group. This is typical of mixed VHF/UHF
radiation patterns, Figure 31.
In following the radiation patterns
appropriate for each type of site these data follow dose response relationships
with radial distance and also between high powered TV, moderate powered TV and
low powered FM radio sites. This is very strong evidence that there is a causal
relationship between low intensity RF exposure and adult leukaemia.
Figure
47: Radial cancer rates around the Sutton Coldfield TV Transmitter.
Figure
48: Radial adult cancer rates around the Sutton Coldfield TV transmission
tower.
Figure 49: Radial cancer incidence around the Sutton Coldfield TV/FM
tower near Birmingham, with both VHF and UHF transmissions, Dolk et al.
(1997a).
The radial cancer incidences around the Sutton Coldfield tower shows
that they are generally high in the 1 to 3 km range, low in the 4-5 km range,
slightly higher in the 6-8 km range and diverging up and down outside 8 km. All
Cancer follows this pattern. Being a high powered tower with VHF FM
transmissions the radial exposure pattern is very likely to be similar to the
Sutra Tower, Figure 29.
15.3.3 Childhood Cancer results:
This study
involves a far smaller sample than the San Francisco study, less than half a
million compared to several million total population, but this study considers a
wide range of cancer types for adults as well as for children. However, the
population of children involved is very small, especially in the exposed" group,
and therefore reaching statistical significance is unlikely. For example, at
Sutton Coldfield there are 97 children with cancer with 10 km of the tower.
Within 2 km of the tower there were two childhood leukaemia cases when 1.1 was
expected. This gives RR = 1.82 which is elevated but non-significant. Hence the
Sutton Coldfield study cannot reliably address the childhood cancer issue. This
problem, of small numbers, also limits the reliability of relationships with
individual cancer types, especially close to the towers where population numbers
are necessarily small.
15.3.4 The 20-Site Study:
Figure 48 (Table 1) shows
in the course radial analysis that Skin Melanoma is higher close to the towers
whereas Bladder Cancer is more broadly elevated, consistent with Sutton
Coldfield. All of these sites show the Type A pattern from above, with leukaemia
rates being low near the tower, rising to a broad, complex peak and then
declining with distance. The rate of decline is slower with the more
high-powered transmitters, Group 1, Group 2, Crystal Palace and
Wenvoe.
Figure 50: Cancer data for the 20 site U.K. study from Dolk et al.
(1997b).
The elevated cancers identified by Dolk et al. include Leukaemia,
Non-Hodgkin's Lymphoma, Skin Melanoma and Brain, Bladder, Male and Female
Breast, Colorectal, Stomach and Prostate Cancer. Some are elevated only in the
0-2 km ring and some in the 0-10 km zone, Figure 50.
Figure 51: Adult
leukaemia as a function of radial distance from regional TV transmission towers,
for all 20 sites and for a number of individual sites throughout the United
Kingdom, Dolk et al. (1997b).
Figure 52: Other cancer sites in the broad
radial analysis from Dolk et al. (1997b).
15.3.5 21-Site Childhood
Cancers:
The ability of these studies to detect childhood cancers was
severely limited by small number of children who live within 10 km of these TV
Transmission Towers. While in the 21 sites there were 3609 adults (( 15 years)
with leukaemia, there were only 317 children ((14 years). Close to the towers,
i.e. inside 2 km there were 101 adults and 10 children 1with leukaemia. The
expected incidence was 94.17 and 8.94 respectively. This gives O/E = 1.073,
95%CI: 0.81-1.42 for adults and O/E = 1.12, 95%CI: 0.61-2.06 for
children.
This the childhood leukaemia rate is elevated around the 21 TV
transmission towers in the United Kingdom, more so than the adult rate, but the
small numbers mean the elevation is not significant.
For brain tumours, the
rate is elevated within 10 km of the towers, for Malignant and Benign Brain
Tumour O/E = 1.06, 95%CI: 0.93-1.20, n=224, and for Malignant Brain Tumours, O/E
= 1.03, 95%CI: 0.90-1.18. It would have been interesting to observe the radial
cancer rates for these tumours for the numbers involved are much higher than for
the Sutra Tower Study. The equivalent data from the North Sydney Study is for
Childhood Leukaemia O/E = 1.8, 95%CI: 1.2-2.5, n=33 and for Brain Tumour O/E =
1.3, 95%CI: 0.7-2.3, n=12. Hocking et al. use a 4 km radius whereas the UK data
is for a 10 km radius. There is a different mix of TV and FM signals and signal
strengths in the North Sydney Study than in the UK Study. Accepting these
differences they all show elevated leukaemia and brain tumor. The very large
output power of the Sutra Tower results in far higher childhood cancer
rates.
15.3.6 Conclusion:
If the authors had known about and applied the
available engineering knowledge about radial exposure patterns, they would have
concluded that there was a significant dose-response relationship between a
number of adult cancers and RF exposure from TV/FM transmission towers. There is
complete internal consistency once the different radiation patterns are
recognized. The study also shows elevations in cancers from sites all over the
body, with dose-response relationships being evident for those presented. Hence
the observations are consistent with the data in Selvin et al.(1992) data and
analysis of Robinette et al. (1980), Milham (1985,1988) and Szmigielski (1996).
This shows a causal relationship between RF exposure and cancer.
Excesses in
cancer are still seen at 10 km, where the direct exposure is 5 to 10 times less
than the UHF peak of 1.3 µW/cm², i.e. between 0.13 and 0.26 µW/cm². Applying the
lifetime mean residential exposure factor of 0.15 reduces the exposure
associated with these adverse health effects to the range 0.02 to 0.034
µW/cm².
The data in Dolk et al. is internally consistent, shows elevated
childhood leukaemia and brain tumor, and a set of dose-response relationships
which are likely to be highly significant, if related to realistic radial RF
patterns, for cancer at a wide range of body sites including All Cancer,
Leukaemia, Non-Hodgkin's Lymphoma, Brain Cancer, Bladder Cancer, Prostate
Cancer, Skin Melanoma, Male and Female Breast Cancer and Colorectal Cancer. This
is also consistent with Robinette et al. (1980), Szmigielski (1996) and Milham
(1985, 1988).
ICNIRP's Cancer Assessment - Conclusion:
Discounting the two
inappropriately included studies, Barron and Barraf (1958) and Rothman et al.
(1996a), all of the remaining studies report significant increases in cancer
incidence and mortality from RF/MW exposure, or total mortality. Significant
dose-response relationships are reported by Robinette et al. (1980) for
Respiratory Cancer and Beall et al. (1996) for Brain Cancer; are contained in
the data of Selvin et al. (1992) for All Childhood Cancer, Leukaemia, Lymphoma
and Brain Cancer; of Dolk et al. (1997a,b) for Adult Leukaemia, Bladder Cancer,
Melanoma; and in the extended analysis of Hocking et al. (1996, 1998) through
McKenzie, Yin and Morrell (1997) and of Szmigielski (1996, 1998). A dose
response relationship for total mortality is also shown by Rothman et al.
(1996b).
The three challenges in this report of the ICNIRP assessment, of
using the wrong methodology and of using Constructive Dismissal to defend their
flawed methodology, and neglecting a large body of epidemiological research,
have been proven.
The first is proven by comparison with the approaches and
levels of evidence used for chemicals and air pollution. The second is proven by
a detailed analysis of the research results cited by the ICNIRP. The
Reproductive and Cancer Assessments of the ICNIRP are very limited in their
scope and very selective in the studies chosen. In both cases inappropriate
studies have been included to incorrectly bolster ICNIRP's case that there is no
reliable evidence of adverse effects. In both cases published material and
author's conclusions have been misquoted with a bias towards finding no effects.
In both assessments the cited papers include elevated, significantly elevated
and dose-response increases in miscarriage and cancer. In the cancer case it is
sufficient to establish cause and effect with the material cited. This is
strongly confirmed when the very large number of studies which are available are
included. For Reproductive Effects, the cited material is indicative, but when
the additional available studies are included and the biological mechanisms are
considered, consistent with the cancer assessment and evidence of neurological
and hormonal influences of EMR, a causal relationship between low level EMR
exposure and reproductive effects is established.
The statements in
opposition to the adoption of the ICNIRP Guideline for use a national standards
is proven to be fully justified. The ICNIRP guideline is many orders of
magnitude above the levels at which known adverse human health effects occur.
Hence the world's population is being put severely at risk by the campaign to
adopt the flawed ICNIRP Guidelines globally.
17. Additional studies
not cited by ICNIRP:
Studies cited in the WHO (1993) review:
There is
a large body of epidemiologic scientific literature that is relevant to the
assessment of RF/MW exposures risk of cancer. Almost all of these studies have
not been referenced in the WHO/UNEP/IRPA review, WHO (1993), that is cited by
ICNIRP to be one of the "more detailed reviews". In fact the ICNIRP review
covers more published studies than does the WHO/UNEP/IRPA review, but both
ignore most of the published epidemiological studies. Three of the studies cited
by WHO (1993) are omitted by ICNIRP. They are the case-study by Archimbaud et al
(1989), and Air Force Base studies of Lester and Moore (1982) and Lester (1985)
and Amateur Radio Study of Milham (1985). WHO (1993) omits the Wichita Kansas
Study of Lester and Moore (1982a) and the Operator Electrical Workers Study of
Milham (1985) and the Amateur Radio Operators study, Milham (1988).
WHO
(1993) and ICNIRP (1998) share many of the flawed methodological approaches and
the assumption of the RF-thermal effect that the only RF/MW effect is heating of
human tissues. The review teams were chaired by the same person during most of
the 1990's, Dr Michael Repacholi.
WHO (1993) states that no significant
effects were found in Lilienfeld et al. (1978). This has been proved here to be
wrong. The U.S. Air Force Bases Studies are described as "contradictory" because
Polson and Merritt (1985) correctly criticize Lester and Moore for relating
cancer rates in counties to the existence of Air Force bases in those counties
when many cities which are close to Air Force bases are in adjacent counties
without Air Force bases. Lester (1985) adjusted the analysis accordingly and
concludes:
"This strengthens the possibility of an association between some
factor associated with AFBs - our original hypothesis was microwave radiation -
and cancer incidence because we now explicitly recognize the use of the county
containing the city nearest the base, which would be expected to be a truer
indicator of the effect produced by some factor emanating from the base than
would a county in which the base is situated but in which the nearest city is
farther away."
The Lester (1985) updated result was in the same journal issue
as Polson and Merritt (1985) and yet WHO (1993) ignores the existence and
significance of the correction. This again reveals the bias towards dismissing
evidence of effects.
WHO (1993) acknowledges that Szmigielski et al. (1988)
and Archimbaud et al.(1989) show a relationship between RF/MW and increased risk
of cancer, including Acute Myelogenous Leukaemia. In the case of Milham (1985)
the increase in Leukaemia is acknowledged. However, the result is questioned
because it is noted that many of the Amateur radio operators are also employed
in the "Electrical Industries". Hence they are exposed to PCBs, solvents, fumes,
and 50/60 Hz magnetic fields and not 300Hz-300GHz radiation. This claim is
challenged by evidence which supports the EMR Spectrum Principle because many
ELF powered appliances also emit RF/MW radiation which is much more
bioelectrically active.
The overall WHO (1993) conclusions include the
statements:
"In summary, the epidemiological and comparative clinical studies
do not provide clear evidence of detrimental health effects in humans from
exposure to RF fields".
And
"The question of whether RF might act as a
carcinogen should be further evaluated in epidemiological studies."
If the
studies available to it had all be included and the proper epidemiological
assessment principles had been followed, then the WHO review should have
concluded that RF radiation is a probable human carcinogen, because they had
more and stronger evidence than the U.S.E.P.A. review team in 1990, and they
concluded that RF/MW was a possible human carcinogen.
Lester and Moore
(1982a) is their initial study which tested the hypothesis that radar might
increase the risk of cancer by noting that Wichita Kansas had radar sets on Air
Force Bases on two opposite sides of Wichita. The tested the hypothesis by
separating populations which were exposed to no radar signals, living in
valleys, one radar signal, on one or other hill slope, and two radar signals by
living on ridges. The cancer incidences are 303, 429 and 470 per 100,000
(1.00:1.42:1.55). The dose-response association persisted through age, sex, race
and socio-economic adjustments.
Dr Sam Milham's two other studies not cited
in WHO (1993) are Milham (1985a), a large study of Electrical Workers in
Washington, and Milham (1988) and updated Amateur Radio Study covering
California and Washington. Milham (1985a) studied cancer rates in 486,000 adult
male workers who were in occupations in Washington State which had potential
exposures to electromagnetic fields. This showed elevated and significantly
elevated cancer rates in many body organs. The results are summarized in Table
23.
Table 23: Summary of all site cancers from Robinette et al. (1980), using
AT/ET except for Brain cancer (FT/ET), Milham (1985a), Szmigielski (1996) and
for Dolk (1997a,b) using the maximum and/or significant result in the radial
patterns.
Robinette Milham Szmigielski Dolk(a) Dolk(b)
Exposure Regime
RF/MW Mixed RF/MW RF/MW RF/MW
High Mod. High Low Low
Relationship RR PMR
RR O/E O/E
Sample Size(N) 202 2649 55,500 17409 13372
Symptoms
All
Malignant Neoplasms 1.66* 106** 2.07* 1.20*
Esophageal and Stomach
3.24**
Respiratory Tract, Lung 1.75 114** 1.06
Colorectal/ bladder (1)
3.19** 1.36/1.76 1.10
Liver, pancreas 117* 1.47
Skin, Melanoma 2.66 1.67*
2.39* 1.11
Thyroid 1.54
Brain, CNS (2) 2.39 143** 1.91* 1.31
1.06
Leukaemia 2.22* 136* 6.31*** 1.74* 1.15
Non-Hodgkins Lymphoma 164**
5.82*** 1.30*
Acute Leukaemia (Lympho) 162** 5.75* 3.57 1.04
Acute
Myeloblastic Leuk. 8.62*** 1.02 1.17
Chronic Myelocytic Leuk.> 13.90***
1.23
Chronic Lymphoblastic Leuk 3.68** 2.56* 1.20>
p-values: *
<0.05; ** <0.01; *** <0.001
Note (1): Colorectal for Szmigielski and
the left Dolk(a) and bladder for the right Dolk(a) and Dolk(b).
Note (2): In
Milham 16 of the unspecified neoplasms were brain tumors which have been added
to this group.
Milham (1988) studied 67,829 amateur radio operators in
Washington State and California. He concludes "The all-cause standardized
mortality ratio (SMR) was 71 but a statistically significant increased mortality
was seen for cancers of the other lymphatic tissues (SMR = 162), a rubric which
includes multiple myeloma and non-Hodgkin's lymphomas. The all leukemia SMR was
slightly elevated but not significant (SMR = 124). However, mortality from acute
myeloid leukemia was significantly elevated (SMR = 176). Elevated cancer rates
were found for Esophagus, SMR = 113 (71-172); Large Intestine, SMR = 111
(89-137); Prostate, SMR = 114 (90-142); Brain, SMR = 139 (93-200), Lymphoma +
Leukaemia, SMR = 123 (99-152); Hodgkin's Disease, SMR = 123 (40-288); Leukaemia,
SMR = 124 (87-172) and Other Lymphatic Tissue, SMR = 162 (117-218).
Table 23
shows a great deal of consistency between several large studies which stand as
proof, backed by many dose-response relationships, even at residential exposure
levels, that RF/MW increases the risk of cancer over the whole body. This stands
in strong contrast with the ICNIRP and WHO review conclusions.
17.2 Studies
not cited by WHO nor ICNIRP:
The following is a brief summary of a number of
relevant epidemiological studies which have been omitted by both WHO (1993) and
ICNIRP (1998).
A broad Summary:
It is not widely recognized that ELF
epidemiological studies have relevance to RF/MW assessments of effects. There
are two primary reasons for this. High voltage power lines are sources of RF
radiation, especially in the 3 to 30 MHz range, Vignati and Giuliani (1997).
This is why you often hear a buzz on your radio as you drive under a powerline.
This is outlined as part of the EMR Spectrum Principle. This evidence proves
that epidemiological studies of RF/MW and ELF show elevated and significantly
increased cancer in many body organs, but especially brain cancer, leukaemia and
breast cancer.
More neurasthenic symptoms (chronic mental and physical
weakness and fatigue) in group exposed to radar (Djordevic et al.,
1979).
Higher frequency of increase in red blood cells (polycythemaemia) with
microwave exposure (Friedman, 1981).
Lin et al. (1985) studied 951 cases of
brain tumors among white male residents of Maryland during the period 1969-1982.
Fifty cases of glioma and astrocytoma were observed among electrical workers
exposed to EMR compared to an expected number of 18, i.e. an risk ratio of 2.8.
While their exposure was mainly to ELF fields it shows the common link over a
wide range of frequencies. A significant dose-response relationship was found:
No exposure: 1.00; Possible exposure OR = 1.44(1.06-1.95); Probable exposure, OR
= 1.95 (0.94-3.91), and Definite exposure, OR = 2.15 (1.10-4.06).
In 1985 an
unusual number of children with leukaemia were identified living in the vicinity
of broadcasting facilities (OR = 3.4: CI=0.70 -16.41), Maskarinec et al.
(1993).
Upper limb paraesthesia and eye irritation among 30 exposed workers
using 27 MHz plastic sealers (Bini et al., 1986);
De Guire et al. (1987)
report increased malignant melanoma of the skin in workers in a
telecommunication industry, affecting only men, SIR = 2.7 CI :
1.31-5.02).
Thomas et al. (1987) report a 10-fold increase in astrocytic
brain tumor among electronics and repair workers employed for 20 years or more.
Some risk was due to solvents, put at a factor of 2, placing RF/MW contribution
at a factor of 5.
Electrical workers in Los Angeles county have a 4.3-fold
increased risk of certain brain tumors (Preston-Martin et al. 1989).
An
increased incidence of malignant brain tumors has been reported in children of
fathers exposed to electromagnetic fields and electronic solvents (Johnson and
Spitz, 1989).
Increased protein band in CSF in exposed group or radar
mechanics (Nilsson et al., 1989).
Hayes et al.(1990) report an Odds ratio for
all testicular cancer of 3.1 (CI: 1.4-6.9) for a small sample of workers who
were occupationally exposed to RF/MW radiation.
Navy Electrician's Mates have
an excess risk of leukaemia, RR=2.4 (1.0-5.0), Garland et al. (1990)
Savitz
and Chen (1990) show significant increased risk of childhood cancer
(Neuroblastoma (OR=11.8*), Brain Tumour (OR=2.7*) and CNS tumors (OR=1.7))
associated with parents who work in electrical and electronic
industries.
Increased risk for all brain tumours (RR=2.9 (1.2-5.9)) and
glioblastomas (RR=3.4 (1.1-8.0)) for assemblers, and repairmen in the radio and
TV industry, Tornqvist et al. (1991)
Microwave heating reduces immune system
factors in human breast milk, compared to conventional heating. Microwave
heating significantly reduces the IgA for E coli bacteria, producing five times
more E coli for 25 (C heating and 18 times more after 3 hours for 98(C heating,
Quan et al. (1992).
Floderus, Tornqvist and Stenlund (1994) found a
significant increase in Brain Tumours, RR = 12.2, 95%CI:2.8-52.5; Breast Cancer,
RR = 4.9, 95%CI:1.6-11.8 and pituitary tumours, RR = 3.2, 95%CI:1.6-6.2, for
electrical railway workers younger than 30 yrs.
Loomis, Savitz and Ananth
(1994) found significant increases in Female Breast Cancer in Electrical
Workers, OR = 1.38 (95%CI: 1.04-1.82). Adjusted Ors for electrical engineers, OR
= 1.73 (95%CI: 0.92-3.75); for electrical technicians, OR = 1.28
(95%CI:0.79-2.07) and for telephone installers, repairers and line workers, OR =
2.17 (95%CI:1.17-4.02).
Women working in the Telephone Industry showed many
excess cancers. Among white women (age <49) Rectum Cancer MOR = 3.3
(1.2-8,7); connective tissue MOR = 4.4 (2.2-8,2); Breast Cancer MOR = 1.6
(1.2-2.1), corpus uteri MOR = 3.3 (1.5-7.5, Ovary MOR = 2.1 (1.3-2.5); and Brain
MOR = 2.1 (1.2-3.7). Excess risks of connective tissue cancer among engineers
and technicians; office workers; telephone operators; and mechanics and
repairers, MOR = 8.5, 4.9, 1.7, and 4.4 respectively, Dosemeci and Blair
(1994).
Significantly increased and dose-response increases of total
Mortality, All Cancer, Leukaemia and Brain Tumour were found in US Utility
Workers (1950-1988) and sub-set of occupations, Savitz and Loomis
(1995).
Increased risk of female breast cancer with exposure to
radiofrequency EMF, RR=1.15 (1.1-1.2), Cantor et al. (1995).
Tynes et al.
(1996) observed an excess risk of Female Breast Cancer for female radio and
telegraph operators exposed to RF (405 kHz-25 MHz), SIR = 1.5 for > 50 yr of
age.
The Skrunda Radar provides a living laboratory for the chronic low level
effects of exposure to RF/MW radiation. To date investigations have revealed a
number of statistically significant changes associated with exposure to the
radar signal. These include:
Impaired physical and scholastic performance of
children in the open field exposure range of 0.0008-0.41 µW/cm², mean measured
level in the range 0.0028- 0.039 µW/cm², Kolodynski and Kolodynska (1996).
A
6-fold increase in broken chromosomes in the peripheral erythrocytes of the
exposed cows (p<0.01). The measured exposure is in the range 0.042 to 6.6
µW/cm² placing the mean exposure in the range 0.157 to 0.63 µW/cm², Balode
(1996).
A statistically significant (P<0.01) negative correlation between
the relative additional increment in tree growth and the intensity of the
electric field. The Pine trees at 4 km were exposed to a range of 0.011 to 0.41
µW/cm², a mean open field exposure of 0.039 µW/cm² and measured distance
exposure of 0.0027 µW/cm² (for the radar signal). A probable biological
mechanism was identified through observed changes in physiological conditions,
Balodis et al. (1996),
Chromosome and reproductive damage in plants exposed
RF/MW in the range 0.042 to 6.6 µW/cm². Magone (1996).
Chronic exposure to
pulsed RF radar signals is associated with chromosome damage in plants and
animals, with associated reproductive aberration in plants, and growth reduction
in pine trees linked to observed physiological changes, and scholastic
impairment of school children occurs in relation to exposure levels which fall
well below 2 µW/cm², below 0.1 µW/cm². and even below 0.01 µW/cm².
Stenlund
and Floderus (1997) identified increased Testicular Cancer in middle ELF
exposure (>0.28 µT) and high exposure (>0.4 µT) compared with low exposure
((0.15 µT) with OR = 1.3 (CI:0.7-2.5) and OR = 2.1 (CI:1.0-4.3) for those ( 60
years and OR = 1.9 (CI:0.8-4.4) and OR = 3.9 (CI:1.4-11.2) for men ( 40 years.
These produce significant (p<0.05) dose-response relationships.
Brain
tumour studies:
The Bioelectromagnetic
principles include the EMR sensitivity of the human brain. This suggests that
brain cancer is a probable result of EMR exposure. In section 16.2 several
studies show significant increases in brain cancer. A literature search,
assisted by MEDLINE, identified over 60 studies showing increased rates of brain
cancer, and over 30 showing significant increases in brain cancer in EMR exposed
populations. The following studies show significant increases in brain tumours
for children and adults, in ELF to RF/MW exposures in residential, occupational,
commercial and military situations.
Sweden, Power lines, Children RR = 3.9,
p<0.05, Tomenius (1986),
Denver, Residential, children, 2-level wire code
Savitz et al. (1988)
OR = 2.04 (1.11-3.76)
U.S., prenatal electric
blanket, Savitz, John and Kleckner (1990)
Brain cancer in children , OR = 2.5
(1.1-5.5)
Finland, power lines Verkasalo et al. (1993)
CNS tumours in boys
SIR = 4.2, (1.4-9.9)
>0.2 µT or > 0.4 µT-years
Denmark, High voltage
installations Olsen et al. (1993)
Children, >0.4 µT Significantly
increased cancer, including CNS tumours.
Denver, Residence Savitz and Kaune
(1993)
Children, Wire Code OR = 2.5 (1.1-5.5)
U.S. Meta Analysis of 13
studies Washburn et al. (1994)
Residential Children, CNS RR = 1.89
(1.34-2.67)
Washington State, Electrical Workers Milham (1985)
All Groups
PMR = 123, p<0.05) n=101
Electrical and electronic technicians PMR = 134
n=7
Power Station Operators PMR = 130 n=3
Electricians PMR = 155
p<0.01) n=46
Maryland, U.S. electrical industries Lin et al.
(1985)
Brain tumours Died significantly earlier n=951
United States, 16
States (Mortality) Loomis and Savitz (1990)
Electrical engineers and
technicians OR = 2.7 (2.1-3.4)
Telephone workers, OR = 1.6
(1.1-2.4)
Electric power workers OR = 1.7 (1.1-2.7)
Electrical workers
in
manufacturing industries OR = 2.1 (1.3-3.4)
Finland, Occupational
exposures Juutilainen, Laara and Pukkala (1990)
CNS tumour, 25-64 year old
male
Probable exposure RR = 1.3 (0.7-2.3)
Possible exposure RR = 1.3
(1.0-1.6)
Germany, electrical workers Schlehofer et. al. (1990)
Women RR =
5.2 (1.4-20.1)
Men RR = 0.9 (0.2-2.3)
Aerospace electromechanical workers
Park et al. (1990)
All workers PMR = 4.2 (p<0.0001) n=583
For hourly
workers with up to
20 years of work PMR = 8.7 (p=0.000003).
Sweden,
Occupational exposure Tornqvist et al. (1991)
Assemblers and repairmen in
radio and TV industry
All brain tumours SMR=2.9, (1.2-5.9)
Glioblastomas
SMR=3.4, (1.1-8.0)
All welders SMR=1.3, (1.0-1.7)
Iron/steel industry
SMR=3.2, (1.0-7.4)
For glioblastomas SMR=1.5 (1.1-2.1).
Norway,
Occupational electric Tynes, Andersen and Langmark (1992)
and magnetic
exposures.
Overall brain tumour SIR = 1.09 (0.9-1.41) n=77
ISCO code weak
magnetic/
electric exposure SIR = 2.20 (1.01-4.18)
Tram drivers SIR = 2.04
(0.42-5.98)
Radio/telegraph operators SIR = 1.20 (0.25-3.49)
Electricians,
installation SIR = 1.23 (0.67-2.07)
Electricians, power supply SIR = 1.16
(0.43-2.53)
Power plant operators SIR = 1.15 (0.24-3.36)
Power line
workers SIR = 1.51 (0.78-2.64)
Telephone installers SIR = 1.22
(0.49-2.51)
Railway track walkers SIR = 2.20 (1.1-4.18)
Total for these
groups SIR = 1.14, (0.9-1.42)
New Zealand, electrical workers Preston-Martin
et al. (1993)
Electricians OR = 4.6 (1.7-12.2)
Electrical engineers OR =
8.2 (2.0 - 34)
Sweden, Occupational exposure Floderus et al. (1993)
Low
exposure RR = 1.0 (0.7-1.6)
Moderate Exposure RR = 1.5 (1.0-2.2)
High
Exposure RR = 1.4 (0.9-2.1) n=261
United States, Telephone industry Dosemeci
and Blair (1994)
Women from 24 states OR = 2.1 (1.2-3.7)
England,
Electrical workers Fear et al. (1996)
PPR = 118 (103-136)
Brazil, San
Paulo, Utility workers Mattos and Koifman (1996)
PCMR = 7.7
(1.02-9.65)
France electrical utility workers Guenel et al. (1996)
Brain
tumour OR = 3.06 (1.08-8.74) n=69
5 year latency OR = 3.69
(1.10-12.43)
Telephone and radio operators, electricians, Kaplan et al.
(1997).
All Brain Tumours OR = 1.2 (0.2-5.2)
Malignant Brain Tumours OR =
1.4 (0.2-8.7)
Danish Utility Workers Johansen and Olsen (1998)
Women SIR =
1.3 (0.7-2.2) n=15
Women >10yrs < 0.09 µT SIR = 1.9 n=4
0.1-0.29 µT
SIR = 9.2 p<0.05 n=2
United States, Occupational Cocco, Heineman and
Dosemeci (1999)
CNS cancer RR=1.2 to 1.3 p<0.05 n =12980
United States:
Microwave repair workers Zarek (1977)
RR = 74.1 (15.0-367), p<0.001
n=2
United States Embassy in Moscow: Lilienfeld et al. (1978)
Radar RF/MW
exposure
Males Working in the Embassy SMR = 20 (2.4-72.2) , p<0.01
n=2
Navy, Korean War, FT/ET groups, RF/MW Robinette et al. (1980)
For
brain, eye and CNS RR = 1.66 (1.06-2.60) n=8
New Zealand, electrical workers
Pearce, Reif and Fraser (1989)
Radio and TV repair OR = 7.86 (2.2-28.1)
n=2
Electricians OR = 1.68 (0.75-3.79) n=6
Total electrical workers OR =
1.62 (1.04-2.52) n=21
Canada, British Colombia pilots Salisbury et al.
(1991)
Elevated PMRs for brain cancer and nervous system cancer.
Canada,
Commecial pilots Band et al. (1990)
ELF/RF SMR = 4.17 (1.4-9.5), p=0.017
n=4
SIR = 3.45 (1.2-7.9), p=0.03 n=4
England, British Airways pilots
Irvine and Davies (1992)
ELF/RF PMR = 2.68, p<0.05
U.S. Air Force
Grayson and Lyons (1996)
Aircrew compared OR = 1.77(1.17-2.68) n=37
with
non-flying crew
Adjusted for rank, socioecom. OR = 1.22 (0.76-1.95)
Polish
Military Szmigielski (1996)
Mortality RR=1.9 (1.08-3.47), p<0.05
n=55,500
U.S. Air Force personnel Grayson (1996)
Age-race-adjusted odds
ratios
ELF fields OR = 1.28 (0.95-1.74)
RF/MW fields OR = 1.39
(1.01-1.90)
Brazilian Naval Personnel Santana, Silva and Loomis
(1999)
Aged <56 yrs OR = 4.63 (2.54-8.45) n=40
Unmarried men OR = 3.18
(1.69-5.99)
This lists 34 separate studies, covering over 56 occupational or
residential groups which have been exposed to EMR and more than 40 show
significant increases in brain cancer incidence or mortality.
Thirteen
studies show dose-response relationships for EMR exposure and brain
tumor:
Denver, United States, power lines Wertheimer and Leeper
(1979)
Childhood ) Birth Address RR = 1.83, p=0.04 n=22
CNS tumors) Death
Address RR = 1.76, p=0.017 n=30
Dose related for children living at same
address.
Eastern U.S. Electronic Industries Thomas et al.
(1987)
Astrocytic brain tumours RR=4.9 (1.9-13.2)
Duration Employed
(yr)
Unexposed <5 5-19 ( 20
RR 1.0 3.3 7.6 10.4>
Solder fume
adjusted RR 1.0 1.65 3.8 5.2
(trend p<0.05)
East Texas, Males Glioma
Speers, Dobbins and Miller (1988)
n=202
Transportation,
communication
and utilities industries OR = 2.26 (1.18-4.32)
Electricity
or electromagnetic fields OR = 3.94 (1.52-10.20) Trend: p<0.01
Los Angeles
County, Occupational exposure Preston-Martin et al.(1989)
High exposure to
electric and magnetic fields n=272
Glioma OR=1.8 (0.8-4.3) p for trend
=0.05
Astrocytoma, >5 years empl. OR=4.4 (1.2-15.6)
Los Angeles
Country, electrical industry Mack et al. (1991)
n=272
Astrocytomas RR =
10.3 (1.3-80.8) Trend, p=0.01
San Francisco, Sutra Tower (FM/TV) Selvin et
al. (1992)
Children < 21 yrs RR = 2.87, (1.30-6.32), p<0.01
n=35
Comparing <4.5km and >4.5 km Trend p <0.0001
Quebec, Ontario
and French Utility workers Theriault et al. (1994)
>=90th percentile,
years of exposure
( 5 years OR = 0.81 (0.3-2.21)
(20 years OR = 1.78
(0.69-4.62)
>=20 (20 years OR = 5.90 (0.37-94.4)
Canada, Provincial
Residential Electric Consumption (REC) Kraut et al. (1994)
Childhood brain
cancer significantly increases with REC in a dose-response manner.
U.S.
Electrical Workers Savitiz and Loomis (1995)
Mortality Dose-response OR =
1.94 per µT-yr
United States, office workers Milham (1996)
Transformer
fields SIR = 389 (156-801) N=410
Employment period trend p<0.05 Exposure
trend p=0.0034
U.S. Computer exposures Beall et al. (1996)
Computer
Programmers (>10 yrs) OR = 2.8 (1.1-7.0) Trend p =
0.04
Engineering/Technical (>10 yrs) OR = 1.7 (1.0-3.0) Trend p =
0.07
Glioma, All subjects, 5yr programme OR = 3.9 (1.2-12.4) Trend p =
0.08
Ontario Hydro male employees (Adjusted ORs) Miller at al.
(1996)
Brain Tumour Mod. Field OR = 1.27 (0.32-5.41)
High Field OR = 1.33
(0.52 -10.8) Both show trends.
Benign Brain Mod. Field OR = 5.38
(0.42-69.3)
Tumour High Field OR = 5.64 (0.3-105)
Norway Tynes and
Haldorsen (1997)
Children <0.05 µT 0.05-<0.14 µT >0.14 µT n=10
RR
= 1.0 2.6 (0.5-12.0) 2.3 (0.8-6.6) p=0.07
Of the thirteen studies showing
dose-response relationships for EMR exposure and brain cancer, at least seven
show significant dose-response relationships. The majority of studies involve
industrial exposures mainly to ELF fields but many appliances, like power lines,
also produce a spectrum of RF signals. One, Beall et al. (1996), involves VDT
exposure that is mixed ELF/RF. Two of the significant dose-response studies
involve RF/MW, Thomas et al. (1987) and Selvin et al. (1992), and Thomas et al.
for workers.
17.5 Leukaemia Overview:
The most frequently identified
cancer associated with ELF EMR and RF/MW EMR is childhood and adult leukaemia.
This is unremarkable in the light of the sensitivity of the whole body to EMR
and the established biological effect of altered cellular calcium ion
homeostasis with the strong implications towards impairment of the immune system
from this. The ICNIRP reviews these studies, and in a very limited selection of
the literature, find that Relative Risks are consistently in the range 1.5 to 3.
The studies suffer generally from small numbers. The ICNIRP notes that a common
cut-off point at 0.2 µT is emerging but from their limited research selection,
it is not strong enough, in "the absence of experimental research to form a
basis for setting exposure guidelines". ICNIRP is consistent. Their inverted
priorities place biological mechanism above epidemiological evidence.
The
ICNIRP finds the evidence for melatonin reduction insufficient to convince them
though a very selective citing of the literature. Hence they retain a guideline
based on limiting induced current. At 50/60 Hz it is close to 100 µT.
As with
the RF/MW assessment, there is a large body of literature not cited by ICNIRP
that strongly confirms the 0.2 µT cut-off for residential studies of childhood
cancer. All of the studies cited by the ICNIRP have mean annual exposures less
than 1-10 µT for occupational studies and <0.6 µT for residential studies.
Hence in a Public Health Protection Approach a cut-off of 0.2 µT would be
identified and then a safety factor would be applied to allow for the
uncertainties produced by small sample sizes and the extent of the exposure
risk, i.e. the whole population. This demonstrated again how severely and
consistently flawed the ICNIRP approach is.
Based on the strongly supported
EMR Spectrum Principle, if ELF exposures are consistently shown to increase
leukaemia then RF/MW exposures are highly likely to also produce leukaemia, and
at lower exposure intensities. Table 24 summarizes RF/MW studies showing
increases in adult Leukaemia.
When the RF/MW studies which have identified
significant increases in Adult Leukaemia are ranked from residential,
recreational, occupational and military exposures, they form a global
dose-response relationship, Table 24.
All of these studies involve
non-thermal exposures. Together they confirm a causal relationship between RF/MW
exposure and adult leukaemia.
17.6 Summary:
The vast majority of these
epidemiological studies are not cited by ICNIRP. They confirm the EMR Spectrum
Principle that health effects occur across the spectrum from ELF to RF/MW and in
mixed exposures. Leukaemia, Brain Tumour and Breast and other hormonal related
cancers are most commonly associated with EMR exposure. Compared to chemical
assessments, the strength of evidence that there is a cause and effect
relationship between EMR and cancer exceeds that of most substances that are
classified as human carcinogens.
Table 24: A summary of epidemiological
studies involving adult leukaemia mortality or incidence, ranked by probable
RF/MW exposure category.
Study Reference Exposure Leukaemia Risk 95%
Conf.
Category Type Ratio Interval
Polish Military Szmigielski et al.,
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 a. (1980) High All Leuk. 2.22 1.02-4.81
(Mortality)
Amateur
Radio Milham (1988) Moderate AML 1.79 1.03-2.85
(Mortality)
UK TV/FM Dolk
et al. (1997a) Mod/Low Adult Leuk. 1.83 1.22-1.74
(Incidence) CML 1.02
0.28-2.60
AML 1.86 0.89-3.42
ALL 3.57 0.74-10.43
CLL 2.56
1.11-5.05
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) CML 1.16
AML 1.17
ALL 1.04
CLL
1.20
Note: ALL : Acute Lymphatic Leukemia; CLL: Chronic Lymphatic Leukaemia;
AML Acute Myeloid Leukaemia; CML: Chronic Myeloid Leukaemia; and All Leuk.: All
Adult Leukaemias.
The studies cited by ICNIRP contain sufficient evidence to
conclude cause and effect between RF/MW and cancer across many body organs,
especially leukaemia and brain tumour, and at chronic lifetime exposures showing
dose-response relationships pointing to a zero level.
This is confirmed by
more than three as many studies as are cited by ICNIRP(1998), thus confirming
the cause and effect relationship between RF/MW exposure and cancer. Support
also comes from ELF studies and those involving "Electrical or Utility"
Occupations because of the validity of the EMR Spectrum Principle.
The
ICNIRP's conclusion is:
Overall, the results from a small number of
epidemiological studies published provide only limited information on cancer
risk."
This is demonstrably wrong and grossly misleading.
18. Recommended Public
RF/MW Exposure Standard:
ICNIRP's thermally based approach has been
proven many times to be wrong in terms of scientific evidence and public health
standard methodology. There is sufficient epidemiological evidence to establish
a cause and effect relationship between chronic low level EMR exposure and many
adverse health effects, including cardiac, neurological, reproductive and cancer
effects. The dose response relationships indicate a cancer and reproductive
problem threshold near zero.
Hence the target for the recommended standard is
10nW/cm².
This is despite the fact that, consistent with the
Bioelectromagnetic Principle 2 which identifies the sensitivity of the brain to
interference by EMR, and there is confirmation from the Swiss, Schwarzenburg
Study. This study identified adverse effects on sleep and a number of other
serious health effects, down to mean RF levels of 0.4nW/cm².
Significant
learning difficulties were measured in children in a school in exposed to the
pulsed radar signal at Skrunda, Latvia, compared to unexposed schools,
Kolodynski and Kolodynska (1996). The RF-exposed children live within a 20 km
radius of the radar. At 3.7 km from the radar the measured field was 0.32
µW/cm². Assuming an inverse square law between 3.7 and 20 km from the radar, at
10 km the exposure is approximately 0.04 µW/cm² and 0.01 µW/cm² at 20 km. Hence
the children are showing significant physical and intellectual impairment when
chronically exposed in the range 10 to 40 nW/cm².
Wever (1974) and Konig
(1974) proved that human brain detect and use the Schumann Resonance signals for
synchronization and maintaining the homeostatic relationship during diurnal
variations. Cherry (2000) shows that the Schumann Resonance signal is a
biological mechanism to many human significant adverse health effects observed
in relation to geomagnetic activity variation. This shows that brains detect the
Schumann Resonance signals intensity and frequency and uses hormones such as
melatonin to communicate with organs and cells to maintain diurnal regulation.
Since the mean Schumann Resonance intensity is close to 0.1 pW/cm², and adverse
health effects are observed for higher and lower intensity levels, then
endogenous ELF and RF/MW modulated signals can interfere with hearts, brains and
cells at extremely low intensities, approaching zero exposure. Hence
minimization of exposure is needed to protect workers and public health.
The
background RF/MW levels in Western cities are already in the range 1nW/cm² -
5nW/cm², except near cell sites and radio and TV towers. A practical option
to avoid these demonstrated effects is to set the initial public exposure limit
at 10
nW/cm² (0.01 µW/cm²).
In all cases all practical attempts should
be undertaken to keep exposures as low as possible, below 10 nW/cm².
A
primary means of achieving public health protection is a strong move away from
"wireless" technology. If major cities moved to fiber-optic cables for all
telephone, fax, radio, TV and internet services, removing the need for broadcast
transmission sites, the mean public exposure could be kept below 10 nW/cm².
Mobile phones, couple with their base stations, pose the highest risk in their
present modes of introduction. The usage of mobile phones should be minimized
and discouraged, and the base station placement should be remote from where
people live and work, from hospitals and schools.
19. Achieving the 10
nW/cm² standard:
A cell site policy which limits the peak exposure to 1
µW/cm² at the boundary of the nearest dwelling property, is likely to have a
mean weekly exposure of 0.3 to 0.6 µW/cm² because of the phone traffic going
through the site. At the house the exposure is smaller, and inside it is about
1/20th to 1/40th of the outside value, i.e. 0.007 to 0.03 µW/cm². Allowing for
an 75% home/away ratio, this becomes 6 to 23 nW/cm². Away from the centre of the
radiated beams the mean exposure is much lower. Hence the peak boundary exposure
limit of 1 µW/cm² achieves a lifetime mean residential exposure of 10nW/cm² for
almost all of the population. This shows that the proposed standard is more
achievable than it initially seems.
Note: Cherry, N.J., 2000: "Schumann
Resonances, a biological mechanism for human health effects of Geomagnetic
Activity". Is under peer-review for publication in the journal, Natural
Hazards.
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