Cellular Phone:
Criticism of the ICNIRP Guidelines

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Posted:
20 March 2000

CRITICISM OF THE HEALTH ASSESSMENT IN THE ICNIRP GUIDELINES FOR RADIOFREQUENCY AND MICROWAVE RADIATION (100 kHz - 300 GHz)

Neil Cherry

Lincoln University

31/1/2000

1 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.

1.2 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

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.

1.3 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.

1.3.1 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:

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), http://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:

1.3.2 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:

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 m g/m³
1 in 100,000               1.3 to 4.5 m g/m³
1 in 1,000,000            0.13 to 0.45 m g/m³

Figure 1: An example of standard setting using Benzene from the Royal Commission on Environmental Pollution, Houghton (1998).

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 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 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 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).

It is also an absolute prerequisite that the exposure takes place prior to the effect occurring (temporality). This is the only viewpoint which could be termed a "criteria".

1.4.1 Viewpoints NOT criteria:

Establishing a cause and effect relationship is a judgement call made on a weight of evidence approach. Guidance as to how to weight the environmental epidemiological evidence is given by Sir Austin Bradford-Hill. Hill (1965) discusses the interpretation of epidemiological evidence from Association to Causation. In many assessments that favour the RF-thermal approach and try to dismiss evidence of adverse health effects, Dr Bradford Hill's guidance is termed the "Bradford Hill Criteria". Bradford Hill's viewpoints are presented as a set of standards to be jointly achieved before a disease agent can be causally related to exposure. Sir Austin himself directly rejects this approach through the statement:

Sir Austin Bradford Hill would have found this conclusions untenable. When he looked closely at the data, which the authors stratified by mean exposure. 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.

1.4.2 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:

1.4.3 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.

1.4.4 First Priority - Dose-Response Relationship:

In relation to dose-response Sir Austin states:

1.4.5 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.

1.4.6 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:

1.4.7 Lowest Priority - Biological Mechanism:

Dr Bradford Hill's comments on "biological plausibility" or "biological mechanism" place them at the lowest priority. He states:

Just two years ago Quinn (1997) noted that:

1.5 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. For this 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.

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.

1.6 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.

The accepted model of cancer development involves initiation, promotion and progression, Figure 3.

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).

1.7 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.

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.

1.8 Dr Goldsmith is critical of ICNIRP standards approach

Eminent, internationally recognized, environmental epidemiologist, the late Dr John Goldsmith, Goldsmith (1997c), states:

(a) Failure to consider both thermal and non-thermal effects especially of non-ionizing radiation.

(b) Interpretation of non-significant results as equivalent to no effect.

(c) Accepting the author's interpretation of a study, rather than examining its data independently for evidence of hazard.

(d) Discounting data on unanticipated effects because of poor fit to preconceptions.

(e) Dependence on threshold assumptions and demonstration of dose response relationships.

(f) Choice of insensitive epidemiological indicators and procedures.

(g) Consideration of each study separately, rather than giving weight to the conjunction of evidence from all available studies.

1.9 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:

1.10 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 often focus the signal more in one direction than another. A cancer rate that is higher on the high emission side than the low emission side is a first indication of a dose-response.

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.

Figure 4: A typical vertical antenna pattern for a 4-element dipole array at about 98 MHz.(VHF), Units in dB.

Figure 5 is street level measurements around the Empire State Building for a 44 MHz VHF transmitter, taken in 1933.

Figure 5: Ground level radiation pattern for the 44 MHz (VHF) signal from the Empire State Building in New York City, from Jones (1933) by merging his figures 6 and 8.
 
 

Figure 6: Variation resulting from field strength with distance and frequency. Antenna height 1000', receiver height 30 ', power 1 kW, Reference data for Engineers, Jordon (1985).

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.

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.

1.11 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 1/15^th of the outdoor exposure. The away exposure is assumed to be 1/30^th 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 0.017m W/cm², respectively. These give reduction factors for street level and inside of 45 and 176 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.

1.12 A more appropriate approach:

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 totally new, fresh and objective scientific approach is needed to be taken to more comprehensively and reliably assess the research results that have been published. 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?

2. History of the RF-Thermal View:

2.1 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.

2.2 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.

2.3 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:

2.4 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."

 

 
"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."
 

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.

2.5 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.

2.6 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.

2.7 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.

2.8 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.

3. The ICNIRP and WHO Approach in the 1990's:

3.1 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".

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.

3.3 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)

3.4 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.

3.5 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:

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:

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.

3.6 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:

A. Alter DNA, initiating cancer.
B. Corrupt cellular growth control, thus acting as cancer promoters.
C. Act with other carcinogenic agents, working as Co-promoters of cancer.

There is evidence that EMR acts in all of these ways.

3.7 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.

3.7.1 ICNIRP misquotes results:

In the ICNIRP (1998) cancer assessment the following statement appears:

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.

3.7.2 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:

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:

Many more ELF health studies have been published since July 1994. Four laboratories have shown that ELF below 1.2 m T reduces the oncostatic protection of melatonin in human breast cancer cells, with a threshold of around 0.1 to 0.2m T. 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 0.2m T 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 0.3m T, 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 0.2m T cut-off and RR=5.1 (95%CI: 2.1-12.6) for 0.5m T 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 0.1m T. 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.

3.7.3 Canada does it 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:

4. ICNIRP's 1998 assessment of the RF/MW Guideline:

4.1ICNIRP 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."

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. (1995), Selvin et al. (1992), Dolk et al. (1997a,b), andMichelozzi et al. (1998).

In the middle of the frequency spectrum, where the ICNIRP Guideline exposure level is at its lowest, 200 m W/cm², there are residential epidemiological studies that give dose-response relationships for adult and childhood leukaemia with a threshold near 0.025 m W/cm². This is 8,000 times lower than the ICNIRP Guideline. In Switzerland, significant sleep disturbance was observed at an RF exposure level of 0.0004m W/cm², Altpeter et al. (1995). For this RF frequency (6.1-21.8 MHz) for which the ICNIRP Guideline is 2000m W/cm². The adverse effect occurs at a factor of 5 million times lower than the Guideline.

4.3 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 2 in terms of electric field strength and exposure intensity, as a function of carrier frequency.

Figure 7: The ICNIRP 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 (m W/cm²). The three plateau regions above 1 kHz are 87, 28 and 61 V/m, corresponding to 2000, 200 and 1000 m W/cm², respectively, ICNIRP (1998).

5. A sports analogy of the different approaches:

5.1 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.

5.2 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):

In his conclusion Dr Adey directly challenges the thermal view.

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 m W/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.

6.2 Calcium ion (Ca²⁺) efflux:

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.

 


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.
 

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."

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:

No change 0.75 2.30 4.50 5.85 7.08 8.19 8.66 10.6 14.7

Enhanced efflux 1.75 3.85 5.57 6.82 7.65 7.77 8.82

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 which 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 m W/cm².

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.

 


Figure 11: Effect of 15 V_rms/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.

"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".
 

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.

6.3 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).

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 600m T. 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.

6.4 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."
 

6.5 EMR Reduces Melatonin in Animals and People

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 m T, 60 Hz field with a 0.06m T DC field, over 10 experiments, averages a 46% reduction in melatonin production from pinealocytes. Stark et al. (1997) observed a significant increase in salival melatonin in a group of 5 cows when the short-wave radio transmitter at Schwarzenberg, Switzerland, was turned off for three days, compared to 5 cows that had much lower RF exposure. Hence there are now nine independent observations of melatonin reduction in animals from ELF and RF exposure.

Ten 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. Nine 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), 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. (1999). The tenth 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.).

 
Hence it is established from multiple, independent studies, that EMR from ELF to RF/MW reduces melatonin in animals and human beings.

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.

6.7 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. 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:

"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).

Figure 13:Electric fields from, I , the Schumann-Resonance, II , Local fields of about 3 Hz and the a (10 Hz) and d (3 Hz) human EEG channels, König (1974).

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 I (10 Hz) signals field intensity, König (1974).

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 m W/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 15: 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).

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.

7.1 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).

7.2 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.

7.2.1 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.

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:

• 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 (sAb ).

• sAb is quickly secreted from cells after production, increasing the levels of sAb in the blood stream. sAb then binds to Apolipoprotein E and apolipoprotein J to be transported to and across the Blood Brain Barrier.

• Over time, when sufficient sAb 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.

7.2.3 Neurological effects of cell phone usage:

In 1998 Mild et al. (1998) survey around 11,000 cell phone users in Norway and Sweden, Figure 16. 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).

7.2.4 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.

Figure 16: The prevalence of symptoms with various categories of calling times/day, A. Norway, B. Sweden, Mild et al. (1998).

Salival melatonin was measured in cows in the Schwarzenburg study in 5 ‘exposed’ cows and 5 ‘unexposed’ cows. The exposed cows had lower mean melatonin levels but the difference was not statistically significant because the sample was too small. Human beings were sampled (using urine analysis. Samples were taken first thing in the morning when melatonin levels are naturally low, instead of at the correct time soon after midnight, when melatonin levels are high and reductions are easier to detect. However, the research team noted "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 of 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).

When the transmitter was off for three days the melatonin in the exposed cow herd reached their highest nocturnal peaks for that week. When the transmitter went on again, on that day the exposed cows’ melatonin was statistically significantly lower than the unexposed cows.

The causal relationship between RF radiation exposure and deterioration in sleep quality is identified through a significant dose response relationship (p<0.001), improvements in sleep quality which changing the direction of the beams and turning the transmitter off, and reduced melatonin as the biological mechanism.

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 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.

7.3 Bioelectromagnetic Principle 3:

Our hearts are electrically sensitive.

7.3.1 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.

7.3.3 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).

7.4 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.

7.5 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.

7.5.2 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).

7.6.2 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 ten human studies show that EMR significantly reduces melatonin, Section 1.4.3 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.

7.6.3 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.

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 m T, men RR = 2.1 0.3-14.1 Feychting et al. (1998)

>0.2 m T, women < 50 yr RR = 1.8 0.7-4.4 "

>0.01 m T, women with RR = 1.6 0.6-4.1 "

+ estrogen receptor

>0.01 m T, women with RR = 7.4 1.0-178.1 "

+ estrogen receptor,

aged < 60 years

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.

7.7 Bioelectromagnetic Principle 7:

The EMR spectrum should be treated as an integrated whole, with biological impacts generally increasing with increasing carrier frequency.

7.7.2 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:

7.8.1 The Intrinsic Free Radical Principle.

7.8.2 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.

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.

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. Chromosome aberrations are a proven risk factor for cancer, Hagmar et al. (1994).

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 (<0.1m W/cm²) 156-162 MHz, 24.4 Hz pulse frequency, radar signal in Latvia produced significant alterations in the immune system factors of exposed villagers, Bruvere et al. (1998).

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.

7.9 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:

8.1 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. In considering the evidence before it, including evidence of actual or potential adverse effects which occurred about 3 m W/cm², the court set a public exposure condition for a cell site at that time and in that case of 2 m W/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.

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 evidence the public exposure condition of 2 m W/cm² was imposed.

8.2 Environment Court Judge's error:

In the 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 who received evidence of potential or actual effects below 2 m W/cm². This included the North Sydney Study, Hocking et al. (1997), presented by Dr Hocking, who recommended an exposure level of 0.2 m W/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). The judges findings accepted that there was a very low risk of childhood leukaemia, sleep disturbance and miscarriage, but allowed the ICNIRP guideline exposure level of 450m W/cm² to be applied.

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. In 1999 the Ouruhia Radio Tower case was settled by a consent order after Radio Network had presented its case and before the residents presented their main evidence. The presiding judge, Judge Peter Skelton. The judge felt it appropriate to record the following statement:

9. The ICNIRP treatment of Biological mechanisms:

9.1 In appropriate 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.

9.2 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 applies to all biological mechanisms, including Ca²⁺ 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".

9.3 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

10.1 The ICNRIP Statement:

There are several major errors and omissions in the ICNIRP (1998) assessment of reproductive effects, ICNIRP (1998), Figure 17.

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 for use in labour, and report on the subjective Apgar Score of the new-born child. The test is carried out about 60 seconds after birth. 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.

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.

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.

10.5.2 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 m W/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.

• 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),

Electric therapies OR=2.2
Shortwaves OR=2.5
Microwaves OR=2.4
Ultrasound OR=3.4
Heavy lifting OR=6.7 .

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
<0.13m T 1.0 Reference
0.13-0.3 m T 1.9 0.9-3.9
>0.3 m T 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 (³ 0,63 m T at the front door), OR = 5.1 (1.0-25).

• 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.

10.5.4 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.

10.5.5 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):

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 0.168m W/cm² and 1.053m W/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:

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.

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 m W/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 which 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 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 18.
 
 

Figure 18: Multigenerational exposure of mice to low level RF leads to complete infertility.

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 m W/cm² over a week. Total infertility occurred in mice after 5 weeks of exposure to 0.17m W/cm².

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 m W/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 course 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 19.

Figure 19: Specific absorption rate (SAR) profile across the uterus for a small woman exposed to 1 mW/cm², from Hocking and Joyner (1995).

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 m W/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).

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.

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 exposure period of 2 minutes is chosen to be associated with the exposure range of 80 - 1200 m W/cm². The dose-response relationship is expressed in terms of treatments per month.

One treatment per month is associated with a mean monthly exposure in the range 0.0038 to 0.056m W/cm², and a mean exposure of 0.03m W/cm².

There is a 5 % increase in miscarriage associated with a mean microwave exposure of 0.08m W/cm². One treatment per month is associated with a monthly mean exposure of 0.03m W/cm², so that this is the Level of Lowest Observed Effect. This is totally consistent with the calcium ion efflux and animal toxicology experiments.

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 19.

Figure 19: 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).

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 20, 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:

1. 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.

2. 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.

3. 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.

4. 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.

5. Beall et al. (1996): Is quoted by ICNIRP as failing to show significant increases in nervous system tumours, when it does, and includes a significant dose-response relationship between years of exposure and rates of brain tumor for computer programmers.

6. 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.

7. 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.

8. 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.

9. 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".

10. 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.

11. 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".

12.2 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, Cooper and Swygert (1994), Band et al. (1996), etc. In addition, the reviews of Goldsmith (1995, 1996, 1997a,b) are ignored. Many other papers are also 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 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.

• It is easier to present biased conclusions than to falsify data.

• 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:

• 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 0.2m W/cm², and hence involve chronic mean exposures in the range 0.015 to 0.03m W/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.

13.1 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.

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.

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:

13.2.3 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.

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).

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

Their 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. 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.

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

This 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.

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. The second data set was from Veterans' Administration Hospitals for the period 1963-76.

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).

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

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 VA compensation data Robinette et al. found significantly increase in sickness for Musculoskeletal system and other organs, including:

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 for when they identified them, and found that they were significant, they could not bring themselves to associate them with 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."

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. A high exposure 'repairer group' (AE), was placed in the 'operator', low exposure control group.

b. All participants are more highly exposed to radar than the average male population of the same age, Lin et al. (1985).

c. Combining the FT and AT groups reduces the exposure separation.

d. All of the three 'high exposure' groups contain a mixture of low, middle and high exposure individuals.

Exposure Dilution weakens and tends to destroy 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:

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.

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 5m W/cm² between 1953 and May 1975, 15m W/cm² between June 1975 and Feb 1976. After this it was a fraction of 1m W/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 m W/cm². Inside the exposure was in the range of 10 to 50 times lower, i.e. 0.04 to 0.2 m W/cm².

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.

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

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)

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:

• 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.

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.

13.4.1 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."

13.4.2 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. 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 21 shows a typical UHF signal taken from an antenna vertical pattern in Hammett and Edison (1997).

 


Figure 21: 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 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 21.

13.4.3 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 1.74m W/cm². When the PEF of 0.15 is applied this becomes 0.26m W/cm².

 
 


 

Figure 22: The measured and estimated power density (exposure in mW/cm²) with distance from the Sutra Tower. Circles show measurements. The line follows measurement points and the radial pattern of Figure 20 beyond 3 km. From Hammett and Edison (1997) and readings taken by the author in 1999.

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 23.

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 23: Spatial map of white childhood (<21 years) leukaemia for San Francisco, 1973-88, from Selvin et al. (1992).

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 23.

It is immediately evident in Figure 23 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.

Figure 23 also reveals the lack of cancer and residence in Golden Gate Park to the WNW of the tower, 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 and the port and industrial area along the eastern coastline. These were all taken into account when the residential population density was calculated below. The cluster 48-51, to the NE are residences on a western facing hill slope, with higher exposure levels from the Sutra 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. This explains some of the scatter about the dose response line.

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 22. 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.

Est. Population 1138 4334 3558 4489 5146 5566 4939 5386 8141 7988

Estimated personal mean dose

in m W/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

Figures 24 and 25 show extremely significant dose-response relationships (p<0.0001) for Childhood brain tumor and All Cancer. The trend line shows an estimated no observed adverse effect level (LOAEL) of 0.05m W/cm². This is of the same order of size of the lowest published calcium ion efflux exposure level (0.08m W/cm²), Schwartz et al. (1990). The trend line for All Cancer has a no exposure threshold near zero and a highly significant linear dose-response relationship. The All Cancer threshold is close to 0.02 m W/cm².

The dose-response trend analysis uses a least squares fit, using the Mantel-Haenszel estimate of t with a two-tailed t-test 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 Lymphoma (t = 1.94, p<0.05) and Hodgkin 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 24: 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 25: 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.

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 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 26.

Figure 26: 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.

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 5m W/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 m W/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.

13.6.1 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:

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.

13.7.1 The Context:

This and the next paper, Rothman (1996 a and b), are used to imply that there is "no excess total mortality was apparent among uses of mobile phones". This is on 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.

13.7.2 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 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 that the present preliminary findings have two major limitations:

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.

Three of the papers, Barron and Baraff (1958) and Rothman et al. (1996 a,b) are inappropriately included when they are not giving epidemiological results of cancer resulting from RF/MW exposure.

The remaining five reports or papers all show statistically significant increases in 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..

Two show these 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 close to zero, about 0.02m W/cm².

14. Studies that are acknowledged by ICNRIP to show increases in cancer from RF/MW exposure:

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".

14.1.1 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."

14.1.2 Cancer Epidemiology:

Most cancer studies are based on using records from cancer registers over several decades because it takes decades for cancer to develop and 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. 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. There 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.

14.1.3 Polish Military Exposure Assessment:

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."

14.1.4 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:

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.

14.1.5.1 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 m W/cm² for 3 months.

14.1.5.4 Integrated evaluation of immunity in MW/RF exposed animals:

Szmigielski et al. proceed to describe their own experiments in this area. They conclude:

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. 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.

They 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:

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:

Figure 28: 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 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 29.

Figure 29: Cancer morbidity rates in RF/MW exposed and "non-exposed" personnel for all types of malignancies at various age groups.

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.

(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

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.

The Haematopoietic and Lymphatic cancers are very highly significantly elevated and so are separated further in Table 17.

(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.

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).

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 1000m W/cm², and 83.7 % below 600m W/cm². This data also includes the all cancer risk ratio for these groups of people.

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:

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.).

15.1 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."

15.2.1 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. 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 30.

Figure 30: 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).

15.2.3 Exposure situation:

Tower 1 has the highest TV/FM output power, 500 kW, while Tower 2 has 290 kW and Tower 3, 110 kW. This shows that the Lane Cove population should experience the highest mean exposure and North Sydney the second highest. The frequencies involved are in the range 63 - 219 MHz and 626-633 MHz. 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 made. Using the output power of the 4 TV transmitters the combined radial exposure was calculated relative to the centre point of the three towers, neglecting ground reflections. At the center between the towers this gave 1m W/cm². The highest calculated exposures were between 4 to 8 m W/cm² in a narrow ring at about 1 km. 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 0.2m W/cm² at 4 km, the limit of the "exposed" population.

The second data set was a number of actual readings taken by the Commonwealth Dept of Communications. These were generally about 1/5^th 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 31.

Figure 31: Logarithm of the calculated power densities (in m W/cm²) for TV signals from the three TV towers against distance from the centre of the towers.  

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.

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 formula which does not produce side lobes, which for elevated VHF/UHF signals do produce and they influence ground level exposures out to beyond 4 km, Figures 4 to 6. 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 (3m W/cm²), in the garden on the street (0.066m W/cm²) and inside the home (0.017m W/cm²). This verifies the factors used for the mean exposure estimates made in section 1.10.

Using these 'representative' calculated exposures for each municipality, McKenzie et al. plotted the total childhood cancer incidence rate as a function of the calculated exposure, Figure 32.

Figure 32: 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 an estimated geographic centroid of each municipality.

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 4km ring, the outer edge of the 'exposed population', is about to 25 nW/cm².

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. 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".

It has already been shown that VHF and UHF broadcast tower transmissions follow a complex radial pattern. For UHF transmissions the ground level exposure, Figure 20, is low near the tower, rises to a broad variable peak between 1 and 5 km and then declines with distance out to 10 km (the limit of the Dolk et al. studies). When VHF signals are involved, Figures 4 and 5, some side-lobe peaks occur within 1km radius of the base of the tower. This immediately changes the approach to the U.K. study results.

15.3.2 U.K. Cancer Study Results:

A wide range of body cancer sites were analysed as a function of radial distance from the Sutton Coldfield transmission Tower, Dolk et al. (1997a). The data was obtained and analysed by the Small Area Health Statistics Unit of the Department of Epidemiology and Public Health of the Imperial College of Medicine, London. They obtained adult (>=15 years) cancer data for a wide range of cancers, but childhood (0-14) data was limited to all cancer and all leukaemia. The period was 1974-1986. The population living with 10 km of the Sutton Coldfield transmitter was 408,000 from the 1981 census. For the complete data set there was a statistically significant 3 % increase in all cancer with 10 km radius of the transmitter compared to regional expected rates (O/E = 1.03, 95%CI: 1.02-1.05 ).

15.3.3 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 but is far from 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.

For adult cancers the results are presented in the following two tables.

Figure 33: Radial cancer rates around the Sutton Coldfield TV Transmitter.

Figure 34: Radial adult cancer rates around the Sutton Coldfield TV transmission tower.

These tables show two radial cancer patterns:
 

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 21.

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 22.

Figure 35: Cancer data for the 20 site U.K. study from Dolk et al. (1997b).

Figure 35 (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.

15.3.4 Site Difference Analysis:

Thus we find a great deal of consistency between the Sutton Coldfield data and the 20-site data. There is only one major exception, the high rate of adult leukaemia near the Sutton Coldfield Tower.

For a cancer rate to be detected as high near an RF transmission tower, three factors must occur:

1. 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.

2. 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.

3. 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).

In addition to leukaemia, both studies, Sutton Coldfield and the 20-site Study, show considerable elevations in a whole range of cancers. It is disappointing that Dr Dolk and her colleagues did not analyze the radial patterns for other cancers in the 20-site study. Their bulk analysis, Figure 35 (Table 1) from the 20-site study and Figure 37 (Table 5) from Sutton Coldfield, shows considerable elevations for a number of cancers. At no point is the combined data from 21-sites analyzed and presented for cancers other than childhood leukaemia and brain tumour, Dolk et al. (1997b).

With the understanding of the residential radiation patterns, favouring a type a pattern (low, elevated, decline), a radial analysis of all of the data for other cancers would be very valuable. The initial indications from the data published thus far is indicative of data which supports the whole body principle, as confirmed by Robinette et al., Milham and Szmigielski.

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 37: Other cancer sites in the broad radial analysis from Dolk et al. (1997b).

15.3.5 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 (³ 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 s 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 Exposure Assessment:

Excesses in cancer are still seen at 10 km, where the direct exposure is 5 to 10 times less than the UHF peak of 1.3m W/cm², i.e. between 0.13 and 0.26m W/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 m W/cm².

This is consistent with the widely identified no observable adverse effect level of 0.025m W/cm².

If the authors had known about and applied the available engineering knowledge 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).

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).

Discounting the three inappropriately included studies, Barron and Barraf (1958) and Rothman et al. (1996a,b), all of the remaining studies report significant increases in cancer incidence and mortality from RF/MW exposure. 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).

The twin charges leveled ion this report, of using the wrong methodology and using Constructive Dismissal to defend their flawed methodology, 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:

17.1 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."

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."
 

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.

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.

The following is a brief summary of a number of relevant epidemiological studies which have been omitted by both WHO (1993) and ICNIRP (1998).

17.2.1 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 (SIR = 2.09: CI=1.08-3.65), Maskarinec et al. (1994).

• 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:

• Stenlund and Floderus (1997) identified increased Testicular Cancer in middle ELF exposure (>0.28m T) and high exposure (>0.4m T) compared with low exposure (£ 0.15m T) 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.

• Occupational risks of Brain Tumours includes telephone and radio operators, electricians, OR = 1.2 (0.2-5.2) for All Brain Tumour and OR = 1.4 (0.2-8.7) for malignant Brain Tumours, Kaplan et al. (1997).

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)

• 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)
>0.2m T or > 0.4m T-years

• Denmark, High voltage installations Olsen et al. (1993)

• Denver, Residence Savitz and Kaune (1993)

• U.S. Meta Analysis of 13 studies Washburn et al. (1994)

• 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)

• 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)

• Sweden, Occupational exposure Floderus et al. (1993)

• United States, Telephone industry Dosemeci and Blair (1994)

• 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)
• Danish Utility Workers Johansen and Olsen (1998)

• 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)

• 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)

• New Zealand, electrical workers Pearce, Reif and Fraser (1989)

• Canada, British Colombia pilots Salisbury et al. (1991)

• 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)

• 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)

Thirteen studies show dose-response relationships for EMR exposure and brain tumor:

• Denver, United States, power lines Wertheimer and Leeper (1979)

• 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 ³ 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)

• Canada, Provincial Residential Electric Consumption (REC) Kraut et al. (1994)

• U.S. Electrical Workers Savitiz and Loomis (1995)
 
Mortality Dose-response OR = 1.94 per m T-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 <0.05m T 0.05-<0.14m T >0.14m T n=10

RR = 1.0 2.6 (0.5-12.0) 2.3 (0.8-6.6) p=0.07

17.2.3 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 0.2m T 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 100m T.

As with the RF/Mw assessment, there is a large body of literature not cited by ICNIRP that strongly confirms the 0.2m T cut-off for residential studies of childhood cancer. All of the studies cited by the ICNIRP have mean annual exposures less than 1-10 m T for occupational studies and <0.6m T for residential studies. Hence in a Public Health Protection Approach a cut-off of 0.2m T 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.

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

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.

17.2.4 Summary and Conclusions:

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.

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 Level of No Observed Adverse Effects threshold of about 20nW/cm².

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:

18. Recommended Public RF/MW Exposure Standard:

ICNIRP's thermally based approach has been proven many times over 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. The dose response relationships indicate a cancer and reproductive problem threshold near 20 nW/cm².

Hence the interim immediate target could be 20nW/cm² to allow industry time to adapt, but the recommended standard of 10nW/cm² adopted in 2010.

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.

Figure 38 shows the dose-response relationship for sleep disturbance from the Schwarzenburg Study, Abelin pers. Comm- seminar.

Figure 38: Sleep disturbance around the Schwarzenburg short-wave radio tower in Switzerland, Altpeter et al. (1995) and Abelin (1998) - seminar. Groups A, B and C were surveyed in 1992. Group R asked to be included in an updated survey in 1996. They fitted into a dose-response curve because their exposure lay between B and C.

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 m W/cm². Assuming an inverse square law between 3.7 and 20 km from the radar, at 10 km the exposure is approximately 0.04 m W/cm² and 0.01 m W/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.

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

Aiming, over 10 years, to reduce it to

9. nW/cm² (0.01m W/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.

References: