Limitations of the ICRP Recommendations
for Worker and Public Protection
from Ionizing Radiation

THE ATOMIC BOMB STUDIES:

The atomic bomb studies followed, and did not precede the setting of the radiation protection guidelines recommended by ICRP and followed internationally until 1990. The main recommendations were set in 1952, and the first doses assigned to A-bomb survivors were not available until 1965. Moreover, the research was designed to determine the effects of an atomic bomb, not the health effects of exposure to ionizing radiation. The research was undertaken by military researchers from both the US and Japan familiar with and primarily concerned with military used of atomic, chemical and biological warfare agents. The research has come too late for standard setting needs, it has focused on cancer deaths, is uncorrected for healthy survivor effect, and is not inclusive of all of the radiation exposures of cases and controls (dose calculations omit fallout, residual ground radiation, contamination of the food and water, and individual medical X-ray), and fails to include all relevant biological mechanisms and endpoints of concern.

It is normally claimed that biological basis of the cancer death risk estimates used by ICRP, is the atomic bomb studies. However, these studies are not studies of radiation health effects, but of the effects of an atomic bomb. For example, the radiation dose received by the Hiroshima and Nagasaki survivors from fallout, contamination of food, water and air, has never even been calculated. Only the initial bomb blast, modified by personal shielding, is included in the US Oak Ridge National Laboratory assigned "dose". This methodology is carried to an extreme. For example, one survivor I know lived within the three kilometer radius of the hypocenter, but was just beyond the three kilometre zone, at work, when the bomb dropped. As soon as she could, she returned home after the bombing and found her parents and brother dead. Then she stayed in her family home for the three following days, not knowing where to go and filled with grief. Although she suffered radiation sickness and many subsequent forms of ill health, she is counted as an "unexposed control" in the atomic bomb data base. By using the "not in the city" population which entered after the bombing as "controls", many of the cancers attributable to the radiation exposure in both cases and controls are eliminated from the outcomes considered related to the bomb. In contrast, in the United States:

"Any veteran exposed to a nuclear bomb test or who was part of the first 11 months of occupation of Hiroshima or Nagasaki is provided coverage for radiation exposure and any such veteran is assured priority of hospital treatment ahead of veterans with non-survivor claims. Occupation of Hiroshima or Nagasaki means official military duties within ten miles of either city, between the dates of 6 August 1945 and 1 July 1946." (Ref. 1)

The difference is obvious: the A-bomb studies measure only cancers due to the bomb blast; veterans are compensated for radiation induced cancers.

The basic radiation protection standards, recommended by ICRP and in effect until 1990, were set by the physicists of the Manhattan Project and presented to the International Association of Radiologists in 1952, when they asked to be allowed to join the organization. They set maximum permissible doses per year as 50 mSv for workers and 5 mSv for the public.

The data base for the Hiroshima and Nagasaki Life Span Study, the basis for the mortality estimates, was first identified in the 1950 Japanese Census. The information was not collected and ready for analysis until around 1957, and because it depends on first cause of death information, it was based on only a small percentage of deaths for the first seven years. It was heavily dependent on the accuracy of death certificates. Deaths in the Hiroshima and Nagasaki population between 1945 and 1950 are not included in the study. Even today, the majority of the 1950 identified survivors are still alive. (Ref. 2)

The first research reports were based on distance from the hypocentre. The doses were not assigned to the survivors until the T65D, (which stand for tentative dose estimates, 1965), compiled by John Auxier of Oak Ridge National Laboratory, became available. Atomic Bomb dose/response studies could not have been the basis of recommendations set in 1952 because they did not exist!

Interestingly, the Atomic Bomb Casualty Commission (ABCC) and its successor organization, the Radiation Effects Research Foundation (RERF), has, since the beginning, collaborated with the Japanese National Institute of Health (JNIH). ABCC was set up be the occupying force in September 1945. Their Japanese partner was responsible for hiring and firing all Japanese scientists who worked on the A-bomb data, although the US assumed singular control of all of the dose assignments once they were available.

The JNIH was actually established by the order of the U.S. Forces (Ref. 3), staffed with scientists from the Institute of Infectious Disease (IID) attached to the University of Tokyo, and containing most of the leading medical scientists from the Japanese Biological Warfare (BW) Institutions and the infamous Unit 731, which was responsible for the gross experimentations with humans in Manchuria during World War II. (Ref. 4) The Japanese scientists who engaged in biological warfare experiments on live human beings, allegedly including allied prisoners of war, were granted immunity by the U.S.Army from investigation for war crimes in return for the results of their experiments.

Kobayashi Rokuzo, advisor to the IID laboratory was attached to the Japanese Army's Medical College headquarters of the BW network, was Director of JNIH from 5/47 to 3/55. His Vice-Director for the same term was Kojima Saburo, who had intensively cooperated with BW Unit 1644 in the vivisection of humans at Nanking, and with the IID unit during the occupation of China. The Director of the JNIH from 3/55 to 4/58 was Komiya Yoshitaka, who was a member of the Institute of Health in Central China during the occupation, part of the BW network of hospitals run by the Military Police. Yanagisawa Ken, Vice-Director from 10/58 to 3/70, conducted experiments on Chinese youths during the occupation, through BW Unit 731. It was through these human experiments that he developed dried BCG, becoming "eminent" in medical circles. The list is much longer, including Directors and Vice-Directors up until 1990, scientists known to have conducted military experiments on humans. (Ref. 5).

Clearly warfare and the results of the nuclear bomb "experiment" were the main guiding principles of the research at Hiroshima and Nagasaki. American researchers were "safe" with the Japanese who had also conducted research on humans in order to further their war tactics. Consequently, it was not until 1994 that the research on cancer incidence rate after the A-bomb exposure was first published, highlighting their neglect the high incidence rate of breast, thyroid and skin cancers (not always fatal). Incidence rate had been unreported up until then. (Ref. 6).

In 1986, we witnessed the release of a complete reassignment of doses to the Hiroshima and Nagasaki survivors, supposedly based both on revised estimates of the neutron component of the dose and new estimates of shielding. According to Dr. Dale Preston, who directed the reassignment of doses, this was not a simple proportional change in all doses, but a true reassignment, often to new categories of exposure. This implies that all of the research based on the earlier assignment of doses is now considered to be wrong.

"The importance of the new research is that it completely changes the scheme of radiation doses that people are supposed to have received in Japan, particularly in Hiroshima." (Ref. 7)

According to this same article, the dispute over dose estimates had been brewing for four years, since 1977, when the US National Council on Radiation Protection asked John Auxier for supporting information for his assignment of doses to atomic bomb survivors. Auxier stated that when his office was moved in 1972, the record division at Oak Ridge mistakenly shipped his files to the shredder. He never reported the loss of these valuable papers. There was no US Government response until 1981 and it took until 1990 to complete this rearrangement of the Hiroshima and Nagasaki data. All of this manipulation of data took place "in house" by the staff of the US Department of Energy. Such sweeping change in a data base is usually considered manipulation, whether deliberate or not.

There are other reasons to challenge the ICRP reported reliance on the atomic bomb studies for its fatal cancer risk estimates. Not only does this research fail to include dose from residual radiation, fallout and food web sources, but it also fails to include medical X-ray data for each survivor. Radiation "dose" in these studies excludes all ionizing radiation exposures except that from the original flash of the bomb. Many survivors were part of special investigations requiring medical X-rays, the Japanese medical doctors X-ray the survivors at their yearly medical examination, the American researchers X-ray them every second year.

Although the A-bomb scientists have now admitted that more cancers were caused per unit dose of radiation than previously thought, ICRP has now given itself risk reduction factors for slow dose rate and low dose. This introduction of an unsubstantiated "correction factor" gives evidence of the inadequacy of the data base to answer important questions about worker and public exposures, which are almost all at low doses and slow dose rate. It also indicates that the ICRP knows that it is inadequate. There is no supporting human evidence for this reduction of the risk factors, and considerable evidence that it is not warranted. (Ref. 9).

I do not have time to go into all of the myriad details involved in forming my judgement, since I have worked in this field for thirty years, but I would generally recommend the article: "Inconsistencies and Open Questions Regarding Low-Dose Health Effects of Ionizing Radiation", by Rudi H. Nussbaum and Wolfgang Kohnliein, and also the fine research papers published by Dr. Alice Stewart on this subject, and on ABCC failure to correct their data for the Healthy Survivor effect. It is my professional opinion that the slow dose rate - low dose reduction factors used by ICRP (and UNSCEAR) are not justified. It is also my professional opinion that the fatal cancer dose rate for an exposure of one hundred Person Gray should be conservatively set at 20, rather than the current 5 as recommended by ICRP. The direct extrapolation for Atomic Bomb data to low dose exposure would predict 17 fatal cancers per Person Gray exposure. They obtain this estimate in spite of losses through failure of death certificate information and elimination of all deaths prior to 1950. This, in the face of under reporting, is in close agreement with nuclear worker data, and should not be reduced with this Dose-Dose Rate Reduction Factor.

BIOLOGICAL MECHANISMS AND ENDPOINTS:

In the early 1950's, when it was generally recognized that using the erythema dose, the dose which actually burnt the skin, was not adequate as a guide to radiation protection, many different biological endpoints were proposed as guides to regulatory standards: reproductive problems, tumors, congenital malformations, cataracts, blood disorders. Other possible biological endpoints were added later: obesity, hormonal disruptions, auto-immune diseases, developmental disorders, mental and physical retardation. ICRP decided that people should only be concerned about fatal cancers, and the only biological mechanism to be considered would be direct damage to DNA. Most of the other endpoints are dismissed as transient, not consequential, not damaging of the gene pool, or not fatal. This is an administrative, not a scientific decision, with which we may well wish to disagree. Even with respect to fatal cancers, those which were promoted or accelerated by the radiation exposure are not counted, because they are not considered to be "radiation induced"(Ref. 10).

Hiroshima and Nagasaki studies of non-cancer effects of exposure to ionizing radiation are either very poor or non-existent. I remember my frustration when I first looked for data on the relationship between exposure to radiation and adult onset diabetes. Diabetes among Hiroshima males had shown a linear trend with dose for causing death (Ref. 11). Since diabetes is not normally a first cause of death, one could well question the relationship of radiation with incidence rate of diabetes. When I located the research paper from the ABCC, I was astonished to find a bold statement that diabetes shows no relationship with radiation exposure in the early part of the paper. There is no supporting evidence for this statement. The remainder of the paper is devoted to a discussion of diabetes among A-bomb survivors with no further mention of or reporting of their doses. Reference is made to negative findings of atomic bomb research in order to discourage further research into the relationship between diabetes and radiation. Diabetes rates are extremely high in the nuclear fall out areas of the Pacific, downwind of the Nevada Test Site, and in areas of heavy fallout in the Arctic. However, no research has been done into the possible causal links with nuclear fallout.

The US studies of the health affects of nuclear fallout were carried out in the Marshall Islands, not (as noted earlier) in Japan (Ref. 12). They are much less publicized. The US began testing nuclear bombs at Bikini Atoll in the summer of 1946, before the territory had been given to it by the UN as a "Strategic Trust Territory". The world community knew that it was the intention of the US to use this territory for nuclear testing, but chose to look the other way. The Australian Ambassador was the exception, and he chose to resign from the UN over this issue. Other nations could hardly have failed to notice! Australia merely replaced their Ambassador, the US was given its testing site in 1947, and everyone looked the other way as the US and UK conducted nuclear tests in the Pacific and Australia (Ref. 13).

On March 1, 1954, the US exploded a 15 Megaton hydrogen bomb at Bikini, and no one informed the Rongelap People, who lived downwind of the testing site. The Weather men stationed at Rongerik Atoll, slightly further away from Bikini than Rongelap, have publicly testified that they warned the military that the winds were traveling in the direction of inhabited Atolls. The US Navy ship, Gypsy, stationed just off the tip of Rongelap, was ordered to move away from the fallout area, but the Rongelap People were not warned.

About 72 hours after the heavy fallout on Rongelap, which polluted the land, drinking water and food, the Rongelap People were evacuated to the Kwajalein Atoll military base for medical examination and care. Many suffered sever radiation sickness, burns, epilation (hair loss), and depleted blood counts. They were forced to stay on Kwajalein for three years, until the US Military declared their Atoll again "safe for inhabitation". In moving this population of about 87 people back to the Rongelap Atoll, the US chose a population of relatives (Rongelapese who were not on the Atoll at the time of the fallout), matched for age and sex, to return to the Atoll as a "control" group for their research.

Money appropriated by the US Congress for the health of the Rongelap People was given to the Brookhaven National Laboratory for their research program. The Laboratory purchased and outfitted a ship which they used in the summer to travel from Long Island, New York, via the Panama Canal, to the Marshall Island, which is about half way between Hawaii and Japan. Their medical program consisted primarily in conducting blood tests of the Rongelap "cases" and "controls", and examinations for thyroid nodules or other thyroid abnormalities. The medical "care" given to the Marshallese consisted of referral slips to local health professionals noting some medical problem which had been found during the examination and recommending medical diagnosis or treatment (often not available in the substandard facilities in the Trust Territory). If they found a thyroid abnormality, this Brookhaven team would recommend flying the Marshallese to the Cleveland Clinic in the US for a thyroidectomy, calling this preventive surgery (preventing thyroid cancer by removal of the thyroid gland).

In 1978, the US Department of Energy conducted an extensive investigation of the residual radiation on Rongelap Atoll. The Rongelap People after seeing the reports of their still contaminated Atoll and food web, evacuated themselves and began a struggle with the US Congress for cleanup and compensation. Finally in the late 1980's, the Congress agreed that the Island was still uninhabitable, although the experimental population had been living there from 1957 to May 1983, some 26 years. The nuclear scientists working for the US Department of Energy and the US Department of Defense claimed that the Rongelap People were irrationally fearful of the radiation and that their evacuation was uncalled for. Eventually the Congress not only commended the Rongelap People, but they ordered a cleanup of the Atoll to a level guaranteeing that exposures of the people would not exceed 0.25 mSv per year, well below the 5 mSv per year standard used in the US. This same standard for cleanup was used by the US on the Johnston Atoll, another US nuclear test site in the Pacific.

The medical examination of the Rongelap People included many reports of "monster" and molar births. According to the People they actually began to photograph these abnormalities, which at first they had hidden thinking it was their own fault to have such abnormal pregnancies. When the photographs were shown the American researchers, the pictures were seized. They burned them in front of the people saying: "This is what we think of your evidence". We heard this story from many different people on the Atoll.

In a cross sectional study which we undertook in 1988 (Ref. 14), we included 297 children, 134 adult females and 113 adult males, randomly chosen from Rongalapese in the US DOE "exposed" category, i.e. in the actual fallout, "control" category, i.e. relocated on the contaminated Atoll with the exposed group in 1957, and "neither" of the above, and their children. We found the following proportions with serious chronic illness among adult Rongelapese born prior to the 1954 hydrogen bomb detonation:

Serious congenital disease or malformation in living children (realizing that with the substandard medical facilities many were miscarried, stillbirths or infant deaths):

* This category had a higher rate of miscarriages and still births. There were 59 (1.6 grandchild per adult) offspring in this category, while the other two categories included 81 (4.1 grandchild per adult) and 84 (3.1 grandchild per adult) children respectively.

** There were only 13 live children (0.36 per adult) in this survivor group, whereas there were about 50 (48, 2.4 per adult and 51, 1.9 per adult) respectively representing the other two exposure categories.

In the survivor population, those over 35 years of age in 1988, 2.4% were found to have congenital diseases or malformations.

Using the three age groups as roughly representing three generations of Rongelapese -- those exposed, their offspring and the third generation -- we find some startling changes in health parameters:

It seems that we should have expected the thyroid abnormalities at Chernobyl! However, the world medical community was completely unprepared for the crisis since this Rongelap data was not widely known by the non-US Government scientists.

These figures likely indicate the teratogenic effects on the first generation born on the contaminated Atoll after the relocation there of the exposed and control population in 1957.

More than 90% of the survivors were under medical service and more than 50% experienced frequent hospitalizations, about 2.5 time higher than in their unexposed peer group. They found the following:

In the early 1970's, when I was part of the analytical team working on the Tri-State Leukemia Survey, I noticed the remarkable statistical regularity of the increase of non-lymphatic leukemia incidence in the population with increasing age. From age 15, when the incidence rate is at a minimum and childhood cancers have played out, one finds an increased rate of about 5% per year of these leukemias. I found the same compound interest type increase in non-lymphatic leukemias in the general population with increased usage of diagnostic medical X-rays, about 4% for trunk examinations. Therefore, I posed a new research question: What exposure to medical X-rays is comparable to one year of natural aging for increasing the risk of non-lymphatic leukemia? I found that the answer was dependent on the part of the body exposed to the X-ray, which turned out to be the amount of the bone marrow exposed by the particular X-ray procedure (Ref. 20).

With one more important piece of information, namely that medical X-ray is measured by the mR in air at skin entrance (rather than by tissue or bone marrow dose as used by the physicist), I will telescope some ten years of research into a few short conclusions:

• For X-ray of arms or legs, and dental X-ray, it requires an accumulated dose of 4000 mR to increase the risk of non-lymphatic leukemia the same amount as one year of natural aging.

• For chest X-ray, it requires an accumulated dose of 1670 mR at skin entrance to simulate one year's natural aging for increasing non-lymphatic leukemia rate.

• For abdominal X-ray it requires an accumulated dose of 1000 mR in air at skin entrance to simulate one year's natural aging for increasing the non-lymphatic leukemia rate.

• The corresponding bone marrow doses for these three sites and these mR doses are: 0.64, 0.72 and 0.83 mSv.

• This is clearly consistent with measurements of the external annual effective dose equivalent for natural background radiation: 0.65 mSv in UNSCEAR 1982 (for normal parts of the world); 0.81 mSv in Solon et al. 1958 (for 124 US cities); 0.61 mSv in Beck et al. 1966 (for 210 locations in the US).

I called this generalized effect of X-ray on the ability to resist non-lymphatic leukemia an "acceleration of the aging process" (Ref. 21). This is a less sophisticated term than "genome instability", but I think that I was measuring the same phenomenon in humans exposed to diagnostic X-rays.

Another important point of this research is that although medical X-ray is low dose, it is given at a fast dose rate, a matter of seconds, whereas the natural background dose is delivered at a very slow rate, spread over the course of a year. There is obviously not a dose rate difference, contrary to what the ICRP would have us believe.

In other research on the Tri-State Leukemia data, I used the natural aging equivalent of each persons medical X-ray exposure history, and added it to their chronological age to obtain what I called the person's "biological age". This was then used in the standard age adjusted statistical procedures rather than the chronological age. It served to elucidate many problems of apparent inconsistency in the data, and proved to be a valuable tool in understanding the complex relationships between environmental factor influencing leukemia rates in a large population. For this reason, namely, its general nature as a factor requiring control (just as one must control for age in epidemiological research) I believe that the aging effect, or genome instability, has broader consequences than just increasing the rate of non-lymphatic leukemia. Again, this implied a need to expand the biological endpoints and low dose mechanisms of concern when dealing with exposure to ionizing radiation.

In addition to these general affects on the whole organism, there are micro-biological effects and biomarkers of exposure which have been neglected by the ICRP because of their focus on cancer death and only one mechanism, namely, direct damage to the DNA molecule initiating a malignant growth. Professor Michael Vicker, University of Bremen, has documented the acute radiosensitivity of blood to micro-Gray doses of radiation, causing the arachidonic acid cascade (Ref. 22). Rather than trying to extrapolate the DNA damage hypothesis from the high dose exposures to radiation into theoretical happenings in the low dose range, researchers would do better to expand the mechanisms studied to include those which actually occur at the low dose and their sequelae.

With all of the sweeping changes which have occurred in biology and microbiology since the 1952 discovery of DNA by Watson and Crick, radiobiology has stayed focused on cancer and direct damage to DNA. Other branches of biology have expanded to consider the entire cell, systems influencing cellular behavior including functional levels and coupled feedback reactions of networks of inter- and intra- cellular responses regulating cell communication. Without a holistic view of biology and physiology, radiobiology has been consumed with detail and elaborate mathematical picture of the small world which was delimited by the very first administrative decisions of the nuclear bomb era.

In an organism, cells communicate with one another through the exchange of specific information, for example through a hormone, and the translation of this signal into intracellular messages. Paracrine (hormones secreted from tissues other than endocrine glands) and endocrine hormones are unable to pass through cell membranes. Therefore their information (the hormone) requires a cellular receptor on the outside surface of the cell, a transmembrane signaling that is connected to the receptor, called a "second messenger-generating enzyme", and a correct interpretation of the second messenger system. Various second messengers are released into the cell after stimulation of a particular receptor enzyme system, and which systems may be activated depends on the genetically determined receptors possessed by the cell. This communication system between cells in complex systems, can be modified, for example by phosphorylating particular proteins, and two second messengers can interact through feedback and cross talk. Ionizing radiation causes many interferences and disruption in this delicately balanced intercellular communication system. In radiobiology, these problems are dismissed and assume to be either trivial or perfectly repaired. Ionizing radiation induces oxidative stress, something admitted by radiobiology but discussed only in terms of its thermal effects. This same oxidative stress induces measurable inflammation, including a massive cascade of fatty acids in various states of oxidation. These mediate inflammatory reactions in the blood and other tissues, such as blood vessel endothelium, and function as second messengers, even controlling such things as pain and chemiluminescence.

The perturbation of cellular communication, regulation and homeostasis by low doses has major consequences for human health and development. It is irrational, as the physicists are now doing, to count on the failure to observe high dose effects at low doses as "proof" that such doses are "safe". DNA damage is a statistical phenomena, called stochastic by the physicists, while the inflammatory response is non-stochastic, or deterministic as it is now called. Unlike skin burns, these internal inflammatory responses occur at microGray doses. The ICRP assumes that deterministic effects do not occur below 500 mGy doses.

The ionizing radiation stimulations are "illicit" in the sense that there is no equivalent stimulation of the arachidonic pathway after non-radiological physiological stimulation, making it pathogenic in character, difficult for the body to regulate and return to homeostasis. This response activates the monocytes, which kill themselves by the oxidants they produce, often ending up as pus along with their digested cellular victims. They can endanger the host by killing other tissue, for example, transplants or infarcted heart tissue.

Activated monocytes are carcinogenic, provoking hitherto latent oncogenic systems and genomic errors to replicate. This may well be one of the mechanisms by which cancers were increased within the first ten years after the Chernobyl disaster. These cancers were dismissed by the IAEA as not radiation related because the ICRP required latency period of ten years had not been completed. These were radiation promoted or accelerated cancers, not radiation induced cancers. Again, we see ICRP recognizing only radiation induced cancers, whereas the victim will experience both mechanisms as due to the disaster.

HORMESIS:

Recently, in a concerted effort to raise the permissible levels of radiation for workers and the public, members of the Heath Physics Society have been actively promoting their theory of Hormesis, namely, that low dose exposures to radiation induce "beneficial" effects such as longevity, robustness, radio-resistance and increased growth. The use of the term "beneficial" implies a judgment, not a scientific fact. Experiments backing these hypotheses have been difficult to reproduce and definitions of "beneficial" have been controversial and appear very subjective. Claims of low dose hormesis have frequently been based on high dose observations, and the only mechanisms offered for these effects has been speculation on repair overshoot at the cellular and genome level. Cell growth as "hormetic" is the most troubling claim, since illicit growth stimulation signifies catastrophe for biological organisms.

What has been sorely neglected in this public relations battle, is that low dose radiation at the cellular level must necessarily affect a large range of molecules in the cellular communication system in any particular cell type. In order to produce one "good" effect, one must endure many other unwanted "bad" effects which will in the long run claim a physiological price perhaps significant, although they evolve to a clinically observable level more slowly (Ref. 23).

Many of the phenomena which have been attributed to radiation exposure by the victims, and those scientists and physicians who have studied the problem from the victims point of view or simply from the available information, can be explained by the low dose effects on inter- and intra cellular communication. In particular, this includes: the high rate of cardiovascular disease deaths in radiologists (Ref. 24); the deaths of infants in the higher fallout areas after the Chernobyl disaster in Germany (Ref. 25); the increased rate of low birth weight infant deaths which I documented in Wisconsin, statistically associated with increases in off gas releases from neighboring nuclear reactors (Ref. 26); and the higher than expected cancer mortality rates for nuclear workers (Ref. 27 and 28).

In therapeutic irradiation to kill cancer cells, there are often unwanted reaction in non-irradiated tissues. Sometime this secondary effect is lethal. Under the dominant theory that the only damage of concern is DNA damage, there is no remedy after the exposure. However, experience in hospitals has shown that corticosteroids, which inhibit one of the second messenger reactions, and aspirin like compounds, which inhibit the inflammatory response, can reduce these secondary effects They have demonstrated that these conditions are treatable.

The internal "sunburn" attributable to low dose ionizing radiation exposure may perturb homeostasis, and aggravate pathological conditions such as allergic or arthritic diseases, heart and circulatory disfunction, and cause death for the embryo, fetus or infant critically dependent on timed signal exchanges between cells for proper development.

It may also be true that in subsistence communities, such as was reported for India, children are more sensitive to the low dose effects. The children in five Indian villages downwind from two nuclear reactors demonstrated four-fold higher rates, statistically significant levels, of congenital malformations than a comparable subsistence control group 50-60 kilometres away. Adults (born before the operation of the nuclear reactors) showed comparable levels of congenital malformations (Ref. 29). There have also been documented reports of teratogenic effects after the Chernobyl disaster (Ref. 30). This has very serious implications for the current push to market this unwanted technology in the economically developing countries.

My own research has pointed out the dramatic reductions of monocytes in ionizing radiation exposed populations in many parts of the world (Ref. 31). It seems to be clearly a biomarker for exposure, similar to the way a sun burn is a biomarker for exposure to visible and ultra violet light. I believe that what I am measuring is both a response to low dose radiation as described by Vickers, and also an effect due to the radiosensitivity of the stem cells in the bone marrow which produce the monocytes. These stem cells, subjected to chronic irradiation by the radionuclide incorporated into bone (strontium 90, plutonium, uranium, radium, lead 210), become depleted, clinically resulting in iron deficient anemia and depression of the cellular immune system.

I hope that I have shown that the very narrow focus of ICRP on one biological mechanism of damage to one type of molecule, namely DNA, and neglect of all other mechanisms and molecular damage from ionizing radiation, is scientifically abhorrent and practically very prejudicial to the victims of radiation. There are now attempts to further restrict this narrow focus to health effects due to doses above 100 mSv, through claims of "hormesis" below this dose. The victims must try to fit their problems into the narrow categories "accepted" by the ICRP. It should be the other way around, namely the ICRP is expected to recognize and protect against all mechanisms, damage to all important molecules, and the serious consequences of such damage for human health subsequent to all doses of radiation.

It should also be noted that studies done in Russia after the Chernobyl disaster, point to doses which are below the stimulation of the cellular repair system. That is, at very low doses of radiation the cellular repair mechanisms are not stimulated and the damage goes unrepaired. This would imply "J" shaped curve for effects at low doses (Ref. 32).

ADEQUACY OF RESEARCH INTO NON-CANCER EFFECTS:

Unfortunately, because of the professional isolation of radio-biologists from their colleagues in microbiology, biology and physiology, they have spent their time in elaborate mathematical modeling of the basic narrow focus determined in 1952: namely reconciling the different types of radiation and energies of the transformation events, relating partial body exposure to whole body exposure, setting tissue weights to reflect the fatal nature of the induced cancers. They have missed the examination of subtle low dose exposure mechanisms, investigations into the reasons for differences in radiation sensitivity between different tissues, different people and the same person at different periods in their life.

The non-cancer effects of radiation have largely been studied outside of the generous funding mechanisms of the nuclear establishment, and these studies often cannot produce accurate dose estimates. For example, the whole field of teratogenic effects of radiation. These effects are well known, and have been demonstrated in medical X-ray case and even more clearly in Kerala, India, and Chernobyl, Ukraine. However, if you have made an administrative decision that there are only two categories of radiation effects worth considering: direct damage to the Standard Man, and damage to the population gene pool, then this damage is of no concern and dose responses are not obtained. Teratogenic damage, embryonic and fetal losses, as well as still births, apparently do not count, because they do not effect the population gene pool and are not an economic cost to society. These damaged offspring never pass on the defect to future generations.

I did a small study on the Tri-State Leukemia data to see if there was a deficit of births in the "irradiated in utero" sub-sample. I found that in the control children, those without leukemia or other life threatening disease, matched to the case children for age, sex and geographical location, there was a deficit of children in every irradiation category (Ref. 33). This is highly significant on a 1% level, that is, it would happen by chance in less than one of a hundred such studies. In all, assuming that the unirradiated children gave the population distribution of pathological factors, and the children with no pathological factors gave the distribution of irradiation categories, 259 children would have been expected in the control population, but there were only 223, a loss of 26 (10%) of the sample. The children with leukemia, on the other hand, were over represented in each of the radiation and pathology categories. There were 151 children, while only 130 were expected, an excess of 21 (14%). Both of these groups of children were controlled for Mother's earlier pregnancy loss and pathologic factors. One can assume that the excess was attributable to diagnostic X-ray at doses below 1 mSv. Usually prenatal X-ray examinations are assumed to give a dose of 0.5 mSv to the fetus. This is one half of the yearly dose to the public permitted by ICRP. Investigation into the mechanisms behind this reproductive loss has been minimal or non-existent.

Research into the genetic effects of exposure to ionizing radiation has also been unsatisfactory, even though this is on the ICRP administrative list of detriment concern. For example, as early as 1957, the World Health Organiztion identified the population exposed to high background radiation in Kerala, India, as the best population in the world for studying the genetic effects of radiation (Ref. 34). This was never followed up with action until a group of independent researchers with a small grant from the World Council of Churches undertook a study in 1988. This data has now been collected but needs more input of money for main frame computer analyses, and publication of the findings. We do know that on the high background monozite sands, with chronic exposures between 3 and 30 mSv per year, there is four times the rate of Down's Syndrome, twice the rate of other mental retardation, epilepsy, congenital blindness and deafness, deformities of the long bones and infertility, than is found in the matching control group on normal background (Ref. 35).

It is scientifically outrageous to keep stating that the RERF research found no genetic effects of radiation! Atomic bomb researchers were aware of the fact that their data base was inappropriate. Their research is clearly poorly designed because of their odd matching of cases and controls, their failure to correct for healthy survivor effect and the shortness of time since exposure, which can mask intergenerational effects. Yet the ICRP has failed to call for support for the research which is universally agreed upon as most likely to show the effects of chronic intergenerational exposures.

Meanwhile, the genetic problems has been reduced by ICRP administrative decision not to deal with recessive genetic damage, or diseases with genetic components, but rather to limit consideration of genetic damage to the most obvious autosomal dominant and X-linked defects, and chromosomal diseases. The risk estimates being used for genetic damage are derived from rat studies. Sometimes the genetic effects "of concern" are limited to the first generation offspring under the pretext the damage to subsequent generations does not cause sorrow to the individual exposed during their life time!

Current urgent research needs in the area of radiation health and safety includes:

• Funding of serious analysis of the Kerala data, with full involvement and credit given to those who have carefully collected this data without proper financial support from either governments or the nuclear industry.

• Research into the dose response estimates appropriate for teratogenic effects of radiation and inclusion of these effects in the administrative category of "detriments".

• Research into dose response relationships between radiation exposure and the occurrence of: cysts; blood abnormalities; autoimmune diseases; hormonal disruptions; reduced fertility; skin cancer (including non-melanoma), and the so-called "transient" effects of exposure which disrupt homeostasis.

One would expect that such research, seriously undertaken, would lead to the use of genetic and teratogenic damage as the basis of radiation protection standards.

In the current application of radiation protection standards, for example at nuclear reactors, it is important to change the focus from maximally exposed individuals (usually the Standard Man who works out of doors near the facility) to maximally susceptible individuals (the embryo, fetus and baby being fed with contaminated milk), in order to truly protect against the most severe detriments. Standards should be protecting the public against the harmful effects of radiation exposure both to the individual (including those unborn) and to the gene pool.

The elegance of the mathematical theory should not take precedence over common sense protection of the most vulnerable.

NEED FOR RADIATION PROTECTION STANDARDS:

I would not like my remarks to be construed to mean that regulation of radiation exposure should not take place. It is of course necessary that standards be set. I believe that the standard setting should be recommended by a professionally established open body, with credentials in occupational and public health. The ICRP is profoundly undemocratic and unprofessionally constituted. It is self- appointed and self-perpetuated. Certainly a recommending body could be composed of individuals elected from professional societies such as international associations of professionals trained in occupational health, epidemiology, public health, neonatology, pediatrics, oncology, etc. Some members could be recommended by the WHO and the ILO.

An organization of users of radiation, such as ICRP, being asked to set standards is like inviting the tobacco industry to regulate tobacco! ICRP is organized by its By-Laws to include only users and national regulators (usually coming from the ranks of users) of radiation.

If it is decided that fatal cancer incidence rate should be the biological endpoint on which the regulations are based, and I do not accept this as the best indicators of problems, then the radiation industry needs to conform to the same standards of injury as is used for regulating the chemical industry.

The State of Minnesota, in the USA, decided that a nuclear waste dump should not be able to cause more than one cancer (fatal of non-fatal) over the life-time (70 years) of an exposed person. This is the standard which the State used for chemical polluters. Based on this, a criteria of no exposure of the public above 0.0005 mSv per year was derived by the State Department of Health. This Standard is being enforced in that State, although it is ten thousand times lower than the current permissible dose to the public per year under US Federal Law, namely 5 mSv per year.

In Ontario, the Advisory Committee on Environmental Standards (ACES) expressed astonishment that the nuclear industry was permitting itself to pollute the drinking water with up to 40,000 Bq of tritium per Litre, under the 5 mSv per year federal radiation dose limit for members of the public. When the ICRP reduced the recommendation to 1 mSv per year, the industry agreed to lower the permissible level of tritium in water to 7,000 Bq per Litre. When the ACES used the industry risk estimates for calculating the expected number of fatal cancers considered to be "permissible" under this Standard, they called for an immediate reduction in permissible levels to 100 Bq per Litre, with a further reduction to 20 Bq per Litre within five years. This was based of the standard setting used for toxic chemicals. This means the radiation protection guide line allows 350 times more fatal cancers than chemical standards would allow.

While I understand mathematically why the nuclear industry, dealing with a mixture of radionuclides sets such unreasonably high permissible values, I see also that these high values are used for public relations reasons to assure the trusting public when there is a spill or abnormal incident at a reactor. Stating that the exposure was less than 10% of the permissible dose, sounds reassuring! Yet if one knew that the permissible dose was 350 times too high based on cancer deaths caused, 10% would be seen as 35 times too high. It is in the interest of the nuclear industry, hiding behind ICRP, to carry on the subterfuge that "permissible" implies "no harm".

The ICRP assume no responsibility for the consequences attributable to a country following its recommendations. They stress that the Regulations are made and adopted by each National Regulatory Agency, and it merely recommends. However, on the National level, governments say they cannot afford to do the research to set radiation regulations, therefore they accept the ICRP recommendations. In the real world, this make no one responsible for the deaths and disabilities caused!

In ordinary public health practice, an industry can be called "safe", if it causes the death of less than one person per million exposed to it per year. Using the nuclear industry's own estimate of risk of fatal cancer, and the 1990 ICRP recommendation to keep exposures of the general public below 1 mSv per year, there is an expectation of 50 cancer deaths per year per million exposed. I believe that the risk estimate used by ICRP is too low by a factor of four, based on research done at the low dose and slow dose rate exposure level. This means the number of deaths per year may be as high as 200. These 200 deaths are likely to be predominantly deaths of women and children, and many of the cancers will be expressed clinically after the local reactor is decommissioned. Women have more cancers per unit exposure than do men because of their high risk breast and uterine tissue, and also because they are more susceptible to radiogenic thyroid cancer than are males. Children pick up more radionuclides from the water and food web, incorporating more in bone because they are growing. Children have less mature immune systems, and have a longer life expectancy during which the cancers of longer latency period can develop. It is the men over 50 years who have the smallest risk!

It would certainly be worthwhile for the Parliament to appoint a serious study of radiation protection standards, considering the current death estimates together with the potential breadth of biological endpoints which are truly of concern to the general public. Mental retardation, epilepsy, blindness and deafness are tragedies as well as social expenses never assumed by this industry. Infertility is spawning expensive in vitro fertilization clinics throughout the world. The economic costs externalized by this industry are very large.

I would personally be opposed to leaving the regulation of radiation completely to each national government, with an international recommendation. The nuclear industry has been trying for several years to have the regulations relaxed even further, and I understand that the next released report from the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) will be devoted to the "belief" in hormesis, the "benefit" of exposure to low level radiation. As a plenary member of the Health Physics Society, I have watched this movement within the industry expand over the past few years. The rallying cry is: "Put your mouth were your money is". Health physicists are trying to keep this industry alive in any way they can. Making radiation more acceptable to the public is part of that plan. In the face of such organized opposition to regulation, it will be necessary to establish an honest, prestigious organization which speaks to health - both of humans and of the ecosystem. It should be independent of the vested interest of users of radiation who make their living from this use. It should not attempt risk-benefit trade-offs, but only clarify and quantify the risks.

Rosalie Bertell, Ph.D., GNSH
International Institute of Concern for Public Health
710-264 Queens Quay West
Toronto ON M5J 1B5 CANADA
Tel: +1-416-260-0575
Fax: +1-416-260-3404
E-mail: IICPH@compuserve.com

REFERENCES:

1. US Code of Federal Law 3.309(d)(3) and the Veterans Health Care, Training and Small Business Loans Act of 1981, PL 97-82 11/3/81, sec.102, 95 Stat 1048, 38 USC 1710 (e)(1)(B).

2. Dale Preston and Donald Pierce. "The effects of changes in dosimetry on cancer mortality risk estimates in the atomic bomb survivors" Radiation Effects Research Foundation, Technical Report RERF TR 9-87.

3. M. Susan Lindee. Suffering Made Real: American Science and the Survivors at Hiroshima. The University of Chicago Press, Chicago 1994.

4. P. Williams and D. Wallace. Unit 731: Japan's Secret Biological Warfare in World War II. The Free Press, New York, 1989.

5. Shibata Shingo. "Japan's National Institute of Health (JNIH) as Heirs of the Tradition of Medical Scientists of the Biological Warfare Network". Documentation by Shibata, Emeritus Professor of the University of Hiroshima, June 1997. This document was prepared in English, and it includes an extensive Bibliography in Japanese to support the documentation.

6. Radiation Research Vol 137, 1994 Contains the four main papers on cancer incidence rate in atomic bomb survivors.

7. "New A-bomb Studies Alter Radiation Estimates", Science Vol.212, 22 May 1981, Page 900.

8. Ibid. Ref. 7.

9. "Inconsistencies and Open Questions Regarding Low-Dose Health Effects of Ionizing Radiation", by Rudi H. Nussbaum and Wolfgang Kohnliein, in Environmental Health Perspectives, Vol 102, No. 8, August 1994.

10. Several studies have shown increases in cancer above the expected value shortly after exposure to radiation, prior to the ICRP designated latency period for radiation induction. This was also observed after the Chernobyl disaster. See US National Academy of Science BEIR III Report, 1980, page 369. They report here on the ankylosing spondylitis patients followed by Sir Richard Doll. There were 28 cancer of colon deaths in the irradiated patients, with 17.3 expected. Of these, six occurred in the first three years with 2.52 expected. The authors conclude: "the early excess was not caused by radiation, but was related to the treated disease. Although the group not treated with radiation showed no such early excess."

11. Beebe, G.W., et al. "Studies of the Mortality of A-bomb Survivors. 4. Mortality and Radiation Dose, 1950-1966" in Radiation Research Vol.48,613-649, 1971.

12. Conard, R. A. "Medical Survey of the People of Rongelap and Utirik Islands, thirteen, fourteen and fifteen years after exposure to fallout radiation." March 1968, March 1969, BNL 50220 (T-562) Brookhaven National Laboratory, New York 1970.

13. Personal discussion with George Ignatieff, Canadian Ambassador to the United Nations at the time of the granting of US Trust Territories in Micronesia.

14. R. Bertell. "A Report to the US Congress on the Health Problems of Rongelap People" June 1989. Available from IICPH, Toronto.

15. Testimony of Dr. Katsumi Furitsu, Internist Medical Doctor and Member of the Investigative Committee of Atomic Bomb Victims, Hannan Chuo Hospital, Osaka, Japan. In: CHERNOBYL: Environmental, Health and Human Rights Implications" Transcripts from the Permanent People's Tribunal Hearing, Vienna, Austria, April 1996. IPB Geneva 1997.

16. Basic National Life Survey, Standard Japanese Population, as reported by the Japanese Ministry of Health and Welfare in 1986.

17. N. Hayakawa et al. "Mortality statistics of major causes of death among atomic bomb survivors in Hiroshima 1962-1982, Proceedings Hiroshima University RINMB 32, 405-424, 1991.

18. The committee for the compilation of materials on damage caused by the atomic bombs in hiroshima and nagasaki:Chapter 9, Aftereffects and Genetic Effects, Other Disorders, 327-332, In: Hiroshima and Nagasaki, The Physical, Medical and Social effects of the Atomic Bombings, Iwanami Shoten Publishers, Tokyo 1979.

19. Y. Shimizu et al. "Non-cancer Mortality in the Life Span Study, 1950-1985", Journal of Hiroshima Medical Association, Vol 44, 1388-1390, 1991.

20. R. Bertell. "X-ray Exposure and Premature Aging". Journal of Surgical Oncology, Vol. 9, Issue 4, 1997.

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22. M. G. Vicker. "Radiosensitivity Mechanisms at Low Dose: Inflammatory Responses to microGray Radiation Levels in Human Blood" International Perspectives in Public Health Vol 9, 4-20, 1993.

23. Biological Effects of Low Level Exposures to Chemicals and Radiation, Editor Edward J. Calabrese, University of Massachusetts School of Public Health, Lewis Publishers, London 1992.

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25. J. Scheer, M. Schmidt and H. Iggel. "Infant Mortality in the Federal Republic of Germany before and after the Chernobyl Nuclear Reactor Explosion" International Perspectives in Public Health Vol.6, 4-9, 1990.

26. R. Bertell. "Epidemiology in Radioactive Contaminated Areas" In: Biomedical and Psychosocial Consequences of Radiation from Man-Made Radionuclides in the Biosphere, Editor: Gunnar Sundes, Royal Norwegian Society of Sciences and Letters Foundation, Trondheim, Norway, 1994.

27. A. M. Stewart and G. W. Kneele. "Risk Factors for Radiogenic Cancers: A Comparison of Factors Derived from the Hanford Survey with those of ICRP" British Journal of Industrial Medicine, Vol. 42, 647, 1985.

28. A. M. Stewart and G. W. Kneele. "An Overview of the Hanford Controversy". Occupational Medicine, State of the Art Review, Vol. 6, No. 4, 641-643, 1991.

29. S. D. Gadekar and S. N. Gadekar. "Congenital Malformations Near a Nuclear Plant in India" International Perspectives in Public Health Vol 10, 3-7, 1994.

30. A. Roche. Children of Chernobyl: The Human Cost of the World's Worst Nuclear Disaster . Harper Collins Fount Paperback, Glasgow 1996.

31. R. Bertell. "Internal Bone Seeking Radionuclides and Monocyte Counts". International Perspectives in Public Health, Vol 9, 21-26, 1993.

32. Consequences of the Chernobyl Catastrophe: Human Health. Editor: E. B. Burlakova, Centre for Russian Environmental Policy and the Scientific Council on Radiobiology, Russian Academy of Science. Moscow 1996.

33. R. Bertell. "Radiation Exposure and Human Species Survival" Environmental Health Review. Vol. 25, No. 2, 1981.

34. The Effect of Radiation on Heredity. Study Group on Radiation and Heredity, World Health Organization, Geneva, 1957.

35. S. Geetha, I. C. Varma and V. T. Padmanabhan. "Cytogenetic Studies in Children with Mental Handicap and their Parents in High Background Radiation Region of Kerala, India." Presented at the International Symposium on Trends in Biological Dosimetry, October 22-27, Lerici, Italy, 1990.