Dr. Rosalie Bertell’s submission to CNSC, regarding SRB Technologies and its proposal to pour tritiated water down the municipal sewer.
Dose Dose-rate Reduction Factor
There are many scientific uncertainties associated with ICRP nominal risk of fatal cancer, currently 5 per 100 person Sv dose, for exposure to ionizing radiation,1,2.
The complexity of the biological response to dose and dose-rate was recognized as early as 1950, when the physicists from the Manhattan Project met with British radiobiologists in London to discuss radiation protection for the atomic age.3 At this meeting, L.H. Gray (1905-1965), M.R.C. Radiotherapeutic Research Unit, Hammersmith Hospital, who is now honored with a radiation unit designation, gave further clear directives to those who hoped to set radiation standards for the atomic era:
“The small number of examples which have been discussed suffice, I think, to show that it is not possible to express by a single number the efficiency of one radiation relative to another even for one type of biological damage. Still less is it possible to express by a single number to generalize over all types of biological damage. Protection recommendations, however, cannot take account in detail of all the complexities of such a situation. The International Protection Commission, at a recent meeting had reached the conclusion that from the point of view of damage to critical tissues, gamma rays, electrons and X-rays may be grouped as of equal efficiency, and that fast neutrons should be regarded as ten times as damaging of tissue. … it is customary in this country (U.K.) and America to regard alpha radiation as somewhat more damaging than neutrons, and to allow a factor of twenty for the efficiency of this radiation relative to gamma and X-ray.”4
This was the beginning of “committee decisions” to reduce the complexity of radiation effects to something to which mathematical functions and computer programs could be easily applied. At the time, they the scientists were not concerned about beta radiation.
There were more approximations, averages and choices of biological endpoints to come.
Later these decisions took on the aura of “scientific fact”, and these approximations, applicable in a crude way to a large group of people exposed to high doses of external radiation, became applied as if they were “scientific truth” to individual workers, military personnel and the public exposed to a wide variety of internal and external radionuclides. These RBE (radiation biological effectiveness) estimates may well be too low at chronic low dose exposures.
According to Gray:
“the largest factor of difference between alpha radiation and X- or gamma radiation is observed when minimal damage is delivered in protracted exposure, which is exactly the condition contemplated in framing protection recommendations.”5
This also appears to be the case when there is minimal exposure from protracted doses of beta radiation. The low dose with unexpected serious response phenomena was not unknown in 1950.
ICRP incorporates a DDRF (dose, dose rate reduction factor) of two below the risk which one would obtain by linear extrapolation from high dose fast dose-rate. ICRP believes that the DDRF is necessary since when the dose is low (under about 100 mSv) and dose-rate of delivery is slow, the body will be able to repair at least some of the damage caused by the radiation. There is no in vivo human data in support of this reduction.
Far from agreeing that the nominal risk of tritium should be reduced by a factor of two at low doses, these quotes imply the reverse:
“For mouse immature oocyte killing tritium administered chronically as HTO is of near maximum possible radiobiological effectiveness. The implication: tritium in the form most commonly encountered as an environmental pollutant may actually be as effective as the most damaging high-LET (linear energy transfer) radiation in reducing the fertility of certain other species as well…. A highly sensitive germ- cell stage exists prenataly in at least some primate species… By implication, such highly vulnerable stage may also exist in the pre-natal human female.”6 (emphases in original)
“The present study clearly demonstrated that HTO (tritium) severely injures human stem cells to the same extent as neutrons, especially in the low dose range.”7
“Although classified among the least toxic of the important radioactive atoms, there is considerable hazard with the ingestion of even low doses of tritium”.8
“The extreme sensitivity of the pre-implanted mammalian embryo to the beta radiation of tritiated compounds of metabolic importance points to the necessity for a re-evaluation of tritium risks for human beings, not only for workers exposed to occupational hazards, but also for those subject to chronic low doses”.9 “The question of main practical concern is… the possibility that significant biological effects may result from protracted exposure to low tritium concentrations in water”10.
“…through various metabolic pathways[tritiated water] may enter any hydrogen position in organic matter including DNA, the most sensitive target for various radiation effects. The low energy of the beta emission from tritium produces relatively dense radiation tracks and causes localized deposition of dose in tissue. Considering these facts, there is concern about the ability of HTO to produce cytogenetic damage”11.
“The tritium content of the chromosome, especially of DNA, is particularly significant since such tritium is likely to cause genetic and somatic damage and to persist for very long periods of time”12.
In addition, the Canadian Researcher Dr. Abram Petkau, has shown that cell membranes collapse in dose of less than 1 mSv beta radiation from radioactive sodium ions (23 Na) producing a sharp supra-linear reaction above the theoretical extrapolated dose based on high dose and fast dose-rate. For increasing doses the membrane again becomes impenetrable, until high doses are reached. The low dose effect appears to be the result of genomic instability by bystander cells, causing the damage rate at low dose slow dose-rate to be greater per unit dose than that at higher dose and faster dose-rate13.
Dr. Elena Burlakova, has shown that a number of different cell culture test systems respond to external low level radiation exposure with a bi-phasic response having a first maximum at very low doses followed by a minimum and then a second maximum as doses increase. Dr. Burlakova explains this effect by assuming the biological repair function is independent of the response to low dose radiation. Hence there may be no repair response to the original assault by the radiation, and repair may not become active until a critical amount of damage is caused. Then, as the repair function reaches its peak, the damage curve decreases. At some point the damage begins to overwhelm the body’s capability to repair and the response curve again rises14.
Dr. Chris Busby has explained this observed phenomenon by speculating that fragile cells are killed first leading to the first maximum. Then a more resistant cell population causes a decrease in response until a minimum is reached and again the response increases with dose. Regardless of the explanation, the phenomena of supra-linearity at low dose irradiation are well demonstrated and present counter-evidence to the DDRF assumption.
Another ICRP assumption, namely that fatal cancer is the only health effect of concern, is also being challenged. As early as 1950, the conference on the Biological Effects of Atomic Energy15 was opened by F. G. Spear, Strangeways Research Laboratory, Cambridge. He addressed the immediate physical changes due to radiation:
“Penetrating rays affect living tissues, as distinct from isolated cells, by a direct action upon individual cells composing the tissue; by an indirect action via the blood circulation; and by a constitutional effect upon the organism as a whole. According to circumstances, these effects may be present together, or one may predominate to the actual or relative exclusion of the others.”16
He went on to identify the observed changes in cytoplasm:
“vacuolation, lysis, and keratinization, changes in mitochondria and in the Golgi apparatus; pigmentation, alteration of permeability and in UV absorption, in pH and in viscosity; increase in cell size, alterations in secretory activity; effects on the mitotic Spindle; surface changes affecting cytoplasmic cleavage (and therefore the distribution of nuclear material between daughter cells), metabolic disturbances, and effects on enzymes. The nuclear effects chiefly concern the chromosomes at division and include various structural abnormalities, breakage, fragmentation, lag in movement, bridges at anaphase, uneven division of nuclear material, clumping of chromosomes, abnormal precipitation of chromatic material, formation of micronuclei and vaculation.”17
This presents a very complex picture of the effects of external radiation, more detailed than current “new (re)discoveries” of the bystander effect and genomic instability. Spear defined the primary effect of external irradiation of higher animals (including, of course, humans) as:
“its [radiation’s] effect on blood-forming organs, the composition of the peripheral blood and the tissues of which the heart and blood vessels are composed”.
Spears measured a ten-thousand-fold difference between extremes of sensitivity among different types of living cells to the lethal effect of radiation.18 The same individual may also vary greatly in sensitivity to radiation at different stages of development. For this reason, the greatest biological change in a complex organism exposed to radiation may not occur at the point of highest dose.
These concepts also apply to tritium, which because of its weak activity requires a tremendous number of tritium atoms invading the interior of the body and bonding with important molecules to reach significant measurable doses.
The person most sensitive to the radionuclides released into the environment may be a person with respiratory difficulty or depressed immune system, a young child or even a fetus. ICRP understands protection for the “most sensitive” means, reduction by a factor of 10 or 20. Between 1952 and 1990, ICRP recommended: a maximum dose to workers of 5 rem/year, and a maximum dose to the public of 0.5 rem/year19. After 1990, the doses recommended were 20 mSv/year to workers and 1 mSv to the general public20. Canada through the CNSC accepts these recommendations.
There are also very broad effects of exposure to radiation, including non-fatal cancers, teratogenic effects and chronic disease. Fatal cancers were chosen as the biological endpoint of atomic bomb research in 1950, even before the Life-Span Data was collected. It is now being questioned even by the current research staff at the Radiation Effects Research Foundation (RERF) in Japan where a broader option of biological endpoints is being proposed. The RERF Department of Clinical Studies wrote:
“The Adult Health Study (AHS) has greatly increased in importance in recent years as a result of the accumulation of an enormous body of data from serial medical examinations, with and without superimposed radiation aspects. Particularly noteworthy is the accumulating evidence of the radiation dose related increase in non-cancer disease morbidity, such as cardiovascular disease, hyperparathyroidism, thyroid diseases, uterine myoma, chronic liver disease, and cataract … Another unexpected finding is the retrospective evidence that radiation is associated with premature menopause, and this in turn, may result in earlier onset of other conditions, such as an increase in cholesterol levels and cardiovascular disease. In addition, most recent findings suggest that diabetes mellitus increases with radiation dose among young survivors of Hiroshima.”21
It seems to be ironical that RERF has just discovered the non-cancer results of radiation exposure, when this was known or suspected by the radiation researchers, victims and their doctors for many years!
Consequently both ICRP’s choice of a biological endpoint as fatal cancer, and its current exclusiveness, are now in question, as well as the effective dose estimates for internal radiation emitters. In such a situation the Precautionary Principle should prevail. The choice of fatal cancer as the exclusive biological endpoint after ionizing radiation exposure is not scientifically acceptable. Equally unacceptable are estimates of equivalent effectiveness made without adequate backing by scientific research.
For all of the above reasons, I consider the application of a DDRF unacceptable when looking at the real life pollution of Pembroke and the Ottawa Valley with tritium. It is unjustified on a scientific basis, and criminal on humanitarian grounds.
In my opinion, the CNSC has loyalty to Canada and to Canadians which is an order of magnitude higher than its allegiance to ICRP. Canadian Universities are among the best in the world, and scholars in Canada are quite able to determine sensible radiation protection policy without blind adherence to ICRP policy recommendation.
References for Appendix II
1 The Person Sievert dose is the number of persons exposed times the average dose received in the group.
2 ICRP 60, 1990.
3 Biological Hazards of Atomic Energy Edited by A. Haddow, Oxford at the Clarendon Press 1952.
4 ibid. Ref. 3, p 15.
5 ibid. Ref. 3, p 10.
6 Straume, T. et al. “Radiolethal and genetic vulnerabilities of Germ Cells in the Female Mammal: Effects of Tritium and other Radiation Compared” Proceedings of the Third Annual Japan-U.S. Workshop on Tritium Radiobiology and Health Physics. Edited by S. Okada, Institute of Plasma Physics, Nagoya University, Nagoya, Japan IPPJ-REV-3, 1989.
7 Shigeta, C. et al. “Effect of Tritiated Water on Human Haematopoetic Stem Cells” Proceedings of the Third Annual Japan-U.S. Workshop on Tritium Radiobiology and Health Physics. Edited by S. Okada, Institute of Plasma Physics, Nagoya University, Nagoya, Japan IPPJ-REV-3, 1989.
8 Killen, H.M. and J. Carroll, “The Effects of Tritium on Embryo Development and Embryotoxic Effects of 3H-Tryptophan”, International Journal of Radiation Biology. 56(2) 139-149, 1989.
9 Clerici, L. et al. “The Toxicity of Tritium: the Effect of Tritiated Amino Acids on Pre-implanted Mouse Embryos”, International Journal of Radiation Biology 45(3) 245-250, 1984.
10 Vulpis, N. “The Induction of Chromosome Aberrations in Human Lymphocytes by In Vitro Irradiation with Beta Particles from Tritium” Radiation Research 97, 511-518, 1984.
11 Ikushima, T. et al. “Sister Chromtid Exchanges in Bone Marrow Cells of Mice Maintained on Tritiated Water”, International Journal of Radiation Biology 45(3) 251-256, 1984.
12 Commerford, S.L., A.L. Carsten and E.P. Cronkite, “The Distribution of Mice Receiving Tritium in Their Drinking Water”, Radiation Research 72. 333-342, 1977.
13 Petkau, A. “Radiation Carcinogenesis from a membrane perspective”, Acta Physiological Scandinaviaca suppl. 492, 81-90, 1980.
14 Burlakova, E.B. et al. “Mechanisms of Biological Action of Low Dose Irradiations”, in Consequences of the Chernobyl Catastrophe for Human Health, Ed. E.B. Burlakova, Moscow Center for Russian Environmental Policy 1996
15 ibid Ref 3, p 1.
16 ibid. Ref. 3, pp 2-3.
17 ibid Ref. 3, p 3
18 ibid. Ref. 3, p 5.
19 ICRP 1, 1952.
20 ICRP 60, 1990.
21 Research Activities Report By Department, Department of Clinical Studies, Hiroshima and Nagasaki, FY2004, RERF.