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15 Billion Bq of Tritium flows to the Pacific every single day / Tepco under-reported 1/15 at press conference

Following up this article.. 5 Billion Bq of Strontium-90 flows to the sea every single day [URL]

 

15 Billion Bq of Tritium flows from Fukushima plant area to the sea every single day. Tepco reported it in the handout submitted to Fukushima fishery cooperative on 8/25/2014.

In the press conference of the same day, Tepco announced it was 1 Billion Bq, which is 1/15 times much as the actual amount.

It is not clear if Tepco tried to under-report it intentionally or not. Tritium cannot be removed by any of the purification systems of Tepco.

 

http://www.tepco.co.jp/nu/fukushima-np/handouts/2014/images/handouts_140825_04-j.pdf#page=8

 

 

You read this now because we’ve been surviving until today.

_____

Français :

15 milliards de Bq de tritium s’écoulent tous les jours dans le Pacifique : Tepco le minimise au 15e à la presse

See also

 

Article lié : 5 milliards de Bq de strontium 90 se déversent dans l’océan tous les jours

15 milliards de Bq de tritium s’écoulent tous les jours de la centrale de Fukushima dans la mer. Tepco le rapporte dans un prospectus remis à la coopérative de pêche de Fukushima le 25 août 2014.

Au cours de la conférence de presse du même jour, Tepco a annoncé qu’il y en avait un milliard, ce qui est 15 fois moins que la quantité réelle.
On ne sais pas si Tepco a intentionnellement tenté de le minimiser ou pas. Le tritium ne peut être retiré par aucun des systèmes de purification de Tepco.

http://www.tepco.co.jp/nu/fukushima-np/handouts/2014/images/handouts_140825_04-j.pdf#page=8

Vous pouvez lire ceci parce que nous avons survécu jusqu’à aujourd’hui.

Mochizuki
Mochizuki
The writer of Fukushima Diary.
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5 Comments

  1. Tritium is also the nuclide that bonds with water to form tritiated water, which evaporates from the ocean and comes down as rainfall. Tritium is very hard to detect and is not usually tested for in most communities.

    2. Tritium – Dr. Rosalie Bertell
      June 26, 2014 at 5:02pm
      http://iicph.org/health-effects-of-tritium-appendix-2 Concern for Public HealthInternational Institute of Concern for Public HealthArticles, reports, statements and published papers.

      Health Effects of Tritium: Appendix I and IIDecember 1, 2006 Appendix I
      Dr. Rosalie Bertell’s submission to CNSC, regardingSRB Technologies and its proposal to pour tritiated water down the municipal sewer.

      Health Base Regulation, Absorbed Dose and Effective Dose
      1: Health Based Regulation:
      Tritium (3H) is the radioactive isotope of hydrogen. It is a beta emitter with a maximum decay energy of 18 keV (average 5.7 keV), and a physical half-life of 12.3 years. Tritium is formed naturally through cosmic ray interaction with H in the upper atmosphere and transfers to the troposphere. However emissions from civil and military nuclear facilities considerably exceed natural sources, and in this paper I will consider only man-made tritium. Tritium most commonly occurs as tritiated water (HTO), organically bound tritium (OBT) and elemental tritium gas.
      Tritium may be considered a very effective distributor of radioactivity in the environment since it is exceedingly mobile as tritiated water, and can travel everywhere that water can travel. The human body, all tissues and cells, are composed of about 70% water. About 80% of the atoms in the human body are hydrogen atoms, which can be replaced by tritium. Tritium has multiple pathways to humans: via inhalation and drinking water, through ingestion of food, and absorbed through the skin. The International Atomic Energy Agency, depending on ICRP, ranks tritium based only on its disintegration energy, which is low in comparison with other known radionuclides. However, the very large emissions of tritium both from hydrogen bomb explosions and from the CANDU nuclear reactors, makes this dose calculation important for humans and their environment. The potential for binding with important molecules in living organisms adds to concerns. A major error in the ICRP estimation implies major health and environmental problems!
      No one doubts either tritium’s ubiquitousness or its radioactivity. Tritium is classified as radioactive, carcinogenic and mutagenic to humans. The Health Based Goal (HBG) of regulation of tritium is zero.* Permission to pollute with tritium, must be regulated by the ALARApolicy: as low as reasonably achievable. Permissible exposure to Tritium must be as close to zero as possible, and must carry a benefit which outweighs the risk.
      2: Calculation of Dose from Tritium:
      a. Absorbed Dose Depends on Biological Half-life:
      Radiation dose depends on the strength of the source and the length of time the person is exposed to the source. It is well know that one’s sun exposure results from both the sun’s energy reaching the earth (time of day) and the length of time spent exposed to this energy. Therefore, although the physical half-life of tritium in known to be 12 years, it is important when calculating dose to consider its biological half-life, i.e. the time needed for one half of the tritium to be emitted from the body in urine, feces or sweat. ICRP considers that most of the tritium formed when tritium gas is released into the environment will be in the form of tritiated water. It assumes that it will be taken up by plants, animals and humans as tritiated water (HTO), and distributed homogeneously with a biological half life of between 6 and 12 days1,2. ICRP recognizes an exchange component which binds with organic molecules, (called here OBT 1) with a biological half life between 21 and 76 days, generally accepted as 40 days. In the Exchangeable OBT’s (OBT1), tritium is bound to oxygen, sulfur, phosphorus or nitrogen atoms, to form hydroxides, phosphides and amines. With chronic environmental HTO exposure, with food web involvement, the two fractions: HTO and OBT 1, become about equal in size. All organic molecules downwind of a tritium (HTO) plume which come in contact with the HTO become tritiated very quickly. This includes all plant and animal species, all water bearing materials and soil, including vegetables and fruit in market places or backyard gardens. The fixed binding of tritium to a carbon atom of theDNA, called here OBT 2, has a longer biological half life between 280 and 550 days3,4. ICRPappears to base OBT half-life calculation on either the cycling time of the carbon, 40 days (which is difficult to document) or a misapplication of research on OBT 1. The estimate of energy deposited in tissue from tritium, incorporated into the body as tritiated water, according to ICRP, would be as HTO with a 12 day biological half-life for 97% and OBT with biological half-life of 40 days for 3%. The alternative, based on published research, proposed by ECRR5 for chronic exposure is: 43.5% HTO with half-life 12 days; 43.5%; OBT 1, with half-life 40 days and 3% OBT2 with half-life 550 days. This will increase the ICRP estimate by about a factor of three.
      The U.S. EPA in 2001 settled this dispute with the ruling:
      “(EPA) currently takes the view that the more cautious, wider definition of OBT to include any organic matter which contains tritium either exchangeably bound or fixed more firmly to the carbon chain, should be used. This will ensure that any dose assessments will take account of both forms of OBT while uncertainty remains. Indeed, this definition more closely describes the OBT fraction which is measured by current laboratory methods.”6
      The OBT 1 includes amino acids, proteins, sugars, starches, lipids, and cell structural material.
      In summary, due to longer half-life of tritium in the human body, and the proportion of each of three components (HTO, OBT 1, and OBT 2) the energy deposit of HTO ingested, inhaled or absorbed would be three times higher than that estimated by ICRP methodology.*
      b. Absorbed Dose with Non-homogeneous Distribution
      There is another factor, important for the calculation of the energy deposited in tissue from HTO. Contrary to the ICRP assumption OBT is not uniformly distributed in the tissues of the body. Homogeneity is clearly not true of either OBT 1 or OBT 2, each delivering highly localized doses. The cells at most risk of tritium would be those dividing at the time of exposure and which afterwards were long-lived, replicating the resultant damage, namely: oocytes, embryos and embryonic nerve cells. Tritiated food is quicker and more effective than HTO in delivering tritium to cells and to the DNA7,8 Proteins (amino acids) are efficiently incorporated into nucleoproteins and localized doses from tritiated proteins to DNA are four times greater than from HTO.
      Because the dose from OBT 1, and OBT 2 is not uniformly distributed and the localized dose can be four times the dose from homogeneously distributed HTO, the effective dose estimate is increased by another factor of three. This means that the current scientific calculation of tritium energy deposited in tissue is nine times greater than that estimated using ICRP methodology.
      c. Effective Dose Equivalent:
      The energy deposited in tissue determines the dose in mGy, and must be converted into mSv, with a relative biological effectiveness (RBE) factor, reflecting its equivalence for cell killing with a comparable dose of 200 kVp X-Ray (the usual reference dose for radiation comparison) or 137 cesium.
      In 1980, the Oak Ridge National Nuclear Laboratory in the U.S. mounted a campaign, based on copious evidence, to recognize the RBE of tritium as two.9,10. In 1986, a joint committee of ICRPand ICRU (International Commission on Radiation Units) recommended an increase in the quality factor for tritium from one to two for microdosimetric reasons11. This recommendation was not implemented by ICRP, which insisted on keeping an RBE of one for tritium12. In 1991 and 199313,14 a comprehensive review of tritium data was developed. Researchers concluded that a radiation weighting factor of three was appropriate for tritiated water (HTO), and that higherRBE’s were appropriate for exposure to tritiated nucleotides such as human lymphocytes (a kind of white blood cell).
      Combining the effects of chemical change (OBT ! and OBT 2) and biological half-life with the weighting factor of two or three RBE, for the energy deposited in tissue by tritium, one can argue effectively that current ICRP dose calculation, used by CNSC and the Canadian nuclear industries, should actually be about 18 to 27 time higher. Damage wrought will also be increased by a transmutation effect currently not well understood. A transmutation effect by which the atom formed when tritium has a nuclear disintegration, namely helium, recoils from the emission of the beta particle and has an associated excitation of energy ruptures the bond to the compound to which the former tritium atom had been attached. This process is of special concern when the tritium atom has been bound to the DNA or DNA precursors, giving it significant mutagenic force. More research is needed to understand this mechanism which enhances the radiation effect especially for OBT 2. Not allowing for this effect makes the present evaluation of dose conservative.
      ICRP methodology significantly ignores these contradictory research findings in favor of its minimizing assumptions. This may be due to its protection of the military nuclear program. When the first large hydrogen bomb was exploded over Bikini Atoll in the Pacific, in March 1954, the Great Lakes, 6000 miles away, registered tritium levels of several hundred tritium units. Prior to that explosion tritium was undetectable in the Great Lakes. This reluctance to deal realistically with tritium has proven fortunate for the Canadian nuclear industry since the CANDU reactor releases much more tritium that do American light-water reactors. The faulty (or biased) calculations ofICRP are now benefiting the SRBT facility in Pembroke, at the cost of the health and common good of citizens of Pembroke and the Ottawa Valley.
      I would point out for the record, that prevalence of Down’s Syndrome was found to be increased by 80% in Pickering (observed 24; expected 12.9 cases) and by 46% at Ajak (observed 14, expected 9.6), a town further from the Pickering Nuclear Station (PNS). This report by the AECB(Atomic Energy Control Board) also found an association between the high tritium releases fromPNS and central nervous system anomalies in births at Pickering.
      Moreover, It is apparent from the IARC study of Nuclear Workers that radiation related cancers among Canadian workers is higher than that of other nuclear workers receiving the same radiation dose. The study on which this was based, done by Lydia Zablotska, J.P. Ashmore and the Radiation Protection Bureau of Health Canada15 was tested with and without tritium exposure (with ICRP calculations). Researchers were unable to account for the difference. They failed to consider a significant underestimation of the effects of tritium exposure as the cause. The IARCstudy was a summary of the experience of 400,000 workers at 531 nuclear reactors internationally. There is evidence that with long term chronic exposure, OBT 1 makes up 50%. In long term mice studies, it was shown that the OBT/HTO ratio after 15 months of HTO feeding was between 0.73 and 1.0716. Other animal studies found the long term ratio between 0.85 and 1.517,18,19, although these animals may have consumed OBT as well as HTO in the natural environment.
      A human who died after eight months chronic exposure to tritiated water had tritium constituents of fat and hair (OBT) higher than that in body water at time of autopsy.20 Eight workers at aCANDU reactor station in India were found to have a much larger fraction of OBT than was predicted by ICRP, and the committed dose equivalent was 3.4 times higher than that based onHTO21.
      Background tritium levels in humans and plants with long term chronic doses of tritiated water have been found to be about 50% OBT and 50% HTO.22,23,24,25,26
      In conclusion, two or three are reasonable quality factors for the RBE of tritium. This implies that doses estimated to be 1 mGy and 1 mSv using ICRP methodology, would actually be 9 mGy and 18 to 27 mSv according to well documented research. It would seem conservative to use the factor 20 to represent the true conversion from ICRPcalculated doses to more realistic research based effective doses. This would imply the need for reducing the 7,000 Bq/litre water permitted by CNSC to about 350 Bq/litre water.
      References for Appendix I:
      1 Rudan, K. et al. “Significance of in Vivo Organic Binding of Tritium following intake of Tritiated Water”. Radiation Protection Dosimetry 25 (1) 5-13, 1988.
      2 Balonov, MI, et al. “Exchange Kinetics and Dosimetry of Tritium Oxide in Man for Different Routes of Administration”. Health Physics 27:367-375, 1974.
      3 Moghissi, A.A., and M.W. Carter. “Long-term Evaluation of the Biological Halflife of Tritium”, Health Physics 21, 57-60, 1971.
      4 Moghissi, A.A., MW Carter and R. Lieberman. “Further Studies on the long term evaluation of the biological half-life of tritium”, Health Physics 23, 805-806, 1972.
      5 Chris Busby, “Tritium Properties, Metabolism and Dosimetry” Paper 8-1, Presented at the 9th meeting, 30 April 2003 of the Committee Examining Radiation Risks of the Internal Emitters (CERRIE), set up under the Blair Government in the U.K. 2003-2004.
      6 U. S. Environmental Protection Agency, “Potential for Bio-accumulation of Organically Bound Tritium in the Environment” Review of Monitoring Data, National Compliance Assessment Service. Technical ReportNCAS/TR/2000/026, 2001.
      7 Commerford, S.L., A.L. Carsten and E.P. Cronkite, “The Distribution of Tritium among AminoAcids of Proteins Obtained from Mice Exposed toTritiated Water”, Radiation Research 94, 151-155, 1983.
      8 Saito, M. and M.R. Ishida, Tritium Metabolism in Animals and Estimation of the Accumulated Dose “, in Radiation Protection Dosimetry 16, (1), 5.13, 1988.
      9 Till, J.E. et al., “Tritium: An Analysis of Key Environmental and Dosimetric Questions”. Department of Energy Report ORNL/TM-6990(AT), Oak Ridge National Laboratory TN, USA, 1980.
      10 Till, J.E., E.L. Etnier, and H.R. Meyer, “Updating the Tritium Quality Factor – The Argumants for Conservatism in Tritium Technology in Fission, Fussion and Isotopic Applications”. Proceedings of the American Nuclear Society Topical Meeting. CONF-800427,p. 1-8, 1980. American Nuclear Society.
      11 “The Quality Factor in Radiation Protection.” Report of a Joint Task Group of the ICRP and the ICRU to theICRP and ICRU. ICRU Report 40, Bethesda, MD, USA, 1986.
      12 ICRP 60, 1990.
      13 Straume, T, “Health Risks from Exposure to Tritium”, Lawrence Livermore Laboratory Report UCRL-LR 105088, University of California Livermore, CA, USA, 1991.
      14 Straume, T. and A.L. Carsten, “Tritium radiobiology and relative biological effectiveness”, Health Physics 65: 657-672, 1993.
      15 Lydia Zablotska, J.P. Ashmore and the Radiation Protection Bureau of Health Canada. Radiation Research 161, 633-641, 2004.
      16 Commerford et al. “The Distribution of Mice Receiving Tritium in Their Drinking Water” Radiation Research 72, 333-342, 1977.
      17 Koranda, J.J. and J.R. Martin, “The Movement of Tritium in Ecological Systems” in Tritium Ed. By Mohissi, A.A. and M.W. Carter. Messengers Graphics, Phoenix, Arizona. 1973.
      18 Hatch, F.T. et al. “Ecology and Radiation Exposure of Kangaroo Rats Living in a Tritiated Environment”. Radiation Research 44, 97, 1970.
      19 Evans, E.G., “New Dose Estimates from Chronic Tritium Exposures”. Health Physics, 16, 57, 1969.
      20 Pinson, E. A. and W.H. Langham, “Physiology and Toxicology of Tritium in Man”, Applied Physiology 10, 108-126, 1957.
      21 Rudran K., “Significance of in Vivo Organic Binding of Tritium following Intakes of Tritiated Water” Radiation Protection Dosimetry, 25 (1) 131-134, 1988.
      22 Bogen, D.C., “Tritium Intake in New York City” in Tritium see Ref. 17, 1973.
      23 Bogen, D.C. et al, “Tritium Distribution in Man and Environment” in Behaviour of Tritium in the Environment , Ed. S. Freeman, p. 567-572, IAEA, Vienna, 1979.
      24 Ujeno, Yi et al. “Tritium Content in Japanese Bodies”, in Tritium Radiobiology and Health Physics, Ed. S. Okada, Proceedings of Third Japan-US Workshop, Kyoto, Japan. November 1988 IPPJ-REV-3, 1989.
      25 Hisamatsu, S. et al., “Transfer of fallout 3H from diet to Humans in Akita, Japan”, in Tritium Radiobiology and Health Physics, See Ref. 24, 1989.
      26 Belot Y. et al. “Distribution of OBT in Vegetation Exposed to Fallout”, Radiation Protection Dosimetry, 16 (1-2) 111-113, 1986.
      — Rosalie Bertell

      Appendix II

      Dr. Rosalie Bertell’s submission to CNSC, regardingSRB 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 DDRFis 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 nearmaximum 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 Energy15was 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. ICRPunderstands 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 RERFDepartment 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 withpremature 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.
      — Rosalie Bertell
      International Institute of Concern for Public Health. Some rights reserved.IICPH, 292 Dupont, P.O. Box 40017, Toronto ON Canada M5R 0A2Concern for Public Health
      Articles, reports, statementsand published papers

    3. Hydrogen naturally occurs in three isotopes, each with 1 proton and with either 0, 1 or 2 neutrons. The chemical properties are identical; and the physical properties, such as freezing point, are extremely similar. Water is two hydrogens, and one oxygen, but can be any combination of H, D & T. Nuclear reactor bombard water with neutrons. Some neutrons are captured, increasing the atomic weight of the water. Hydrogen H Atomic Weight 1, Deuterium D Atomic Weight 2 and Tritium T Atomic Weight 3. HHO is light water. All the others HDO, DDO, HTO, DTO, TTO, are heavy water. Tritium is the only naturally common radioactive hydrogen isotope.

  2. The entire world has been poisoned. Within 20 years most everyone will be dying of cancers of multiple forms if an immediate intervention does not occur All wars must immediately stop. All entertainments must stop. All able-bodied adults must pay attention.http://www.ccnr.org/tritium_1.html

    What is a curie?

    A curie is a unit of radioactivity, corresponding to 37 billion disintegrations per second. Thus 3,500 curies corresponds to 129.5 trillion disintegrations per second (1.295 x 1014 dps, or 129,500,000,000,000 dps). That is a great deal of radioactivity.

    One disintegration per second (dps) is called a “becquerel”.
    Thus one curie is 37 billion (37,000,000,000) becquerels.
    A microcurie is one millionth of a curie, or 37,000 becquerels.
    A picocurie is a trillionth of a curie; that is, 0.037 becquerels.

    What is tritium?

    Tritium is a weakly radioactive form of hydrogen, with a half-life of 12.3 years. The radiation emitted by tritium is not penetrating; it is a very low-energy form of radiation. About 99 percent of all tritium occurs in the form of “tritiated water” (HTO or DTO); see the explanation given below.

    The letters in parentheses are based on a kind of chemical shorthand:

    H = an atom of normal hydrogen (hydrogen-1), known as “protium”.
    Hydrogen is the lightest and most abundant element in the universe.
    It is essential to life, forming an integral part of every organic molecule.

    D = an atom of heavy hydrogen (hydrogen-2), known as “deuterium”.
    D behaves exactly like H, except that it’s twice as heavy as H.
    For technical reasons, it is used in the CANDU reactor.
    (“CANDU” means “CANadian Deuterium Uranium”.)

    T = an atom of radioactive hydrogen (hydrogen-3), known as “tritium”.
    It behaves like H, but it’s three times as heavy, and it is also radioactive.
    When a deuterium atom (D) absorbs a neutron it becomes a tritium atom (T); this happens often inside every CANDU nuclear reactor.

    H2O = a molecule of ordinary water (or “light water”).
    An ordinary water molecule is formed when two ordinary hydrogen atoms (H + H = H2) combine with one oxygen atom (O).

    D2O = a molecule of heavy water.
    In every molecule of “heavy water”, both of the ordinary hydrogen atoms in ordinary water have been replaced by heavy hydrogen atoms.
    Heavy water is used in the core of a CANDU reactor as a “moderator” (to slow down the neutrons) and as a “coolant” (to remove the heat produced by the nuclear fuel).

    HTO or DTO = a molecule of tritiated water.
    If one of the ordinary hydrogen atoms (H) in ordinary water (H2O)
    — or one of the heavy hydrogen atoms (D) in heavy water (D2O) —
    is replaced by a tritium atom (T) , “tritiated water” is created.
    This happens when one or two neutrons are captured.

    Where did the contaminated NPD cooling water get dumped?

    The tritium-contaminated water was eventually pumped from the boiler room back into the reservoir from which it came, but it was contaminated with grit and oil as well as with radioactivity. In order to clean out the reservoir, Ontario Hydro officials decided to dump the dirty water into the Ottawa River. Many communities downstream from the reactor site draw their drinking water from the Ottawa River. Tritium cannot be filtered or otherwise removed from drinking water by any standard water-treatment processes.

    Is this kind of radioactive dumping allowed?

    According to the United Nations Scientific Committee on the Effects of Atomic Radiation, radiation protection policies are supposed to be based on “the principle of eliminating any exposures which are not necessary and of keeping all doses as low as is reasonably achievable” (UNSCEAR 1977 p.14). Evidently, the Atomic Energy Control Board (AECB) does not enforce this principle rigorously; instead, it sets limits and establishes guidelines on how much radioactivity can be released by the nuclear industry into the environment, wehether it is necessary or not. In this particular case, the resulting radiation exposure of people downstream was clearly unnecessary, but was nevertheless allowed.

    Do the radiation guidelines prevent biological damage?

    No. In the case of cancer, leukemia, and genetic damage, the scientific consensus is that every additional exposure to radiation adds to the total risk and therefore to the incidence of these diseases in exposed populations. In the case of developmental damage to unborn babies exposed in the womb, scientists have so far found it impossible to determine what level of exposure to tritium constitutes a “damaging dose”.

    According to a 470-page report published by the British Columbia Medical Association (BCMA) in 1980, existing AECB standards for public exposure to another radioactive substance — radon — “may well be viewed as tantamount to allowing an industrially-induced epidemic of cancer”. Chapter XXII of the BCMA Report is entitled “Atomic Energy Control. Board — Unfit to Regulate”, based on the AECB’s poor record of protecting the public health and safety (BCMA p.283).

    What is the AECB limit for tritium emissions from NPD?

    According to the AECB, the maximum permissible release limit from the NPD reactor into the Ottawa River is 220,000 curies of tritium per month, or 2.64 million curies per year. As an operating target, the AECB tries to keep releases to within 1 percent of this limit; that is, 2,200 curies of tritium per month or 26,400 curies per year (equivalent to an average of 7.3 curies per day).

    Did the NPD dumping meet the AECB operating target?

    Obviously not. Since 3,500 curies is larger than 2,200 curies, the dumping exceeded the AECB operating target by about 60 percent (if calculated on a monthly basis). However, since the 3,500 curies were dumped in less about five days, at an average rate of more than 700 curies per day, the AECB operating target was exceeded by about 1000 percent if calculated on a daily basis.

    Does it matter if tritium is released slowly or quickly?

    According to Dr. Edward Radford, Chairman of the U.S. National Academy of Sciences’ Third Committee on the Biological Effects of Ionizing Radiation (BEIR-III), a sudden burst of tritium in the drinking water may be much more dangerous to a female embryo in the early stages of pregnancy than the same amount of tritium spread out over a longer period of time (testimony to the Select Committee on Ontario Hydro Affairs, July 10 1979).

    Where does tritium come from?

    Tritium is produced in nature by the action of cosmic rays from outer space. It is also produced by atomic explosions and by nuclear power plants. Each CANDU reactor produces from 30 to 100 times as much tritium as a comparable American light water reactor, because the heavy water in a CANDU “breeds” tritium while the reactor is operating.

    How much tritium is produced globally?

    Before the advent of nuclear energy, it is estimated that the global inventory of naturally-occurring tritium was about 34 million curies, of which 22.2 million curies were contained in the oceans and 9.2 million curies were present in inland areas (UNSCEAR p.55).Nuclear weapons testing has added about 3,600 million curies of tritium in the northern hemisphere. By 1970, only about 2,900 million curies was left, mostly in the oceans; the rest had undergone radioactive disintegration to become helium-3 (UNSCEAR p.117).

    American light-water reactors generate about 15 to 23 curies of tritium per megawatt-year, of which no more than 1 curie is normally released into the environment. CANDU reactors generate about 620 curies per megawatt-year, of which about 20 curies are normally released into the environment (16 curies to the air, 4 curies to the water — UNSCEAR p.180).

    At that rate, one would expect the Pickering nuclear complex (2,000 MW) to release about 32,000 curies of tritium into the air each year, yet in 1978 only 26,000 curies were released. One would expect the NPD reactor (20 MW) to release about 80 curies of tritium into the Ottawa River each year.

    Is tritium a biological hazard?

    The radiological significance of tritium is not related to its inherent toxicity, as it is a very low energy form of radiation, but to its easy incorporation into all parts of the body that contain water (Select Committee Report p.15).

    Tritiated water can be ingested in the liquid form. It can also be inhaled or absorbed through the skin in the form of water vapour or steam, which makes tritium an occupational hazard in CANDU nuclear power plants. In pregnant females, tritium ingested by the mother can cross the placenta and be incorporated directly into the foetus.

    Like all radioactive substances, tritium can cause cancer, genetic mutations, or developmental defects in unborn children (the latter following pre-natal exposure of the foetus). No threshold or “safe dose” of tritium has been scientifically established for any of these effects.

    What scientific evidence is available?

    “There is now experimental evidence, both in terms of changes in the developmental effects on foetuses in utero in animals and also in studies of cancer induction, that tritium [is] four or five times more effective than would be predicted just on the basis of its energy alone” (Dr. Edward Radford, testimony to the Select Committee on Ontario Hydro Affairs, July 10 1979).

    “Concerning the passage of tritium administered under the form of tritiated water from the mother through the placenta and into the foetus … several statistically significant effects were found at various HTO levels, in no apparent relationship with dose. These included microcephaly [shrunken heads, also observed at Hiroshima], sterility, stunting, reduction of the litter size, …” (UNSCEAR p.695 — these are, of course, animal studies).

    “During the past few years, there has been a growing interest in the study of the biological effects of radio-isotopes, particularly of plutonium-239 and tritium. A number of genetic and cytogenic [i.e. cellular] studies that have so far been carried out in mice demonstrate that these isotopes are capable of inducing dominant lethal mutations, chromosome aberrations and point mutations (for the last category, only the effects of tritium have been studied)” (UNSCEAR p.477).

    Bibliography

    BEIR III (National Academy of Sciences: Third Committee on the Biological Effects of Ionizing Radiation). The Effects on Populations of Exposure to Low Levels of Ionizing Radiation. Academy Press. Washington: 1982.

    UNSCEAR (United Nations Scientific Committee on the Effects of Atomic Radiation). Sources and Effects of Ionizing Radiation. Report to the UN General Assembly. United Nations, New York: 1977.
    Annex H: Genetic Effects of Radiation. Part 2: Tritium.
    Annex J: Developmental Effects of Radiation. Part V-B: Tritium

    Select Committee on Ontario Hydro Affairs. The Safety of Ontario’s Nuclear Reactors. Ontario Legislature, Toronto: 1980.

    BCMA (British Columbia Medical Association). Health Hazards of Uranium Mining. BCMA, Vancouver: 1980.
    Chapter XXII: AECB — Unfit to Regulate.

    back to [ Table of Contents ]

    Reference #2:
    The Effects on Populations
    of Exposure to
    Low Levels of Ionizing Radiation

    published in 1980 by
    The U.S. National Academy of Sciences’
    BEIR-III Committee
    (BEIR = Biological Effects of Ionizing Radiation)

    Excerpt from pp. 485-486:
    “Somatic Effects Other Than Cancer”

    Because tritium (hydrogen-3) is a potential pollutant from nuclear-energy production, it’s effect on development [of unborn babies] has been the subject of a number of studies.

    Tritiated water (HTO) is a common chemical state of tritium, and it has easy and rapid access to living cells, including those of the embryo or foetus.

    HTO administered in the drinking water to rats throughout pregnancy produced significant decreases in relative weights of brain, testes, and probably ovaries, and increases in norepinephrine concentration, at doses of 10 microcuries per millilitre (estimated at 3 rads per day), and produced weight decreases in a number of [other] organs at higher doses.

    Because the length of the critical period [of vulnerability to damage] for various organs is not known, the total damaging dose cannot yet be estimated. Relative brain weight was found to be reduced at only 0.3 rads per day (one microcurie per millilitre of drinking water) when exposure began at the time of the mother’s conception.

    Even lower exposures (0.003 rads per day and 0.03 rads per day) have been implicated in the induction of behavioral damage, such as delayed development of the righting reflex and depressed spontaneous activity. However, because the data fail to show a clear dose dependence, there is some doubt about the validity of this suggestion.

    Tritiated drinking water has been used to study the effects of radiation on development of a sensitive cell type, the oocyte. Oocyte counts were made in serial sections of exposed and control animals. In squirrel monkeys continuously exposed from conception to birth, the LD-50 was 0.5 microcuries per millilitre of body water, giving a foetal dose rate estimated at 0.11 rads per day. Because the sensitive period for oocyte development is probably the last trimester, the LD-50 was calculated to be 5 rads. In the mouse, the sensitive period occurs during the first two weeks after birth, and, by a similar calculation, the LD-50 from tritiated drinking water at that time is slightly below 5 rads.

    . . . from the Summary section, page 493
    Until an exposure has been clearly established below which even subtle damage does not occur, it seems prudent not to subject the abdominal area of women of child-bearing age to quantities of radiation appreciably above background, unless a clear health benefit to the mother or child from such an exposure can be demonstrated.

    Ed. note: This does not refer to tritium only, but to any form of radiation exposure.

    back to [ Table of Contents ]

    Reference #5:
    Sources and Effects of Ionizing Radiation

    1977 UNSCEAR Report
    to the U.N. General Assembly

    [ UNSCEAR = U.N. Scientific Committee on the Effects of Atomic Radiation ]

    ANNEX H
    Genetic effects of radiation

    2. Tritium
    (a) Induction of dominant lethal [mutations] in mice

    Paragraph 372.

    Carsten and Commerford and Carsten and Cronkite have published the results of their studies on the induction of dominant lethals [dominant lethal mutations] in mice (random-bred, Hale-Stoner-Brookhaven strain) fed with tritiated water (HTO).

    The HTO test animals were first-litter mice resulting from breeding of eight-week-old animals that had been maintained on HTO (3 microcuries per millilitre) since weaning at four weeks of age. The control animals were first litter mice taken from the colony and maintained on tap water.

    From the second generation animals, four experimental groups were established for dominant lethal tests.

    Group 1 consisted of animals
    where both the male and female were on HTO.

    Group 2 females received HTO,
    males, tap water.

    In Group 3, the situation
    was the reverse of that in Group 2, and

    Group 4 received only tap water
    (both males and females).

    At eight weeks of age, in each group, each male was mated to five females for a 5-day period, the females were killed and their uterine contents examined for assessing dominant lethality.

    Paragraph 373.

    The results, based on 366 pregnant females in the controls, 764 in Group 1, 315 in Group 2, and 316 in Group 3, clearly demonstrated that dominant lethals are induced by HTO in both sexes.

    Significantly fewer viable embryos were found when either both mating partners or only the female was maintained on the tritium regimen. Similarly, when both the partners were on tritium, the incidence of early death (dark mole) is significantly higher than in the control group. Treatment of the males only gave similar effects, but these were not [statistically] significant.

    When post-implantation mortality (early plus late deaths in the authors’ terminology) is used as the basis for comparison, the increased mortality due to HTO in Groups 2 and 3 is of the same magnitude in both sexes, and in Group 1 (both sexes on HTO) the effect is nearly twice that in Groups 2 or 3.

    Current experiments are directed at repeating these studies with a lower concentration of 1.0 microcuries per millilitre.

    (b) Induction of specific-locus mutations in male mice

    Paragraph 374.

    Cumming et al. (128) have completed the first series of experiments on tritium-induced specific locus mutations in mice, providing the only data available on such gene mutations in any mammal.

    In view of possible levels of tritium release, not only from existing nuclear installations but also from contemplated controlled thermonuclear reactors, these data are of great relevance.

    A total of 14 groups of males was used. Two groups were injected with 0.75 millicuries , and the 12 others with 0.50 millicuries , of tritiated water per gram of body weight.

    The results demonstrate that beta radiation from the decay of tritium can induce specific-locus mutations in spermatogonia as well as in post-meiotic stages: 16 mutations have been recovered among a total of 20,626 offspring derived from germ cells irradiated as spermatogonia and 11 in 7,943 offspring from irradiated post-meiotic stages.

    The mean absorbed dose to the spermatogonial cells has been estimated to be 700 rad and that to post-meiotic cells, 430 rad. These data thus permit mutation-rate estimates of 1.58 x 10-7 per rad per locus for spermatogonia and 4.60 x 10-7 per rad per locus for the other stages. These rates are within the statistical limits of what would have been expected from a comparable external dose of x [-irradiation] or gamma irradiation.

    The point estimate of the RBE [Relative Biological Effectiveness] for post-spermatogonial stages is close to 1, with fairly wide confidence intervals; that for spermatogonia is slightly above 2, with confidence intervals that include 1.

    There are some indications that the distribution of mutants among the seven loci may differ from that produced by gamma rays; noteworthy is the observation that only one of the mutations was at the s locus (the expectation would be about 5 or 6).

    In more recent studies, currently in progress at Oak Ridge, Cumming and W.L. Russell (129) are engaged in collecting more extensive data on tritium irradiation, focusing attention on the induction of mutations in spermatogonia.

    (c) Induction of chromosome aberrations
    in human lymphocytes by tritiated water (HTO)

    Paragraph 375.

    Hori and Nakai (233) and Bocian et al. (39) have reported on the induction of chromosome aberrations in human lymphocytes exposed to tritiated water in vitro. Exposures were carried out by the addition of whole blood to the culture medium containing tritiated water.

    In the work of Hori and Nakai, the concentration of tritium ranged from one millionth of a microcurie per millilitre to one hundredth of a microcurie per millilitre, and the cells were exposed during their entire period in culture (48 hours).

    Bocian et al., used two regimens: in one (“acute exposures” in the authors’ terminology), the lymphocytes were exposed for a 2-hour period prior to PHA stimulation (range of concentrations, 1.71 to 14.36 millicuries per millilitre), after which they were washed and cultured (53-hour cultures); in the other (“protracted series”) the cells were exposed during 53 hours (concentration range, 0.063 to 0.51 millicuries per millilitre).

    Paragraph 376.

    The results indicate that with protracted exposures (48 or 53 hours) the [chromosome] aberrations produced were mostly of the chromatid type, such as gaps, deletions and fragments, and there were relatively few chromatid exchanges.

    In the concentration range used by Hori and Nakai, the dose-effect curve for the number of [chromosome] breaks induced was quite complex at low concentrations. In the work of Bocian et al. and with the range of concentrations they used, the frequency of chromatid aberrations increased linearly with dose.

    A quantitative comparison of the frequencies between the two groups of authors is, however, not possible because each group used only one (but different) fixation time, and in addition, the ranges of concentration were different.

    Paragraph 377.

    In the 2-hour exposure experiments of Bocian et al., chromosome-type aberrations were found to be induced (dicentrics, centric rings, terminal and interstitial deletions). The data for dicentrics plus rings, as well as those on deletions, gave a good fit to a linear plus quadratic model.

    Using the data obtained in x-irradiation experiments (acute doses of 50 to 300 rad), Bocian et al. have estimated that the RBE [Relative Biological Effectiveness] for the induction of dicentrics plus centric rings is about 1.2 .

    3. Summary and conclusions
    [Annex H: Genetic Effects]

    Paragraph 378.

    During the past few years, there has been a growing interest in the study of the biological effects of radioisotopes, particularly of plutonium-239 and tritium.

    A number of genetic and cytogenetic studies that have so far been carried out in mice demonstrate that these isotopes are capable of inducing dominant lethals [i.e. lethal mutations] , chromosome aberrations and point mutations (for the last category, only the effects of tritium have been studied) .

    Paragraph 379.

    Autoradiographic studies have shown that in mice, intravenously injected plutonium-239 (as citrate solution) is inhomogeneously distributed in the testis and is largely localized in the interstitial tissue outside and between the seminiferous tubules. A consequence of this is that the alpha-irradiation dose rate to the spermatogonial stem cells is from 2 to 2.5 times greater than the average for the testis as a whole.

    Paragraph 380.

    When plutonium-239-injected males are mated to females, there is a significant excess of intra-uterine mortality relative to controls and the effect persists in matings up to five weeks after injection (post- and peri-meiotic stages sampled). In addition, the effect appears to be unrelated to the amount of plutonium-239 injected (in the range of 0.05-0.5 microcuries per mouse).

    Paragraph 381.

    Dominant lethal [mutation] tests performed on F1 males sired by fathers which received plutonium injection (and derived from matings during the ninth, fourteenth and sixteenth weeks) showed that here again there was an increase in intra-uterine mortality relative to controls.

    Paragraph 382.

    Relative to chronic gamma irradiation, alpha particles from plutonium-239 seem to be more than 20 times as effective in inducing dominant lethality (post-implantation) in meiotic and post-meiotic stages.

    Paragraph 383.

    In male mice exposed to alpha particles from plutonium-239 (intravenously injected citrate solution) for a duration of 6 to 34 weeks, reciprocal translocations (in spermatogonia) and chromosome fragments (in spermatocytes) are induced.

    Relative to chronic gamma irradiation, alpha-particle irradiation from plutonium-239 is more than 20 times as efficient for the induction of these effects. This finding is similar to that recorded for the induction of dominant lethals in meiotic stages.

    These calculations do not take into account the inhomogeneous distribution of plutonium-239 in the testis.

    Paragraph 384.

    Male and female mice fed on tritiated water, show, in dominant lethal tests, an increased amount of intra-uterine death.

    Paragraph 385.

    In specific-locus tests, mutations have been found to be induced in male mice fed with tritiated water. The data currently available suggest that the rate of induction [of mutations] per unit dose of irradiation with beta particles from tritium is about the same as that of x-irradiation. The estimates are 1.58 x 10-7 per rad per locus for spermatogonial mutations and 4.60 x 10-7 per locus for post-spermatogonial stages. These estimates have wide confidence limits. There is some evidence that the distribution of mutants among the seven loci may be different from that after x-irradiation.

    Paragraph 386.

    In human lymphocytes exposed to tritiated water in vitro, both chromosome- and chromatid-type aberrations are induced, depending on the concentration of tritium and the duration of exposure.

    back to [ Table of Contents ]

    [ Tritium Dangers ~ Part 2 ]

    [ Nuclear Accidents at Chalk River — The Human Fallout ]

    [ No Safe Dose of Radiation — Nuclear Authorities ]

    [ CCNR SHORT DIRECTORY ] [ CCNR COMPLETE DIRECTORY ]

    ccnr@web.net

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About this site

This website updates the latest news about the Fukushima nuclear plant and also archives the past news from 2011. Because it's always updated and added live, articles, categories and the tags are not necessarily fitted in the latest format.
I am the writer of this website. About page remains in 2014. This is because my memory about 311 was clearer than now, 2023, and I think it can have a historical value. Now I'm living in Romania with 3 cats as an independent data scientist.
Actually, nothing has progressed in the plant since 2011. We still don't even know what is going on inside. They must keep cooling the crippled reactors by water, but additionally groundwater keeps flowing into the reactor buildings from the broken parts. This is why highly contaminated water is always produced more than it can circulate. Tepco is planning to officially discharge this water to the Pacific but Tritium is still remaining in it. They dilute this with seawater so that it is legally safe, but scientifically the same amount of radioactive tritium is contained. They say it is safe to discharge, but none of them have drunk it.

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